Journal of Scientific Dentistry Vol 8 Iss 2 July-Dec 2018 by Dept of Medical Informatics

P-ISSN No: 2277-7687 E-ISSN No: 2278-3865

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JOURNAL OF SCIENTIFIC DENTISTRY An official publication of

Indira Gandhi Institute of Dental Sciences, Puducherry

Volume 8 Issue 2 July-Dec 2018

The whole purpose of education is to turn 'mirrors'into 'windows'- Sydney J Harrison

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P-ISSN No: 2277-7687 E-ISSN No: 2278-3865

JOURNAL OF SCIENTIFIC DENTISTRY Website: http://igids.ac.in/jsd/jsdindex.html

 MISSION STATEMENT Journal of Scientific Dentistry, published by Indira Gandhi Institute of Dental Sciences, Sri Balaji Vidyapeeth, Puducherry, is a peer-reviewed, indexed, bi-annual journal with an aim to reinforce the scientific foundation of the art of Dental Sciences, by providing a platform for sharing and disseminating high quality, evidence based knowledge among the clinicians and the academicians of all branches of this fraternity.

 PATRON

Shri. M.K. Rajagopalan

 ADVISOR

Prof. S. C. Parija

 EDITOR IN CHIEF

Prof. R. Saravana Kumar

 EDITOR

Prof. M. Shivasakthy

SECTION EDITORS

 Narrative review

Prof. G. S. Prathima Prof. N. Vezhavendhan

 Original research

Prof. P.S. Manoharan Prof. B. Pratebha

 Case report

Prof. R. Sathyanarayanan Prof. A. Santha Devy

 Technical report / Short communication

Prof. U. B. Rajasekaran Prof. C. Dhanavel

 Product Profile

Prof. M. Senthil Prof. W. David Livingstone

 Ombudsman

Mr. L. Swaminathan

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2. Books and Other Monographs Personal author(s): Ringsven MK, Bond D. Gerontology and leadership skills for nurses. 2nd ed. Albany (NY): Delmar Publishers; 1996. Editor(s), compiler(s) as author: Norman IJ, Redfern SJ, editors. Mental health care for elderly people. New York: Churchill Livingstone; 1996.

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Article should be sent to : Prof. Saravanakumar R Editor in Chief Journal of Scientific Dentistry IGIDS, Sri Balaji Vidyapeeth, Puducherry. Phone: 9840887003 Email id: jsdigids@gmail.com Disclaimer : "The Statements and opinions in the Journal of Scientific Dentistry are solely those of the individual authors and editors as indicated"

JOURNAL OF SCIENTIFIC DENTISTRY Web site: http://igids.ac.in/jsd/jsdindex.html

 CONTENTS Journal of Scientific Dentistry, Volume 8, Issue 2 From the Editor’s desk

Saravanakumar. R

Krishnapriya. V, Vikneshan. M, Senthil. M

Singh. V, Kumar. N, Gauba. K

Contemporary Dentin Bonding Agents A Review

Nandini Pugal, Praveen rajesh, Dhanavel chakravarthy, Padmaraj S.N, Vijayaraja

Evolution of The Efficiency of Various Methods of Fixation for Zygomatico Maxillary Complex Fractures

Sarath.K, Sathyanarayanan .R, Nithin Joseph Jude

Role of Immunology in Periodontal Disease: A Brief Review

Vinoth Kumar B Na, Arvina R, Sivaranjani K S, Hema P, Arun Varghese R

The Role of Stromelysin-3 (ST-3) in Progression of Oral Squamous Cell Carcinoma- A Narrative Review

Muthukumaran R, Vezhavendhan N, Vidyalakshmi S, SanthaDevy A, Premlal K R, Gayathri C

Surface Conditioning and Silanization for Ceramic Adhesion

Nandini Pugal, Praveen Rajesh, Preethe P M, Padhmaraj S N, Dhanavel Chakravarthy

Role of Dna Repair Pathways in Aging A Review

C Gayathri, A Santhadevy, N Vezhavendhan, Premlal K R, S Vidyalakshmi, R Suganya

 Original Article Knowledge and Awareness About Effects of Sesame Oil Pulling and Its Health Benefits Among Dental Students of Igids, Puducherry: A Cross Sectional Study

 Case Report Removable Mandibular Retractor- An Effective Treatment for Early Class III Malocclusion: A Case Report and Review

 Review Article

 CONTENTS Journal of Scientific Dentistry, Volume 8, Issue 2

 Review Article Microbiological Profile of Chronic and Aggressive Periodontitis- A Review

Hema P, Saravanakumar R, Shahinas begum.B, Nandini Dimple, Vinoth kumar B.Na, Sivaranjani KS

XP-endo Shaper : One File Shaper System

Limly Bal T, Dhanavel Chakravarthy, Padmaraj. S N

Relevance of C- reactive protein (CRP) and other inflammatory markers as valuable tool in oral and systemic diseases

N. Chitra, A. Santhadevy, K. R. Premlal, Selvaraj Stephen

Self-Ligating Brackets in Orthodontics A Narrative Review

Lijin James, U B Rajasekaran, Aniruddh Yashwant.V, Lidhiya Alexander, Helen Rachel Xavier, Basil Joseph

Effect of Behavioural counselling in Tobacco Cessation

Manjula D.C, Vandana Shekar, Jagat reddy R.C

Genetic Aspects of Chronic and Aggressive Periodontitis

Sivaranjani KS, Bijivin Raj .V, Vinoth Kumar B.Na, Arvina .R, Hema .P, Ananya Sweta .V

Iatrogenic Effects of Bonding in Orthodontics - A Narrative Review

Helen Rachel Xavier, U B Rajasekaran, Aniruddh V Yashwant, Vijay Kumar V, Lijin James, Basil Joseph

JOURNAL OF SCIENTIFIC DENTISTRY From the Editorâ&#x20AC;&#x2122;s desk.... Bruce J. Baum suggested that dental schools should aim to produce a graduate who: 1. I s a lifelong learner, capable of being able to grow and adapt as change occurs in our science base and health care systems; 2. Has a sense of community responsibility; 3. Is technically competent at dental surgical procedures; 4. Is competent at managing oral medical disorders; and 5. Is competent treating ambulatory, medically compromised individuals. Such a graduate will be able to function in a health care system in which oral health truly is integrated with total health. Interest in competencies and measuring specific learning is accelerating throughout the world. Many dental schools in the west are gradually undergoing a paradigm shift and transitioning to a competency based education (CBE) curriculum. Schools must be released from departmental courses, a fixed 4-year time course, technical requirements, and classical lecture formats; i.e., schools must move from a teacher-centered curriculum to a student-centered one. To accomplish this change, dental school faculty members need to become educational professionals, learning how to educate adults for a professional career. In order to introduce CBE, Hendricson and Smith have described three questions: 1. What knowledge, skills, and values must the student possess at the time of graduation, so that he/she is ready for the next level (PG/practice)? 2. What learning experience will enable the student to acquire these competencies? 3. What proof or evidence is needed to establish that the student has attained these competencies? Three models of competency-based curricula have been described in literature: Top down planning, readiness model, and horizontal curriculum structure. The top down planning is a need-based approach in which the needs of the community drive the curriculum and learning. The readiness model moves away from the traditional calendar-based system; in this system, no fixed time is allotted to attain competencies. The students remain in training until he/she demonstrates the skills required for patient care without assistance. The horizontal curriculum incorporates integration across disciplines. The Association for Dental Education in Europe (ADEE) has prepared a document with competency statements for the graduating dentist. This document was prepared to promote convergence of standards of dental education in Europe. This report titled Profile and Competencies for the Graduating European Dentist (PCD) â&#x20AC;&#x201D; update 2009 has defined seven domains which are: 1. Professionalism. 2. Interpersonal, communication, and social skills. 3. Knowledge base, information and information literacy. 4. Clinical information gathering. 5. Diagnosis and treatment planning. 6. Therapy: Establishing and maintaining oral health. 7. Prevention and health promotion. Faculty must dedicate time to work together to convert the haphazard curriculum of the past to the now-accepted organized, competency-based curriculum. This process of conversion includes examination of course content for gaps, redundancies, and proper sequencing, and the consideration of teaching methods which integrate scientific principles with clinical practice. Formative and summative assessment of student performance need to be criterion based; the integral parts of clinical practice must be evaluated in addition to the end product. Furthermore, the means of evaluating program effectiveness must give direction to the ongoing process of revision as technology and consumer demands change. The use of competencies in curriculum design provides direction for program course goals whose achievement produces a competent graduate. Prof. R. Saravana Kumar Editor-in-chief Journal of Scientific Dentistry

Original Research

Knowledge and Awareness About Effects of Sesame Oil Pulling and Its Health Benefits Among Dental Students of Igids, Puducherry: A Cross Sectional Study Krishnapriya.V1, Vikneshan.M2, Senthil.M3

ABSTRACT The purpose of this study was to evaluate knowledge and awareness about effects of sesame oil pulling and its health benefits among dental students. A Questionnaire containing 16 questions was distributed to 200 clinical dental students (under graduates from 3rd year to interns and postgraduates). They were asked about their attitudes toward oil pulling in general and their knowledge regarding specific sesame oil pulling. Of the 200 students responding to the survey, 77.5% know what is oil pulling. However, 12.5% don’t know what is oil pulling. 53.5% agreed to the statement “Dentist (practitioner) should advise oil pulling for patient with moderate oral health for maintenance”, whereas 10.5% of the disagreed and 36% were not sure whether dentist should advise oil pulling for patient with moderate oral health for maintenance. The results of this survey provide insight into the Knowledge and awareness of clinical students both undergraduates and postgraduates towards effect of sesame oil pulling and its health benefits. This study highlights need for educational interventions and the importance of providing awareness about sesame oil pulling among clinical students.. Key Words: Oil pulling, Sesameoil, Chlorhexidine, Dental Caries , Halitosis.

Introduction Mouth is considered as the mirror of the general health of human body. Many general disease conditions also have oral manifestations that increase the risk of oral disease which, in turn, is a risk factor for a number of general health conditions1.So it is very important to maintain oral health. Antibiotic resistance, adverse effects and toxicity to modern medicines has prompted scientists to research on natural products. Oil pulling is claimed to improve oral health2. Sesame oil is considered to be the queen of oil seed crops because of its beneficiary effects3. Sesame oil has various advantages over chlorhexidine Such as no staining, no lingering aftertaste, and no allergy. Sesame oil is cost-effective than chlorhexidine and is readily available in the household. There are no disadvantages for Oil pulling therapy except for the extended duration of the procedure compared with chlorhexidine4. Sesame oil has increased polyunsaturated fatty acids, and lipid per oxidation is reduced there by reducing free radical injury to the tissues. Sesame oil was found to be active in the reduction of bacteria causing dental caries Sesame oil pulling showed a significant reduction in plaque, gingivitis and reduction in bacteria causing dental caries and halitosis. The aim of this study is to evaluate the knowledge and awareness about the importance of sesame oil pulling and its effect on health of human among dental students. The objective of this 2

studywere to assess the knowledge and awareness among dental students about the importance of sesame oil pulling and its effect on health of human

Materials and methods This descriptive cross sectional study was conducted at Indira Gandhi Institute of Dental Sciences, Puducherry, among the postgraduate and undergraduate students. The study was approved by the Institutional ethical committee and was conducted for a period of 2 months. The sample size included all the students who will be present on the day of examination. Selection criteria was based on students who volunteered themselves for the study and if they fit into inclusion criteria which was dental college students from Third years, Fourth Year, interns and Postgraduates who were present on the day of study. For data collection pre-structured questionnaire was used. A 16 –item questionnaire with 15 closed items and 1 open ended item was included, the questions were obtained from a pre-validated questionnaire. Explanations were given if the subjects could not understand the items. The instrument used was questionnaire on, knowledge, attitude toward oil pulling and the principal investigator had made herself available for clarifications on the doubts raised by the subjects. To ensure confidentiality all subjects’ identity

Journal of Scientific Dentistry, 8(2), 2018

Knowledge and Awareness About Effects of Sesame Oil Pulling and Its Health Benefits Among Dental Students of Igids, Puducherry: A Cross Sectional Study

was coded and stored safely. Subjects were assured of the confidence in the handling of their responses5.

Ethical Clearance "Ethical approval for this study was provided by (ECR/290/Indt/PY/2018)Institutional Ethical Committee of Indira Gandhi Institute Of Dental Sciences, puducherry, IGIDSIEC2018NRP14UGKPPHD on 9 April 2018."

Statistical analysis For data Analysis and Statistical assessment, data collected were tabulated and compiled in MS Excel. Data collected were grouped into data for undergraduates, postgraduates and total summation of the entire sample. Descriptive statistics was used in terms of the frequency and percentage5

Result This study is the first questionnaire study done among dental students, puducherry regarding knowledge and awareness about effects of sesame oil pulling. In this study 200 students had participated in which 182students were undergraduates and 13 students were postgraduates the mean age of the undergraduates participating in the study was 21.648 years and the postgraduates had a mean age of 26.625 years (Table 1). The number of correct answers given for each question in the questionnaire was calculated and the percentage of correct answers for each question were calculated for the entire sample (Table 2). The sample was unbiased.77.5% of the participants responded that they are aware about oil pulling, where as 12.5%responded that they don’t know what is oil pulling and 9.5%responded not sure.It is found that most of the students are aware about oil pulling from the maximum percentage of answer given for first question (77.5%) Do you know about oil pulling? Nearly 38% think oil pulling can replace usage of chemical mouthwashes for maintenance of oral health.82.5% of the participants said that sesame oil is the most commonly used oil to perform oil pulling.Though 77.5% of them said they know what is oil pulling and 59% of them accepted that oil pulling can be practiced daily. But when it comes to practice based question 35.5% gave wrong answer for the question when oil pulling should be done either morning, before or after brushing or should be done in night before bed (question 4).nearly 29.5% agreed the statement that “chronic usage of oil pulling stains the teeth” and 45%were not sure for the above statement.48.5%gave wrong answer for the question (question no 6) Ideal time to spit oil after doing oil pulling.47% were not sure whether chronic Journal of Scientific Dentistry, 8(2), 2018

Krishnapriya et al

usage of sesame oil pulling has effect on systemic disease like peptic ulcer, GERD.68% of participants agreed that practicing sesame oil pulling improves both general and oral health. But nearly 11% disagreed and 34.5% were not sure to the statement “oil pulling aids in reduction of halitosis”. Question number 16 for the statement “Dentist (practitioner) should advise oil pulling for patient with moderate oral health for maintenance”. Nearly 53.5% agreed the statement in which 2.5% justified their answer saying that oil pulling has good effect, 10.5% said oil pulling is natural and good effect comparing to chemical mouth washes, 2% said that it is easy to perform and also healthy, 1.5%said since it is a mouth refreshners and another 1.5% justified saying that it is cost effective. But 10.5% disagreed the same statement in which 1.5% justified their answer saying that sesame oil pulling STAINS teeth and another 1.5% said that chemicals are more effective than oil pulling and some said when there are many gold standard chemical mouthwashes why oil pulling should be used. 36% responded not sure for the above statement and 69% did not justify their answer.

Discussion On the whole the results of the study are in have shown that a gap exists between attitude, the knowledge and practice of sesame oil pulling among the dental students5. The results of this study Show that the students of different categories have shown a positive attitude towards the necessity of practicing however the percentage of right answers goes down for knowledge and practice related questions. Oil pulling is a traditional folk remedy practiced in ancient India4. The concept of oil pulling was familiarized by Dr. F. Karach in the 1990s in Russia. It is claimed to cure about 30 systemic diseases ranging from headache, migraine to diabetes and asthma[15] when practiced regularly and as directed. Due to occurrence of side effects to modern medicines and oral hygiene products, people are increasingly attracted towards complementary and traditional practices. Oil pulling or oil swishing, in alternative medicine, is a procedure that involves swishing oil in the mouth for oral and systemic health benefits[13,15].The exact mechanism of the action of oil pulling therapy is not clear. It was claimed that swishing of oil in the mouth activates enzymes and draws the toxins out of the blood [14,18].Oil pulling should be ideally performed daily morning on empty stomach before brushing teeth and care should be taken that oil is not swallowed7. It is contraindicated for children below 5 years due to risk of aspiration10. In addition to maintaining oral hygiene it has been claimed to have systemic health benefits and cure systemic diseases. An improvement in oral hygiene is noticed within two weeks of practicing 3

Knowledge and Awareness About Effects of Sesame Oil Pulling and Its Health Benefits Among Dental Students of Igids, Puducherry: A Cross Sectional Study

correct method of oil pulling. Sesame oil is more palatable when compared to other refined edible oils4. Oil pulling, this process makes oil thoroughly mixed with saliva. Swishing activates the enzymes and the enzymes draw toxins out of the blood. The viscosity of the oil can inhibit bacterial adhesion and plaque coaggregation. Sesame oil is found to be effective in reducing bacterial growth and adhesion. Toxins and bacteria from the body might be expelled through the tongue and trapped in the oil and removed from the body. It contains high amounts of unsaturated fatty acids. Linoleic acid and oleic acid are the predominant compositions. Oil-pulling therapy with sesame oil significantly reduced S. mutans counts in plaque and saliva of adolescents within 1 week 8. It was claimed that the swishing activates the enzymes and draws the toxins out of the blood. Sesame oil has three lignans sesamin, sesamolin, and sesaminol - that have antioxidant properties and potentiate Vitamin E action9. Sesame oil has increased polyunsaturated fatty acids and the lipid peroxidation is reduced thereby reducing free radical injury to the tissues. Emulsification is the process by which insoluble fats like sesame oil can be broken down into minute droplets and dispersed in water. Emulsification greatly enhances the surface area of the oil thereby increasing its cleansing action. Sesame oil is relatively high in unsaponifiable substances. The unsaponifiable fraction, a class of substances not found in other fats (sesamin or sesamolin) can probably protect the oral cavity from infection and inß ammation by its antioxidant property. A study done by Asokan et al. [15] have cocluded that Sesame oil pulling therapy has been equally effective like chlorhexidine on halitosis and organisms, associated with halitosis7. Oil pulling therapy has been as equally effective As chlorhexidine against plaque-induced gingivitis. Sesame oil has the following advantages over chlorhexidine: no Staining, no lingering after-taste, and no allergy. Sesame oil is 5 to 6 times more cost effective than chlorhexidine and is readily available in most households3.in some cases like the cases of mouth ulcer, those who have tendency to vomit, asthma, cough, thirst where brushing is considered to be contraindicated Oil pulling can be used to clean the oral cavity[10,17]. A group of researchers compared oil pulling method using sesame oil with chlorhexidine mouthwash for two weeks on twenty adolescent subjects. There was statistically significant reduction in the S.

Krishnapriya et al

mutans count in the plaque samples of oil pulling group after one and two weeks. Also there was reduction in the mean scores of salivary S. mutans count after two weeks. However the study noted that the reduction in S. mutans count is more in chlorhexidine group than oil pulling group[11,12].A study done by Nilufar Nekuzada et al[16] showed that the use of Sesamum indicum in patients under chemotherapy has decreased the phlebitis incidence[16]. There are no disadvantages for oil pulling therapy except for the extended Duration of the procedure compared with chlorhexidine. It can be used as a preventive home therapy to maintain oral hygiene.

Conclusion The questionnaire has on the whole given us a view into the general attitude of dental students on sesame oil pulling. We have observed a huge gap between the positive attitudes Expressed by the students towards sesame oil pulling and the Knowledge and actual practice of this procedure. This study further stresses the need to conduct more educational programmes and create awareness among dental students who are the future clinicians about the about effects of sesame oil pulling and its health benefits. So that practitioners can advice patients to practice sesame oil pulling which helps them to maintain their oral health in cost effective way, overcoming the disadvantage of chronic usage chemical mouth washes and also improving both Oral health and general health simultaneously. Table 1: Details of participants Number of students (n) 200 Undergraduates 182 III year IV year Interns 70 62 50 Postgraduates 13 Gender Male 47 Female 153 Age (yrs) Mean age Ug 21.648 Mean age Pg 26.625

Journal of Scientific Dentistry, 8(2), 2018

Knowledge and Awareness About Effects of Sesame Oil Pulling and Its Health Benefits Among Dental Students of Igids, Puducherry: A Cross Sectional Study

Table 2: Physiciansâ&#x20AC;&#x2122; responses to questions regarding KNOWLEDGE AND AWARENESS ABOUT EFFECTS OF SESAME OIL PULLING AND ITS HEALTH BENEFITS and outcomes No

Questions

Responses

% of right

Oil pulling works under 43.5% ______________ mechanism? 30.5% a) Emulsification 23% b) sapnofication c) none of the above

30.5%

Do you think chronic usage 32.5% of sesame oil pulling has 20% effect on systemic issues like 47% GERD, peptic ulcers, diabetes, migraine a) Yes b) No c) Not sure

32.5%

Oil that is used to swishing 20% around the mouth can be 59.5% swallowed instead of spiting 20% it out. a) Agree b) Disagree c) Not sure

59.5%

% of right

Do you know about OIL 77.5% PULLING? 12.5% a) Yes 9.5% b) No c) Not sure

Questions

Answer

Krishnapriya et al

Do you think oil pulling can 38% replace the usage of chemical 17.5% mouthwashes to prevent and 44.5% maintain oral health a) Yes b) No c) Not sure

38%

According to you which of 82.5% the following oil is most 7% commonly used for oil pulling? 10% a) Sesame oil b) Mustard oil c) Coconut oil

82.5 %

Oil pulling should be done 67.5% __________ 7.5% a) Early morning (empty 4.5% stomach) before brushing b) Early morning (empty stomach) after brushing c) Night time before bed

67.5%

10 Practicing Sesame oil pulling 68% improves both general health 11% and oral health. 20.5% a) Agree b) Disagree c) Not sure

68%

Is it advisable for childrenâ&#x20AC;&#x2122;s 15% below 5 years to practice oil 48.5% pulling 35% a. Yes b. No c. Not sure

48.5%

11 Oil pulling aids in reduction of 54% halitosis. 11% a) Agree 34.5% b)Disagree c) Not sure

54%

Ideal time to spit oil after doing oil pulling? 38% a) After 10 minutes 10.5% b) After 20 minutes 51% c) Once oil loses its viscosity and becomes thin and milky

51%

12 Chronic usage of sesame oil 29.5% pulling stains teeth. 25% a) Agree 45% b) Disagree c) Not sure

25%

Journal of Scientific Dentistry, 8(2), 2018

Knowledge and Awareness About Effects of Sesame Oil Pulling and Its Health Benefits Among Dental Students of Igids, Puducherry: A Cross Sectional Study No

Questions

Responses

13 13. Oil pulling is very 49.5% effective against plaque 9.5% induced gingivitis. 39.5% a) Agree b) Disagree c) Not sure

49.5%

25%

15 Sesame oil pulling can be practiced daily. a)Agree b) Disagree c) Not sure

59%

16 Dentist (practitioner) should 53.5% advise oil pulling for patient 10.5% with moderate oral health for 36% maintenance. a) Agree b) Disagree c) Not sure

1.50%

7 = MAY STAIN TEETH

1.50%

8 = CHEMICALS ARE MORE EFFECTIVE THAN OIL PULLING

1.50%

1. Amith HV, Ankola AV, Nagesh L. Effect of oil pulling on plaque and gingivitis. J Oral Health Community Dent. 2007 Jan; 1(1):12-8.

3. Asokan S, Emmadi P, Chamundeswari R. Effect of oil pulling on plaque induced gingivitis: A randomized, controlled, triple-blind study. Indian Journal of Dental Research. 2009 Jan 1;20(1):47. 4. Pathak S. Oil pulling therapy in dental practice: A short review. SRM Journal of Research in Dental Sciences. 2016 Jan 1;7(1):33. 5. Krishnapriya,Therese BA, Suresh V,Sathyanaraynan R. knowledge and awareness about hand hygiene practices among dental studentsof dental college, puducherry: a cross sectional study, International Journal of Current Research. 2016 Nov ;8(11): 42473-42476

53.5%

6. Wahner-Roedler DL, Vincent A, Elkin PL, Loehrer LL, Cha SS, Bauer BA. Physicians' attitudes toward complementary and alternative medicine and their knowledge of specific therapies: a survey at an academic medical center. Evidence-Based Complementary and Alternative Medicine. 2006; 3(4):495-501. 7. Lakshmi T, Rajendran R, Krishnan V. Perspectives of oil pulling therapy in dental practice. Dental Hypotheses. 2013 Oct 1;4(4):131. 8. Ciancio SG. Current status of indices of gingivitis. Journal of Clinical Periodontology. 1986 May;13(5):375-8.

FOR

9. Shanbhag VK. Oil pulling for maintaining oral hygieneâ&#x20AC;&#x201C;A review. Journal of traditional and complementary medicine. 2017 Jan 1;7(1):106-9.

Justifiation for Question (16) Were

6 = cost effective

2. Shanbhag VK. Oil pulling for maintaining oral hygieneâ&#x20AC;&#x201C;A review. Journal of traditional and complementary medicine. 2017 Jan 1;7(1):106-9.

59% 17.5% 23%

Responses

% of Answers

References

14 Oil pulling inhibits growth of 25% malignant tumor. 23.5% a) Agree 49.5% b) Disagree c) Not sure

JUSTIFICATION QUESTION 16

Responses

% of right Answer

Krishnapriya et al

% of Answers

1 = oil pulling --) good effect

2.50%

2 = Natural and good effect comparing to chemical mouth washes

10.50%

3 = helps in maintaining good oral hygiene

10%

4= easy and healthy

5 = mouth refresher

1.50%

10. Asokan S. Oil pulling therapy. Indian Journal of Dental Research. 2008 Apr 1;19(2):169. 11. Tomar P, Hongal S, Jain M, Rana K, Saxena V. Oil pulling and oral health: A review. IJSS Case Report & Reviews. 2014 Aug; 1(3):33-7. 12. Asokan S, Rathan J, Muthu MS, et al. Effect of oil pulling on Streptococcus mutans count in plaque and saliva using Dentocult SM Strip mutans test: a randomized, controlled, triple-blind study. J Indian Soc Pedod Prev Dent. 2008;26:12e17. 13. Asokan S, Rathinasamy TK, Inbamani N, Menon T, Kumar SS, Emmadi P, Raghuraman R. Mechanism of oil-pulling therapyin vitro study. Indian Journal of Dental Research. 2011 Jan 1;22(1):34

Journal of Scientific Dentistry, 8(2), 2018

Knowledge and Awareness About Effects of Sesame Oil Pulling and Its Health Benefits Among Dental Students of Igids, Puducherry: A Cross Sectional Study 14. Asokan S, Emmadi P, Chamundeswari R. Effect of oil pulling on plaque induced gingivitis: A randomized, controlled, triple-blind study. Indian Journal of Dental Research. 2009 Jan 1;20(1):47. 15. Asokan S, Kumar RS, Emmadi P, Raghuraman R, Sivakumar N. Effect of oil pulling on halitosis and microorganisms causing halitosis: A randomized controlled pilot trial. Journal of Indian Society of Pedodontics and Preventive Dentistry. 2011 Apr 1;29(2):90.

Address of Correspondence

Vikneshan.M, Department of Public Health Dentistry, Indira Gandhi Institute of Dental Sciences, Email id: drvikneshan@gmail.com Phone no: 950520798

Krishnapriya et al

16. Nekuzad N, Torab TA, Mojab F, Alavi-Majd H, Azadeh P, Ehtejab G. Effect of external use of sesame oil in the prevention of chemotherapy-induced phlebitis. Iranian journal of pharmaceutical research: IJPR. 2012;11(4):1065. 17. Singh A, Purohit B. Tooth brushing, oil pulling and tissue regeneration: A review of holistic approaches to oral health. Journal of Ayurveda and integrative medicine. 2011 Apr;2(2):64 18. Hebbar A, Keluskar V, Shetti A. Oil pullingâ&#x20AC;&#x201C;Unraveling the path to mystic cure. J Int Oral Health. 2010 Dec 1;2(4):11-5.

Authors CRRI, Indira Gandhi Institute of Dental Sciences.

Reader, Department of Public Health Dentistry, Indira Gandhi Institute of Dental Sciences.

Professor, Department of Public Health Dentistry, Indira Gandhi Institute of Dental Sciences.

How to cite this article : K rishnapriya.V, Vikneshan.M, Senthil.M. Knowledge and Awareness About Effects of Sesame Oil Pulling and Its Health Benefits Among Dental Students of Igids, Puducherry: A Cross Sectional Study. Journal of Scientific Dentistry 2018;8(2):2-7 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Case Report

Removable Mandibular Retractor- An Effective Treatment for Early Class III Malocclusion: A Case Report and Review Singh V1, Kumar N2, Gauba K3 ABSTRACT Developing class III malocclusion presents a challenge to clinicians due to its varied etiology. Several treatment modalities have been developed over the years to tackle this anomaly. However, most of the appliances are either difficult to fabricate and use or not tolerated well by the patient. Removable mandibular retractor is a simple and convenient yet often overlooked appliance for management of early class III malocclusion. Only a few case reports of the appliance in use are present in the literature. This case report presents the case of a 10 year old patient treated successfully with this appliance. Key words: Developing class III, removable mandibular retractor, simple appliance.

Introduction Angleâ&#x20AC;&#x2122;s class III malocclusion although, a well recognized entity, remains one of the most difficult to treat. Globally, its prevalence ranges from 0%- 26.7% amongst different populations and ethnic groups.1 In India, class III malocclusion affects 1.4%- 3.4% of the population with the average being lower than the global average.2 Time and again, various modalities have been put forth to manage class III malocclusion but none has demonstrated significantly greater benefit as compared to others.9 Removable mandibular retractor, first described by Tollaro in 19958, is a simple, low cost appliance with favourable results.5,9 This case report, presents the case of a female patient successfully treated with removable mandibular retractor highlighting the relative efficacy of this simple appliance over other more complex treatment modalities in management of developing class III malocclusion.

Figure 1: Pre-treatment frontal view showing anterior crossbite

Figure 2: Pre-treatment frontal view showing anterior crossbite and a protruding chin button

Case A 10 year old female reported to the Unit of Pedodontics and Preventive Dentistry, Oral Health Centre, PGIMER, Chandigarh with the chief complaint of irregularly erupting teeth. The history vis-Ă -vis trauma or deleterious oral habits was non-contributory. On examination, the patient was in the mixed dentition stage with erupting 11,21 in crossbite with teeth 31,41,42 (figure 1). The molar relationship was mesial step bilaterally with a developing end-on relation. The DMFT+deft was 7 with teeth 74,75,85,52,54 being carious and 64 and 84 being root 8

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Removable Mandibular Retractor For Treatment Of Early Class- III Malocclusion

Figure 3: Post appliance delivery

Figure 4: Corrected incisor relation post appliance therapy

Vishwendra Singh et al

Figure 6: 11 months follow up frontal view showing retained corrected incisor relationship

Figure 7: Cephalograph superimposition depicting preand post-treatment changes

Figure 5: Post treatment cephalogram showing corrected incisor relation

Discussion Class III malocclusion needs to be tackled at an optimum time to achieve favorable results.6 The general consensus, however, for treating a cross-bite is as soon as its discovered especially during eruptive stages of the maxillary incisors.10

stumps. Also mild crowding was present in the mandibular anterior region. Cephalometric analysis (Figure 2, Table 2) did not reveal any skeletal discrepencies. Hence, it was decided to use a Removable Mandibular Retractor (RMR) for correction of developing anterior crossbite along with carrying out restorative work (Figure 3). The patient was monitored at regular 3 weekly intervals and at 4 months post initiation of appliance therapy the anterior crossbite was corrected (Figure 4) and was retained by the natural incisor alignment. The patient displayed no signs of relapse or other occlusal problems at 11 months follow up (Figure 6). Journal of Scientific Dentistry, 8(2), 2018

Various appliances have been described in literature for intercepting class III malocclusion vis-Ă -vis maxillary expansion, removable plates with springs, fixed or removable inclined planes, functional appliances, chincups, simple fixed appliances etc. However, most of them are difficult to fabricate and not tolerated well by the patients. Removable mandibular retractor is a simple, low cost, appliance which has been shown to produce favorable growth changes in the mandible.3-6,8,9 The results achieved in the present case correspond to that of other authors.3-6,8,9 There was an improvement in SNA angle and Wittsâ&#x20AC;&#x2122; appraisal and no change in SNB angle (Table 2) demonstrating a favorable growth pattern. Majanni et al7 conducted a randomized controlled trial comparing bone anchored inter-maxillary traction 9

Removable Mandibular Retractor For Treatment Of Early Class- III Malocclusion

Vishwendra Singh et al

Table-1: Review of literature present on Removable Mandibular Retractor Author/ Year/ Country Almeida/ 2011/ Brazil

Nature of Study Case Report with 10 year follow up

Sample size and age N=1

Baccetti T, Tollaro I/ 1998/ Italy

Retrospective

2 groups

Age: 9 years, Female

Group I (deciduous dentition): N=20

Appliance used

Conclusions

Removable Mandibular Retractor with chin cup and comprehensive orthodontic treatment

Corrected functional class III malocclusion remained stable with only minor corrections done by fixed orthodontic treatment. Treatment using mandibular retractor allowed proper facial growth and development and prevented worsening of malocclusion. Removable More favourable changes in mandibular mandibular rotation and mandibular retractor used length were achieved by the in both groups appliance in the deciduous dentition and compared group. Thus the optimum time with control for intervention using functional group in which appliance appeared to be in the no treatment was deciduous dentition period. used.

Mean age: 5 years ± 7 months Group II (mixed dentition): N=18

Loli D/ 2017/ Rome

Machado/2016/ Brazil

Majanni MR/2016/ Syria

Mean age: 8 years ± 9 months -

Systematic review conducted using studies on PubMed and Scopus Case report N=1

Age: 6 years, Male

Randomized controlled trial

4.5 years follow up N=38 Mean Age: 11.46 ± 1.28 years

Removable mandibular retractore

Removable mandibular retractor is a simple, low cost device capable of producing favourable changes in mandibular positioning and growth

Removable mandibular retractor

Removable mandibular retractor is a simple modality to treat early class III malocclusion with favourable retention

Removable mandibular retractor and Bone Anchored Intermaxillary Traction

Bone anchored intermaxillary traction appeared to be better than removable mandibular retractor in correcting mild to moderate class III malocclusion in growing patients

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Removable Mandibular Retractor For Treatment Of Early Class- III Malocclusion

Author/ Year/ Country Tollaro I/ 1995/ Itally

Nature of Study Longitudinal

Sample size and age N=38 (18 test, 18 control) Mean Age: 5.47Âą1.14 years

Woon SC/2017/ United Kingdom

Systematic review and meta analysis

Studies collected from Cochrane Database of Systematic Reviews, Embase, MEDLINE

Appliance used Removable mandibular retractor

Chin cup, facemask, modified tandem traction bow, appliance, tongue plate, removable mandibular retractor, bite block appliance, bionator III, maxillary protractor

Vishwendra Singh et al

Conclusions Statistically significant upwardforward rotation of mandible was observed in the treated group which compensated for the excessive mandibular growth. Thus the appliance showed favourable results. There is moderate evidence to suggest that early facemask treatment results in positive skeletal and dental changes. However, there is a lack of evidence about its long term effectiveness. There is some evidence for chin cup, tandem bow, removable mandibular retractor but the studies have a high risk of bias.

Table 2: Pre- and Post- treatment Cephalograph readings

(BAIMT), which is a fixed modality, with the removable mandibular retractor. They concluded that BAIMT was superior to the retractor. However, we feel that it is not pragmatic to compare a fixed bone anchored modality with a removable one as the former has the added steps of fixing the units surgically thus increasing morbidity and also the mechanism of action and indication of both the appliances is different. A few clinical trials have been conducted using the removable mandibular retractor (RMR), however,

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literature mostly contains case reports on this appliance (Table 1). By the time of the penning of this case report, a clinical trial on evaluating the efficacy of the removable mandibular retractor was recruiting patients.11 This will probably shed better light on the efficacy of this humble appliance. The present case demonstrated favorable changes in the growth pattern post appliance therapy. The corrected cross-bite was also retained naturally by the positive overjet and remained stable at 11 months follow up.

Removable Mandibular Retractor For Treatment Of Early Class- III Malocclusion

Conclusion This case report shows that developing class III malocclusion, with minor skeletal involvement, can be easily treated with RMR. The appliance induces a favorable anterior morphogenetic rotation of the mandible leading to positive inclination of the maxillary incisors. The stability of the results achieved depends on the correct diagnosis and early treatment.

Acknowledgement: None Conflict of interest: None References: 1. Hardy DK et al. Prevalence of Angle Class III Malocclusion : A Systematic Review and Meta- Analysis. Open Journal of Epidemiology. 2012; 2, 75-82. 2. Agarwal SS, Jayan B, Chopra SS. An Overview of Malocclusion in India. J Dent Health Oral Disord Ther 3(3): 00092. DOI: 10.15406/jdhodt.2015.03.00092 3. Almeida MR et al. Early Treatment of Class III Malocclusion: 10 year Clinical Follow Up. J Appl Oral Sci. 2011;19:431-439.

Address of Correspondence

Vishwendra Singh, Oral Health Centre, Block- D, GMCH, Chandigarh, Email id: vishwendra89@gmail.com Phone no: +91 8728947189#

Vishwendra Singh et al

4. Bacetti T, Tollaro I. A Retrospective Comparison of Functional Appliance Treatment of Class III Malocclusions in the Deciduous and Mixed Dentitions. European Journal of Orthodontics. 1998; 20:309-317. 5. Loli D. Removable mandibular retractor: a simple and usefool tool to treat anterior crossbite. WebmedCentral ORTHODONTICS 2017;8(11):WMC005396 6. Machado AR. Early Correction of a Developing Class III Malocclusion with a Removable Appliance. Dent Oral Craniofac Res. 2016; 2(5):359-61 7. Majanni AMR, Hajeer MY. The Removable Mandibular Retractor vs the Bone- anchored Intermaxillary Traction in the Correction of Skeletal Class III Malocclusion in Children: A Randomized Controlled Trial. J Contemp Dent Pract. 2016;17(5):361-371. 8. Tollaro I et al. Mandibular Skeletal Changes Induced By Early Functional Treatment of Class III Malocclusion: A Superimposition Study. American Journal of Orthodontics and Dentofacial Orthopedics. 1995;108(5): 525-32. 9. Woon SC, Thiruvenkatachari B. Early orthodontic treatment for Class III malocclusion: a systematic review and meta-analysis. Am J Orthod Dentofacial Orthop. 2017;151(1):28-52. 10. Proffit WR (2000) Contemporary Orthodontics. (3rd edn.) Philadelphia: Mosby; 511- 513. https://clinicaltrials.gov/ct2/ show/NCT03354442

Authors Senior Resident, Oral Health Centre, GMCH, Chandigarh.

Ex-Senior Resident, Oral Health Sciences Centre, PGIMER, Chandigarh.

Professor & Head, Oral Health Sciences Centre, PGIMER, Chandigarh.

How to cite this article : S ingh V, Kumar N, Gauba K. Removable Mandibular Retractor- An Effective Treatment for Early Class III Malocclusion: A Case Report and Review. Journal of Scientific Dentistry 2018;8(2):8-12 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

Contemporary Dentin Bonding Agents-A Review Nandini Pugal1, Praveen rajesh2, Dhanavel chakravarthy3, Padmaraj S.N4, Vijayaraja5 ABSTRACT The purpose of contemporary dentin bonding agent is to know or understand the clinical effectiveness of contemporary resin-based dentin bonding agents primarily focusing on the longevity of restoration. Despite the significant improvements of adhesive systems, the bonded interface remains the weakest area of tooth-colored restorations. The most important reasons for the failure of adhesive restorations with earlier adhesives are the loss of retention and the deficient marginal adaptation. However, the introduction of reliable adhesive restorative materials has subsequently reduced the need for extensive tooth preparation. Dentin bonding has evolved from no-etch to total-etch to self-etch systems. The development of self-etching primer adhesive systems has greatly simplified resin bonding procedures, as a separate etching step is no longer required. There is much interest and activity nowadays with dentin bonding agents. More focus has been laid upon conservative approach of tooth preparation. Therefore, introduction of adhesive restorative materials has reduced the need for an extensive tooth preparation. Modern dental bonding systems come as a “three-step system”, where the etchant, primer, and adhesive are applied sequentially; as a “two-step system”, where the etchant and the primer are combined for simultaneous application; and as a “one-step system”, where all the components should be premixed and applied in a single application (so-called seventh generation of bonding agents So, now the newer generations of bonding agents, self-etch, total etch and their mechanisms and their inner microscopic changes are explained in detail in the forthcoming pages. Key-words: Dentin bonding agent, etch and rinse, wet bonding.

Introduction The traditional drill and fill approach is largely a concept of past for the younger generation. Today’s operative dentistry primarily involves “minimally invasive” care because the dental profession now recognizes that an artifact is of less biological value than the original healthy tissue. The adhesive materials have revolutionized dentistry by opening up conservative cavity preparation options. Also, adhesive techniques promote “maintenance and repair” instead of changing the entire restorations which has further boosted its use in varied applications of everyday clinical practice.(1,2) The primary factor in the premature failure of moderate to large composite restorations is secondary caries at the margins, particularly the gingival margin of the restorations due to unreliable dentin bonding.(3,4)These resin based materials tend to have a major weak link at the resin-dentin interface. Although bonding to enamel has been quiet predictable, bonding to dentin poses a million-dollar challenge till date. Modern adhesive system is superior to their predecessors especially in terms of retention that is no longer a major cause of premature clinical failure.(5) Though the current adhesive systems

Journal of Scientific Dentistry, 8(2), 2018

have tremendously improved the complex dentin bonding there are still changes that are needed to be addressed. Over the last 40 years, there seemed to be an expansion of knowledge in this area major advances have been made in both adhesive monomer formulations and in pre-treatment of dentin to improve resin penetration inside the tissue matrix. It is hoped that this review will stimulate critical thinking in this area and encourage new research into problems yet unsolved. (7). The concept of adhesive has been essentially the most noteworthy development in ever progressing sciences, over the past three decades bonding of resin-based composite filing has been revolutionized by advances in dental bonding technology.(8) There has been a noteworthy alteration in the principles of cavity preparation design, from the age old principles of “extension for prevention” defined by G.V. Black to a more carious lesion-centered method. This lesion-centered method is promising through the innovations in adhesive restorative materials and through the introduction of computer-assisted ways and means of caries detection, an enhanced understanding of the role of magnification, digital radiography and caries 13

Contemporary Dentin Bonding Agents-A Review

risk assessment of the patient to permit for developed conservative caries management. (10)

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4-META (4-methacryloyloxyethyl1 tri mellitic anhydride)

Composition Of Dentin Bonding Agents

MAC-10(11methacryloyloxy-1,1-undecanedicarboxylic acid

Etchants:

Solvent:

Etchants are strong acids which are used to remove smear layers and open tubules, increase retention of resin sealant and promote mechanical retention. They dissolve minerals and allow the formation of micromechanical interlocking in enamel and dentin 30-50% of phosphoric acid can be used but exactly 37% of phosphoric acid is preferred for etching to produce consistent etching pattern which do not damage the pulp. If the concentration is at 50% or greater than 50%then it results in the deposition of adherent layer of mono-calcium phosphate monohydrate on the etched surface which inhibits further dissolution. Etchant is supplied as an aqueous gel to allow placement over a specific area. Composition of these gels is colloidal silica or polymer beads. Other materials used as etchants are maleic acid, tartaric acid, citric acid, EDTA, acidic monomers, polyacrylic acid, hydrochloric acid, nitric acid and hydrofluoric acid.

The addition of solvents to resin is indispensable to the composition of adhesives that needs to be bonded to the dentine. Primers/adhesives have low viscosity due to dissolution of monomers in a solvent that improves their diffusion ability in the micro retentive tooth surface. Most commonly used solvents are water, ethanol and acetone. Water ionizes acid monomers and re-expands the collagen network which had already collapsed. Ethanol is used instead of water as co-solvent. Water-alcohol combination mixtures start the formation of hydrogen bonds between water and ethanol molecules which leads to better evaporation of water ethanol aggregate than plain water. Acetone consists of high vapor pressure. The advantage is that the pressure is four times higher than ethanol. It is highly volatile which has a less shelf life by rapid evaporation. Both ethanol and acetone can remove water easily as they have better miscibility with hydrophobic monomers. So they are called “water chasers”.

Patterns of etching: Type 1

Type 2 Type 3

Most common etching pattern. This involves removal of enamel prism cores with prism peripheries remaining leaving intact Here peripheries are removed leaving the cores intact. This is associated with the presence of prism less enamel

Primers: Primers are solutions containing hydrophilic monomers that get dissolved in a solvent like acetone, ethanol or water. Such monomers exhibit hydrophilic properties through HEMA- Phosphate, phenyl p{(2-methacryloyloxyethy) phenyl hydrogen phosphate)}-Phosphate, carboxylic acid, alcohol. 10-MDP (metharyloyloxydecyl dihydrogen phosphate) 4-meta (4-methalacryloyloxyethyl tri mellitic acid) 14

The main purpose of adhesive is to fill inter-fibrillar spaces of the collagen network that created a hybrid layer and resin tags for micromechanical retention. Adhesive is composed of BIS-GMA-Bisphenol Glycidyl Methacrylate TEGDMA-Tri Ethyl Glycol Dimethacrylate UDMA –Urethane Dimethacrylate and small amounts of HEMA -2 Hydoxy Ethyl Methacrylate Initiators: The main purpose of the initiator is polymerization. Polymerization can be initiated by photo initiator system which consists of camphorquonine a photo sensitizer and an initiator –tertiary amine through a self-cure system a chemical initiator like benzoyl peroxide or through dual cure initiator system, fillers: these fillers are added to the resin to reinforce the adhesive it gives a strengthening effect other reason is to modify the viscosity of the adhesive to a thicker to pastier consistency.

Journal of Scientific Dentistry, 8(2), 2018

Contemporary Dentin Bonding Agents-A Review

Mechanism of action: Many trials have been made to achieve this type of bonding, but till now there are very few evidence that such bonds form. The reason simply is that the tooth surface is poorly standardized regarding chemical composition and that the bonds are not stable when other ions, diffuse along the interface and compete with the different bond sites. Bonding to Hydroxyapatite: The formula M-R-X) shows the chemical bonding in dentistry. M - Stands for the methyl methacrylate group including the -CO-O- bond). R - stands for a spacer consisting of a hydrocarbon chain, X - is the group capable of bonding to calcium present on the tooth surface. HYBRID LAYER: The distinct zone between the bulk adhesive and nondemineralized dentin (i.e.,) consisting of 50%collagen matrix and 50%resin is termed as hybrid layer. Hybrid layer is formed when an adhesive resin penetrates a de-mineralized or acid etched dentin surface infiltrates the visible collagen fibrils (fig:1). The hybrid layer is very tough when it is correctly formed and shows good micromechanical retention for resin (13) Infiltration of demineralized collagen fibers with resin and formation of hybrid layer results in Successful bonding. Development of hybrid layer is a vital part of dentin bonding. The superiority of the hybrid layer that is formed decides the strength of resin-dentin interface. In2009, Ana Paula Martin specified that micromechanical behavior of hybrid layer along with voids should lower bond strength of self-etching adhesives then in 2011 they concluded that bonding agent with simplified application procedure were less successful compared to conventional totaletch adhesives. (14) Traditional enamel bonding theory postulates that resin tags mechanically lock into undercuts in the etched enamel. The hybrid concept proposes that bonding stability will increase if the resin tags are supplemented by a thin zone of hybrid layer (resin-reinforced tissue). The hybrid layer forms an acid resistant envelope that seals the dentin, preventing from hypersensitivity and secondary caries. Journal of Scientific Dentistry, 8(2), 2018

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Three characteristics are necessary for the formation of hybrid layers

1. The aggressive acid expose collagen below the hybrid layer and leaves a zone of weak dentin that leads to long term degradation 2. The bonding resin must include monomers with both hydrophilic and hydrophobic groups that can penetrate the dentin and combine with that. 3. The catalyst present here should allow polymerization process in the presence of oxygen and water. There are three different zones in hybrid layer:

1. Top zone: It consists of loosely arranged collagen fibrils with inter-fibrillary spaces filled with the adhesive resin 2. Mid-zone: This consists of collagen fibrils infiltrated with resin with residual hydroxyapatite crystals between collagen 3. Bottom zone: It shows an abrupt transition to the underlying unaltered dentin with partially de-mineralized dentin containing hydroxyapatite crystals enveloped by adhesive resin. The resin monomers are not able to fully infiltrate the de-mineralized dentin, only a part of de-mineralized dentin remains susceptible to hydrolytic degradation. The remaining water gets entrapped in the hybrid layer and deteriorates the bond strength. The hydrophilic monomers act as a semi permeable membrane which allows the movement of water, classically known as â&#x20AC;&#x153;water treeâ&#x20AC;? phenomenon. This exposes both resin and exposed collagen fibers to degradation by hydrolysis. (17) Hybrid layer is formed by the penetration of monomer in dentin and its polymerization in situ which is essential for a good bonding to dentin. The other one is the reverse hybrid layer in which the hybrid layer is surrounded by more inorganic material. The hybrid layer degrades coincidently with decreasing bond strength which contributes to the ageing of dentin 15

Contemporary Dentin Bonding Agents-A Review

bond integrity. This is caused by the activation of MMP’s which denature the collagen in the hybrid layer. (1) As the smear layer is a porous substrate, the expectation is that thick smear layers could work as water reservoir and accelerate the degradation of the bonds. The hybridized smear layer has as much attraction toward water. Various advancements in the properties of adhesive systems have been developed to reduce micro leakage by strengthening the adhesion between the tooth surface and the restoration, such as increasing the acid potential of the etchant, addition of Nano fillers, and change in resin composition.

Total Etch Technique Fusayama advocated etching enamel and dentin simultaneous. This was a very opposing concept in the United States and Europe. acid-etching dentin produces pulpal death. A review of the literature indicated that the pulpal reactions which occurred after acid etching were largely because of inadequate sealing of etched cavities, and were the consequence of bacterial leakage. Few years ago they found, reduction in etching time and improvements in bonding formulations and techniques have eliminated the acid-etching controversy. Bonding was a 3-step process:

1. Total etch and rinse 2. Priming and evaporation of solvent and 3. Application of the adhesive then light curing. 1. Acid- it uses 35-37% phosphoric acid which removes the smear layer and de-mineralizes the most superficial hydroxyapatite crystals, thus exposing both intertubular and peritubular collagen. 2. Primer- Includes bi-functional molecules (hydrophilic and hydrophobic). 3. Resin- Includes monomers that are mostly hydrophobic; such as Bis-GMA. The resin monomers permeate the water filled spaces between adjacent dentin collagen fibers that used to be occupied by hydroxyapatite crystals. Several dental product manufacturers brought fourthgeneration bonding systems that etch dentin with phosphoric acids and some other acids. Examples include All- Bond 2, Amalgam bond, 16

Nandini pugal et al

Clearf~l Liner Bond OptiBond (Kerr), ProBond and Scotchbond Multi-Purpose Plus (3M). Many investigators have reported shear bond strengths for these materials that approach or exceed the typical enamel bond strength of 20 MPa. In addition, micro leakages studies indicate that they provide a better marginal seal than earlier generations of adhesives. A separate acid-etching step is still needed in “totaletch” wet-bonding techniques. This is done by application of two layers of bonding agent to wet dentin. The first layer is the same purpose as did the original primer. It removes much of the residual water and starts into penetrate adhesive monomer into acid etched dentin. If the acid-etched dentin surface is too wet, the change of phase occurs. Generally, when the second layer of bonding agent is applied, fresh monomers and their solvent re-dissolve the resin globules, leaving a more homogeneous film.

Ethanol Wet Bonding: The Ethanol wet-bonding concept was emerged from the tissue embedding techniques in which hydrated organic tissues are chemically dehydrated with ethanol for a few hours and then they will be embedded into epoxy resin. Due to the presence of water in the current wet-bonding techniques, there is a risk for phase separation of the hydrophobic Bis-GMA monomer from the hydrophilic resin monomers, which has limited water solubility. To avoid these problems, the wet-bonding technique involved the use of hydrophilic monomers, such as Hydroxyethyl methacrylate (HEMA). These hydrophilic monomers absorb moisture after polymerization, which causes plasticization of the resin polymer chains and thereby decreases the resin-dentine bond strength. Then the ‘‘ethanol-wet bonding (EWB)’’ concept was developed to replace water with ethanol to support the de-mineralized dentine collagen fibrils. (26) This ethanol dehydration process is known as “full chemical dehydration protocol” given by Sadek et al. and takes more time and it is too complex to perform properly in a clinic daily. When dentin is treated with an acidic conditioner is rinsed with water, the solubilized calcium and phosphate ions and reaction products should be extracted from the spaces between the collagen fibrils. When “wet bonding” techniques applied, the collagen fibril network is suspended in water, blocks the penetration of resin half way. Unlike the conventional water-wet-bonding Journal of Scientific Dentistry, 8(2), 2018

Contemporary Dentin Bonding Agents-A Review

technique, this method uses ethanol instead of water to saturate and to prevent the collapse of de-mineralized dentin matrices before to resin application. Water is replaced from inter-fibrillar spaces with ethanol during saturation of de-mineralized dentin matrices with ethanol before the application of the adhesive. The rationale behind this is that miscibility of adhesive resin monomers in the ethanol-saturated dentin matrices is better than those in the water-saturated dentin matrices. So ethanol is used as a saturation solvent for de-mineralized dentin matrices which allows intimate encapsulations of collagen fibrils with adhesive resin monomers. Therefore, ethanol-wet bonding might destroy enzymatic degradation of collagen fibrils and improve durability of resin dentin bonds (27) The advantage of Ethanol-wet bonding technique is that it can successfully persuade less hydrophilic monomers into the dentine matrix, creating a more hydrophobic hybrid layer that could absorb less water. Adhesives should be applied on time to ethanol-wet dentine to permit better infiltration of the adhesive monomers. The timeliness results in the avoidance of the collapse of the collagen network caused by the quick Evaporation of ethanol. (28).

Self Etch Adhesive Self-etch adhesives are developed for reduction in application steps and for hemical interaction with hydroxyapatite-coated collagen fibers. (32) Instead, bonding to dentin with additional phosphoric acid etching still remains controversial. The idea of self-etching approach was created approximately 20 years ago, though, the first and second generations of bonding agents can be considered self-etch materials since no acid etching/rinsing or conditioning step were used. Self-etch adhesive systems also comprise HEMA monomer because most of the acidic monomers are low water-soluble and to rise the wettability of dentin surface. Bi- or multi-functional monomers are added to provide strength to the cross-linking formed from monomeric matrix (5). Because self-etch adhesive systems do not need a separate acid conditioning step and moist post-rinse control, they are considered simplified adhesive materials. (32) self-etch approach may have the best future perspective. They are categorized as Ultra mild self-etc., Mild self-etch, Intermediate self-etch, Strong self-etch

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Gic Based Adhesive Glass-ionomers continue as the only materials that are self-adhesive to tooth tissue without any surface pretreatment. Pre-treatment with a feeble poly- alkenoicacid conditioner significantly improves bonding. Glassionomer approach can be achieved following a one- or two-step application procedure The extra conditioning step becomes more important, when coarse cutting diamonds are used and, so, thicker and more compact smear layers are produced. Poly-alkenoic-acid conditioner is applied for 10-to-20 seconds and gently rinsed off, followed by gently air-drying without dehydrating the surface. The increase in bonding efficiency must be partially attributed by • “Cleaning” effect, by which cutting debris is removed, a partial “demineralization” effect, by which the surface area is enlarged • Micro porosities for micromechanical meshing or hybridization are visible • Chemical contact of poly-alkenoic acid with residual hydroxyapatite (31) Glass ionomer cements (GIC) are often used as a lining or base material under resin composite restorations as a dentin replacement to seal the dentin with a material demonstrated to form a dependable bond. There is presently very little research data on the topic of bonding of GIC and resin-based adhesives, even if this technique is widely recommended for the restoration of large proximal cavities. Micromechanical bond is also significant to bond to a conventional GIC. In the case of resin-modified GICs, there is also a chemical bond between the resin constituent of the resin-modified GIC and resin of the enamel/dentin adhesive.

Conclusion Improvements have been made for aesthetic appeal, ease of use and reduction of technique sensitivity. The innovation of dentin bonding agents has solved many issues like the application procedure and bonding and thus making the procedure minimally time conducive. As we enter the new millennium it is important to examine the past keeping abreast of the fast rapidly spreading progresses in the drill of adhesive dentistry with the hottest trend.

Contemporary Dentin Bonding Agents-A Review

References 1. Van Meerbeek B, De Munck J, Yoshida Y, Inoue S, Vargas M, Vijay P, Van Landuyt K, Lambrechts P VGB. Adhesion to enamel and dentin: current status and future challenges. Oper Dent. 2003;28:215–35. 2. Van Niuwenhuysen JP, D’Hoore W, Carvalho J, Qvist V. Longterm evaluation of extensive restorations in permanent teeth. J Dent 2003; 31: 395-405 (Pub Med: 12878022). 3. Hunter AR, Treasue ET, Hunter AJ. Increases in cavity volume associated with the removal of class2 amalgam and composite restorations. Operat Dent 1995; 20:2–6 4. Kleverlaan CJ, Feilzer AJ. Polymerization shrinkage and contraction stress of dental resin composites. Dent Mater 2005;21:1150–1157.

Nandini pugal et al interface and protection of tooth structures. Jpn Dent Sci Rev. 2011;47(1):31–42. 19. Aggarwal V, Singla M, Sharma R, Miglani S, Bhasin SS. Effects of simplified ethanol-wet bonding technique on immediate bond strength with normal versus caries-affected dentin. J Conserv Dent [Internet]. 2016;19(5):419–23. Available from: http://www.ncbi. nlm.nih.gov/ pubmed /27656059 20. Van Landuyt K, De Munck J, Coutinho E, Peumans M, Lambrechts P, Van Meerbeek B. Bonding to dentin: Smear layer and the process of hybridization. Dental Hard Tissues and Bonding: Interfacial Phenomena and Related Properties. 2005. 89-122 p. 21. Tjäderhane L, Nascimento FD, Breschi L, Mazzoni A, Tersariol ILS, Geraldeli S, et al. Optimizing dentin bond durability: Control of collagen degradation by matrix metalloproteinases and cysteine cathepsins. Dent Mater [Internet]. 2013;29(1):116–35.

5. Abedin F, Ye Q, Parthasarathy R, Misra a., Spencer P. Polymerization Behavior of Hydrophilic-Rich Phase of Dentin Adhesive. J Dent Res [Internet]. 2015;94(3):500–7. Available from: http://jdr. sagepub. com/ cgi/doi/ 10.1177/ 0022034514565646YiuC

22. Liu Y, Tjäderhane L, Breschi L, Mazzoni A, Li N, Mao J, et al. Limitations in bonding to dentin and experimental strategies to prevent bond degradation. J Dent Res. 2011;90(8):953–68.

6. An overview of solvents in resin-dentin bonding. 2014;(January) 7. On AF, Disease S. Current Concepts. 2009;2(2):1–8

24. Parmar G. Review article : Hybrid layer : Foundation of Dental bonding. 2014;(October):46–50.

8. Gupta S, Biswal SS, Kaushik SV. Review Article Dentin Bonding Agents : An Overview. :82–4.

25. Swift EJ. Dentin/enamel adhesives: review of the literature. Pediatr Dent. 2002;24(5):456–61.

9. Communication S. Dentin Bonding Agents I : Complete Classification — A Review. 2011;2(December):367–70.

26. Ekambaram M, Kar C, Yiu Y, Pekka J, Wen J, Chang W, et al. ScienceDirect Effect of chlorhexidine and ethanol-wet bonding with a hydrophobic adhesive to intraradicular dentine. J Dent [Internet]. 2014;1–11. Available from: http://dx.doi.org/10.1016/j. jdent.2014.02.006

10. Strassler HE, Mann M. Dental Adhesives for Direct Placement Composite Restorations : An Update. 11. Journal of esthetic dentistry and restorative dentistryvol 27,n0.6.331- 334.2015doi.10.1111/jerd.12185 by Jorge perdigao,edwardnj.swift.j.r.dmd,ms 12. Phillips ciences of dental materials Anusavice/shen/rawls/Elsevier 13. Agee K, Chiba A, Tagami J. HHS Public Access. 2016;28(6):706– 21 14. Roberson TM. EDITORS.-sturdevants operative dentistry book 15. Inoue G, Nikaido T, Foxton RM, Tagami J. The acid-base resistant zone in three dentin bonding systems. 2009;28(6):717–21 16. Di Francescantonio, M., de Oliveira, M. T., Shinohara, M. S., Ambrosano, G. M. B., & Giannini, M. (2007). Bond strength evaluation of self-etch and total-etch adhesive systems on intact and ground human enamel. Brazilian Journal of Oral Sciences, 6(23), 1462–1466 17. Helvey G a. Creating super dentin: using flowable composites as luting agents to help prevent secondary caries. Compend Contin Educ Dent [Internet]. 2013;34(4):288–300. Available from: http:// www. ncbi.nlm. nih.gov/ pubmed/23895566 18. Nikaido T, Inoue G, Takagaki T, Waidyasekera K, Iida Y, Shinohara MS, et al. New strategy to create “Super Dentin” using adhesive technology: Reinforcement of adhesive-dentin

23. The Evolution of Dentin Bonding | Dentistry Today [Internet]. Available from: http://dentistrytoday.com/materials/1483

27. Ekambaram M, Kar C, Yiu Y, Pekka J, Martyn N, Russell F. ScienceDirect Adjunctive application of chlorhexidine and ethanol-wet bonding on durability of bonds to sound and cariesaffected dentine. J Dent [Internet]. 2014;42(6):709–19. Available from: http://dx. doi.org/ 10.1016/ j.jdent.2014.04.001 28. Effect of simplified ethanol-wet bonding on microtensile bond strengths of dentin 2adhesive agents with different solvents. 2016;(October). 29. Pei D, Huang X, Huang C, Wang Y. Ethanol-wet bonding may improve root dentine bonding performance of hydrophobic adhesive. J Dent [Internet]. 2012;40(5):433–41. Available from: http://dx.doi. org/10. 1016/j. jdent.2012.02.005 30. Article R, Pathology M. From dry bonding to water-wet bonding to ethanol-wet bonding. A review of the interactions between dentin matrix and solvated resins using a macromodel of the hybrid layer. 2007 Swift j. Review. 1998; 31. Kenshima S, Francci C, Reis A, Dourado A, Eloy L, Filho R. Conditioning effect on dentin , resin tags and hybrid layer of different acidity self-etch adhesives applied to thick and thin smear layer. 2006;34:775–83.

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Contemporary Dentin Bonding Agents-A Review 32. Giannini M, Makishi P, Almeida Ayres AP, Moreira Vermelho P, Marin Fronza B, Nikaido T, et al. S e l f - E t c h Ad h e s i v e S y s t e m s : A Literature Review. Braz Dent J. 2015;26(1):3–10.

Nandini pugal et al 34. Carious Dentin Treatment For Glass Ionomer Cement Adhesion : A Comparative Study Carious Dentin Treatment For Glass Ionomer Cement Adhesion : A Comparative Study. 2010;1–11.

33. Zhang Y, Burrow M, Palamara J, Thomas C. Bonding to Glass Ionomer Cements Using Resin-based Adhesives. Oper Dent. 2011;36:618–25.

Address of Correspondence

Dr. Nandini pugal, Final Year Postgraduate Department of Conservative dentistry and endodontics Indira Gandhi institute of dental sciences. Email id: nandini26588@gmail.com Phone no: 9952184648

Authors Final year postgraduate, department of conservative dentistry and endodontics, Indira Gandhi institute of dental sciences

2,4 Reader, Department of Conservative dentistry and endodontics, Indira Gandhi institute of dental sciences

Professor and Head, Department of Conservative dentistry and endodontics, Indira Gandhi institute of dental sciences

Senior lecturer, department of conservative dentistry and endodontics, Indira Gandhi institute of dental sciences

How to cite this article : N andini Pugal, Praveen rajesh, Dhanavel chakravarthy, Padmaraj S.N, Vijayaraja. Contemporary Dentin Bonding AgentsA Review. Journal of Scientific Dentistry 2018;8(2):13-9 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

Evolution of The Efficiency of Various Methods of Fixation for Zygomatico Maxillary Complex Fractures Sarath.K1, Sathyanarayanan.R2, Nithin Joseph Jude3 ABSTRACT Back Ground: Despite the prevalence of zygomaticomaxillary complex (ZMC) fractures, there is no consensus regarding the best approach to management. The aim of this review is to discuss the evolution and compare the efficiecy of various fixation methods of zygomatico maxillary complex fractures. Objective: To discuss the evolution and compare the efficiecy of various fixation methods of zygomatico maxillary complex fractures. Data Sources: A detailed search was undertaken on major electronic databases. The search was restricted to English language. Review Methods: Randomised controlled trials, experimental studies were included in the review. Conclusions: This narrative review concluded that there was enough evidence to suggest that patients may benefit from rigid and semirigid internal fixation using miniplates in zygomatico maxillary complex fractures Key words: Zygomatic complex fractures, Semirigid fixation, drill free screws.

Introduction

Literature Review

Maxillofacial trauma by their varying nature imparts and a high degree of emotional as well as physical trauma to the patients. The anatomy of the cranio facial skeleton is complex where it functions as a three dimensional unit. As a result of the complexity isolated fractures of the facial bone is a rare incidence.(1)

A thorough literature review available for relevant literature in English language was done. The number of articles reviewed for this review is around 40â&#x20AC;&#x201C;45 articles , articles selected were on English language.

Midfacial fractures can either occur alone or combined with other injuries such as mandibular, ophthalmologic, cranial, thoracic as well as upper and lower long bone injuries(2).The existing data regarding fracture of the face varies in site, extent and etiology depending on the subjects studied.These diverse causes of fracture of oral and maxillofacial region can be because of differences in risk as well as traditional and cultural factors among countries which in turn is influenced by the severity of injury.(3)

Objective To discuss the evolution and compare the efficiecy of various fixation methods of zygomatico maxillary complex fractures

Studies Related To Conventional Methods Of Fracture Reduction And Fixation A comprehensive report of the use of transmaxillary Kirschner wire is done on 1952 which stated that it provide stability after the reduction of zygomatic fractures. The main disadvantages were that the wire technique puts at risk the structures of the contralateral orbit. Rotation of the malar bone against the frontal process is possible as the pin is usually inserted parallel with the frontal and horizontal planes. Later in 1964 selfcure acrylic is used to manufacture the splints and cemented them on the teeth. Acrylic splints can be ready to effect immobilization within two hours of taking impressions as compared to cast metal splints (6-8 hours). This results in very early immobilization of the fractured bones, with considerable benefit to the patient. This reduced time factor is also a great advantage in the Journal of Scientific Dentistry, 8(2), 2018

Evolution of The Efficiency of Various Methods of Fixation for Zygomatico Maxillary Complex Fractures

treatment of the patient with skeletal damage and facial lacerations. In 1972 box frame fixation offers simple immobilization of the midfacial fracture, with or without associated mandibular injury. The technique does not require complicated apparatus and is very easy. No dressings are required and patients can be mobilesed immediately after the operation. Although they have to sleep on their backs, the patients are comfortable. The removal of the apparatus at the end of 6 weeks is painless, and can be done in minutes in an outpatient unit. The resulting scars are not usually unaesthetic. Minimal pin tract infection has been encountered. Box frame is usually applied between the 6th and 12th day, when the swelling has subsided. On performing a clinical study, in 1976 proved that internal wiring fixation is better than fixation of pack in the antrum when stay in the hospital, restoration of infraorbital nerve function, position of the orbits, bilateral palpebral fissure symmetry and the final easthetic results are considered. However, in the antral packing group, the result was better when jaw movem,.ents and occu.rrence of permanent double vision were compared. Retrospective examination of 21 subjects having maxillary fractures treated at the Medical Center Hospital of Vermont in Burlington in 1983 by thorough comprehensive dental and ent clinical analyses, revealed no nonunion in any patient examined and compared each patient's lateral ceph with computerized norms suggested that elongation of face did not occur when Inter maxillary fixation alone was the principal method of repair. In a study conducted using Champy miniplates in the treatment of facial fractures and in the correction of the post traumatic deformities, in birth craniofacial deformities, and bony deformities occurring secondarily, the advantages of plating are summarized as reduced time of operation , rigid fixation during the surgery, adequate and good fixation of bone grafts, and the skill to take out the intermaxillary fixation in children after the procedure or during the immediate postoperative days. Klotch and Gilliland 1987 evaluated internal fixation using AO miniplates compared to the already existing therapy (utilizing a combination of IMF, and interosseous wiring, or bone grafting) for the treatment of serious mid third fractures. They concluded that internal fixation gives very good stabilization and correction of serious mid third injuries with less complications and fast return to routine job for most patients.

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Wu et al 1998 evaluated the stability of miniplate osteosynthesis for midface fractures and found that RIF provided good three dimensional stability. The fixation of zygomatico frontal suture and zygomatico maxillary suture were the key for obtaining sufficient stability, and at least two fixation screws were required above zygomatico frontal suture.

Studies Related To Various Advancements In Midface Fracture Reduction And Fixation Manson and coworkers 1985 have proved that immediate extensive ORIF with bone grafting done primarily provides superior aesthetic results in midthird of face. fractures in poly trauma patients. Orbital reconstruction most frequently requires bone grafts. They concluded that extended ORIF and bone grafting simultaneously has an added advantage over the aesthetic results obtained from facial fracture treatment. Also, structural bone union and pre operative facial structure could be restored if soft tissue contraction is not present In a study done by Rudolf and Coworkers(39) 1987, treating unstable zygomatic fractures with resorbable poly (L-lactide) (PLLA) plates and screws, the results showed that this method of fixation gives good stability over a sufficiently long period to enable undisturbed fracture healing. Francel TJ in 1992(40) summarized the complications of rigid fixation in the management of craniomaxillofacial trauma as prominence, infection, exposure, and migration of the osteosynthesis appliances. The frequency of infection and exposure may be decreased with antiseptic irrigation, correct placement of plates, attention to proper mucosal closure, and mucosal-saving techniques. In a retrospective study by Niessen et al(41) 1996 comparing the late results of patients with an isolated zygomatic fracture and dislocation, who have been treated with the Gillies procedure alone or with stabilizing transosseous wires, proved that even the stabilized zygomatic complexes (22%) could, due to the pull of the muscle masseter, still rotate around the axis of stabilization and this causes asymmetry in 60% of the cases. Unstable fractures and dislocations, however, need an open reduction and an adequate stabilization with miniplates at the frontozygomatic suture and infraorbital rim. Lee et al(42) 1997 utilized endoscopic-assisted technique of open reduction and rigid fixation for managemet of complex midfacial fracture to facilitate 21

Evolution of The Efficiency of Various Methods of Fixation for Zygomatico Maxillary Complex Fractures

the anatomic repair of associated zygomatic arch and orbital floor fractures. The results obtained proved that the technique minimized ocular globe manipulation and concominantly eliminated the need for coronal scalp and lower eyelid incisions. In 1997 stated that in case of significant midface retrusion due to bone loss, a framework reconstruction using 2.0mm titanium mesh molded and fixed rigidly in place, followed by application of hydroxyapatite cement onto the mesh allow restoration of normal skeletal structure. No overcorrection is required if this method of reconstruction is used. In a study by Enislidis and coworkers 1998, a new material for osteosynthesis fixation of zygomatic fractures was used and after six month follow-up period, there was uneventful bone healing with no complication regarding the hardware. advantages of the new material is that its malleable when heated, and adapting fast to the bone surface, and second operation can be avoided for implant removal. In another study of 44 patients by Schortighuis et al 1999 with maxillofacial trauma treated by open reduction and internal fixation using 1.0 and 1.5-mm microplates for fixation revealed a perioperative complication rate of 1.2% for the 1.0-mm screws, primarily malposition. No complications were observed with the 1.5-mm system and there was no instance of exposed hardware In a study by Park and his co-workers 2001, for the repair of 39 orbital fractures, Titanium mesh screen 1.0 (SYNTHES) were used either as an onlay implant or as cover implant to repair severely crushed fracture on the orbital rim or maxillary wall segments. The advantages of using titanium mesh screen were its high rigidity and malleability, fewer artifacts on the follow up CT scans and ability to restore and fix easily even crushed tiny bony pieces without loss and achieve more accurate three dimensional anatomical reconstruction of orbital wall fracture. Paludetti et al 2003 conducted a study comparing various techniques for midface fracture fixation, it is concluded that the use of titanium mini and microplates, are easy to apply and offer optimal reduction and stabilization and hence well-suited for surgical application. Resorbable mini-plates are more advantageous in paediatric patients since titanium plates interfere with cranial-facial growth and, also make both CT and MRI artifacts. Moreover, these could create problems, in the event of oncologic disease that requires radiotherapic treatment. Use of 22

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absorbable materials reduces the risk of inflammatory complications following titanium implant rejection requiring removal of these devices. Marcin Kozakiewicz 2009 used 3-D virtual and anatomical models on the basis of computed tomography images. Using rapid prototyping, these were used as templates to form titanium mesh implants, which are then used intra operatively as guides to aid correct implant placement in the orbit for the reconstruction of orbital floor defects. Kloss et al 2011 stated that in the management of midfacial fractures complications occur after 6 and 12 months. Nerve parasthesis and sensitivity to the material were most prominent. Hence careful decision should be taken regarding surgical treatment Vijay Ebenezer 2012 in his study stated that microsystem has good and paramount use in midface fractures. The advantages noted are adequate fixation of fractures, with negligible palpability in the thin midfacial region, minimal thermal conductivity, high malleability to easily adapt to complex facial contours and high biocompatibility. Inaddition, it gives a very good access and easy placement without disturbing adjacent anatomic structures. In a study by Mehra 2013, craniofacial suspension using POP head cap is found to be a quick, simple and efficient immobilization of middle third fracture with/ without associated mandibular fracture. Carron and co-workers 2014 ultrasonically vibrated the pin to fill the pilot holegrooves created by the drill with the pin material. The material fills the grooves completely even at less than 90Â° angles and behaves analogous to screw threads. This provides a tremendous advantage in hard-to-reach midface areas because pilot holes may be drilled at less than 90Â° angles and the plate screw construct will maintain stability, unlike its titanium counterpart. The two properties of the absorbable system may help overcome the issue of achieving stability when perpendicular placement would be difficult.

Studies Related To Self Tapping And Drill-Free Screws Drill Free Screws (DFS) were developed in 1998 by Heidemann as having a cork screw and cutting flutes which are specially formed which enable insertion of the screws without drilling. Tests performed to analyze the holding power of drill free screws and self-tapping Journal of Scientific Dentistry, 8(2), 2018

Evolution of The Efficiency of Various Methods of Fixation for Zygomatico Maxillary Complex Fractures

titanium screws showed that the holding power of drill free screws is between 70 and 104% of the holding power of self-tapping titanium screws. In a prospective study performed by Heidemann 1999 to investigate the clinical efficiency of mini and microdrill free screws (DFS) and also to determine areas in maxillofacial traumatology and orthognathic surgery, where this new type of screw may be recommended for clinical use; this study proved that micro- and mini-DFS has adequate rigidity and stabilty for the fixation of bone fragments in the central and lateral midface and in the anterior mandibular area. However, the application of DFS in the mandibular angle region is not recommended. In a study evaluating the clinical use of self drilling screws in the craniomaxillofacial area, Ralf Schon et al 2000 found that ease of insertion without previous drilling and less use of instruments reduced the operating time. Screw fractures occured, when the screws were inserted forcefully in the periorbital area. They concluded that miniplate osteosynthesis and the fixation of cortical and cortico-cancellous bone grafts using self-drilling screws proved to be reliable. Holmes and co-workers 2000 suggested the technique for the use of bicortical screws that two forward turns followed by one backward turn excludes the shaft from the pitch of the screw during insertion and removal. Heidemann 2001 on comparing the metal/osseous interface and bone remodeling after insertion of selftapping screws and drill free screws found that DFS had higher screw/bone contact and significantly more residual bone in the region of the screw threads. The greater amount of original bone in the threads of drill free screws demonstrated that the insertion of drill free screws did not cause harm to the surrounding bone. Both the results obtained are important for osteosynthesis in regions where thin cortical bone is present, such as the central midface. Coburn 2002 recommended the placement of selftapping IMF screws with careful bur hole drilling, with slow bur speed and copious irrigation with sterile saline. Also, the screw insertion speed should be judicial and should not be forced once resistance is felt. Alpert and his coworkers 2003 stated that self-drilling, self-tapping screws areshowing much superior quality while fixing screws into asoft and cancellous bone graft. The self-drilling principle has an added advantage of

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avoiding the a drill hole thus shortening the process of orif and requiring less instruments. Gibbons AJ 2003 stated that drill free IMF bone screws may be used as temporary IMF to support the fracture during definitive plating for military purposes. At the end of the surgery the IMF is released, the occlusion checked and the screws removed. If postoperative elastic traction is required, for example in mandibular condylar fractures, the screws may be left in place and removed at a later date. Yan Chen et al 2008 compared the influences of self drilling and self tapping titanium implant modalities on orthodontic microimplants and surrounding tissues biomechanically and histologically. The tendency to fracture and the percentage of bone-to-implant contact values was greater in the self-drilling group. It proved that self-drilling microimplants can provide better anchorage and hence can be recommended for use in the maxilla and in thin cortical bone areas of the mandible. Mischkowski RA et al 2008 in their study were campared with four miniscrew types for anchorage of the skeleton regarding the property such as biomechanical, contributing to primary stability. A drill-free screw having a conical design can achieve better and higher primary stability compared with self-tapping screws which is cylindrical. This effect was more visible during the insertion of torque estimations compared to pull-out tests. The Dual Top screws, were highly susceptible to fractures. Jin-Seo Park and coworkers 2009 did 3D finite element analysis to evaluate the strain induced in the cortical bone surrounding an orthodontic microimplant during insertion in a self-drilling manner reported that the upper limit for normal bone remodeling, were observed in the peri-implant bone along the whole length of the microimplant. Level of strains in the vicinity of either the screw tip or the valley part was similar. The study concluded that bone strains from a microimplant insertion in a self-drilling manner might have a negative impact on the physiological remodeling of cortical bone. In an animal study using scanning electron microscopy by Juliana GG and co-workers 2010, comparing selfdrilling and self-tapping screws the bone debris formed with self-drilling screws is not the result of the heat generated, but rather the result of biologically active bone tissue capable of reacting with the screw and improving its performance and hence, bone debris formed during 23

Evolution of The Efficiency of Various Methods of Fixation for Zygomatico Maxillary Complex Fractures

the installment of the self-drilling screws is considered beneficial. Nandini and colleagues 2011 compared the use of selftapping IMF screws to the conventional Erich arch bars for intermaxillary fixation in the treatment of mandibular fractures. Self tapping IMF screws reduce the operating time and the risk of needle stick injuries. Oral hygiene maintenance and patient compliance were good with IMF screws as compared to arch bar Sumit Yadav 2012 in a study evaluating microdamage accumulation after mini implant placement by selfdrilling (without a pilot hole) and self-tapping (screwed into a pilot hole) insertion techniques found that the selfdrilling technique resulted in greater total crack lengths in both the maxilla and the mandible.

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References 1. Naveen Shankar A, Naveen Shankar V, Hegde N, Sharma, Prasad R. The pattern of the maxillofacial fractures – A multicentre retrospective study. Journal of Cranio-Maxillofacial Surgery. 2012;40(8):675-79. 2. Simpson DA, Mclean AJ: Mechanisms of İnjury. In: David DJ, Simpson DA (Eds) Craniomaxillofacial Trauma, Vol. 101. Churchill Livingstone, 1995 pg.92. 3. Killey H C. Fractures of the Middle Third of the Facial Skeleton. Bristol: John Wright & Sons Limited, 1977 pg.77 4. Thomas DW, Hill CM: Etiology and Changing Patterns of Maxillofacial Trauma. In: Booth PW, Schendel SA, Hausamen JE (Eds) Maxillofacial Surgery, Vol. Churchill Livingstone, 3, 2000 pg.273. 5. Mouzakes J, Koltai P, Kuhar S, Bernstein D, Wing P, Salsberg E. The Impact of Airbags and Seat Belts on the Incidence and Severity of Maxillofacial Injuries in Automobile Accidents in New York State. Arch Otolaryngol Head Neck Surg. 2001;127(10):1189.

Conclusion

6. Norton N S. Netter’s Head And Neck Anatomy For Dentistry. Philadelphia: Saunders Elsevier, 2007 pg.56.

Results of the narrative review of literature shows that semi rigid internal fixation using self tappig screws is the best method of fixation of zygomatico maxillary complex fracture and drill free screws can be used as an alternative to self tapping screws which is evidenced y similar success rate of both screws.

7. Le Fort R. Etude experimentalesur les fractures de la machoiresuperiore. Rev Chir 1901; 23:208–27. 8. Le Fort R. Etude experimentalesur les fractures de la machoiresuperiore. Rev Chir 1901;23:360–79. 9. Le Fort R. Etude experimentalesur les fractures de la machoiresuperiore. Rev Chir 1901;23:479–507. 10. Gassner R, Tuli T, Hächl O, Rudisch A, Ulmer H. Craniomaxillofacial trauma: a 10 year review of 9543 cases with 21067 injuries. Journal of Cranio- Maxillofacial Surgery. 2003;31(1):5161.

Address of Correspondence

K. Sarath, Department of Oral & Maxillofacial Surgery, Indira Gandhi Institute of Dental Sciences Email id: sarathsreenivasan@gmail.com Phone no: +91 90472 99004

Authors Post Graduate, Department of Oral & Maxillofacial Surgery, Indira Gandhi Institute of Dental Sciences.

Professor, Department of Oral & Maxillofacial Surgery, Indira Gandhi Institute of Dental Sciences. 2

Associate Professor, Department of Oral & Maxillofacial Surgery, Indira Gandhi Institute of Dental Sciences.

How to cite this article : S arath.K, Sathyanarayanan.R, Nithin Joseph Jude. Evolution of The Efficiency of Various Methods of Fixation for Zygomatico Maxillary Complex Fractures. Journal of Scientific Dentistry 2018;8(2):20-4 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

Role of Immunology in Periodontal Disease: A Brief Review Vinoth Kumar B Na1, Arvina R2, Sivaranjani K S3, Hema P4, Arun Varghese R5 ABSTRACT Periodontitis is a highly complex and multifactorial disease. In recent years, researchers began to focus on bacterial-host interactions. It had been recognized that though the bacteria present in plaque initiates the periodontal inflammation, the host response to these pathogens equally matters in the progression of the disease. Therefore, the severity of this disease is due to a variety of factors, including the presence of periodontopathic bacteria, high levels of proinflammatory mediators and low levels of antiinflammatory mediators. However, the immune response initiated by periodontal disease seems to be much broader. This review attempts to enlighten the various immune mechanisms involved in periodontal disease initiation and progression. Key Words: Immunology, Periodontitis, Pathogens, Cytokines, Antibodies.

Introduction

Innate Immunity

Periodontitis is one of most common inflammatory diseases and it can be of inflammatory, traumatic, metabolic, developmental and/or genetic origin.1 Till date, two principal forms of periodontitis have been recognized (chronic and aggressive periodontitis). Chronic periodontits is an inflammatory response in the periodontal tissue by the presence of microorganism in the dental plaque.2 Aggressive periodontitis is a rapidly progressive form of periodontal disease, characterized by severe destruction of the hard tissue support of the dentition in early age and there is a high tendency for diseases to occur in families.3

The epithelial tissues play a key role in innate response, because they are in constant contact with bacterial products. It is now recognized that epithelial cells also constitutively express a diverse range of antimicrobial peptides and their synthesis is upregulated in response to periodontal bacteria. These peptides belong to four families (Îą-defensins, Î˛-defensins, cathelicidins, saposins) that have been found in humans.6

Bacteria present in the plaque, are the primary etiological factor but the host immune response to these bacteria is the fundamental factor for the destruction of both soft and hard tissues in chronic and aggressive periodontitis.4 Bacteria that colonize the subgingival plaque biofilm encounter both innate and acquired immunity. Host immune system response to the periodontopathic pathogens is believed to be the major part in periodontitis by the interaction between periodontopathic bacteria and host immune system.5 The paradigm of the pathogenesis of periodontitis is shifting. It is important to understand how oral bacteria alters the host immune responses and how periodontium is affected by the protective factors induced by host response. This review article highlights the major role of host immune system in chronic and aggressive periodontitis.

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Innate recognition of bacteria and their products by the host involves a sophisticated array of receptors providing specificity to pathogen detection. Through these receptors, cells can directly respond to conserved pathogen-associated microbial patterns (PAMPs) and host danger-associated molecular patterns (DAMPs). These molecular motifs are recognized by pattern recognition receptors (PRRs) on immune cell surfaces.7 PAMPs associated with periodontal disease are bacterial lipoproteins, lipopolysaccharide, peptidoglycan, fimbriae, flagellin, heat shock proteins, DNA. The toll-like receptor (TLR) family is the best characterized class of PRRs and detects multiple PAMPs. In the context of periodontal disease, TLR-2 and TLR-4 play important roles in bacterial antigen sensing.8,9 TLR signaling occurs in a manner that is dependent on the adaptor molecule myeloid differentiation primary response gene (MyD88) or occurs independently via TIR-domain-containing adapter inducing Interferon-Î˛ (TRIF). All TLRs with the exception of TLR-3 signal 25

Role of Immunology in Periodontal Disease

via MyD88; however, TLR-4 engages both MyD88 and TRIF signaling pathways.10 Neutrophils are the ďŹ rst innate immune cells to migrate to the site of infection. Neutrophils utilize relevant Tolllike receptors to recognize and respond to different types of microbial challenge. Like neutrophils, macrophages/ monocytes also play a key role in host defense by recognizing, engulďŹ ng and killing microorganisms.11

Role Of Neutrophils In Innate Host Defence a) CHEMOTAXIS Circulating neutrophils can be quickly mobilized to infection or inlammation sites through a systematically controlled process known as transendothelial migration.12 This leukocyte adhesion cascade is positive regulated by tissue-derived cytokines and by tissue-derived chemokines. Once neutrophils move into tissues, they follow chemoatractant gradients to reach infection or inlammation sites through a process called chemotaxis. Some chemoatractants for neutrophils are activated by complement components, such as the anaphylatoxin C5a, and bacterial components, such as formyl-methionylleucyl-phenylalanine (fMLF).13 b) PHAGOCYTOSIS Phagocytosis occurs when the neutrophil encounters the bacteria. Phagocytosis is greatly enhanced by coating of the bacteria with antibody or complement. These coating molecules (collectively called opsonins) facilitate binding and internalization via cell surface receptors including Fc receptors (receptors for the Fc fragment of IgG) and receptors for complement, specifically CR1and CR3.14 During phagocytosis, the phagosome fuses with lysosomes to become phagolysosomes, within which bacteria are killed and fragmented by a variety of toxic substances, antimicrobial agents and enzymes. The bacteria are killed by a mechanism termed as intracellular killing which results in sequestration of the enzymes responsible for bacterial cell death. Killing can also occur through release of the granules into the tissues in the vicinity of the invading bacteria. This killing is termed as extracellular killing.15

Antigen Presentation If the early lesion persists without resolution, bacterial antigens are processed and presented by lymphocytes, macrophages and dendritic cells. Broadly, two different subsets of lymphocytes have evolved to recognize 26

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extracellular and intracellular pathogens after being presented with antigens by the innate immune cells: T-lymphocytes and B-lymphocytes.16 B-lymphocytes have immunoglobulin molecules on their surface, which function as antigen receptors. Activation of the T-cell receptor requires the major histocompatibility complex, which is also a member of the immunoglobulin superfamily. Two classes of major histocompatibility complex molecules are required for the activation of distinct subsets of T-cells. Various T-cell subsets kill infected target cells and activate macrophages, B-cells and other T-cells. Thus, T-cells are essential for the regulation of both humoral and cell-mediated responses.17 Classically, T-lymphocytes have been classified into subsets based on the cell-surface expression of CD4 or CD8 molecules. CD4+ T-cells (T-helper cells) were initially subdivided into two subsets, designated T-helper 1 and T-helper 2, on the basis of their pattern of cytokine production.18 Activation of B-cells is an important step in the maturation of the antibody response. This event is mediated mainly by the tumor necrosis factor family of proteins and their receptors.19 In addition to their role in presenting antigen, B-cells also function as effectors, through cytokine secretion, lysosomal components, reduced oxygen metabolites, nitric oxide and antibodies. This is also important because in severe periodontal lesions, B-cells are the predominant antigen-presenting cells, suggesting that B-cell antigen presentation may allow further activation and clonal expansion of already activated T-cells.20

Adaptive Immunity The adaptive immunity is activated when there is a breach in epithelial barrier, with its antimicrobial peptides and other components of innate systems. The immune response in periodontal disease is governed by the net effect of T-helper 1 (Th1) and T-helper 2 (Th2) cytokines.21,22 The differentiation of Th1 and Th2 T cell subsets is determined by antigen, nature of the antigen-presenting cell and co-stimulatory molecules.23 IL-18, as a cofactor with IL-12, is able to enhance the maturation of naive T cells to Th1 cells. Th1 cytokines include interleukin-2 and Interferon-Îł and promote cell-mediated immunity, while the Th2 cytokine, interleukin-4, suppresses cell-mediated responses and enhances humoral immunity.24 However, there are controversial data about the Th1/ Th2 immune response in periodontal disease. Studies over the past decade or so have supported the hypothesis Journal of Scientific Dentistry, 8(2), 2018

Role of Immunology in Periodontal Disease

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that Th1 cells are associated with the stable lesion and Th2 cells are associated with disease progression.25-29 However, other studies have reported a predominance of Th1-type cells or reduced Th2 responses in diseased tissues.30-32 Recently, a new subset of T-helper cells, Th17 cells, characterized by the production of interleukin-17, has been described. This subset may have both destructive and protective effects in periodontal diseases.33,34

periodontal disease which will enable new treatment paradigms and prevention strategies.

On the other hand, the integrity of bone tissues depends on the interdependency between the osteoclasts and osteoblasts. The major regulatory mechanism of osteoclast activity is modulated by three novel members of TNF family of receptors, RANK (receptor activator of nuclear factor-Î˛), osteoprotegerin (OPG) and the RANK ligand (RANKL).35 RANK is expressed on osteoclasts and its precursors, while RANKL is expressed particularly on osteoblasts under homeostatic conditions. Interactions between RANK and RANKL are required for the differentiation and activation of osteoclast precursor cells to osteoclasts. OPG, a soluble decoy receptor produced by osteobalsts, marrow stromal cells and other cells, strongly inhibits bone resorption by preventing RANK-RANKL interaction.

3. Albandar JJ, Brown LJ, Loe H. Clinical features of early-onset periodontitis. J Am Dent Assoc 1997; 128: 1393-99.

RANKL also induces the production of some substances, such as MCP-1/CCL2, which could contribute to bone resorption.36 Osteoblasts are found to express chemokine receptors during synthesis, which can modulate their function through the binding of chemokines. Additionally, an osteoclast can produce important chemokines which are involved in the recruitment of neutrophils and different lymphocyte subsets, suggesting a role for osteoblasts in the development of the inflammatory immune reaction.37 Furthermore, the production of chemokines, with the consequent chemoattraction of inflammatory cells, may contribute to the disruption of bone homeostasis, resulting in bone resorption.

Conclusion In this review, a brief introduction of periodontal disease, focusing on the participation of host immune system including both innate and adaptive systems, which may interfere in the development and progression of the periodontal disease, was described. The available data show that the host response is critical in protecting the periodontium from the pathological sequelae of bacterial colonization and invasion. However, till date no consensus regarding the pattern of the immune response in controlling the periodontal disease has been documented. Therefore, more researches are warranted to understand the intricacies of the immunological background of Journal of Scientific Dentistry, 8(2), 2018

References 1. Page RC, Schroder HE. Pathogenesis of inflammatory periodontal disease: A summary of current work. Lab Invest 1976; 4: 235-49 2. Lindhe J, Hamp SE, Loe H. Experimental periodontitis in the beagle dog. J Periodontal Res 1974: 8: 1-10.

4. Genco RJ. Host responses in periodontal diseases: Current concepts. J Periodontol 1992: 63: 338-58. 5. Page RC, Kornman KS. The pathogenesis of human periodontitis: An introduction. Periodontol 2000 1997: 14: 9-11. 6. Hancock RE, Scott MG. The role of antimicrobial peptides in animal defenses. J Clin Periodontol 2000; 97(16): 8856-61. 7. Lien E, Sellati TJ, Yoshimura A, Flo TH, Rawadi G, Finberg RW, et al. Toll-like receptor 2 functions as a pattern recognition receptor for diverse bacterial products. J Biol Chem 1999; 274(47): 33419-25. 8. Brightbill HD, Libraty DH, Krutzik SR, Yang RB, Belisle JT, Bleharski JR, et al. Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors. J Immunol 1999; 285(5428): 732-6. 9. Takeda K, Kaisho T, Akira S. Toll-like receptors. J Immunol 2003; 21(1): 335-76 10. Sugawara Y, Uehara A, Fujimoto Y, Kusumoto S, Fukase K, Shibata K, et al. Toll-like receptors, NOD1, and NOD2 in oral epithelial cells. J Dent Res 2006; 85(6): 524-9. 11. Mocsai A: Diverse novel functions of neutrophils in immunity, inflammation and beyond. J Exp Med 2013; 210: 1283-99. 12. Amulic B, Cazalet C, Hayes GL, Mezler KD, Zychlinsky A. Neutrophil function: From mechanisms to disease. Annu Rev Immunol 2012; 30: 459-89. 13. Summers C, Rankin SM, Condlife AM, Singh N, Peters AM, Chilvers ER. Neutrophil kinetics in health and disease. Trends Immunol 2010; 31: 318-24. 14. Faurschou M, Borregaard N. Neutrophil granules and secretory vesicles in inflammation. Microbes Infect 2003; 5: 1317-27. 15. Sengelov H, Follin P, Kjeldsen L, Lollike K, Dahlgren CNB. Mobilization of granules and secretory vesicles during in vivo exudation of human neutrophils. J Immunol 1995; 154: 4157-65. 16. Gemmell E, Carter CL, Hart DN, Drysdale KE, Seymour GJ. Antigenâ&#x20AC;?presenting cells in human periodontal disease tissues. Oral Microbiol Immunol 2002; 17(6): 388-93. 17. Cekici A, Kantarci A, Hasturk H, Van Dyke TE. Inflammatory and immune pathways in the pathogenesis of periodontal disease. Periodontol 2000. 2014; 64(1): 57-80. 18. Gemmell E, Yamazaki K, Seymour GJ. The role of T cells in periodontal disease: homeostasis and autoimmunity. Periodontol 2000. 2007; 43(1): 14-40.

Role of Immunology in Periodontal Disease 19. Mackler BF, Frostad KB, Robertson PB, Levy BM. Immunoglobulin bearing lymphocytes and plasma cells in human periodontal disease. J Periodontal Res 1977; 12(1): 37-45.

Vinoth Kumar et al 29. Lappin DF, MacLeod CP, Kerr A, Mitchell T, Kinane DF. Antiinflammatory cytokine IL-10 and T cell cytokine profile in periodontitis granulation tissue. Clin Exp Immunol 2001: 123: 294-300.

20. Taubman MA, Valverde P, Han X, Kawai T. Immune response: The key to bone resorption in periodontal disease. Journal Periodontol. 2005; 76: 2033-41.

30. Ebersole JL, Taubman MA. The protective nature of host responses in periodontal diseases. Periodontol 2000 1994: 5: 112-41

21. Taubman MA, Kawai T. Involvement of T-lymphocytes in periodontal disease and in direct and indirect induction of bone resorption. Crit Rev Oral Biol Med 200; 12(2): 125-35.

31. Salvi GE, Brown CE, Fujihashi K, Kiyono H, Smith FW, Beck JD, et al. Inflammatory mediators of the terminal dentition in adult and early onset periodontitis. J Periodontal Res 1998: 33: 212-25.

22. Nakajima T, Ueki-Maruyama K, Oda T, Ohsawa Y, Ito H, Seymour GJ, et al. Regulatory T-cells infiltrate periodontal disease tissues. J Dent Res 2005; 84(7): 639-43.

32. Takeichi O, Haber J, Kawai T, Smith DJ, Moro I, Taubman MA. Cytokine profiles of T-lymphocytes from gingival tissues with pathological pocketing. J Dent Res 2000: 79: 1548-55.

23. Eastcott JW, Yamashita K, Taubman MA, Harada Y, Smith DJ. Adoptive transfer of cloned T helper cells ameliorates periodontal disease in nude rats. Oral Microbiol Immunol 1994; 9(5): 284-9.

33. Gaffen SL, Hajishengallis G. A new inflammatory cytokine on the block: re-thinking periodontal disease and the Th1/Th2 paradigm in the context of Th17 cells and IL-17. J Dent Res 2008; 87(9): 817-28.

24. Yamashita K, Eastcott JW, Taubman MA, Smith DJ, Cox DS. Effect of adoptive transfer of cloned Actinobacillus actinomycetemcomitans-specific T helper cells on periodontal disease. Infect Immun 1991; 59(4): 1529-34. 25. Aoyagi T, Sugawara-Aoyagi M, Yamazaki K, Hara K. Interleukin 4 (IL-4) and IL-6-producing memory T-cells in peripheral blood and gingival tissues in periodontitis patients with high serum antibody titers to Porphyromonas gingivalis. Oral Microbiol Immunol 1995: 10: 304-10. 26. Bartova J, Kratka Opatrna Z, Prochazkova J, Krejsa O, Duskova J, Mrklas L, et al. T helper type 1 and Th2 cytokine profile in patients with early onset periodontitis and their healthy siblings. Mediators Inflamm 2000: 9: 115-20. 27. Manhart SS, Reinhardt RA, Payne JB, Seymour GJ, Gemmell E, Dyer JK, et al. Gingival cell IL-2 and IL-4 in early-onset periodontitis. J Periodontol 1994: 65: 807-13.

34. Adibrad M, Deyhimi P, Ganjalikhani Hakemi M, Behfarnia P, Shahabuei M, et al. Signs of the presence of Th17 cells in chronic periodontal disease. J Periodontal Res 2012; 47(4): 525-31. 35. Takahashi N, Udagawa N, Suda T. A new member of tumor necrosis factor ligand family, ODF/OPGL/TRANCE/RANKL, regulates osteoclast differentiation and function. Biochem Biophys Res Commun 1999: 256: 449-55. 36. Lorenzo J. Interactions between immune and bone cells: New insights with many remaining questions. J Clin Invest 2000: 106: 749-52. 37. Liu D, Xu JK, Figliomeni L, Huang L, Pavlos NJ, Rogers M, et al. Expression of RANKL and OPG mRNA in periodontal disease: Possible involvement in bone destruction. Int J Mol

Med 2003: 11: 17-21.

28. Gemmell E, Seymour GJ. Cytokines and T cell switching. Crit Rev Oral Biol Med 1994: 5: 249-79.

Address of Correspondence

Dr. Vinoth Kumar. B.Na, Department of Periodontology, Indira Gandhi Institute of Dental Sciences, Email id: vinothmessi@gmail.com Phone no: 9843353089

Authors Final year post graduate student, Department of Periodontology, Indira Gandhi Institute of Dental Sciences.

Senior Lecturer, Department of Periodontology, Saveetha Dental College and Hospitals, Chennai.

Final year post graduate student, Department of Periodontology, Indira Gandhi Institute of Dental Sciences. 3,4

Final year post graduate student, Department of Periodontology, Indira Gandhi Institute of Dental Sciences.

How to cite this article : V inoth Kumar. B.Na, Arvina R, Sivaranjani. K S, Hema P, Arun Varghese R. Role of Immunology in Periodontal Disease: A Brief Review. Journal of Scientific Dentistry 2018;8(2):25-8 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

The Role of Stromelysin-3 (ST-3) in Progression of Oral Squamous Cell CarcinomaA Narrative Review Muthukumaran R1, Vezhavendhan N2, Vidyalakshmi S3, SanthaDevy A4, Premlal K R5, Gayathri C6

ABSTRACT Matrix metallo proteinases (MMP) are zinc dependent endopeptitases. The role of MMP have been implicated in various physiological and pathological process including oraganogenesis, inflammation, vascular disease, wound healing, auto immune disease and cancer progression. Several MMPs was over expressed in head and neck squamous cell carcinoma (HNSCC) and the MMP found to have correlating with cell proliferation, angiogenesis, invasion, and metastasis. Epithelial–mesenchymal interactions involving cell–cell, cell–Extra cellular matrix (ECM), multistep process of carcinogenesis. ECM remodelling in tumor progression is mediated by MMPs. MMP 1,2,3,7,8,9,10,11,13,and 19 are most over expressed in HNSCC. The role of MMP 11(ST-3) in human breast carcinoma, ovarian cancer are well established whereas the expression of role of MMP 11 in oral squamous cell carcinoma (OSCC) gives varied observations. Hence the current review is aimed to various studies involved the immunohistochemical expression of MMP 11 in OSCC. Key Words: Oral Sqaumous Cell Carcinoma, Matrix Metallo Proteinases(MMP), Stromelysin-3 (ST3), MMP-11.

Introduction

Materials and Methods

One of the major extracellular matrix-degrading enzyme implicated in cancer development is matrix metalloproteinases(MMPs), also called matrixins. A group of zinc and calcium-dependent endopeptidases, with a broad spectrum of proteolytic activity toward extracellular matrix components1 The expression of MMP11 is regulated by numerous growth factors, cytokines, stress, hormonal regulation, irreversible cellular changes etc. MMP’s are set to have their own inhibitors that decide in the tissue (TIMPs), which in turn control the sustained expression of MMP. Matrix metallo proteinases (MMPs) regulate tumor invasion by remodeling the host tissue.2 An imbalance between the various MMPs and their TIMPs attributes to pathological remodeling in cancer progression and metastasis. MMP-11 (Stromelysin-3) discovered in breast cancer, interacts with the stromal components and contributes to the early and late stages of tumor progression.3 These matrix degrading enzymes also hold apoptotic and anti- apoptotic roles. Expression of MMP-11 is noted in cancers that undergo metastasis. MMP-11 is a marker more profoundly used in therapy as well as assessing the prognosis.4 The role of MMP11 in human breast carcinoma, ovarian cancer are well established whereas the expression of role of MMP11 in HNSCC is not been studied to the fullest. Hence the current review is aimed at allude on varies studies involved the immunohistochemical expression of MMP 11 in oral sqamous cell carcinoma.5

The period of 1995 to 2017 medical and dental articles were reviewed by using the search engines like Pubmed (PMC), Research gate, Elsevier, Google scholar etc.

Journal of Scientific Dentistry, 8(2), 2018

Classification of Matrix Mettalo Proteinases: MMPs are classified into collagenases, gelatinases, stromelysins, matrilysins, metalloelastase, membranetype MMPs, and others on the basis of their substrate speciﬁcity. In the collagenases type includes MMP 1,8,13, in gelatinases 2,9, stromelysins comprises of 3,10,11, matrilysins is MMP 7 and membrane type MMPs were also included which are MT1,2,3,4,5, and other MMPs. Commonly MMPs are degrades the extra cellular matrix and promotes the degradation this will led to progression of tumor and invaded to the adjacent structure as well as metastasis.6

Mechanism Action 0f Mmp 11: Matrix metalloproteinase (MMP)-11or Stromelysin-3, are Zinc dependent endopeptidases. Which are widely expressed in both physiological and pathological conditions. Such as osteogenesis, spinal cord morphogenesis, embryonic implantation, interdigitation, placentation, epithelial growth and inflammation, wound healing.7 And pathologically involved in matrix 29

The Role of Stromelysin-3 (ST-3) In Progression of Oral Squamous Cell CarcinomaA Narrative Review

degradation and tissue remodeling and helps the tumor progression. Among the other MMPs, MMP-11 only secreted under active form, this characteristics have role in tumor progression and tissue remodeling processes.9 And it interacts with stromal component that contribute to cancer in the early and late stages of tumor progression in human. MMP-11 always expressed in the fibroblast around the invaded tumor islands.10

mmp-11 (Stromelysin-3) in oscc Polymorphism of numerous MMP genes are functional and they may contribute to tumorigenesis of OSCC. Studies have also shown that polymorphism of MMP-1 and MMP-2 is associated with head and neck carcinoma risk, whereas polymorphism of MMP-9 and MMP-13 are associated with increased risk of aggressive form of oral cancer. MMP-11 gene polymorphism found to exhibit synergistic effect of environment factors like betel nut and tobacco in OSCC formation.10 When there is a change in binding affinity between the promoter of Polymorphic MMP-11 gene and in betel nut or in tobacco constitutes, it can lead to alteration in expression or in activity of MMP-11. This in turn unregulated extra cellular proteases which promotes the development of OSCC. MMP-11 also found to play role in metastasis.10 Depending upon the spatio-temporal factors the role MMP-11 in metastasis will occur. In a study they also found that there is a increased frequency of lymphnode metastasis in OSCC patients with at least one polymorphic allele of MMP-11. MMP-11 which contain cysteine that binds with catalytic zinc ion and inhibiting the enzyme, when this cysteine ion is dissociated from zinc ion, releases peptide which activates the enzyme which in turn found to affect the function of MMP-11 this leads to increased activity of MMP-11 in tumor cells and surrounding fibroblast which in turn enhances the proliferation and metastasis of oral cancer.11 When expression of MMP- 11 in tumor specimen of 177 OSCC patients where study they found positive expression for 70 percentage of samples. in another study when 220 OSCC patients and 90 precancerous lesions where studied for MMP 11 expression and they found that expression of MMP-11 and pro angiogenic factors are indicators for progression from free cancer stage to frank malignancy. also there is evidence in study conducted in Taiwan that strongs expression of MMP-11 is correlated 30

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with poor survive in OSCC patients also that study they found that a FAK/src a signalling pathway is involved in MMP-11 mediated cell metastasis in oral squamous cell carcinoma.11 In a study it has been found that expression of ST3 in stromal fibroblast also in, epithelial cells that are undergoing mesenchymal transition.12 this has been related with progression of phenotypic alteration which are required yearly during malignant transformation of oral epithelium pathway.13 Thus stating that MM-11 can serve as a potential target in designing molecular therapeutics in early intervention of oral tumorigenesis.

Conclusion MMP’s are one of the proteins that remodel the host tissue, by degrading various ECM components. MMP’s also promote the proliferation and invasion of cancer cells. MMP-11(ST-3) favours epithelial proliferation in areas of intense remodeling, where the regenerating cells remain viable through an anti apoptotic signal. This physiological role of ST-3 is hampered in malignancy. Need further studies to well establish the role of MMP-11 in Oral squamous cell carcinoma.

References 1. Matrisian LM. The matrix-degrading metalloproteinases. Bioassays 1992;14:455–63. 2. Birkedal-Hansen H. Proteolytic remodeling of extracellular matrix. Curr Opin Cell Biol 1995;7:728–35. 3. Nagase H, Woessner JF Jr. Matrix metalloproteinases, minireview. J Biol Chem 1999;274: 21491–4. 4. Dano K, Andreasen PA, Grondahl-Hansen J, Kristensen P, Nielsen LS, Skriver L. Plasminogen activators, tissue degradation, and cancer. Adv Cancer Res 1985;44:139 –266. 5. Mignatti P, Rifkin DB. Biology and biochemistry of proteinases in tumor invasion. Physiol Rev 1993;73:161–95. 6. Savita JK, Kumar BY, Nayak VN. Matrix metalloproteinases in oral squamous cell carcinoma-A review. Journal of Advanced Clinical and Research Insights. 2018 Jul 1;5(4):124. 7. Matziari M, Dive V, Yiotakis A. Matrix metalloproteinase 11 (MMP‐11; stromelysin‐3) and synthetic inhibitors. Medicinal research reviews. 2007 Jul;27(4):528-52. 8. Nakopoulou L, Panayotopoulou EG, Giannopoulou I, Alexandrou P, Katsarou S, Athanassiadou P, et al. Stromelysin-3 protein expression in invasive breast cancer: Relation to proliferation, cell survival and patients’ outcome. Mod Pathol. 2002;15(11):1154– 61. 9. Boulay A, Masson R, Chenard MP, El Fahime M, Cassard L, Bellocq JP, et al. High cancer cell death in syngeneic tumors

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The Role of Stromelysin-3 (ST-3) In Progression of Oral Squamous Cell CarcinomaA Narrative Review developed in host mice deficient for the stromelysin-3 matrix metalloproteinase. Cancer Res 2001;61:2189–93. 10. Lin CW, Yang SF, Chuang CY, Lin HP, Hsin CH. Association of matrix metalloproteinase‐11 polymorphisms with susceptibility and clinicopathologic characteristics for oral squamous cell carcinoma. Head & neck. 2015 Oct;37(10):1425-31. 11. Hsin C-H, Chou Y-E, Yang S-F, Su S-C, Chuang Y-T, Lin S-H, et al. MMP-11 promoted the oral cancer migration and FAK/Src activation. Oncotarget [Internet].2017;8(20):32783–93.

Address of Correspondence

Dr. R Muthukumaran, Department of Oral pathology and microbiology, Indira Gandhi Institute of Dental Sciences, Email id: mthkumaran85@gmail.com Phone no: 9042184953

Muthukumaran et al

12. Arora S et al. Stromelysin 3, Ets-1, And Vascular Endothelial Growth Factor Expression in Oral Precancerous and Cancerous Lesions: Correlation with Microvessel Density, Progression, And Prognosis.Clin Cancer Res. 2005;11(6):2272-84. 13. Soni S, Mathur M, Shukla Nk, Deo Sv, Ralhan R. Stromelysin-3 Expression Is An Early Event In Human Oral Tumorigenesis.Int J Cancer. 2003;107(2):309-16.

Authors Post graduate student, Department of Oral pathology and microbiology, Indira Gandhi Institute of Dental Sciences.

Professor, Department of oral pathology and microbiology, Indira Gandhi Institute of Dental Sciences.

Reader, Department of oral pathology and microbiology, Indira Gandhi Institute of Dental Sciences.

Professor and Head , Department of Oral Pathology and Microbiology, Indira Gandhi Institute of Dental Sciences.

Reader, Department of Oral Pathology and Microbiology Indira Gandhi Institute of Dental Sciences.

Post graduate, Department of Oral Pathology and Microbiology, Indira Gandhi Institute of Dental Sciences.

How to cite this article : M uthukumaran R, Vezhavendhan N, Vidyalakshmi S, Santha Devy A, Premlal K R, Gayathri C. The Role Of Stromelysin-3 (ST-3) In Progression of Oral Squamous Cell Carcinoma- A Narrative Review. Journal of Scientific Dentistry 2018;8(2):29-31 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

Surface Conditioning and Silanization for Ceramic Adhesion Nandini Pugal1, Praveen Rajesh2, Preethe P M3, Padhmaraj S N4, Dhanavel Chakravarthy5

Introduction Bonding of two dissimilar materials require the substrate and adherent to have a clean surface for maximum bond strength. Removal of impurities from the surface results in, increase in surface energy and wettability of the surfaces to be bonded. The process of removing impurities and increasing the surface area is known as surface conditioning. Several surface conditioning techniques exist, namely acid etching, air abrasion, tribo chemical coating, grit blasting, etc. However, conditioning alone did not result in sufficient bond strengths between composites and metals/ceramics. A chemical component was required in the bonding process to enhance bond strengths. The chemicals that promote adhesion between two dissimilar molecules are called coupling agents. Most widely used coupling agents are organo metallic compounds such as organosilanes, titanates, zirconates and thiones. Coupling agents played a vital role in adhesion of matrix (resin) and fillers (silica) to form dental composites. This provides composites the necessary physical properties to withstand the adverse oral conditions. Organosilanes are the most commonly used coupling agent in dentistry. Silanes are derivatives of silicon compounds that contain Si-C and Si-H bond(s). The silanes are of two main types: functional silanes and non-functional silanes.the former contains two functional groups that can react with both organic and inorganic surfaces. Silica based ceramic and resin composites (an organic substrate), are uniďŹ ed by silanes showing that they can bring about adhesion of two chemically different materials while the non-functional Silanes that are not intended to impart chemical reactivity to the substrate used for surface modification. Non-functional silanes have only one reactive group which is capable of reacting with the hydroxyl groups of the inorganic substrate only. The main aim of this article is to discuss about the different methods of surface conditioning and the mechanism of how a silane modifies the surface of a substrate.

Methods of Surface Conditioning 1. Tribo-chemical silica coating 2. Pyro-chemical silica coating 3. Acid etching and electrolytic coating 4. Grit blasting 5. Selective infiltration etching 6. Nanostructured alumina coating 7. Chemical vapor deposition 8. Internal coating method 9. Gel-sol form 10. Plasma fluoridation 11. Nano silica coating 12. Silicon based coating Surface conditioning: Conditioning of the surface increases the critical surface energy for adhesion. when surface tension of a liquid is less than the surface energy of particular surface, the contact angle is 0Ě&#x160; degree and therefore the liquid can spread immediately. Adequate wetting of the substrate with bonding agent is essential for micro-mechanical retention, resistance to fatigue and stress relief. (6) Tribochemical silica coating: This method was introduced in 1989 as an improvement of the pyrochemical silica coating. A tribochemical Rocatec System (3M ESPE, Seefeld, Germany) was designed for surface conditioning of dental restorative materials like ceramics, metals and metal alloys. The substrate surface is grit-blasted under compressed air using silica-coated alumina powder (alumina particles act as the carrier) and this causes the melting of the surface microscopically. The impact of the powder particles changes the surface topography and then the powder particles also gets embedded onto the substrate surface. A silica coated surface is then subjected to follow salinization. The produced bond strength is affected by the blasting pressure applied. Recently it was reported that the grit blasting angle might be one of the cause which can affect the resin bonding. However, no significant effect with the change of angle or distance during sandblasting is provided.

Journal of Scientific Dentistry, 8(2), 2018

Surface Conditioning and Silanization for Ceramic Adhesion

Currently, the widely used surface-conditioning method is Tribochemical silica coating in which, a layer of silica is created on the surface so that the silane coupling agent will re-join chemically to make a strong bond with nonsilica-based materials. Due to the increased surface roughness there will be improved micro-mechanical retention. Silanes were used as adhesion promotors in ceramic restorations and their repairs with resin composites \glass fibre, reinforced polymer composites, glassy fillers in resin composite to form durable bonds between resin composite to silica-coated metal and metal alloys. Silanes lack intrinsic toxicity. (7) Silicatization provides a chemical basis to enhance composite bonding since silica rich surface is required for strong organic matrix to make bond with resin composite filling materials (8) These days, dental resin composites are composed of a resin matrix that contain monomers and cross-linking monomers, a free-radical initiator, colouring pigments such as glass, silica, hydroxyapatite and a silane coupling agent. The latter improves the bonding between the filler particles and resin matrix. The filler particles which are added to the resin matrix also recover the physical and mechanical properties of the resin composite. Additionally, the incorporation of fillers reduces the volume shrinkage after polymerization and improves the radio-opacity, aesthetic appearance. Also, this treatment will increase surface roughness, which will improve micromechanical interlocking for bonding.(8) Pyrochemical silica coating This technique is done based on the utilization of elevated temperatures eg: silicatermd, silicoater tm classic. The suface of the substrate is sandblasted and introduced into flame. A pyro-chemical silica coating is thus obtained of roughly 0.1-1.o mu thickness. The coating solution consists of tetra-ethoxysilane. (6)(9) The basic principle of the pyro-chemical silica-coating is the chemical reactions of silane at high temperature to form silica. Silicoater Classical, Silicoater MD and Siloc (heraeuskulzer, Wehrheim, Germany) systems were used since 1984. Base metal alloys, noble metal alloys and porcelain had been silica-coated by this method. In the Silicoater system, tetraethoxysilane, Si(OCH2CH3)4, TEOS, is injected into a flame. A series of pyrochemical reactions take place which can be summarized as follows Si(OCH2CH3)4(g) → sio2(s) + aco2(g) + bh2o(g)

Journal of Scientific Dentistry, 8(2), 2018

Nandini Pugal et al

The processing temperature is 150–200◦C. The reactive silane intermediates, Si(OH)C (where m = 1, 2, 3) deposits on the substrate surface. After cooling, a silane coupling agent is applied onto the silica coating to react. This method is however, no longer used in dental technology. A modification of the Silicoater technique was introduced later on as Silano Pen or pyrosil Pen (Bredent, Senden, Germany) for extra-oral use in dental laboratories. It is applied by a hand-held device with a flame treatment. Traditional surface treatment methods discussed above are applied in dental laboratories. Researches on other surface treatments is in progress in an attempt to improve adhesion and its durability in the oral cavity. (2) Acid etching and electrolytic coating: Acid etching of ceramic restorations prior to bonding is important to create the appropriate surface structure needed to maximize retention of the resin cement. This method involves etching of the surface with hydrofluoric acid (5%HF),lithium disilicate (e.max): 20 second etch with 5% HF..Leucite ceramic (Empress Esthetic, Authentic, etc.): 60 second etch with 5% HF.Feldspathic ceramic (d.SIGN, Ceramco, etc.): 120 second etch with 9% HF Base metal alloy of fixed partial denture is electrolytically etched to reinforce the adhesion of resin composite luting cements by creating irregularities on the metal surface. The etched surface is difficult to assess with the naked eye. Another modification is that the electrolytical tin plating is done before veneering metal crown followed by which sandblasting is completed and this enhances micro-mechanical retention (6) Ceramic restorations and repairs: Silane coupling agents are used for dental reestablishments, like ceramic repairs of on-lays, in-lays, crowns and bridges. Mostly the repair is less expensive and time-saving unless the damage due to fracture is beyond repair. The clinical procedure for mending ceramic restoration sometimes involves the subsequent steps (1) • • • •

Roughening the surface with diamond burs Sand-blasting the surface Acid etching, silanization Finally bonding to resin composite

Surface Conditioning and Silanization for Ceramic Adhesion

Grit blasting In dental laboratory the routine procedure for surface pre-treatment of some indirect restorative materials is grit blasting with aluminum oxide powder with particle size of eg:110µ under a constant pressure of 380 k pa, this cleansing action will increase the surface roughness that enhances the bonding by micromechanical interlocking (retention). However, the surface is also contaminated with aluminum oxide powder particles throughout grit blasting. A thin layer of aluminum oxide coating is also formed onto the substrate surfaces during grit-blasting. The quantity of aluminum oxide deposited is directly proportional to the blasting pressure applied. Al- O -Si linkages is also formed The linkages are rather weaker than -Si-O-Si- and are more susceptible to hydrolysis. A drawback of this method is an induction of subsurface damage causing surface micro-cracks due to the impact of the powder particles. This would possibly compromise the mechanical strength at the surface layer that successively affects the long run clinical performance.(10) Selective infiltration etching This is a comparatively new approach where the zirconia surface is coated with thin layer of a glassconditioning agent. The coating is fired above the glass transition temperature and also the molten glass particles penetrate into the surface grain boundaries. Surface tension phenomenon is developed which causes the surface grains movements: an inter-grain porosity is formed when treated with acid and the glass particles are removed. Therefore, an extremely reactive and retentive zirconia surface is created. Resin zirconium bonding is considerably improved with the selective infiltration etching treatment followed by a silane application. (10) Nano-structured alumina coating Alumina nano-particles are formed by the hydrolysis of aluminum nitride (aln) powder heated at 75◦C, resulting in nano-boehmite (alooh) particles deposited on oxide surface. Once the coating is thermally treated in air at 900◦C, the boehmite undergoes a series of phase transformation to alumina causing an increase in the surface area enhancing the micro-mechanical interlocking for resin bonding. The improvement in resin zirconia bonding is obtained when water aging process begins even without a silane application (3) 34

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Chemical vapor deposition In molecular vapor deposition system, a mixture of tetra-chlorosilane (sicl4) and water is heated. The vapor is passed onto zirconia surface in a vacuum chamber. Silane undergoes hydrolysis to form hydroxylated silica and HCl gas is produced as a byproduct. A silica seed-layer (sixoy) is formed on the zirconia surface. The coating thickness can be adjusted by the time of deposition. The silica seed coating is reported to form durable bonding to zirconia with an application of silane coupling agent (11) Laser treatment There are three types of laser used in dentistry for clinical use and surface treatment: 1. Erbium: yttriumaluminum-garnet (Er: YAG), 2. Neodymium: yttriumaluminum-garnet (Nd: YAG), and 3. Carbon dioxide (CO2). The substrate surface is irradiated with a laser beam. This laser energy is absorbed and are converted into heat energy which causes the melting of the substrate surface and produces surface irregularities. Surface topography changes take place and enhanced adhesion promotion was observed. (12) Internal coating method Silica coating on the zirconia surface is achieved by thermal fusion. Porcelain powder is mainly composed of silica with small percentage of Al2O3, Na2O, and K2O. The zirconia surface is grit-blasted with alumina powder. The porcelain powder is mixed with distilled water to form a paste and is applied onto the grit-blasted zirconia surface. It is then fired at 800◦C in vacuum followed by silanization and resin bonding. (12) Sol-gel coating The basic principle of this method is the hydrolysis of silicon. Certain precursors, mostly tetra-ethoxy silane form silica sol gel in an acidic or alkaline medium. Hydrolysis of tetra-ethoxysilane produces silica and ethanol as a by-product. The silica sol gel deposits on the substrate surface through the surface hydroxyl groups and forms silica coating Plasma fluorination An extremely reactive coating is created on the zirconia surface by using plasma spray technique. Zirconia surface is exposed to continuous flow of Sulphur hexafluoride (SF6) gas at a continuous pressure in an inductively

Journal of Scientific Dentistry, 8(2), 2018

Surface Conditioning and Silanization for Ceramic Adhesion

coupled plasma reactor. Under plasma irradiation, the Sulphur hexafluoride molecules are converted to reactive species and they react with zirconia after deposition on the surface. Once silane coupling agent is applied onto the reactive surface, surface silanation happens. (12) Nano-silica coating Other silica precursors will react to create silica by chemical reaction however in additional reaction conditions. In a recent study, silica coating was formed on zircionia by the hydrolysis of silicon nitride(sin)under a strong alkaline medium alongside heating. The silicate species are formed from a suspension of silicon nitride nanoparticles in concentrated sodium hydroxide solution and heated to 90◦C. The hydrolyzed silicon oxide nanoparticles deposit on the zirconium surface. When drying the coating is heated to 1400◦C to create the silica coating by condensation of the hydroxylated silica species (13) Silicone-based coating Silicone polymers like polydimethylsiloxane that contains a repeating unit of siloxane can form silica upon thermal oxidization and decomposes in air when a thin layer of polydimethylsiloxane gel is applied on to a titanium surface.(13)

How are Surfaces Modified Using Silane? Most widely used organosilanes have one organic substituent and three chemical substituents. In majority of surface treatments, alkoxy group of the tri-alkoxysilanes are hydrolysed to form silanol-containing group. The reaction occurs in 4 stages:

Nandini Pugal et al

• Hydrolysis of the labile groups • Condensation to oligomers. • The oligomers and hydrogen bonds with -OH group of the substrate. • Finally, through drying or solidification, a covalent linkage is made with the substrate with concomitant loss of water.(3) Coupling mechanism of organfunctional alkoxysilane: It includes synthetic direct =si-h and =si-c bonds(siliconhydrogen, silicon-carbon) These are non- functional silanes that have non- reactive group hydrolysis reaction is by the removal of organic solvents and water: Water is the principal product of condensation reaction among silanes and ceramics and therefore the removal of each residual water and organic solvents is very important to enhance the adhesion of resin cement to dental ceramics. Manufacturers have suggested just blowing the air after the application of silane , is not enough to eliminate the residual water and organic solvents in order to reinforce the adhesion between lithiuim disilicate-based ceramic and resin cement.(4) To achieve adequate cement/ceramic bond strength, numerous treatments on the ceramic surface can be performed. Use of a silane coupling agent is suggested for an adhesive cementation. Silane is a monomer with reactive organic radicals and a hydro-soluble monovalent group that produces bonding between both inorganic phase of the ceramic and the organic phase of the bonding agent and is coupled to the ceramic surface by a siloxane bond. Additionally, the silane agent increases the surface

Figure 1: mechanism of adhesion (12)

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Surface Conditioning and Silanization for Ceramic Adhesion

energy of ceramic substrates and improves the adhesive and/or cement wettability. A suitable silane procedure should be used to assure the bond strength achievement and longevity of the dental restoration. During the application of silane on the ceramic, the surface is dried and an interphase layer is formed. Eliminating the outermost layer of the silane film and leaving the most constant and chemisorbed layer on the ceramic surface improves the bond strength along with the restorative interface. (1) Though described in sequence, these reactions can occur all together after the initial hydrolysis step. Particularly at the interface, there is formation of one bond of each silicon of the organo-silane to the substrate surface. The remaining two silanol groups are present either in condensed or free form. The R group remains available for covalent reaction or physical interaction with other phases. (4) Silanes can modify surfaces in anhydrous conditions by monolayer and vapour phase deposition. Methoxy silanes and cyclic azasilanes are effective devoid of catalysis for vapour deposition. (5) Figure 2: Silane coupling agents (2)

Nandini Pugal et al

stability of bonding better than using silane coupling agents. The chief problem of resin composites that are bonded to silica-coated restorative materials with the application of commercial silane coupling agents is the bond degradation over time under artificial ageing. To upsurge the hydrolytic stability of the bonding at the interfacial layer, innovative surface treatments of restorative materials and the advanced silane monomers are used. Silane coupling agents by means of extended hydrocarbon chains are more hydrophobic than those with small hydrocarbon chains. The bonding at the interfacial layer is more resistant to thermal and water ageing. These two approaches may decide the problems. (10) (14)

Conclusion Therefore, it could be said that silane coupling agents can satisfy the clinical requirements for dental restorations. A standard laboratory protocol for dental restorations entails surface conditioning of dental materials, silanization and cementation. The problem of hydrolytic stability of the siloxane linkage formed from silane coupling agents with resin composites and dental restorative materials is currently being hold forth. It is not an overestimation to claim that silane coupling agents have wide application in industry, such as dentistry and medicine and that it will play an important role in biomaterial sciences.

References 1. Irving W, Road P. Bonding of Resin Materials to All-Ceramics : A Review Liang Chen and Byoung In Suh Research and Development, BiscoInc,. 2012;3(1):7–17. 2. Fuchigami K, Fujimura H, Teramae M, Nakatsuka T. Precision Synthesis of a Long-Chain Silane Coupling Agent Using Micro Flow Reactors and Its Application in Dentistry. 2016;(March):35–46. 3. Amdjadi P, Ghasemi A, Najafi F, Nojehdehian H. Pivotal role of filler / matrix interface in dental composites : Review. 2017;28(3):1054–65.

2 Types of Silane Coupling Agents: Contemporary Trends and Future Development in Dentistry: In the recent times, alternate coupling agents (such as phosphate ester) that are used in dental restorations in addition to self-adhesive resin cements are adhesive primers, metal, alloy primers, and carboxylic acid primers. Phosphate esters can bond straight to non-silicabased ceramics such as zirconia. It has been stated that using this phosphate ester one can enhance the hydrolytic 36

4. Aguiar TR, Franco W, Barbosa DS, Francescantonio M Di, Giannini M. Effects of ceramic primers and post silanization heat treatment on bond strength of resin cement to lithium disilicate based ceramic. ApplAdhesSci [Internet]. 2016; Available from: "http://dx.doi.org/10.1186/s40563-016-0078-0 5. Reddy SM, Vijitha D, Deepak T, Balasubramanian R, Satish A. Evaluation of Shear Bond Strength of Zirconia Bonded to Dentin After Various Surface Treatments of Zirconia. 2012; 6. Matinlinna JP, Ying C, Lung K, Kit J, Tsoi H. Silane adhesion mechanism in dental applications and surface treatments : A review. Dent Mater [Internet]. 2017;34(1):13–28. Available from: https://doi.org/10.1016/j.dental.2017.09.002 7. Attia A, Kern M. Long-term resin bonding to zirconia ceramic with a new universal primer. J Prosthet Dent [Internet]. Journal of Scientific Dentistry, 8(2), 2018

Surface Conditioning and Silanization for Ceramic Adhesion 2010;106(5):319–27. Available from: http://dx.doi.org/10.1016/ S0022-3913(11)60137-6 8. Hooshmand T, Matinlinna JP, Keshvad A, Eskandarion S, Zamani F. Bond strength of a dental leucite-based glass ceramic to a resin cement using different silane coupling agents. J MechBehav Biomed Mater 2013;17:327-332. 9. Silva EA, Trindade FZ, Nagib H, Feres J, De JRC. Heat treatment following surface silanization in rebondedtribochemical silica-coated ceramic brackets : shear bond strength analysis. 2013;21(4):335–40. 10. Ying C, Lung K, Matinlinna JP. Aspects of silane coupling agents and surface conditioning in dentistry : An overview. Dent Mater [Internet]. 2012;28(5):467–77. Available from: http://dx.doi. org/10.1016/j.dental.2012.02.009

Address of Correspondence

Nandini Pugal, Department of Conservative Dentistry and Endodontics, Indira Gandhi Institute of Dental Sciences, Email id: nandini26588@gmail.com Phone no: +91 95667 17443

Nandini Pugal et al 11. Effect of Silanization on Microtensile Bond Strength of Different Resin Cements to a Lithium Disilicate Glass Ceramic. 2016;17(February):149–53. 12. Agents SC. Silane Coupling Agents Combination of Organic and Inorganic Materials to enhance the quality and functionality of. 13. Chen, L., B.I. Suh, J. Kim and F.R. Tay, 2011a. Evaluation of silica-coating techniques for Zirconia bonding. Am. J. Dent., 24: 79-84. PMID: 21698986 14. Nihei T. Dental applications agents.2016;58(2):151–5.

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Authors Final Year Postgraduate, Department of Conservative Dentistry and Endodontics, Indira Gandhi Institute of Dental Sciences.

Reader, Department of Conservative Dentistry and Endodontics, Indira Gandhi Institute of Dental Sciences. 2,4

Intern, Department of Conservative Dentistry and Endodontics, Indira Gandhi Institute of Dental Sciences.

Professor and Head, Department of Conservative Dentistry and Endodontics, Indira Gandhi Institute of Dental Sciences.

How to cite this article : N andini Pugal, Praveen Rajesh, Preethe P M, Padhmaraj S N, Dhanavel Chakravarthy. Surface Conditioning and Silanization for Ceramic Adhesion. Journal of Scientific Dentistry 2018;8(2):32-7 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

Role of Dna Repair Pathways in Aging- A Review C Gayathri1, A Santhadevy2, N Vezhavendhan3, Premlal K R4, S Vidyalakshmi5, R Suganya6 ABSTRACT Aging is a process where decrease of function occurs followed by DNA damage. DNA replication or transcription are affected because of structural damage to DNA, which leads to alteration or elimination of fundamental cellular process. To overcome this defect cell develop certain repair mechanisms. They are Base Excision Repair, mismatch repair, nucleotide excision repair, and double-strand break repair, homologous recombination, non-homologous end joining. Cancer cells can have increased rate of proliferation capacity, reduced apoptosis and increased capacity to invade basement membrane and metastasize. Because of genomic instability of cancer cell they easily break and reform chromosome and stimulate fusion of new oncogene and tumor suppressor gene are inactivated. To overcome this cancer cells should have capacity to withstand DNA damage. Key Words: DNA, Aging, Repair pathways.

Introduction Aging can be defined as progressive decline in function and increase in mortality over a period of time. DNA is considered as precious molecule as it helps in encoding information about cellular contents. If chromosome is lost it is difficult to replace it and because of its irreplaceable nature, it makes itself as a critical target especially to the damage that occurs during aging.DNA damage if not corrected prior to replication it results in cytotoxic development1. Hence DNA replication should be checked properly in cell cycle. DNA damage can occur because of external and internal sources. The external sources are the ionizing radiation and genotoxic drugs and internal sources includes the replication errors, spontaneous chemical changes to DNA programmed double-strand breaks also DNA damaging agents that are normally present in the cells such as reactive oxygen species, super -oxide anion, hydroxyl radical, hydrogen peroxide. ROS cause lipid peroxidation, protein damage and many DNA lesions. This ROS cause persistent damage to cell further which pave way for DNA damage.1

Dna Repair Pathways in Aging MISMATCH REPAIR Mispaired bases occur because of replication errors, recombination of imperfectly matched sequences and deamination of 5-methyl cytosine. Role of mismatch repair is to remove this Mispaired bases. DNA replication that had overcome this point mutation occur when DNA 38

replication cross a mismatched base repair. Mismatch repair found to play a role in repairing oxidative damage2. Mismatch repair (MMR ) is needed for the maintenance of repeated sequence. Mutation in MMR genes leads to destabilization of microsatellites, which in turn causes this microsatellite instability to increases with age. In a study, when cells that are of different passages treated with mismatch â&#x20AC;&#x201C;inducing agent and when detected using alkaline comet assay, they found MMR declined as age increases. Thus age related alteration occurs in mismatch repair. Mismatch repair play role in correcting mutations associated with DNA replication. Microsatellite instability occurs because of missing gene or mutation of MSH2, MSH6 or PMS2 gene and this dysfunction is found to be associated with hereditary non-polyposis colon Cancer3.

Base Excision Repair Lesions that affect only one DNA strand is removed by excision repair and complementary strand fill the gap. Base excision repair (BER) repairs minimal alteration in DNA such as oxidized bases or incorporation of uracil which will not distort overall structure of DNA helix. Damage that are induced by reactive oxygen species is corrected by BER. Excision repair is classified as short patch base excision repair, in which one nucleotide is replaced, whereas in long patch where 2-23 nucleotides are replaced4. Journal of Scientific Dentistry, 8(2), 2018

Role of Dna Repair Pathways in Aging- A Review

DNA glycosylaes initiates BER, that in turn cleave N-glycosylaes BER, that in turn cleave N-glycosylic bond of damaged bases sparing apurinic/ apyrimidinic site. AP endonucleases process abonic site leaving single stranded gap. This gap is then filled by DNA polymerases beta and ligated by DNA ligase.4 The levels and kinetics of AP site, after DNA damage in nuclear DNA revealed that higher basal level of AP in senescent human fibroblast and leukocytes compared to young cells. Deficiency in DNA glycosal activity was found in old cells, when treated with H2O2 or MMS, as the level of AP site increase in younger cells when compared to old cells. When oxidized guanine was measured after exposure to gamma radiation the level was increased, because of BER enzyme activity is altered followed by altered response to DNA damage. In younger mice expression of DNA polymerase and AP endonuclease found to be induced by DNA damage to young mice, whereas in aged mice there is lack of inducibiity. There was deficient in translocation of oxoguanie DNA glycosylase and AP endonuclease in to both nuclei and mitochondria of old mice and senescent human fibroblast. Efficiency of BER is sequence-specific where their gene expression is down regulated with age when compared with young individuals5.

Nuceotide Excision Repair DNA oligo nucleotides that contains damaged base is removed by nucleotide excision repair(NER). The bulky lesions that are caused by carcinogenic compound, covalent linkages between adjacent pyrimidine as a result of UV exposure is recognized by NER. Nucleotide excision repair is classified as global genome repair which has been found to occur everywhere in genome and transcription coupled repair that removes lesions in transcribed strand. Damage in XPC-HR23B is recognized by GG-NER damage, further verified by XPA. XPB, XPD, helicases in complex with TF11H basal transcription initiation factor, unwound DNA and further incision is made in XPF and XPG damage strand. DNA polymerase and DNA ligase remove and repair damaged strands. Repair process is initiated by TCR pathway stabled RNAPOIII along with TCR specific proteins and CSB and CSA.6 In a study they measured the disappearance of cyclobutane pyrimidine dimers from genomic DNA in human fibroblast, by treating the cells with UV and genomic DNA is removed and incubated with T4 endonuclease, which cleave priymide dimmers of DNA. Journal of Scientific Dentistry, 8(2), 2018

Gayathri et al

Restriction enzymes cleave the DNA, that is separated on a alkaline gel and intensity of band to specific gene is determined by southern hybridization.6 They found nucleotide excision repair activity decreased in old or senescent individuals.

Double Strand Break Most lethal of all DNA lesions is double strand break. In unrepaired double strand break (DSB) chromosome segments is lost and affects survival of cell. DSBs destabilize the genome and cause genomic rearrangements if its misrepaired7. Deregulation of transcription and malignancies occur because of genomic rearrangement which is common in aging. Homologous recombination and Non-homologous end rejoining (NHEJ) repair Double strand break in DNA . HR mediated repair of DSB occur in template of sister chromatid which is used to copy missing information in to broken locus. RAD52 mediates repair by HR along RAD52 group. DNA damage can be repaired without genetic consequences as sister chromatids are similar to each other, whereas NHEJ fuses two broken ends without regard for sequence homology. KU70/KU80 hetero dimer along with NHEJ binds with broken DNA ends. Artemis â&#x20AC;&#x201C;DNA PKAS complex are recruited by KU and prepare them for ligation. When DNA polymerase of POLX fill the gap by ligase forms a complex leading to deletion or insertion of filler DNA. Single strand annealing can repair double strand break between two direct repeats which is a mutagenic, mechanism in which sequence between the repeats is deleted. As cancer is associated with genomic rearrangements and loss of Increase in heterozygosity, incidence of cancer is found to be first indication of agerelated changes in DSB repair 8. In a study they found age related decline in efficiency of rejoining x-ray induced DNA breaks in lymphocytes that are normal in humans. When genes involved in DSB repair are disrupted it leads to premature aging phenotype. DSB repair were found to be less efficient during normal aging, the same pathway will also contribute in subtle way in onset of aged phenotype.9-10

Conclusion All the pathways become less efficient with age, leading to mutation accumulation. The reason of DNA repair enzyme to get decreased with aging is because of DNA repair and DNA damage. When alteration in this response occur it leads to DNA damage. Another mechanism apoptosis which is triggered by DNA damage is down regulated in aging or senescence in turn altering p53 39

Role of Dna Repair Pathways in Aging- A Review

activity. Beyond DNA damage response old organisms are sensitive to stress leading to alterations, mutations in DNA repair gene which is the main reason for premature aging syndrome, therefore it is assumed that normal aging is caused as a part of decline in DNA repair capacity. Imbalance between cell death and cell renewable leads to exhaustion of stem cell pool. Loss of tissue cellularity and declined function is main reason for accelerated aging. Also DNA damage and mutation may alter chromatin structure and cause epigenetic changes. Thus there is no reason why DNA repair cannot be improved. To conclude more research to be needed on mechanism of age-related changes in DNA repair, which will help us to up-regulate DNA repair and prevent further delay in aging and cancer.

References 1. Gorbunova V, Seluanov A, Mao Z, Hine C. Changes in DNA repair during aging. Nucleic acids research. 2007 Oct 2;35(22):7466-74. 2. Skinner,A.M. and Turker,M.S. (2005) Oxidative mutagenesis, mismatch repair, and aging. Sci. Aging Knowledge Environ., 2005, re3.

Address of Correspondence

C. Gayathri, Post Graduate, Department of Oral and Maxillofacial Pathology & Oral Microbiology, Indira Gandhi Institute of Dental Sciences, Email id: gayathri02.bds@gmail.com Phone no: +91 9003417067

Gayathri et al 3. Karran,P. (1996) Microsatellite instability and DNA mismatch repair in human cancer. Semin. Cancer Biol., 7, 15–24. 4. Wilson.D.M, III and Bohr,V.A. (2006) The mechanics of base excision repair, and its relationship to aging and disease. DNA Repair (Amst).81. 5. Szczesny,B, Hazra,T.K, Papaconstantinou.J, Mitra,S. and Boldogh,I. (2003) Age-dependent deficiency in import of mitochondrial DNA glycosylases required for repair of oxidatively damaged bases. Proc. Natl Acad. Sci. USA, 100, 10670–10675. 6. Hanawalt,P.C.(2002) Subpathways of nucleotide excision repair and their regulation. Oncogene, 21, 8949–8956. 7. Jackson,S.P. (2002) Sensing and repairing DNA double-strand breaks. Carcinogenesis, 23, 687–696. 8. Helleday,T. (2003) Pathways for mitotic homologous recombination in mammalian cells. Mutat. Res., 532, 103–115. Lieber,M.R. (1999) The biochemistry and biological significance of nonhomologous DNA end joining: an essential repair process in multicellular eukaryotes. Genes Cells, 4, 77–85. 9. Lieber,M.R., Ma,Y., Pannicke,U. and Schwarz,K. (2003) Mechanism and regulation of human non-homologous DNA endjoining. Nat. Rev. Mol. Cell Biol., 4, 712–720. 10. Gorbunova,V. and Seluanov,A. (2005) Making ends meet in old age: DSB repair and aging. Mech. Ageing Dev., 126, 621–628.

Authors Post Graduate,Department of Oral and Maxillofacial Pathology and Oral microbiology, Indira Gandhi Institute of Dental Sciences.

Professor and Head , Department of Oral and Maxillofacial Pathology and Oral microbiology, Indira Gandhi Institute of Dental Sciences.

Professor, Department of Oral and Maxillofacial Pathology and Oral microbiology, Indira Gandhi Institute of Dental Sciences.

Reader,Department of Oral and Maxillofacial Pathology and Oral microbiology, Indira Gandhi Institute of Dental Sciences. 4,5,6

How to cite this article : C Gayathri, A Santhadevy, N Vezhavendhan, Premlal K R, S Vidyalakshmi, R Suganya. Role of Dna Repair Pathways in AgingA Review. Journal of Scientific Dentistry 2018;8(2):38-40 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

Microbiological Profile of Chronic and Aggressive Periodontitis- A Review Hema P1,*, Saravanakumar R2, Shahinas begum.B3, Nandini Dimple4, Vinoth kumar B.Na5, Sivaranjani KS6 ABSTRACT Periodontitis is an microbial oral infection associated with the destruction of gingiva, cementum, periodontium and alveolar bone process. Periodontitis is broadly classified into chronic and aggressive forms. Both are distinguished in terms of microbiology, immunology, genetic influences and clinical presentation. The etiology of periodontitis would be because of accumulation of bacterial plaque, harbouring variety of pathogenic bacteria termed as periopathogens or periodontopathogens. The periopathogens ivolved in periodontitis are anaerobic bacteria such as Porphyromonas gingivalis, Prevotella intermedia,Tannerella forsythia, Treponema denticola, Fusobacterium nucleatum and Aggregatibacter actinomycetemcomitans. The microbiota of subgingival plaque contains more than 500 species of bacteria, nevertheless research has shown that Porphyromonas gingivalis, a Gram negative anaerobic bacterium, is the etiological agent which contributes to chronic periodontitis and is considered the keystone. Aggressive periodontitis is also influenced by microbiological, genetic, and host factors. The a comparative microbial profile between the two forms of periodontitis with the microbiological aspects of chronic and aggressive periodontitis can be explained in detail in this article. Key words: Chronic periodontitis, Aggressive periodontitis, Microbiology, Periodontitis.

Introduction Periodontal disease is a chronic bacterial infection characterized by persistent inflammation of connective tissue breakdown and alveolar bone destruction. (1-3) Biofilms that colonize the oral cavity are the most complex in nature. Besides pathogenic microorganisms, genetic, environmental factors like smoking, systemic diseases, medications such as steroids, antiepileptic, and drugs for cancer therapy, poor placement of dental bridges, dental crowding, lack of teeth, pregnancy and use of contraceptive pills can contribute to periodontitis(4). In recent research 800-1000 species were found to colonize the oral cavity among those about 50 species were strongly associated with periodontal disease (5). The primary bacterial colonizers present in the gingival sulcus produce cytotoxic substances which alter the environment and enhance the colonization of secondary colonizers. These secondary colonizers being more pathogenic exceed its threshold levels in periodontal disease (6).The factors which initiates the periodontal disease might be the virulence factor, their activity, the composition of microbiota and the host immune factors. (7). The causative organisms that are commonly found in periodontitis are Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia, Campylobacter Journal of Scientific Dentistry, 8(2), 2018

rectus; Eikenella corrodens, Fusobacterium nucleatum, Actinobacillus actinomycetemcomitans, Peptostreptococcus micros, Treponema denticola, and Eubacterium spp (8, 9) amongst which the most predominant are the Gram-negative anaerobes are capnophiles, spirochetes which enhances the initiation and progression of the inflammatory process. The bacteriaâ&#x20AC;&#x2122;s in the subgingival area increases in count invading the pocket epithelial cells and the underlying tissues. This review is focussed on the microbiological aspects and differences between chronic and aggressive periodontitis

The Implication of Microorganism in Periodontitis One of the important paradigm shifts that have taken place in the last decade is the recognition and acceptance of the formation of dental plaque as a bioďŹ lm. (10) Van Leeuwenhoek in 1683 described micro-organisms in tartar and they called them as animalcules. The role of microorganisms in periodontal disease has been demonstrated through experimental gingivitis and models. Non-specific plaque hypothesis theory states that periodontal disease is a result of noxious product from the entire plaque. (11, 12) But later it was modified as a specific plaque hypothesis stating that destruction to the periodontal structures is caused with minimal deposits. (13, 14)

Microbiological Profile of Chronic and Aggressive Periodontitis- A Review

Hema et al

Earlier studies demonstrated that the number and proportion of different subgingival bacterial groups varied from periodontal health to disease (14). Bacteria present in periodontally healthy sites were gram-positive facultative rods and cocci (75%) followed by a gradual decrease depending on the site say, gingivitis (44%) and periodontitis sites (10%) similarly there was a proportional increase in gram-negative rods from gingivitis (40%) and periodontitis (74%). (15)

A separate group of bacteria forms a green complex, which includes species: Capnocytophaga sputigena, C. gingivalis, and Eikenellacorrodens. These species are also associated with disease symptoms in adult periodontitis, but with a milder clinical course in contrast to the red complex (21, 22).

Instead of being associated with one particular etiologic agent, many chronic diseases appear to follow the “microbial shift” hypothesis. Microbial shift (symbiosis) refers to the concept that some diseases are due to a decrease in the number of beneficial symbionts and/or an increase in the number of pathogens. This is termed as ecologic shift hypothesis.(16)

Porphyromonas gingivalis

The term “periodontal diseases” includes any inherited or acquired disorders of the tissues that are supporting the teeth (gingiva, cementum, PDL, and alveolar bone) (17) . Chronic periodontitis is characterized by a low to moderate rate of progression that may include episodes of rapid destruction. (17, 18) It is subdivided according to the percentage of the involved sites into localized (<30%) and generalized (>30%). Furthermore, it can be subdivided according to the severity of the disease into mild (1-2 CAL), moderate (3-4 CAL). (19) The most predominant periopathogen are anaerobic bacteria: Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Treponema denticola, Fusobacterium nucleatum, and the relative anaerobe Aggregatibacter actinomycetem comitans. These organisms express a number of potential virulence factors and induce host inflammatory mediators, eventually leading to connective tissue breakdown and alveolar bone resorption (19.20). Currently, based on the research of Socransky team stands out specific groups of bacteria (called complexes) with particular importance in the pathogenesis of periodontitis. Porphyromonas gingivalis creates with the species of Tannerella forsythia and Treponema denticola so called red complex, which appears to be associated with disease symptoms in chronic periodontitis (20). The second important group of bacteria forms a orange complex, comprising 13 species, including Fusobacterium nucleatum and Prevotella intermedia. Orange complex bacteria are an essential link in allowing the colonization of periodontal tissue by a red complex (21, 22) . 42

Microbial Profile Associated with Chronic Periodontitis

Porphyromonas gingivalis is an intensively studied periodontal pathogen. Isolates of this species are gramnegative, anaerobic, nonmotile, asaccharolytic rods that usually exhibit coccal to short rod morphologies of gingivalis is a member of the much investigated black pigmented Bacteroides group. Organisms of this group form brown to black colonies on blood agar plates and were initially grouped into a single species, Bacteroides melaninogenicus. (23) P. gingivalis is has the ability to secrete some virulence factors which penetrates the gingiva and destroys the tissue directly or indirectly, by inflammation. This microorganism has been shown to have extensive virulence factors, including a true collagenase, endotoxin, IgA, proteases, and low-molecular weight compounds including hydrogen sulfide and ammonia which induce bone resorption, destroy connective tissue, induce a variety of cytokines, and inhibit host protective mechanisms. (24) P. gingivalis lypopolyssacharrides inhibits osteoblastic differentiation and mineralization in periodontal ligament stem cells which participate in periodontal tissue regeneration (24, 25).The “trypsin-like” enzymes cleave polypeptides at the C-terminal after arginine or lysine residue. These proteinases are commonly known as gingipains, namely gingipain R and K that cleave after arginine and lysine, respectively. ( 25) P. gingivalis involve directly in the colonization of the periodontal pocket, leading to the destruction of supporting periodontal tissue. In addition, the proteases also confer high resistance of the microorganisms to host defense mechanism. (26-28) Gingipain, a virulence factor was found to degrade fibrinogen and host haem proteins which contribute to inhibition of blood coagulation and increase bleeding, thereby enhancing the availability of hemin for bacterial growth (29). There is a high proliferation rate of P. gingivalis within periodontal pockets in which the count of erythrocytes are huge. Gingipains are also considered important in its capacity to degrade antibacterial peptides, such as neutrophil-derived α-defensins, complement Journal of Scientific Dentistry, 8(2), 2018

Microbiological Profile of Chronic and Aggressive Periodontitis- A Review

factors, such as C3 and C4, T cell receptors, such as CD4 and CD8 (30). P. gingivalis is the main causative for chronic periodontitis. This secondary colonizer is found to express a plethora of virulence factors involved in colonizing the sub gingival plaque and modulating the immune responses of the host cells. In order to increase survival into the host, P. gingivalis is able to locally invade periodontal tissue, thereby avoiding the immune surveillance while maintaining its viability. (29) Tannerella forsythia T. forsythia has been noted in periodontal health and disease for its fastidious and anaerobic growth requirements for cultural detection. T. forsythia with periodontal and other oral infections has used non cultural approaches. (31) T. forsythia possesses a surface-layer (S-layer) consisting of serrated structural subunits (about 10 nm wide and 10 nm high) in either oblique or tetragonal lattices and it lacks surface appendages such as fimbriae. (13) The S-layer has been shown to be composed of at least two high molecular weight glycoproteins of 220 and 210 kDa size encoded by the tfsA and tfsB genes, respectively (32). They provide a protective shield containing ion-traps and molecular sieves for metabolites in the environment. T.forsythia S-layer has been shown to promote epithelial cell adherence and invasion (33). This might promote multiple species biofilm formation observed between the two species and could lead to disease severity (34).

Hema et al

type I, IV, and V collagens, play a role in adherence and colonization by this microorganism. (39) leucine-rich repeat protein (LrrA) play a role in binding to T. forsythia, but not to P. gingivalis or F. nucleatum, and to mediate binding to epithelial cells of p.gingivalis.(39,40)They are also important for epithelial cell invasion and virulence in a mouse alveolar bone loss model by T. forsythia.(40,41) In both of these species, the leucine-rich repeat proteins are members of the CTD family of proteins that are secreted and attached to the surface by novel mechanisms. (40) HbpA and HbpB are two low iron protein secreted by outer membrane which bind to hemin. These proteins are necessary for efﬁcient iron utilization, although this microorganism has the ability to replace the function of these proteins by accessing a variety of sources of host iron for nutrition (41). Fusobacterium nucleatum F. nucleatum belongs to the family bacteroidaceae. Gram-negative, an anaerobic, spindle-shaped rod that has been recognized as a part of the subgingival microbiota for about 100 years (42, 43). F.nucleatum reacts on an inflammatory response during periodontal disease. Within the gingival epithelium,bacterial biofilm forms at the surface of the tooth containing antimicrobial peptides have a crucial role in the maintenance of periodontal health. Among periodontopathogenic bacteria, all F. nucleatum strains tested and showed the highest sensitivity to hβD-3 and LL37 when compared with those of other bacteria. (44) Campylobacter rectus

Treponemes are members of the Spirochaetes phylum, it is from both Gram-positive and Gram-negative bacteria.T. denticola is one member of the oral treponemes. (35) A large body of experimental evidence supports the importance of the oral treponemes, including T. denticola, in the progression of periodontal diseases.(36)

Campylobacter rectus is a putative gram-negative anaerobic, motile, short and rod bacterium which is associated with several forms of human periodontal disease.(45) The surface layer(S-Layer) and cytotoxic activity have been characterized and thought to be a major virulence factors.This s –layer protein is assumed to be involved in résistance of C.rectus to phagocytic uptake and to bactericidal activity of the serum (46,47).

T. denticola bind to a variety of oral surfaces, including the tooth surface, to extracellular matrix proteins, including laminin, ﬁbronectin, and heparin and host cells, such as human gingival ﬁbroblasts. This adherence likely plays an important role in the localization of many bacteria along the matrix border, in close proximity to membrane proteins and other molecules. (37, 38) The collagen binding proteins of T. denticola bind

These S- layer proteins consists of a single layer, forms regularly arranged structures on the outer surface of various bacteria. They play a role in virulence of several pathogens by rendering the bacteria resistant in killing and providing structure for adherence to host cells. It was reported that the S-layer negative bacteria were more adherent to human gingival fibroblasts than were other starins of C.rectus with intact S-layer (48, 49).

Treponema denticola

Journal of Scientific Dentistry, 8(2), 2018

Microbiological Profile of Chronic and Aggressive Periodontitis- A Review

Bacterial adherence is modified by bacterial cell surface structures called adhisions which recognize specific receptors on the particular host cell surface present on the outer membrane (50).

Microbial Profile Associated with Aggressive Periodontitis Aggressive periodontitis is a disease characterized by a rapid loss of alveolar bone around more than one tooth of the permanent dentition.(14) The amount of destruction is associated with the number of local irritants (15). Aggressive periodontitis which was called as â&#x20AC;&#x153;juvenile periodontitisâ&#x20AC;? is considered to be prevalent in children and adolescents during the circumpubertal period. It is characterized by rapid loss of connective tissue attachment and alveolar bone with familial aggregation. It is caused by both pathogenic microflora and abnormality in host defense mechanisms. Aggressive periodontitis can be subdivided into localized (LAP) and generalized. Actinobacillus actinomycetemcomitans was first isolated from a cervicofacial actinomycotic lesion in and initially designated Bacterium actinomycetemcomitam. (51)

Studies have shown that (Faveri M in 2009) the proportions of Aggregatibacter actinomycetemcomitans were elevated in shallow and intermediate pockets of localized aggressive subjects. Actinobacillus actinomycetemcomitans This is the primary pathogen for aggressive periodontitis, especially in its localized form. Six serotypes of A.a (a, b, c, d, e, and f) are described based on the composition of O polysaccharide of their lipopolysaccharide and there are phenotypically nonserotypeable strains of A.a which lack expression of serotype-specific polysaccharideantigen.(52) A highly leukotoxic clonal type of A. A serotype b was first isolated, in the early 1980s, from an 8-year-old male child with localized aggressive periodontitis. A significant feature of A.Actinomycetemcomitans is its surface ultrastructure which includes fimbriae, vesicles, and extracellular amorphous material. (53, 54) A prominent feature of the surface of A. actinomycetemcomitans is vesicles. These structures, which are lipopolysaccharide in nature, originate from

Hema et al

and are continuous with the outer membrane. Vesicles are also released into the external environment in large numbers. (56) Virulence factors are attributes of a microorganism that enable it to colonize a particular niche in its host, overcome the host defenses and initiate a disease process. These factors frequently involve the ability to be transmitted to susceptible hosts. The virulence of A.a has strong assocation with periodontal diseases and related extra oral infections. Many of these virulence factors may be involved in the pathogenesis of periodontitis (55). In most cases, adhesions are proteinaceous structures found on the surface of the bacterial cell (56). The adhesion of A. actinomycetemcomitans to the gingival crevice epithelium helps in the colonization of this organism and destruction associated with periodontal disease. A. actinomycetemcomitans strains that have been tested adhere strongly to epithelial cells (57). LPS causes enormous destruction to host cells and tissues leading to periodontal disease. it was found that the prevalence of A.a was less in patients with LAP whereas elevated levels of P.g, Tannerella forsythia, T.denticola, P.intermedia, and Campylobacterrectus for detection of microorganisms in subgingival using polymerixzation chain reaction(pcr)( Takeuchi) .

Summary and Conclusion However, it is clear that chronic and aggressive forms of periodontitis are not monoinfections. Periodontal disease occurs when there is a disruption in the host microbe homeostasis associated with health. Comparisons of the microbiology of chronic and generalized aggressive forms of periodontitis are in the early phases. It is clear that chronic and generalized aggressive periodontitis are not only caused by gramnegative anaerobic infections, but are also caused by gram-positive bacteria and even non-bacterial microbes from the Archaea domain. Studies have suggested that individuals with generalized aggressive periodontitis have higher subgingival levels of Selenomonas sp. and T. lecithinolyticum compared to patients with chronic periodontitis. However, more microbiological data could be generated by combined culture and culture-independent methods from patients with unambiguously deďŹ ned cases of generalized aggressive periodontitis or chronic periodontitis.

Journal of Scientific Dentistry, 8(2), 2018

Microbiological Profile of Chronic and Aggressive Periodontitis- A Review

Hema et al

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23. Hajishengallis, G., Darveau, R. P., and Curtis, M. A. The keystonepathogen hypothesis. Nat. Rev. Microbiol. 2012; 10, 717–725. 24. Van Steenbergen, T. J., Delemarre, F. G., Namavar, F., and De Graaff, J. Differences in virulence within the species Bacteroides gingivalis. Antonie Van Leeuwenhoek 1987; 53:233–244. 25. Travis, J., Pike, R., Imamura, T., and Potempa, J. Porphyromonas gingivalis proteinases as virulence factors in the development of periodontitis. J. Periodontal. Res. 1997; 32, 120–125. 26. Andrian E, Grenier D, and Rouabhia M. In vitro models of tissue penetration and destruction by Porphyromonas gingivalis. Infect. Immun. 2004; 72: 4689–4698. 27. Dubin G, Koziel J, Pyrc K, Wladyka B, and Potempa J. Bacterial proteases in disease–role in intracellular survival, evasion of coagulation/fibrinolysis innate defenses, toxicoses and viral infections. Curr. Pharm. Des. 2013; 19, 1090–1113. 28. Potempa J, Banbula A, and Travis J. Role of bacterial proteinases in matrix destruction and modulation of host responses. Periodontol 2000.2012; 153–19. 29. Hajishengallis G, Abe T, Maekawa T, Hajishengallis E, and Lambris J. D. Role of complement in host–microbe homeostasis of the periodontium. Semin. Immunol. 2013; 25, 65–72. 30. Nikaido H. Molecular basis of bacterial outer membrane permeability revisited. Microbiol. Mol. Biol. Rev. 2003; 67: 593–656. 31. Dzink JL, Tanner AC, Haffajee AD, Socransky SS. Gram negative species associated with active destructive periodontal lesions. J Clin Periodontol 1985; 12: 648–659. 32. Lee SW, Sabet M, Um HS, Yang J, Kim HC, Zhu W. Identification and characterization of the genes encoding a unique surface layer of Tannerella forsythia. Gene. 2006; 371:102–111 33. Sharma A, Inagaki S, Sigurdson W, Kuramitsu HK. Synergy between Tannerella forsythia and Fusobacterium nucleatum in biofilm formation. Oral Microbiol Immunol. 2005; 20:39–42 34. Sharma A, Sojar HT, Glurich I, Honma K, Kuramitsu HK, Genco RJ. Cloning, expression, and sequencing of a cell surface antigen containing a leucine-rich repeat motif from Bacteroides forsythus ATCC 43037. Infect Immun. 1998; 66:5703–5710. 35. Grenier D. Characterization of the trypsin-like activity of Bacteroides forsythus. Microbiology 1995: 141: 921–926. 36. Cimasoni G, McBride BC. Adherence of Treponema denticola to modified hydroxyapatite. J Dent Res. 1987; 66:1727–1729. 37. Haapasalo M, Muller KH, Uitto VJ, Leung WK, McBride BC. Characterization, cloning, and binding properties of the major 53-kilodalton Treponema denticola surface antigen. Infect Immun. 1992; 60: 2058–2065.

Microbiological Profile of Chronic and Aggressive Periodontitis- A Review 38. Li M, Liu Z, Umemoto T. Collagen-binding proteins of human oral spirochetes. Zhonghua Kuo Qiang Yi Xue Za Zhi 1999: 34: 165–167. 39. Ikegami A, Honma K, Sharma A, Kuramitsu HK. Multiple functions of the leucine-rich repeat protein LrrA of Treponema denticola. Infect Immun. 2004; 72:4619-4627. 40. Rosen G, Genzler T, Sela MN.Coaggregation of Treponema denticola with Porphyromonas gingivalis and Fusobacterium nucleatum is mediated by the major outer sheath protein of Treponema denticola. FEMS Microbiol Lett. 2008; 289:59-66. 41. Hofstad T. The genus Fusobacterium, In M. P. Starr, H. Stolp, H. G. Tru¨per, A. Balows, and H. G. Schlegel., the procaryotes. A handbook on habitats, isolation, and identiﬁcation of bacteria. 1981. Springer Verlag p. 1464–1467. 42. Moore, W. E. C., L. V. Holdeman, and R. W. Kelley. Genus II. Fusobacterium Knorr 1922, In N. R. Krieg and J. G. Holt (ed.), Bergey’s manual of systematic bacteriology. 1984 vol. 14 A, p. 631–637. 43. Dzink JL, Tanner ACR, Haffajee AD, Socransky SS. Gram negative species associated with active destructive periodontal lesions. J Clin Periodontol. 1985; 12: 648-659 44. Kolenbrander PE. Oral microbial communities: biofilms, interactions, and genetic systems. Annu Rev Microbiol. 2000; 54: 413-37. 45. Vandamme P, falson E, Rossau R et al revision of camphylobacter, helicobacter, and wolinella taxonomy: emendation of generic descriptions and proposal of arcobacter gen. nov. int J syst bacteriod. 1991;41(1): 88-103. 46. Dzink JL. Socranskey SS. Haffajee AD,the predominant cultivable microbiota of active and inactive lesions of destructive periodontal disesases. J clin periodontal. 1988:15(5); 316-323.

Address of Correspondence

Hema P, Final year postgraduate, Department of Periodontology, Indira Gandhi Institute of Dental Sciences, Email id: hemaselvamp@gmail.com Phone no: +91 94428 04426

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47. Rams TE, Feik D, Slots J. campylobacter rectus in human periodontitis. Oral microbiol immunol. 1993; 8(4): 230-235. 48. Beveridge TJ, Pouwels PH, Sara M.et al. Functions of S-layer. FEMS Microbiol Rev. 1997; 20: (1-2)99-149. 49. Nitta H, Holt SC, Ebersole JL,. Purification and characterization of campylobacter rectus surface layer protein. Infect Immun. 1997;65(2): 478-483. 50. Pei ZH, Ellison RT, 3rd, Blaster MJ. Identification, purification, and characterization of major antigenic proteins of campylobacter jejuni. J boil chem. 1991; 266(25): 16363-16369. 51. Zambon JJ. Actinobacillus actinomycetemcomitans in human periodontal disease. J Clin Periodontol. l985; 12: 1-20. 52. Meyer DH, Fives-Taylor PM. Characteristics of adherence of Actinobacillus actinornyceterncomitans to epithelial cells. Infect Immun. 1994; 62: 928-935. 53. Holt SC, Tanner AC, Socransky SS. Morphology and ultrastructure of oral strains of Actinobacillus actinomycetemcomitans and Haemophilus aphrophilus. Infect Immun. 1980; 30: 588-800. 54. Holt SC, Tanner AC, Socransky SS. Morphology and ultrastructure of oral strains of Actinobacillus actinomycetem comitans and Haemophilus aphrophilus. Infect Immun.1980; 30: 588-800. 55. Fives-Taylor P, Meyer D, Mintz K. Characteristics of actinobacillus actinomycetemcomitans invasion of and adhesion to cultured epithelial cells. Adv Dent Res. 1995; 9: 55-62. 56. Rosan B, Slots J, Lamont RJ, Listgarten MA, Nelson GM. Actinobacillus actinornyceterncornitans fimbriae. Oral Microbiol Immunol. 1988; 3: 58-63. 57. Meyer DH, Fives-Taylor PM. Characteristics of adherence of Actinobacillus actinornyceterncomitans to epithelial cells. Infect Immun. 1994; 62: 928-935.

Authors Final year postgraduate, Department of periodontology, Indira Gandhi Institute of Dental Sciences. 1,5,6

Professor& Head, Department of Periodontology, Indira Gandhi Institute of Dental Sciences.

3,4 Final year postgraduate, Department of Endodontics and concervative , Indira Gandhi Institute of Dental Sciences.

How to cite this article : H ema P, Dr.Saravanakumar R, Shahinas begum.B, Nandini Dimple, Vinoth kumar B.Na, Sivaranjani KS. Microbiological Profile of Chronic and Aggressive Periodontitis- A Review. Journal of Scientific Dentistry 2018;8(2):41-6 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

XP-endo Shaper : One File Shaper System Limly Bal T1, Dhanavel Chakravarthy2, Padmaraj. S N3 ABSTRACT XP-endo Shaper is a truly innovative shaping instrument which can be used to radically simplify endodontic sequences. The unique feature of this file is its 3D canal shaping ability and less invasive cleaning and shaping procedures. The XP-endo Shaper is the instrument of choice for the treatment of complex canal configurations. It is the latest addition to the XP-endo range. It is a One File Shaper system.

Introduction The need for an excellent 3D canal cleaning and minimal invasive treatments has led to the development of XP-endo Shaper. It is introduced by FKG Swiss endo. It is a single file for complete shaping. The MaxWire and Booster Tip techniques combined together for the excellent features of XP-endo Shaper. The ISO diameter changes from 15 to 30 during cleaning and shaping procedures of root canal. Using only one instrument, it does the canal shaping of minimum 30/.04 (1) Characteristic features of XP-endo Shaper: It has an ISO No 30 and is intended for single use only. The optimal speed ranges from 800-1000 rpm. It is available in 21 mm, 25 mm and 31 mm. It has a minimum taper of 4 %. It is available in 3 files and 4 files sequences.

XP-endo Shaper sequences It consist of 4 and 3 file sequences. The first system known as XP-endo Shaper Plus sequence consist of K File (10 and 15), XP-endo Shaper and XP-endo Finisher. It is used for comprehensive treatment, from glide path to canal cleaning, as well as excellent shaping respectively. The 3 file system consist of K File (10 & 15) and XP-endo Shaper. It is used for glide path, and shaping respectively. Dentists use varieties of NiTi files. XP-endo Shaper (XP), Protaper Gold (PTG), Self-adjusting file (SAF) are extensively used for cleaning and shaping of root canals. Due to excessive instrumentation during chemomechanical preparation, microcracks occurs on the dentin. Based on the usage of the above-mentioned files, it does not create microcracks. Vertical root fracture

Journal of Scientific Dentistry, 8(2), 2018

occurs in many root canal treated teeth. It may lead to loss of tooth structure.(2, 3) Over instrumentation also results in the formation of craze lines. Due to the continuous masticatory forces, it results in the vertical root fracture (2, 4). Presently announced files known as the XP-endoShaper (XP)(FKGDentaire,LaChaux-de-Fonds,Switzerland) has a rotary NiTi snake shaped instrument. The file has an initial taper of .01 in its M phase when it is cooled. The taper of the file varies to 0.04, when it is exposed to 35ยบC. If the file is used separately, it has a minimum canal preparation of 30/.04. The pressure that is applied on the dentin is extremely less by XP. This feature helps in the significant reduction of microcracks. It is the best file system which can be used in complex canals due to its high flexibility. Cyclic fatigue is relatively lesser in this file system(5). XP has a unique feature of 3-dimensional cleaning and shaping. It helps in the complete chemomechanical preparation in the complex canals. It is made up of NiTi MaxWire (Martensite-Austenite). The unique feature of this alloy is that it provides excellent flexibility. (5) The defects in dentin triggered by the NiTi file systems which ranges between (4%-80%) (3, 6-8). when the percentage of taper increases, it results in the higher incidence of dentinal defects. It occurs due to the stress on the canal walls. None of the literature has mentioned about the crack formation in dentin due to the usage of XP. The design of XP results in increased flexibility during high rotational speed (i.e., 800 rpm). (6) The excellent flexibility of XP results in prevention of microcracks in dentin due to the heat treated NiTi instruments. This feature differentiates XP from the traditional NiTi file systems. 47

XP Endo Shaper- One File Shaper System

References 1. Melik et al. Effect of ProTaper Gold, Self-Adjusting File, and XP-endo Shaper Instruments on Dentinal Microcrack Formation: A Micro–computed Tomographic Study. JOE 2017; 43:7 2. Versiani M, Souza E, De-Deus G. Critical appraisal of studies on dentinal radicular microcracks in endodontics: methodological issues, contemporary concepts, and future perspectives. Endod Topics 2015; 33:87–156. 3. Karatas E, Gunduz HA, Kirici DO, Arslan H. Incidence of dentinal cracks after root canal preparation with ProTaper Gold, Profile Vortex, F360, Reciproc and ProTaper Universal instruments. Int Endod J 2015; 3:12541.

Limly Bal et al 5. FKG XP-endo Shaper. Available at: http://www.fkg.ch/sites/ default/files/201607_ fkg_xps_brochure_en_web.pdf. Accessed October 25, 2016. 6. Bier CA, Shemesh H, Tanomaru-Filho M, et al. The ability of different nickel-titanium rotary instruments to induce dentinal damage during canal preparation. J Endod 2009; 35:236–8. 7. Abou E, Nasr HM, Abd E, Kader KG. Dentinal damage and fracture resistance of oval roots prepared with single-file systems using different kinematics. J Endod 2014;40: 849–51. 8. Ustun Y, Topcuoglu HS, Duzgun S, Kesim B. The effect of reciprocation versu rotational movement on the incidence of root defects during retreatment procedures. Int Endod J 2015; 48:952–8.

4. Yoldas O, Yilmaz S, Atakan G, et al. Dentinal microcrack formation during root canal preparations by different NiTi rotary instruments and the self-adjusting file. J Endod 2012; 38:232–5.

Address of Correspondence

Limly Bal. T, Final year postgraduate, Department of Conservative Dentistry and Endodontics, Indira Gandhi Institute of Dental Sciences, Email id: drlimlybal@gmail.com Phone no: +91-9500573031

Authors Post graduate, Department of Conservative Dentistry and Endodontics, Indira Gandhi Institute of Dental Sciences.

Professor & Head, Department of Conservative Dentistry and Endodontics, Indira Gandhi Institute of Dental Sciences.

Reader, Department of Conservative Dentistry and Endodontics, Indira Gandhi Institute of Dental Sciences.

How to cite this article : L imly Bal T, Dr. Dhanavel Chakravarthy, Dr. Padmaraj. S N. XP-endo Shaper : One File Shaper System. Journal of Scientific Dentistry 2018;8(2):47-8 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

Relevance of C- reactive protein (CRP) and other inflammatory markers as valuable tool in oral and systemic diseases N. Chitra1, A. Santhadevy2, K. R. Premlal3, Selvaraj Stephen4 ABSTRACT Oral and systemic infections are posing crucial and overwhelming problems to the individuals. Inflammation has been found to play a vital role in the pathogenesis of various oral and systemic diseases such as gingivitis, periodontitis, cardiovascular diseases, atherosclerosis, cerebrovascular ischemia, preeclampsia etc. Hence it is essential to be aware of the existing disease, careful identification of the etiological factors and diagnosis, treatment and regular follow up. Once inflammation is triggered, within few hours, a group of diverse proteins termed as acute phase proteins are synthesized by the liver and excreted into circulation as a host defense and adaptive response which is termed as acute phase response. These proteins serve as inflammatory markers and measurement of these help in identifying the status of the underlying infection.

Introduction Acute phase proteins include various proteins such as CRP, hsCRP, fibrinogen, ferritin, serum amyloid protein A, alpha-1 antichymotrypsin, alpha -1 antitrypsin, haptoglobulin, alpha â&#x20AC;&#x201C; acid glycoprotein, ceruloplasmin and C3 and C4. CRP is the most widely used protein in clinical practice. Other proteins are being used mainly for research purposes. The limitations for their application in routine practice could be attributed to the complexity in estimation, varying ranges among the population and prolonged plasma half life.(1,2) CRP has a wide range of advantages as it exhibits immediate intensified response and declines sharply reflecting the exact inflammatory status and the values remain unaffected by the other components in blood and collected samples can be stored and evaluated at a later date effectively.(3) hsCRP(high sensitive CRP) is also an analyte in measuring inflammatory levels owing to its efficiency in detecting even traces of CRP, even below 0.3mg/dL, detecting low-grade inflammation. (4-6) . Various acute and chronic inflammatory conditions such as infections, rheumatoid arthritis, and cancers could cause release of interleukin-6 and other cytokines that can trigger the elevated levels of CRP and hs-CRP.(5) The advantages of using hsCRP has been attributed to its accuracy of measurement, easy availability, its usage in various oral and systemic infections as periodontitis, cardiovascular diseases, stroke, myocardial infarction etc. (4-6) Journal of Scientific Dentistry, 8(2), 2018

In a study conducted in a private institution to assess the inflammatory status among preeclamptic pregnant women using CRP in the serum of these individuals, it was found that CRP level was elevated in individuals with moderate periodontitis when compared to those with mild periodontitis. It was also found that these individuals showed increase in dental caries when compared to the others with mild periodontitis. There are studies relating the association of increase in CRP with periodontitis, dental caries and preeclampsia. But there are are no studies associating the existence of all these components together. Since hsCRP is capable of detecting even trace amounts of CRP, even less than 0.3mg/dL, it could be of much use in identifying the inflammatory status in preeclamptic patients. Preeclampsia is a life threatening disorder of pregnancy causing both foetal as well as maternal complication such as still birth, low birth weight, foeto maternal death etc. It could be triggered by inflammatory conditions as periodontitis and vice versa since preeclampsia could also stimulate periodontitis and the exact cause for this still remains unclear..

Conclusion: Obstetrics care for women does not involve oral cavity examination including dental caries and periodontal examination. In addition to this, there are limited studies available regarding the association of dental caries and periodontitis in preeclamptic pregnant women. Hence it would be an eye opener as well as could help many individuals in enabling them to know about their disease 49

Relevance of C- reactive protein (CRP) and other inflammatory markers as valuable tool in oral and systemic diseases:

status at the earliest , whereby proper monitoring of the disease status could be done which could avoid many foetal and maternal complications. Repeat CRP or sequential CRP estimations are of diagnostic value rather than single CRP estimation. Neonatal sepsis is one important condition where fall in CRP levels (to the baseline) is indicative of successful response to therapy and good prognosis. More studies are required to compare CRP and hsCRP to arrive at a proper conclusion.

References 1. Kilicarslan A, Uysal A, Roach E C. Acute phase reactants. Acta Medica. 2013;2:2-7.

Santhadevy et al

3. Hansson L O, et al. Measurement of C-reactive protein and the erythrocyte sedimentation rate in general practice. Scand J Prim health Care.1995;13:39-45. 4. Knight M L. The Application of High-Sensitivity C-Reactive Protein in Clinical Practice: A 2015 Update. US Pharm. 2015;40(2):50-53. 5. Bennet N R.et al. High-sensitivity C-reactive protein is related to central obesity and the number of metabolic syndrome components in Jamaican young adults. Front. Cardiovasc. Med. 2014;16. 6. Kim J, Pyo S, Yoon D W, Lee S, Lim J Y, Heo J S, et al. (2018) The co-existence of elevated high sensitivity C-reactive protein and homocysteine levels is associated with increased risk of metabolic syndrome: A 6-year follow-up study. PLOS ONE.2018; 13(10): e0206157.

2. Chia-Siu Wang, Chien-Feng Sun. C-reactive Protein and Malignancy: Clinico-pathological Association and Therapeutic Implication. Chang Gung Med J. 2009;32(5):471-482.

Address of Correspondence

A.Santhadevy, Professor and Head Department of Oral Pathology and Microbiology, Indira Gandhi Institute of Dental Sciences, Email id: drsantha73@gmail.com Phone no: +91 9443634624

Authors Post Graduate, Department of Oral Pathology and Microbiology, Indira Gandhi Institute of Dental Sciences.

Professor and Head, Oral Pathology and Microbiology, Indira Gandhi Institute of Dental Sciences.

Reader of Oral Pathology and Microbiology, Indira Gandhi Institute of Dental Sciences.

Professor of Microbiology, Mahatma Gandhi Medical college and Research Institute.

How to cite this article : N . Chitra, A. Santhadevy, K. R. Premlal, Selvaraj Stephen. Relevance of C- reactive protein (CRP) and other inflammatory markers as valuable tool in oral and systemic diseases. Journal of Scientific Dentistry 2018;8(2):49-50 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

Self-Ligating Brackets in Orthodontics- A Narrative Review Lijin James1, U B Rajasekaran2, Aniruddh Yashwant.V3, Lidhiya Alexander4, Helen Rachel Xavier5, Basil Joseph6

ABSTRACT Self-ligating brackets are a ligature less brackets system that has a mechanical device incorporated with the brackets to close off the slot. The idea of Self-ligating brackets was not new to orthodontics. It was existing for shockingly lengthy time-frame in orthodontics. Russell lock edgewise attachment being depicted by Dr Jacob Stoltenberg in 1935. More up to date structures of these brackets have on seemed even today. This proceeded with prevalence of self-ligating brackets has pulled in excess of a little level of brackets producers, deals and clients. This narrative review focuses on the different structures, rationalities and movement of self-ligating brackets. Key words: Self ligating, Active, Passive, Interactive, Time, Speed.

Introduction The information of self-ligating brackets has interested and captivated the orthodontist since the season of Edward Point.1 The asserted advantages relate on a fundamental level to each self-ligating brackets, while the distinction may fluctuate in their office to convey these favourable circumstances continually.2 A secure passive or active ligation mechanism that ensures predictable full brackets engagement, decreased friction between the arch wire and the brackets that permits progressively quick tooth movement, great control of tooth position through a sufficiently dimensioned brackets, less chair side time, quicker arch wire removal and ligation.3 These improvements offer the likelihood of a significant decrease in normal treatment span and in anchorage necessities especially in cases requiring extensive tooth movements.4 This survey focuses on the different Designs, methods of insight and advancement of self-ligating brackets.5

Properties The idea that brackets are ligated by means of tie wings has been prevalent to the point that it is profitable considering a list of ideal properties of any ligation system. Ligation must to be secure and robust, ensure full brackets engagement of the arch wire, display low friction among brackets and arch wire, fast and simple to use, allow simple attachment of elastic chain, assist good oral cleanliness, and delightful for the patient.6

Journal of Scientific Dentistry, 8(2), 2018

Regularly Proposed confines of Conventional Ligation are inability to give and keep up full arch wire engagement brought about poor control of tooth movement, frictional qualities are expanded, for elastomeric module, inferable from force decay tooth control was not ideal, both wire and elastomeric ligatures some of the time are dislodged, oral cleanliness was conceivably hindered and wire ligation was a time consuming procedure.7 (Table 1)

Definition A self-ligating bracket is defined as “a bracket, which utilizes a permanently installed, movable component to entrap the arch wire”.8 A self-ligating bracket is “a ligature-less system with a mechanical device built in to close off the edgewise slot”.9 “Brackets with a mechanism to clip on to the arch wire so that no additional ligature’s required. The arch wire slides more freely through such brackets, possibly making tooth movement easier”.10

Philosophy Light forces are key to self-ligation. Defenders propose that low force, low-friction systems enable teeth to venture out to their physiologic position since they don't overwhelm the musculature or giveaway the periodontal tissues. Ischemia isn't actuated in the encircling periodontal tissues on the grounds that the forces created by the small dimension, modern arch wires are excessively low to totally block the periodontal vascular supply. Substantial 51

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forces on teeth cause hyalinization in the periodontal ligament field which conveys tooth movement to a stop.11

with both active and passive elements known as interactive.15 It was presented by American Orthodontics (Time brackets). This brackets system and its mode of function seemed to consolidate all of the desirable features that were inadequate in the systems, for example, minimal force and friction (passive) in the beginning time of treatment, torque and rotation all control (active) in the middle and completing phases of treatment. Low profile (low inout relationships), easy to open-close clip system for simplicity of wire changes and ability to accomplish completing details in a controlled manner in all three planes of space. (Figure 1.4)

Classification There are three sorts of self-ligating brackets system, Active, passive & interactive being used in contemporary orthodontic practices. Systems that are totally passive through all phases of treatment, Systems that are totally active all through all phases of treatment, Systems that are Interactive, that is, they can display either passive or active properties throughout any phase of treatment at the carefulness and course of the clinician.12

Active Self-ligating brackets have an flexible segment to hold the arch wire. This flexible segment compels the arch wire slot and can store and subsequently release energy through elastic deformation. (Table 2) This delicate activity gives a light however continuous level of force on the tooth and its supporting structures, bringing about exact and controlled movement.13 (Figure 1.1) Passive self-ligating brackets use an rigid, movable segment to hold the arch wire. The passive self-ligating brackets have two designs Passive self-ligated brackets with rigid slide (Figure 1.2) and Examples of passive self-ligated brackets with integral “C” clip over the years.14 (Figure 1.3), (Table 3 & 4)

Evolution of Self- ligating brackets The Russell attachment was the first self-ligating brackets was introduced and designed by Dr Jacob Stoltenberg in 1935 who was an orthodontic pioneer in New York.16 This brackets contains a flat-head screw fitted in a round, threaded opening in the surface of the brackets. This alteration in the arch wire supports the orthodontists in simple and quick. The horizontal screw might be adjusted using a simple watch repair screw driver to achieve the required movement of tooth. Unfortunately, this design was not accomplished the correct acknowledgment nearly and completely cleared out from the market. (Figure 2.5)

The one of the fundamental defining moment in self-ligating is the hybrid self-ligating brackets

In 1972, Dr. Jim Wildman of Eugene, Oregon, built up the Edge lock brackets, which had a round body with a rigid labial sliding top.17

Figure 1: 1. Active Self Ligating Brackets. 2. Passive Self Ligating brackets with rigid slide. 3. Passive Self Ligating brackets with “C” clip. 4. Interactive Brackets.

Figure 2: 5. Russell attachment 6. Edge lock 7. Mobillock 8. Speed 9. Time 10. Twin lock 11. Damon 2 12. Damon 3MX 13. In-Ovation R

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A special opening tool was used to move the slide occlusally for arch wire insertion. At the point when the cap was close over the arch wire with finger pressure, the brackets slot was changed converted to a tube. The rigid nature of this external fourth wall rendered the brackets "passive" in its interplay with the arch wire. The Edgelok was the first selfligating brackets, and the first to appreciate any kind of business achievement. (Figure 2.6)

alone; when close, the rigid external mass of the mobile arm changed over the bracket slot into a tube.

A comparative bracket, found out by Dr. Franz Sander of Ulm, Germany, was presented two years after the fact. The Mobil-lock in 1980 required a special tool to rotate the semi-circular labial disk away from any detectable hindrance or close position.18 Likewise with the Edgelok, the passive changed the brackets slot into a cylinder that inexactly contained the arch wire. Maybe as a result of the synchronous presentation of elastomeric ligatures, nonetheless, neither the Edgelok nor the Mobil-lock gained much of popularity. (Figure 2.7) At about a similar time, Dr. Herbert Hanson of Hamilton, Ontario, was making models of selfligating brackets that by 1980 turned into the basic speed design. The Speed Brackets highlights a curved, flexible "Super-Flexible Spring Clip" that wraps occlusogingivally around a scale down brackets body.19 The clip is moved occlusally utilizing either a universal scaler at the gingival part of the brackets body or a curved explorer inserted into the labial window to allow arch wire placement, at that point situated gingival with finger pressure. (Figure 2.8) The Spring clip, through elastic deformation, carefully imparts a light continuous level of force on the arch wire, resulting exact and controlled tooth development. Hanson depicts this as the "homing movement of the spring" the capacity of the speed brackets to reorient itself three-dimensionally until the arch wire is totally placed in the slot. Any ensuing pivot, tipping, or torqueing, amid the tooth development of any sort, results in a labial avoidance of the spring that reactivates this homing behaviour.18 In 1986, Self- ligating Activa Brackets in 1986, planned by Dr. Erwin Pletcher, offered another option. The Activa brackets had a rigid, curved arm that turned occluso gingivally around the cylindrical brackets body.20 The arm could be moved into a "slot open" or "slot close" position with finger pressure Journal of Scientific Dentistry, 8(2), 2018

In 1994, another self-ligating model entered the commercial centre. Structured by Dr. Wolfgang Heiser of Innsbruck, Austria, Time brackets is comparable in appearance to the SPEED brackets however its design and method of activity are fundamentally different.21 A special instrument is used to pivot the arm gingivally into the slot open position or occlusally into the opening close position. The stiffness of the brackets arm keeps any significant interaction with the arch wire, subsequently rendering Time a passive bracket. (Figure 2.9) The Twin Lock brackets, a second undertaking by Dr. Jim Wildman, were presented in 1998. Its level, rectangular slide, housed between the tie wings of an edgewise twin brackets, is moved occlusally into the slot open position with a universal scaler.18 It then slides gingivally with finger pressure to hold the arch wire in an passive arrangement. Comparative self-ligating brackets plans were presented in 1996 and 1999 by Dr. Dwight Damon of Spokane, Washington. (Figure 2.10) Damon SL brackets Damon SL brackets ("An" Organization, San Diego, CA;) likewise wound up accessible in the mid-1990s and had a slide that folded over the labial surface of the brackets. A micro U-shaped wire spring lay under the slide and clicked into the two labial "bulges" on the slide to give positive open and close position These brackets were a positive advance forward, however endured two huge issuesâ&#x20AC;&#x201D;the slides some of the time opened unintentionally and they were inclined to breakage. By and by, these brackets produced a considerable increment in the valuation for the capability of selfligation.22 Damon 2 brackets in 2000 (Ormco Corp.) were acquainted with location the defects of Damon SL. They held a similar vertical slide activity and U-shaped spring to control opening and closing, yet set the slide inside the safe house of the tie wings.22 Joined with the introduction of metal injection moulding assembling, which allows nearer resiliences, these improvements totally wiped out unintentional slide opening or slide breakage and prompted a further increasing speed in the utilization of self-ligation. (Figure 2.11)

Self-Ligating Brackets in Orthodontics- A Narrative Review

Lijin James et al

Damon 3 and Damon 3 MX brackets in 2004 (Ormco Corp.) Have an alternate area and activity of the holding spring, and this has delivered a simple and secure system for opening and closeting. What's more, Damon 3 brackets are semi-esthetic. Be that as it may, early creation Damon 3 brackets endured three critical issues: a high rate of bond failure, partition of metal from reinforced resin components and broken tie wings.22 This was presumably because of the incredibly expanded valuation for what selfligation could do and furthermore to the more prominent ability of makers to put resources into discovering solutions. (Figure 2.12)

Smart clip - In 2004, 3M Unitek presented the Smart Clipâ&#x201E;˘ self-ligating brackets, which is not the same as other self-ligating brackets in that it doesn't have a slide or clip to hold the wires.25 Rather it contains a nickel-titanium cut on each side of the twin brackets that secures in the wire. The arch wire is embedded by utilizing finger pressure to push it past the flexible clip. This requires a specially designed instrument from 3M Unitekâ&#x201E;˘. (Figure 3.16)

GAC In-Ovation brackets - These are fundamentally the same as the SPEED brackets in origination and configuration, however are of a twin design.18 They are a decent, hearty structure, and no breakage of the clips has been actually experienced or revealed. Some moderately minor burdens in brackets dealing with are clear. In the first place, a few brackets are difficult to open. In 2002, littler brackets for the front teeth ended up accessible In-Ovation R (Reduced). This smaller width is exceptionally welcome as far as more prominent between brackets length, In-Ovation brackets have an active clip.18 (Figure 2.13) Lingual Self- ligating Brackets In-Ovation L In-ovation C (Ceramic) is presently accessible with incomplete ceramic face for better esthetics.23 (Figure 3.14) Philippe self-ligating brackets was presented in 2002 by Aldo Macchi.24 These brackets can be bonded directly to the lingual tooth surfaces. These brackets do not have slots, just first and second request movements are conceivable. Four sorts of Philippe brackets are available: A standard medium twin (routinely use), a narrow single-wing brackets (lower incisors), a huge twin, and A three-wing brackets for the attachment of intermaxillary elastics and utilization of basic third order movements. These brackets wings are opened with a Haideman spatula. Brackets are close with a Weingart utility plier. (Figure 3.15)

Phantom is a polychromic self-ligating bracket which was additionally presented at the ESLO congress in Venice, June 2006. These brackets are bonded directly in the mouth after arrangement of the lingual surfaces of the teeth by reshaping and filling all inconsistencies with flowable composite.18 Opal (Ultradent)- The Opal brackets is an aloof brackets which was made in year 2004. It comprises of a translucent fibre-reinforced composite polymer. It has a smooth and adjusted one-piece design with an incorporated lid mechanism for self-ligation. Opening occurs with a special instrument from the incisal direction.18 The Opal brackets are smooth and delicate on the delicate tissues and initially it was very esthetics. It is sensibly simple to position and has simple to peruse, great markings. Cleaning of the brackets is best embraced by a hygienist or other dental human services proficient. The bracket stains effectively. Opal M (Ultradent)- The Opal M brackets is a passive brackets and is delivered utilizing the metal injection moulding system (MIM) and was produced Figure 3: 14. In-Ovation C, 15. Philippe Brackets 16. Smart clip 17. Bio-Quick 18. Clarity SL 19. Alias

Oyster Self-ligating Brackets was the first translucent self-ligating Brackets which was presented in 2003. It was produced using a Strong fibre glass reinforced Polymer. Cap can be evacuated and put once more. Mushroom hook for auxiliary attachments.18 54

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Table 1 Self-Ligated Brackets vs Conventionally Ligated Bracket. Parameters Esthetics Force Level Force Delivery Friction Infection Control Instrumentation Ligation Ligation Stability Office Visits Oral Hygiene Patient Comfort Sliding Mechanics Treatment Time

Self-Ligated Some designs permits significant miniaturization Permits use of lighter forces Light initial force

Conventionally Ligated Limited miniaturization Requires heavier force levels High initial force Stainless steel: High

Predictable, very low Significantly reduced risk of percutaneous injury Fewer instruments required during arch wire changes Movable, integral component creates outer fourth wall Retains original form throughout treatment Shorter, less frequent visits Wingless designs easy to clean Only slight discomfort with wire Changes Ideally suited for efficient tooth translation Overall treatment reduced by about four months

Table 2. The following are active self-ligating brackets.

Active self-ligating brackets Wall she in

1962

Speed

1973

Time

1994

In-Ovation

2000

Evolution LT

2002

In-Ovation R

2002

Table 3. Examples of passive self-ligating brackets with rigid slide over the years.

Passive self-ligating brackets with rigid slide Boyd and Richardson

1933

Laskin

1945

Johnson

1954

Rubin & Rubin

1963

Brunson & Davis

1966

Edgelok

1973

Journal of Scientific Dentistry, 8(2), 2018

Elastomeric: Very high Increased risk of percutaneous Injury Many instruments required during arch wire changes Stainless steel or elastomeric Ligatures Loses initial shape and tightness Longer, more frequent visits Difficult to clean—food traps Teeth usually sore after Ligation Slow due to binding of arch wire Longer, especially in extraction cases.

Mobil lock

1974

Foerster

1980

Activa

1986

Damon SL 1

1997

Twinlock

1997

Damon 2

1999

Opal

2004

Oyster

2004

Damon 3

2005

Table 4. Examples of passive brackets with integral “C” clips over the years Passive brackets with integral “C” clips Brusse and goddard

1941

Kesling

1959

Brader

1967

Fogel and magill

1989

Smart clip

2004

Self-Ligating Brackets in Orthodontics- A Narrative Review

Lijin James et al

in 2006. The moulding is trailed by sintering.12 The brackets are smooth, as the edges are pleasantly adjusted, and it has a "lid" that covers the opening. Opening is from the incisal, utilizing a uniquely structured instrument.

procedure, and treatment objectives. A few inquiries are moderately simple to research. Others are progressively hard to measure, yet are drawing in a lot nearer and increasingly able consideration on the grounds that their clinical significance is a lot more significant.

Bio Quick LP (Forestadent)- The Quick brackets is a functioning brackets. It is a one-piece design using metal injection shaping (MIM), trailed by sintering. The elastic clip is produced using chromium– molybdenum composite. This brackets can be opened with an exceptionally structured instrument either from the gingival or labial viewpoints.14 The clip instrument is anything but difficult to work. The problems of these brackets are esthetic; likewise with every metal bracket, it may not meet patients’ highest necessities. (Figure 3.17)

Abbreviations

Clarity SL (3M Unitek) - The clarity SL brackets is a passive system that comprises of a ceramic body and was produced in year 2007. This has a metal slot joined in the ceramic base to improve the frictional attributes. As in the Smart Clip brackets,18 the selfligating mechanism comprises of a NiTi cut that is fixed to the mesial and distal parts of the twin brackets. Special tools are accessible for inseting and removing arch-wires. (Figure 3.18) Recent advances of Self- ligating brackets, ALIAS lingual straight wire appliance bracket system was created by Takeyomoto and Scuzzu with world first passive self- ligating lingual brackets with square slot takes into consideration improved movement and the more significant interbrackets distances make the aligning stage easier. 26 (Figure 3.19) Recycling of self-ligating brackets results Carburizing of spring clips which prompts fragile crack. Normally it isn't prescribed.27 Conclusion The narrative review in this article demonstrates a portion of some self - ligating systems that will replace the ligating systems in future. In the meantime these are minimal costly this can be weighed against the numerous long stretches of clinical time they spare. While further refinements are attractive and further examinations basic, current brackets can convey quantifiable advantage without lifting a finger of use. The long, slow, yet quickly accelerating ascend to noticeable quality of self-ligation has accordingly brought up a plenty of issues about brackets design, treatment 56

ESLO

European Society of lingual orthodontics

NiTi

Nickel titanium

References 1. Harradine NWT: Self-ligating brackets: where are we now? J Orthod 2003; 30:262-273 2. Wolfgang Heiser. A new orthodontic philosophy. J Clin Orthod 1998; 35: 44-53 3. Pizzoni L, Ravnholt G, Melsen B. Frictional forces related to self-ligating brackets. Eur J Orthod 1998; 20:283-91. 4. Paduano S, Cioffi I, Iodice G, Rapuano A, Silva R. Time efficiency of self-ligating vs conventional brackets in orthodontics effect of appliances and ligating systems. Prog Orthod 2008; 9:74-80. 5. Matasa CG. Self-engaging brackets: passive vs. active. The Orthodontic Materials Insider.1996; 9:5-11. 6. Baccetti T, Franchi L. Friction produced by types of elastomeric ligatures in treatment mechanics with the preadjusted appliance. Angle Orthod 2006; 76:211-6. 7. Gandini P, Orsi L, Bertoncini C, Massironi S, Franchi L. In vitro frictional forces generated by three different ligation methods. Angle Orthod 2008; 78:917-21 8. Woodside DG, Berger JL, Hanson GH 2005 'Chapter 17: SelfLigation Orthodontics with the SPEED Appliance' in T.M. Graber, R.L. Vanarsdall, K.W.L. Vig (Editors) Orthodontics: Current Principles & Techniques St. Louis: Elsevier Mosby p. 717-752 9. Cacciafesta V, Sfondrini MF, Ricciardi A, Scribante A, Klersy C, Auricchio F; Evaluation of friction of stainless steel and esthetic self-ligating brackets in various bracket-arch wire combinations. Am J Orthod Dentofacial Orthop. 2003; Oct; 124(4):395-402. Paduano S, Cioffi I, Iodice G, Rapuano A, Silva R. Time efficiency of self-ligating vs conventional brackets in orthodontics: effect of appliances and ligating systems. Prog Orthod 2008; 9 10. Ludwig B, Bister D, Baumgaertel S. Self ligating in orthodontics. Newyork: Thieme Book, 2012. Pizzoni, L.; Ravnholt, G.; Melsen, B. (1998). 11. Frictional forces related to self-ligating brackets. European Journal of Orthodontics, Vol. 20, No. 3, pp. 283-29 12. Brauchli LM, Steineck M, Wichelhaus A. Active and passive self-ligation: a myth? Part 1: torque control. Angle Orthod. 2012 Jul; 82(4):663-9. 13. Pandis N, Polychronopoulou A, Eliades T. Active or passive selfligating brackets? A randomized controlled trial of comparative

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efficiency in resolving maxillary anterior crowding in adolescents. Am J Orthod Dentofacial Orthop. 2010; 137:12.e1–12.e6

21. Wolfgang Heiser. A new orthodontic philosophy. J Clin Orthod 1998; 35: 44-53

14. Chen, SS, Greenlee GM, Kim J, Smith CL, Huang GJ. Systematic review of selfligating brackets. AJO-DO. 2010. 137:6, 726.e1726.e18

22. Damon DH. The Damon low friction bracket: a biologically compatible straight-wire system. J Clin Orthod.1998; 32:670-80.

15. VALANT, JR Time: a self-ligating interactive bracket system. Semin. Orthod. , Philadelphia, v. 14, no. 1, p. 46-53, 2008. 16. Stolzenberg J: The Russell attachment and its improved advantages. Int J Orthod Dent Child 21:837-840, 1935 17. Wildman, A.J.; Hice, T.L.; Lang, H.M.; Lee, I.F.; and Strauch, E.C. Jr.: Round Table: The Edgelok bracket, J. Clin. Orthod.1972; 6:613-623 18. Harradine N. The History and Development of Self-Ligating Brackets. Semin in Orthod.2008; 14 (1): 5-18. 19. Hanson GH. The SPEED system: a report on the development of a new edgewise appliance. Am J Orthod. 1980;78(3):243-65. 20. Harradine NWT, Birnie DJ. The clinical use of Activa self-ligating brackets. Am J Orthod Dentofac Orthop 1996;109:319–28.

Address of Correspondence

Lijin James, Post graduate, Department of Orthodontics, Indira Gandhi Institute of Dental Sciences, Sri Balaji Vidyapeeth Deemed University. Email id: lijinjames14@gmail.com Phone no: +91 9037376937

23. S. Geron, Self-Ligating Brackets in Lingual Orthodontics, Seminars in Orthodontics, Vol 14, No 1 (March), 2008: pp 64-72 24. Aldo Macchi et al, Philippe self-ligating lingual brackets. J Clin Orthod 2002; 36: 42- 45. 25. Trevisi and Bergstrand: The SmartClip Self-Ligating Appliance System; SeminOrthod2008;14:87-100. 26. Scuzzo G, Takemoto K, Takemoto Y, Scuzzo G, Lombardo L. A new self-ligating lingual bracket with square slots. J Clin Orthod 2011; 45:682-90. 27. M. F. Sfondrini, E. Xheka, A. Scribante, P. Gandini, and G.Sfondrini, “Reconditioning of self-ligating brackets A shear bond strength study,” Angle Orthodontist, vol. 82, no. 1, pp. 158–164, 2012.

Authors Post Graduate Student, Department of Orthodontics and Dentofacial Orthopaedics, Indira Gandhi Institute of Dental Sciences, Sri Balaji Vidyapeeth Deemed University. 1,5,6

Professor and Head, Department Of Orthodontics and Dentofacial Orthopaedics, Indira Gandhi Institute of Dental Sciences, Sri Balaji Vidyapeeth Deemed University.

Senior Lecturer, Department Of Orthodontics and Dentofacial Orthopaedics, Indira Gandhi Institute of Dental Sciences, Sri Balaji Vidyapeeth Deemed University. 3,4

How to cite this article : L ijin James, U B Rajasekaran, Aniruddh Yashwant.V, Lidhiya Alexander, Helen Rachel Xavier, Basil Joseph. Self-Ligating Brackets in Orthodontics- A Narrative Review. Journal of Scientific Dentistry 2018;8(2):51-7 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

Effect of Behavioural counselling in Tobacco Cessation Manjula D.C1, Vandana Shekar2, Jagat reddy R.C3 ABSTRACT Tobacco cessation is an important component of a comprehensive tobacco control strategy since quitting tobacco is the single most important intervention that can improve the duration and quality of life of every tobacco user. Behavioural counselling is the cost effective way of reducing ill health by providing both immediate and long-term health benefits at the community, national and individual levels. This short communication highlights and provides guidelines to strengthen tobacco cessation activities and various management methods of tobacco cessation in tobacco users. Key words: Behavioural counselling,Tobacco,Quitting.

Tobacco cessation is an important component of a comprehensive tobacco control strategy since quitting tobacco is the single most important intervention that can improve the duration and quality of life of every tobacco user. Various other methods are self-help materials such as handouts, pamphlets, videos, and computer programs, school-based and community-based programs, and the use of the standard “5As” and 5 R’s. 5 A’s is a brief intervention method of counseling and a very popular approach used to guide the clinician in tobacco cessation counseling. In Indian scenario and global scenario, cancer patterns in India reveal that the predominance of tobacco related cancers are habit associated so health education in the form of individual counseling is the most essential methods of prevention at the primary level. Behavioural counselling is the cost effective way of reducing ill health by providing both immediate and long-term health benefits at the community, national and individual levels. This short communication highlights and provides guidelines to strengthen tobacco cessation activities and various management methods of tobacco cessation in tobacco users. Aveyard et al (2012) in a review on individual psychological counselling for cessation of tobacco stated that this type of counselling includes planned personal activities by a qualified cessation counselor and counselling is of 10 minutes duration. This method is very effective in helping the tobacco user by first asking about tobacco users interest in quitting date, Generally sessions lasts for a episode of 4 weeks following a quit 58

date.Multiple and lengthier meetings are found to be more successful.1 Group or individual psychological support can also help people to quit.2 The five major steps in this intervention are: 5 A’S They are as follows Ask-about tobacco use. Advice- to quit Assess-commitment and barrier to change.Assist-users committed to change. Arrange-follow up to monitor progress.3 5 R’s model has been advocated for tobacco users who were unwilling to quit.

They were Relevance, Risks, Rewards,Roadblocks and Repetition. Relevance : motivate the tobacco user to signify why stopping is personally significant, to be clearly defined as possible. Motivational information has the maximum impact if it is important to the person’s disease status or health concerns, age, gender and other vital features e.g; previous experience of using tobacco and individual obstacles in cessation. Risks: Inform the users to recognize negative consequences of sustained tobacco usage and highlight those that are very significant to the patient.. emphasise on smoking less– nicotine cigarettes or use of various tobacco forms will not eliminate the risks. Severe risks: breathlessness, asthma, pregnancy, loss of potency, loss of fertility, increased carbon-monoxide. Extended Risks: heart attacks and strokes, lung and other cancers (larynx, oral cavity, pharynx, oesophagus,), Journal of Scientific Dentistry, 8(2), 2018

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chronic bronchitis and emphysema),long-term disability and need for comprehensive care. Environmental risks: greater risks of lung cancer and heart diseases in spouses; higher risks of smoking by children of tobacco users: increased rate for low birth weight, SIDS, asthma, ear disease and respiratory infections in children of smokers. Rewards: The Therapist should ask the tobacco users to categorize the probable benefits of stopping tobacco use and converse specific benefits of quitting like improved health, good sense of smell, saving their cash,, feel better about yourself. home, car,garments, breath will smell better as a replica for children have healthier babies feel better physically, perform higher in physical manners, decreased aging of skin. Roadblocks: The Physician should tell the users to find out the barriers to quitting and note specific obstacles to quitting and note essentials of therapy that could deal with problems associated with it.Distinctive barriers are withdrawal symptoms, fear of disappointment, weight gain, unsupported, dejection, on using tobacco. Repetition: This motivational therapy should be repetitive constantly when an uninterested patient reports the clinic. Tobacco users who were unsuccessful in their past quit attempts should be told that most of them make repeated quit attempts before they are successful.4 In a systematic (transtheoretical) model developed in 1982 by Prochaska et al., individuals using tobacco products are evaluated in 5 stages with regard to their views and behaviour towards quitting smoking based on nicotine dependence.

a. People who do not plan to quit smoking (pre-contemplation phase) b. People who have begun to think about giving up smoking (contemplation phase). c. People who are ready or in the preparation phase to quit smoking (preparation phase). d. Quitting, trying to quit (action). e. Maintaining not smoking (maintenance)5

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The most common intervention physicians make is to advise cessation (because it will prevent ill health), but a systematic review of randomised controlled trials show that offering support for smoking cessation (such as medication or behavioural support) enhances the rate at which people attempt to stop smoking.6 The prime aim of interventions to promote cessation at the individual level is to improve health and reduce the ill-health consequences of smoking.7Achieving lifelong tobacco abstinence is an important public health goal. Most studies use 1-yearfollow-ups, but little is known about how good these are as proxies for long-term and life-long abstinence. Also,intervention intensity is an important issue for development of efficient and cost-effective cessation treatment protocols.8

Conclusion Tobacco cessation facilitates health benefits like improved mental and physical health. Behavioural counselling of two to three minutes can help the quitters to quit than other pharmacotherapy methods like Nicotine replacement therapy where adverse effects are more. However, evidence suggests that a combination of psychotherapy and medication increase the success of quitting success than either of them taken alone.

References 1. Aveyard P, Raw M. Improving smoking cessation approaches at the individual level. Tob Control.2012; 21(2):252–7. 2. Lancaster T, Lf S. Individual behavioural counselling for smoking cessation ( Review ) Summary of findings for the main comparison.2018;(3):2017–19. 3. Fiore MC, McCarthy DE, Jackson TC, Zehner ME, Jorenby DE,,Mielke M,Smith SS,Giuliani TA,Baker TB, et al. Integrating smoking cessation treatment into primary care : an effectiveness study.Prev Med 2004;38(4):412– 20. 4. Clinical Practice Guideline Treating Tobacco Use and Dependence Update Panel, Liaisons, and Staff. A clinical practice guideline for treating tobacco use and dependence: 2008 update. A U.S. Public Health Service report. Am J Prev Med 2008;35:158-76. 5. Prochaska JO, DiClemente CC, Velicer WF, Rossi JS. Standardized, individualized, interactive, and personalized selfhelp programs for smoking cessation.Health Psychol.1993; 12: 399-405. 6. Aveyard P, Begh R, Farley A, West R.. Brief opportunistic smoking cessation interventions: a systematic review and meta-analysis to compare advice to quit and offer of assistance. Brief opportunistic smoking cessation interventions : a systematic review and metaanalysis to compare.Addiction 2012;107(6):1066-73

Effect of Behavioural counselling in Tobacco Cessation 7. Wannamethee SG, Shaper AG, Perry IJ, et al. Smoking as a modiﬁable risk factor for type 2 diabetes in middle-aged men. Diabetes Care 2001;24:1590-95.

Address of Correspondence

Manjula D.C , Post graduate, Oral medicine and Radiology, Indira Gandhi Institute of Dental Sciences, Email id: manjulasiva1@gmail.com Phone no: +91 9791057645

Manjula et al 8. Nohlert E, Öhrvik J, Tegelberg Å, Tillgren P, Helgason ÁR. Longterm follow-up of a high- and a low-intensity smoking cessation intervention in a dental setting- a randomized trial. BMC Public Health 2013;13(1):592.

Authors Post Graduate Student, Oral Medicine and Radiology, Indira Gandhi Institute of Dental Sciences. 1,5,6

Reader, Oral Medicine and Radiology, Indira Gandhi Institute of Dental Sciences.

Professor and Head, Oral Medicine and Radiology, Indira Gandhi Institute of Dental Sciences.

How to cite this article : M anjula D.C, Vandana Shekar, Jagat reddy R.C. Effect of Behavioural counselling in Tobacco Cessation. Journal of Scientific Dentistry 2018;8(2):58-60 Source of support : Nil, Conflicts of Interest : None declared

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Review Article

Genetic Aspects of Chronic and Aggressive Periodontitis Sivaranjani KS1, Bijivin Raj.V2, Vinoth Kumar B.Na 3, Arvina.R4, Hema. P5, Ananya Sweta. V6 ABSTRACT Evidence suggests that there is some genetic basis for the periodontal diseases. The molecular abnormality and its genetic inheritance has been established in some cases of generalized aggressive periodontitis. Family studies indicates that this disorder is transmitted by autosomal recessive genes. Recent evidence also suggests that susceptibility to periodontal disease may be related in part to genetically determined immune responsiveness to bacteria. Although specific genetic risk factors have not been identified for the chronic periodontitis, recent studies indicate that there is significant genetic variance in the population. More precise definitions of disease phenotypes will facilitate future genetic epidemiologic studies of the periodontal diseases. Key words: Gene, Aggressive Periodontitis, Chronic Periodontitis, Polymorphism

INTRODUCTION Periodontitis is a complex multifactorial disease. Complex human diseases are typical that they mostly have a relatively mild phenotype and are slowly progressing and chronic in nature. The phenotype of the complex diseases is determined by both genetic and the environmental factors that aﬀect the individual. Although pathogenic bacteria and various other environmental factors (e.g., smoking and stress)(1) are involved in pathogenesis of periodontitis, genetic factors are proved to be evident in the aetiology of periodontitis. Understanding of the interplay between the host and oral bacteria is a must to the understanding of the pathogenesis of periodontal disease. The first evidence that genetics plays a role in periodontal disease emerged in the 90’s. This new information introduced new concepts such as susceptibility and predisposition to periodontal disease(2,3). A key determinant of whether individuals develop periodontitis appears to be governed by the way they respond to their microflora(4). Therefore, genetic factors modulate how individuals interact with many environmental agents, including biofilm, to determine susceptibility to periodontitis. It’s the interplay between genetic and environmental factors, and not the genes alone, which determines the outcome, ie) the periodontal disease. The differential response is influenced by the individual's genetic profile There are significant clinical and scientific evidences that genetic factors are important determinants of periodontitis susceptibility and progression (5). Support for this statement comes from studies of humans and Journal of Scientific Dentistry, 8(2), 2018

animals which indicate that genetic factors influence inflammatory and immune responses in general as well as in periodontitis. Disease modifying genes are responsible for susceptibility to periodontitis. Mendelian principles do not apply to these disease modifying genes, because both heterozygous and homozygous subjects for a given genetic variation in a gene or locus may not necessarily develop the disease. In such a complex and multifactorial disease as periodontitis, other genetic risk factors and behavioural factors must also exist simultaneously to be determinants of an individual’s propensity to developing periodontitis(6). Thus, it is possible that periodontitis could be polygenic (gene–gene interactions) and multifactorial (gene–environment–life style interactions such as oral hygiene, smoking, stress and diet)(7,8). This review article focuses on the most studied genetic influences on Chronic and Aggressive Periodontitis.

Polymorphism in Relation to Periodontal Diseases 1. Cytokine gene polymorphisms IL-1 gene polymorphism TNF-α gene polymorphism IL-10 gene polymorphism 2. Receptor and other gene polymorphisms FCgR gene polymorphisms 61

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FcgRIIa-131 H/R polymorphism FcgRIIIa-158 F/V polymorphism FcgRIIIb polymorphism Cytokine and chemokine receptor gene polymorphisms Immune receptor gene polymorphism 3. Metabolism - related gene polymorphism Vitamin D receptor gene polymorphism Calcitonin receptor gene polymorphism 4. Antigen - recognition related gene polymorphism HLA gene polymorphism 5. Polymorphisms in the innate immunity receptors TLR2 and TLR4 gene polymorphisms CD 14 gene polymorphism CARD 15 gene polymorphism 6. Miscellaneous gene polymorphisms

Cytokine Gene Polymorphism a. IL-1 gene polymorphism Kornman et al 1997 , in Caucasian population reported that IL-1 composite genotype could be considered a putative severity factor for periodontitis and the "Genotype positive" model was depicted. Diehl et al, 1999(10) showed the IL-1 gene as a putative susceptibility factor for chronic periodontitis and aggressive periodontitis. Ethnicity also has a role to play in IL-1 gene polymorphism(11). Poulsen et al(12) demonstrated that in localized aggressive periodontitis patients, allele 2 of IL - 1 RN VNTR was associated. But also, no clear evidence has emerged, and there are currently too many conflicting and negative results. Large cohort studies of homogeneous composition should be initiated in which all of the currently accepted non-genetic (putative) risk factors are included. Multivariate analysis should be employed to estimate relative contributions of all factors(13). In summary for the global population, polymorphisms in the IL-1 gene (9)

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cluster cannot be regarded as (putative) risk factors for Periodontitis or severity of periodontal destruction. b. TNF-α gene polymorphism: From the studies by Craandijk, 2002 (14) Shapira, 2001 (15) Schulz Machulla 2008 (16), there is no indication that any of the related gene variations are related to susceptibility/ severity of periodontitis. In 2008, Stefan Reichert et al (17) found that IL - 12 RB2 were significantly higher in aggressive periodontitis patients as compared with healthy controls or chronic periodontitis patients. Investigations into severity of Periodontitis in relation to any of the TNF- α gene R -alleles also did not reveal a positive association. Lack of association of TNF- α genetic polymorphisms with Periodontitis severity was also reported by others(18). To summarize, based on the available literature to date, there is only limited data to support associations between any of the reported TNF- α gene variations and Periodontitis. c. IL-10 gene polymorphism: IL-10 can stimulate the generation of auto-antibodies(19) which play a role in Periodontitis(20,21). Functional disturbance in the IL-10 gene due to genetic polymorphisms could be detrimental to host tissues and could be linked to Periodontal disease susceptibility, with altered IL-10 production. The IL-10-1087 polymorphism (N-allele) is more abundant in Periodontitis as particular in nonsmokers(22,23). These observations have led the authors to speculate that the N-allele prevalence in Periodontitis patients may result in higher levels of auto-antibodies, which may lead to increased periodontal destruction. In summary, a limited number of studies have investigated genetic variations at three positions in the IL-10 promoter region. For all three positions some significant differences in the allele carriage rates between patients and controls have been reported. Further studies on IL-10 as candidate gene seems to be justified.

Receptor and Other Gene Polymorphisms a. FCgR gene polymorphism: FcγR are found on a wide variety of immune cells in the Periodontal tissues(24). In the pathogenesis of Periodontitis, it acts as a bridge between the cellular and humoral branches of the immune system. Microorganisms and bacterial antigens, opsonized with antibody, can be phagocytosed via FcγR on neutrophils or internalized via FcγR by a variety of antigen presenting cells (APC), Journal of Scientific Dentistry, 8(2), 2018

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including monocytes, macrophages and B cells. T cells, and natural killer (NK) cells may become activated, when IgG-opsonized bacteria are bound to these cells via FcγR, a variety of cytokines and chemokines may also be released (25). The leukocyte FcγR genes are found on chromosome 1 and encode three main receptor classes: FcyR1 (CD64), FcγRII (CD32) and FcγRIII (CD16). These classes are further subdivided into subclasses: FcγRI a and b, FcγRII a, b and c, and FcγRIII a and b. To summarize, Polymorphisms in the genes encoding the low affinity receptors may result in variations in antibody binding and phagocytosis and hence susceptibility to periodontitis is documented. FcRIIa-131 H/R polymorphism: FcγRIIa-H131 binds IgG2 immune complexes efficiently, whereas the FcγRIIa-R131 allotype, cannot mediate, this interaction(26). The G to T transition polymorphism in the FcγRIIIa gene, results in an amino acid 158-valine (V) (N-allele) substitution for 158-phenylalanine (F) (R-allele). Patients with FcgRIIa-R/R genotype could be more susceptible for periodontitis due to decreased capacity to phagocyte IgG2 opsonized Actinobacillus actinomycetemcomitans(27). But this hypothesis got rejected since Loos et al (28) found that FcgRIIa-H/H genotype is higher in aggressive periodontitis subjects than in controls. A recent study by Nicu et al also proved that H/H genotype is associated with more periodontal destruction than H/R or R/R genotype. FcgRIIIa-158 F/V polymorphism: The V/V variant is capable of efficient binding of IgG 1, 3, 4 relative to F/F variant in both monocytes and natural killer cells. This substitution was also associated with recurrence of adult periodontitis compared to individuals without recurrence(29). The FcγRIIIa-V158 has a higher affinity for IgGl and 3 than FeγRIIIa-F158. Moreover, FcγRIIIa-V158 can bind IgG4, while FcγRIIIa-F158 is unable to do so. A bi-allelic polymorphism in the FcγIIIb gene underlies the FcγRIIIb neutrophil antigen (NA) 1 or NA2 allotype (the N- or R-allele respectively). This is caused by 4 amino acid substitutions in the Fc-binding region resulting in differences in glycosylation. The NA2 type binds less efficiently human IgGl and IgG3 immune complexes than FcγRIIIbNA1(30). FcgRIIIb polymorphism: In neutrophils, FcgRIIIb exists in two allelic forms, NA1 and NA2 as a result of nucleotide substitutions Journal of Scientific Dentistry, 8(2), 2018

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resulting in changes in four aminoacids. FcgRIIIb-NA1 displays more efficient interaction with IgG1 and IgG3 opsonized bacteria compared with FcgRIIIb-NA2 and was found to be associated with increased resistance to periodontitis in an elderly Japanese population(31). To summarize, the possibility that genes encoding for FcgR are associated with susceptibility and severity of several forms of periodontitis in different ethnic groups seems promising.. However, to date no clear and convincing data are present to definitively assign one or more of the FcγR gene polymorphisms as true risk factors for Periodontitis. Further research is recommended in larger group of subjects from different populations(32). b. Cytokine and Chemokine receptor gene polymorphisms: Receptors are important constituents of the whole cytokine system. Through these membrane bound or circulating proteins, cell responses to various cytokines are elicited or blocked. The soluble form of TNF -receptor 2, which is shed from the cell surface significantly reduced the loss of connective tissue and alveolar bone in experimental periodontitis(33). c. Immune receptor gene polymorphism: FMLP receptor polymorphism depressed chemotactic response to n-formyl-1-methionyl-1-leucyl-1phenylalanine peptides has been confirmed in studies done by Van Dyke et al and Serhan CN et al (34).

Metabolism Related Gene Polymorphism a. Vitamin D receptor gene polymorphism: The 3' portions of the VDR gene includes a cluster of linked polymorphisms(35). The first two sites are in the region of the gene from intron 8 to the 3' untranslated region. A silent mutation within codon 352 of the ninth exon alters the site. VDR gene polymorphisms are normally determined by polymerase chain reaction (PCR) and restriction enzyme digestion. The VDR gene polymorphisms are commonly present. If these polymorphisms influence the level or function of the VDR, they may be pathogenic(36). Li et al (37) found in his study that FOKI polymorphism of vitamin D receptor gene might be associated with generalized aggressive periodontitis in Chinese patients. The carriage of F allele increases the risk of developing generalized aggressive peridontitis. Nibali et al(38) found that Vitamin D receptor Taq - 1 TT polymorphism was 63

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moderately associated with both the presence and the progression of periodontitis in smokers, while no association was detected in non-smoking individuals. To summarize, the VDR gene affects both bone metabolism and immune functions. Moreover some encouraging results have been found for different ethnic populations. b. Calcitonin receptor polymorphism: Nosaka et al(39) have found that patients with this polymorphism were 20 times more likely to suffer buccal marginal bone loss than patients who were calcitonin receptor genotype negative.

ANTIGEN RECOGNITION RELATED GENE POLYMORPHISM Human leukocyte antigen (HLA) is involved in genetically predetermined humoral response via recognition of foreign antigens. The various alleles associated with disease in Periodontics are: HLA-DRB1.1501-DQB1.0602 genotype, HLA-DR4 and its subtypes(40,41)

Polymorphisms in Innate Immunity Receptors The innate immune response is the first line of defense in infectious diseases. The host is challenged, to detect the pathogen and to mount a rapid defensive response. a. TLR2 and TLR4 gene polymorphisms: The TLR2 Arg677Trp and Arg753Gln gene polymorphisms have been reported to abrogate the ability of TLR2 to mediate a Response to bacterial cell wall components(42). Two common co-segregating polymorphisms of TLR4, Asp299Gly and Thr399Ile, affect the extracellular domain of the TLR4 protein leading to an attenuated efficacy of LPS signaling and a reduced, capacity to elicit inflammation(43). The TLR4 Asp299Gly gene polymorphism has been correlated with hypo-responsiveness to inhaled. LPS, sepsis and infections caused by Gram-negative bacteria(44). One study has attempted to associate these above named TLR polymorphisms with Periodontitis(45). However, despite the perceived importance of these functional. TLR polymorphisms, no relation with Periodontitis has been observed(46). b. CD 14 gene polymorphism: The R-allele in the promoter region of CD14 at position -260 (-159) enhances the transcriptional activity of the 64

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gene. Individuals homozygous for the R-allele have increased serum levels of soluble (s) CD14 and an increased density of CD14 in monocytes. The CD 14260 SNP has previously been associated of increased risk with myocardial infarction and Crohnâ&#x20AC;&#x2122;s disease.(47) Furthermore, increased serum levels of CD14 have been associated with Periodontitis. There are contradictory findings from the studies of Holla et al (49) and Yamazaki et al(48) which did not find any association between CD14 genome polymorphism and chronic periodontitis. A higher frequency of the N-allele and the N/N genotype of the CD14-1359 polymorphism was found in patients with severe Periodontal disease than in patients with moderate Periodontitis. The importance of this finding requires further study. c. CARD 15 gene polymorphism: The 3020 insC and 2104 C>T polymorphisms of the. CARD 15 (NOD2) gene leads to impaired activation of nuclear factor-Ň&#x203A; B, resulting in altered transcription of pro-inflammatory cytokine genes and reduced expression of these cytokines. These polymorphisms are strongly associated with Crohn's disease. However, to date, these CARD 15 polymorphisms have not been associated with Periodontitis (50). No role for the CARD15 3020insC and 2104 C>T polymorphism was found for Periodontitis in Caucasians. Although genes of the innate immunity processes seem good candidates for their association with Periodontitis, investigations have not yielded any strong indications that they might be associated with this condition.

Miscellaneous Gene Polymorphisms a. Cathepsin C gene polymorphism: Cathepsin C is a proteinase and is expressed in the hyperkeratotic epithelial lesions such as palms, knees and oral keratinized gingiva. Hart et al. identified a gene on chromosome 11 containing the cathepsin C gene, responsible for prepubertal periodontitis as well as Papillon - Lefevre syndrome (PLS). All patients with pre-pubertal periodontitis were found to be homozygous for an A-G mutation at gene position +1040, resulting in a substitution of the amino acid tyrosine by a cysteine. This gene polymorphism was shown to be functional as there was a diminished activity of cathepsin C in PLS. Another study by Noack et al(51) reported two novel gene mutations at positions 947 and 1268, which were associated with these two diseases. Journal of Scientific Dentistry, 8(2), 2018

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b. MMP gene polymorphism: Ustun K Alptekin et al(52) examined the association between MMP-1-1607 1G/2G polymorphism and chronic periodontitis susceptibility in a Turkish population. The results concluded that there was no significant association between this polymorphism and susceptibility to periodontitis. c. Polymorphism in smokers: Cytochrome P450 (CYP) enzymes, CYP1a1 and CYP2E1, are important in the activation of xenobiotics, especially tobacco-derived substances such as polycyclic aromatic hydrocarbon(111) and nitrosamines. Glutathione S-transferase (GST) MI and N-acetyltransferase (NAT1 and NAT2) are involved in detoxification of these associated metabolites. Polymorphism of CYP1A1 and CYP2E1 are associated with enhanced catalytic activities of these enzymes. In addition, the null GSTM1 genotype and mutation in NAT gene result in the inability to efficiently detoxify xenobiotics(53). Itâ&#x20AC;&#x2122;s evident that the slow acetylator genotype of NAT2 is associated with a higher risk of periodontitis, particularly in smokers(54). Therefore, polymorphism of other xenobiotics metabolizing enzymes, CYPs and GSTs may also contribute to individual susceptibility to develop periodontitis. Kocher et al(55) and Meisel et al(56) conducted studies in Caucasian population which demonstrated that the N-acetyl transferase slow phenotype was significantly associated with severity of bone loss. Meisel et al(57) noted that the possible protective effects seen in non-smokers might be due to an allele of myeloperoxidase (MPO), which is not obvious in smokers. d. Other polymorphisms: Other polymorphisms include ACE (Angiotensin converting enzyme), ER2 (Endothelein receptor 2), IL (Interleukin) 2, IL4, IL6, IFN-GR (Interferon gamma receptor) 1, MMP (Matrix mettaloproteinase)-1, MMP3, MMP9, MPO (Myeloperoxidase), RAGE (Receptor for advanced glycation end products), TGF (Transforming growth factor) b, TIMP (Tissue inhibitor of metalloproteinase) 2, Plasminogen activation, Mannose binding lectin, Osteoprotegrin and TNFR (Tumor necrosis factor receptor) 2 gene polymorphisms. Association between these polymorphisms and periodontal disease is yet to be proved(58).

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Summary THE ROLE OF GENETICS IN CHRONIC PERIODONTITIS: Evidence for the role of genetic component in chronic (adult) periodontitis has been conducted from twin and family studies. The twin model is probably the most powerful method to study genetic aspects of any disease, including periodontal disease. Michalowicz et al (59) evaluated the periodontal conditions (attachment loss, pocket depth, gingival index, and plaque index) of 110 adult twins indicated that between 38% and 82% of the population variance for these measures may be attributed to genetic factors. In a study on 117 adult twin pairs the analysis included the evaluation of the environmental factors like smoking and utilization of dental services. The results showed that chronic (adult) periodontitis was estimated to have approximately 50% heritability, which was unaltered following adjustments for behavioral variables including smoking. Velden et al (60) studied with a family study design the effect of sibling relationship on the periodontal condition in a group of young Indonesians deprived from regular dental care. The results of the analysis suggest that also in less severe forms of periodontitis there may be a genetic background for the disease. Also epidemiological studies in a Dutch population have suggested that chronic (adult) periodontitis aggregates in families. From both the twin and family studies it can be concluded that the basis for familial aggregation of periodontitis appears not bacterial/ environmental/ behavioral in nature. Rather, genetics seem to form the basis for the familial aggregation of periodontitis.

Genetic Associations In Aggressive Periodontitis The genetic association study approach is useful for identifying genetic variants that affect susceptibility to common complex diseases(61). A leading hypothesis of increased susceptibility to aggressive periodontitis entails deficient host response to periodontal infection, particularly infections with virulent periodontal pathogens. It is now established that genetic factors regulate the innate immune system and that certain genetic polymorphisms may render the immune system defective and unable to successfully fend off assaults by infecting microorganisms. Genetic factors may play a more significant role in the pathogenesis of aggressive periodontitis than in chronic periodontitis, and this may be attributed, to a certain extent, to the significance of the innate immune system in the pathogenesis of this disease. Although local etiological factors are less prevalent in aggressive periodontitis than in chronic periodontitis, 65

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alveolar bone loss and tooth loss are significantly more pronounced in aggressive periodontitis. Periodontal tissue destruction in aggressive periodontitis commences at an early age, shows a rapid rate of progression and has a unique pattern where it affects multiple teeth and occurs bilaterally. In addition, differences in the microbiologic flora or in other environmental factors do not fully explain the variance in the severity and age of onset between these two diseases. In the quest to identify genetic risk markers of aggressive periodontitis, association studies have focused on genetic factors that regulate the immune response(62).

Conclusion Research on genetic polymorphisms in the recent years has had limited success in unravelling significant and reproducible genetic factors for susceptibility to CP. Taken together the data published so far on gene polymorphisms, some evidence is emerging that polymorphisms in the IL1, IL6, IL10, VDR, and CD14 genes may be associated with Chronic and Aggressive Periodontitis susceptibility in certain populations. Future studies should apply more strict disease classification, larger study cohorts, adjust for relevant risk factors, and include analysis of multiple genes and polymorphisms. Novel statistical methods may allow a better assessment of multiple genes and polymorphisms within the same pathway and interactions with environmental factors. The possibility to include data from multiple genes and polymorphisms or haplotypes and environmental data, and to model their interactions, will give us a better assessment and pathophysiology. Identifying genes can result in novel diagnostics for risk, early detection and individualized treatment approaches(63). Identifying genes that contribute to the pathogenesis of periodontitis can have significant public health, therapeutic and scientific repercussions. Environmental factors involved in the causation of periodontal diseases can be modified or eliminated.

References 1. Gomez RS, Dutra WO, Moreira PR. Epigenetics and periodontal disease: future perspectives. Inflamm Res. 2009; 58(10):625. 2. Taba M, Jin Q, Sugai JV, Giannobile WV. Current concepts in periodontal bioengineering. Orthod Craniofac Res. 2005; 8(4):292-302. 3. Kinane DF, Hart TC. Genes and gene polymorphisms associated with periodontal disease. Crit Rev Oral Biol Med. 2003; 14(6):430-49. 4. Pihlstrom BL, Michalowicz BS, Johnson NW. Periodontal diseases Lancet 2005; 366: 1809–1820. 66

Sivaranjani et al 5. Sofaer JA. Genetic approaches in the study of periodontal diseases. J Clin Periodontol. 1990; 17(7):401-8. 6. Hart TC. Genetic risk factors for early-onset periodontitis. J Periodontol. 1996; 67(3):355-66. 7. Michalowicz BS. Genetic and heritable risk factors in periodontal disease J Periodontol. 1994; 65(5):479-88. 8. Hassell TM, Harris EL. Genetic influences in caries and periodontal diseases. Crit Rev Oral Biol Med.1995; 6(4):319-42. 9. Kornman KS, Crane A, Wang HY, Giovlne FS, Newman MG, Pirk FW, et al. The interleukin‐1 genotype as a severity factor in adult periodontal disease. J Clin Periodontol. 1997; 24(1):72-7. 10. Diehl AM, Yang S, Zhu H, Li Y, Lin H, Gabrielson K, Trush MA,. Mitochondrial adaptations to obesity-related oxidant stress. Ar Biochem Biophysics. 2000; 378(2):259-68. 11. Havemose-Poulsen A, Sørensen LK, Stoltze K, Bendtzen K, Holmstrup P. Cytokine profiles in peripheral blood and whole blood cell cultures associated with aggressive periodontitis, juvenile idiopathic arthritis, and rheumatoid arthritis. J Periodontol. 2005; 76(12):2276-85. 12. Moreira PR, Lima PM, Sathler KO, Imanishi SA, Costa JE, Gomez RS. Interleukin‐6 expression and gene polymorphism are associated with severity of periodontal disease in a sample of Brazilian individuals. Clin Exper Immunol. 2007; 148(1):119-26. 13. Fraga MF, Ballestar E, Paz MF, Ropero S, Setien F, Ballestar ML. Epigenetic differences arise during the lifetime of monozygotic twins. Nat Acad Sci. 2005 Jul 26; 102(30):10604-9 14. Diehl SR, Wang Y, Brooks CN, Burmeister JA, Califano JV, Wang S, Schenkein HA. Linkage disequilibrium of interleukin-1 genetic polymorphisms with early-onset periodontitis. J Periodontol. 1999; 70(4):418-30. 15. Craandijk J, van Krugten MV, Verweij CL, van der Velden U, Loos BG. Tumor necrosis factor -γ gene polymorphisms in relation to periodontitis. J Clin Periodontol 2002; 29:28-34. 16. Shapira L, Stabholz A, Rieckmann P, Kruse N. Genetic polymorphism of TNF-a promoter region in families with localized early-onset periodontitis. J Periodontal Res 2001; 36:183-6. 17. Schulz S, Machulla HK, Altermann W, Klapproth J, Zimmermann U, Gläser C, et al. Genetic markers of tumor necrosis factor alpha in aggressive and chronic periodontitis. J Clin Periodontol 2008; 35: 493-500. 18. Holla LI, Fassmann A, Augustin P, Halabala T, Znojil V, Vanek J. The association of interleukin-4 haplotypes with chronic periodontitis in a czech population. J Periodontol 2008; 79:192733 19. Reichert S, Machulla HK, Klapproth J, Zimmermann U, Reichert Y, Gläser C, et al. Interferon gamma and interleukin 12 gene polymorphisms and their relation to aggressive and chronic periodontitis and key periodontal pathogens. J Periodontol 2008; 79:1434-43. 20. M. Donati, T. Berglundh, A.-M. Hytonen, M. Hahn-Zoric, L.-A. Hanson, and L. Padyukov. Association of the −159 CD14 gene polymorphism and lack of association of the −308 TNFA and Q551R IL-4RA polymorphisms with severe chronic periodontitis in Swedish Caucasians. J Clin Periodontol. 2005; 32(5): 474–479.

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Genetic Aspects of Chronic and Aggressive Periodontitis 21. N. G. de Menezes and A. P. V. Colombo. Lack of association between the TNF-α −308 (G/A) genetic polymorphism and periodontal disease in Brazilians. Braz Oral Res. 2008; 22(4): 322–327. 22. Kinane DF, Hodge P, Eskdale J, Ellis R, Gallagher G. Analysis of genetic polymorphisms at the interleukin-10 and tumor necrosis factor loci in early-onset periodontitis. J Periodontal Res 1999; 34:379-86. 23. Yamazaki K, Tabeta K, Nakajima T, Ohsawa Y, Ueki K, Itoh H, et al. Interleukin-10 gene promoter polymorphism in Japanese patients with adult and early-onset periodontitis. J Clin Periodontol. 2001; 28:828-32.

Sivaranjani et al 36. Nibali L, Parkar M, D'aiuto F, Suvan JE, Brett PM, Griffiths GS, Rosin M, Schwahn C, Tonetti MS. Vitamin D receptor polymorphism (− 1056 Taq‐I) interacts with smoking for the presence and progression of periodontitis. J Clin Periodontol. 2008; 35(7):561-7 37. Nosaka Y, Tachi Y, Shimpuku H, Kawamura T, Ohura K. Association of calcitonin receptor gene polymorphism with early marginal bone loss around endosseous implants. Int J Oral Maxillofac Imp. 2001; 17(1):38-43. 38. Takashiba S, Ohyama H, Oyaizu K, Kogoe‐Kato N, Murayama Y. HLA genetics for diagnosis of susceptibility to early‐onset periodontitis. J Periodontal Res. 1999; 34(7):374-8.

24. E. A. Nicu, U. Van der Velden, V. Everts, A. J. Van Winkelhoff, D. Roos, and B. G. Loos. Hyper-reactive PMNs in FcγRIIa 131 H/H genotype periodontitis patients. J Clin Periodontol. 2007; 34(11):938–945.

39. Bonfil JJ, Dillier FL, Mercier P, Reviron D, Foti B, Sambuc R, Brodeur JM, Sedarat C. A “case control” study on the role of HLA DR4 in severe periodontitis and rapidly progressive periodontitis. J Clin Periodontol. 1999; 26(2):77-84.

25. W.-L. van der Pol and J. G. J. van de Winkel. IgG receptor polymorphisms: risk factors for disease. Immunogen. 1998; 48(3):222–232.

40. Arbour NC, Lorenz E, Schutte BC, Zabner J, Kline JN, Jones M, et al. TLR4 mutations are associated with endotoxin hyper responsiveness in humans. Nat Genet 2000; 25:187-91.

26. N. M. van Sorge, W.-L. van der Pol, and J. G. J. van de Winkel. FcγR polymorphisms: implications for function, disease susceptibility and immunotherapy. T Ant. 2003; 61(3): 189–202.

41. Agnese D, Calvano J, Hahm SJ, Lowry SF. Human toll-like receptor 4 mutations but not CD14 polymorphisms are associated with an increased risk of gram-negative infections. J Infect Disease 2002; 186:1522-5.

27. McGuire MK, Nunn ME. Prognosis versus actual outcome. IV. The effectiveness of clinical parameters and IL-1 genotype in accurately predicting prognoses and tooth survival. J Periodontol. 1999; 70(1):49-56. 28. Loos BG, Leppers-van de Straat VV. U. Fcg receptor gene polymorphisms in relation to periodontitis. J Clin Periodontol. 2003; 31:345-50. 29. T. Kobayashi, K. Yamamoto, N. Sugita, et al. The Fcγ receptor genotype as a severity factor for chronic periodontitis in Japanese patients. J Periodontol. 2001; 72(10):1324–1331.

42. Folwaczny M, Glas J, TÖRÖK HP, Limbersky O, Folwaczny C. Toll‐like receptor (TLR) 2 and 4 mutations in periodontal disease. Clin Exper Immunol. 2004; 135(2):330-5. 43. James JA, Poulton KV, Haworth SE, Payne D, McKay IJ, Clarke FM, Hughes FJ, Linden GJ. Polymorphisms of TLR4 but not CD14 are associated with a decreased risk of aggressive periodontitis. J Clin Periodontol. 2007; 34(2):111-7. 44. Hayashi J, Masaka T, Ishikawa I. Increased levels of soluble CD14 in sera of periodontitis patients. Infect Immunol 1999; 67:417-20

30. N. Sugita, K. Yamamoto, T. Kobayashi, et al. Relevance of FcγRIIIa-158V-F polymorphism to recurrence of adult periodontitis in Japanese patients. Clin Exper Immunol. 1999; 117(2): 350–354.

45. L. I. Holla, D. Buckova, A. Fassman, T. Halabala, A. Vasku, J. Vacha, Promoter polymorphisms in the CD14 receptor gene and their potential association with the severity of chronic periodontitis. J Med Gen. 2002; 39(11):844–848.

31. Armitage GC, Wu Y, Wang HY, Sorrell J, di Giovine FS, Duff GW. Low prevalence of a periodontitis-associated interleukin-1 composite genotype in individuals of Chinese heritage. J Periodontol. 2000; 71(2):164-71.

46. Yamazaki K, Ueki-Maruyama K, Oda T, Tabeta K, Shimada Y, Tai H, et al. Single nucleotide polymorphism in the CD14 promoter and periodontal disease expression in a Japanese population. J Dent Res 2003; 82:612-6

32. Van Dyke TE, Serhan CN. Resolution of inflammation: a new paradigm for the pathogenesis of periodontal diseases. J Dent Res. 2003; 82(2):82-90.

47. Hugot JP, Chamaillard M, Zouali H, Lesage S, Cιzard JP, Belaiche J, et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. Nat Gen 2001; 4(11):599-603

33. Wang C, Zhao H, Xiao L, Xie C, Fan W, Sun S, Xie B, Zhang J. Association between vitamin D receptor gene polymorphisms and severe chronic periodontitis in a Chinese population. J Periodontol. 2009; 80(4):603-8.

48. Noack B, Görgens H, Hoffmann TH, Fanghänel J, Eickholz P, Schackert HK. Novel mutations in the cathepsin C gene in patients with pre-pubertal aggressive periodontitis and Papillon-Lefevre syndrome. J Dent Res. 2004; 83(5):368-70.

34. Selvaraj P, Chandra G, Jawahar MS, Rani MV, Rajeshwari DN, Narayanan PR. Regulatory role of vitamin D receptor gene variants of BsmI, ApaI, TaqI, and FokI polymorphisms on macrophage phagocytosis and lymphoproliferative response to mycobacterium tuberculosis antigen in pulmonary tuberculosis. J Clin Immunol. 2004; 24(5):523-32.

49. Ustun K, Alptekin NO, Hakki SS, Hakki EE. Investigation of matrix metalloproteinase 1 - 1607 1G/2G polymorphism in a Turkish population with periodontitis. J Clin Periodontol 2008; 35:1013-9

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Genetic Aspects of Chronic and Aggressive Periodontitis 51. Park KK, Kim JS, Park JY, Chung WY, Choi MA, Cho KS. Polymorphisms in genes encoding for enzymes metabolizing smoking-derived substances and the risk of Peridontitis. J Clin Periodontol 2004; 31:959-64 52. Meisel P, Timm R, Sawaf H, Fanghδnel J, Siegmund W, Kocher T. Polymorphism of the N-acetyl transferase (NAT2), smoking and the potential risk of periodontology. Arch Toxicol 2000; 74:343-8 53. Kocher T, Sawaf H, Fanghδnel J, Timm R, Meisel P. Association between bone loss in periodontal disease and polymorphism of N-acetyltransferase. J Clin Periodontol 2002; 29:21-7 54. Meisel P, Siegemund A, Dombrowa S, Sawaf H, Fanghaenel J, Kocher T. Smoking and polymorphisms of the interleukin-1 gene cluster in patients with periodontal disease. J Periodontol 2002; 73:27-32 55. Shapira L, Wilensky A, Kinane DF. Effect of genetic variability on the inflammatory response to periodontal infection. J Clin Periodontol 2005; 32:72-86 56. Cullinan MP, Westerman B, Hamlet SM, Palmer JE, Faddy MJ, Lang NP, Seymour GJ. A longitudinal study of interleukin‐1 gene polymorphisms and periodontal disease in a general adult population. J Clin Periodontol. 2001; 28(12):1137-44.

Address of Correspondence

Sivaranjani KS , Final year post graduate student, Department of Periodontology, Indira Gandhi Institute of Dental Sciences, Email id: shivaks.dr@gmail.com Phone no: +91 77080 78424

Sivaranjani et al 57. Nibali L. Suggested guidelines for systematic reviews of periodontal genetic association studies. J Clin Periodontol. 2013; 40(8):753-6. 58. Nield-Gehrig Foundations of Periodontics for the Dental Hygienist 3rd ed. 2011:195-207 59. Ding C, Ji X, Chen X, Xu Y, Zhong L. TNF-α gene promoter polymorphisms contribute to periodontitis susceptibility: Evidence from 46 studies. J Clin Periodontol. 2014; 41(8): 748759. 60. Hu YY, Liu JH, Jiang GB, Yuan RX, Niu YM, Shen M. Association between interleukin-1β gene -511c>t/+3954c>t polymorphisms and aggressive periodontitis susceptibility: Evidence from a metaanalysis. Med Sci Monit. 2015; 21: 1617-1624. 61. Han MX, Ding C, Kyung HM. Genetic polymorphisms in pattern recognition receptors and risk of periodontitis: Evidence based on 12,793 subjects. Hum Immunol. 2015 Jul; 76(7): 496-504. 62. Chrzęszczyk D, Konopka T, Ziętek M. Polymorphisms of toll-like receptor 4 as a risk factor for periodontitis: A meta-analysis. Adv Clin Exp Med. 2015; 24(6): 1059-70. 63. Lindhe, Karring, Lang. Genetics in relation to Periodontitis. Clinical Periodontology and Implant Dentistry 2003; 4:387-97.

Authors Post graduate student, Department of Periodontology, Indira Gandhi Institute of Dental Sciences.

1,3,5,6

Senior Lecturer,Department of Periodontology, Saveetha Dental College, Chennai.

Senior Lecturer (Public Health Dentist), Sree mookambika institute of dental science, Nagercoil.

How to cite this article : S ivaranjani KS, Bijivin Raj V, Kumar B.Na, Arvina R, Hema P, Ananya Sweta V .Genetic aspects of Chronic and Aggressive Periodontitis. Journal of Scientific Dentistry 2019;8(2):61-8 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018

Review Article

Iatrogenic Effects of Bonding in Orthodontics - A Narrative Review Helen Rachel Xavier1, U B Rajasekaran2, Aniruddh V Yashwant3, Vijay Kumar V4, Lijin James5, Basil Joseph6 ABSTRACT Various procedures performed from the start till the end of orthodontic treatment such as bonding and debonding involve profound care and caution by the clinician. This can prevent iatrogenic effects of bonding procedures such as occurrence of white spot lesions, enamel cracks, tearouts and irreversible damage to the pulp. This review focuses on the various iatrogenic effects encountered and the possible precautions to be taken to prevent these effects from occurring. Key words: Iatrogenic, Enamel cracks, White spot lesions (WSL).

Introduction The success of orthodontic treatment depends upon the clinical efficiency of the orthodontist in procedures right from start of bonding procedure until debonding and retention reviews. Though the clinician aims to deliver the ideal and non iatrogenic treatment to the patient, inadequate attention to bonding and debonding procedures might cause more harm to the enamel and surrounding dentoalveolar structures at the end of treatment. The common iatrogenic effects of orthodontic treatment as a whole involves local (discoloration of teeth, decalcification of teeth, periodontal problems and root resorption) 1, 2, 3 and systemic (allergic reactions) 4.Both the clinician and the patient should be aware of these risks so that they can fulfill their responsibilities during the treatment period. This helps to bring a successful result without any adverse effects. This narrative review will provide an overview on the precautions taken during procedures in orthodontic bonding and the iatrogenic effects that may occur in orthodontic bonding procedure.

Orthodontic Bonding Procedure Direct or indirect bracket bonding on both facial and lingual surfaces involves cleaning, conditioning of the enamel surface, microscopic sealing and bonding of the bracket/ buccal tube1. Cleaning Cleaning of the teeth with pumice prior to bonding removes plaque and also the organic pellicle which might interfere with bonding by getting trapped at the Journal of Scientific Dentistry, 8(2), 2018

Figure 1: Removal of excess adhesives during bonding

enamel-resin interface. Proper supervision must be given to prevent trauma to the marginal gingiva which can cause bleeding. Acid etching of enamel removes about 10-20nm of enamel. Porosities are filled by saliva over time. An additional 6-50nm of enamel is estimated to be lost on debonding. The remaining resin tags in the enamel post debonding procedure may change in color with time1. Removal of Excess Excess adhesives cannot be removed by tooth brushing or by other mechanical forces. It must be removed with a probe or an explorer before the setting of the adhesive [Figure 1]. After setting, the adhesives can be taken off with burs or scalers. Excess adhesives must be removed to minimize the occurrence of irritation to the gingiva and to prevent plaque buildup around the bracket base, 69

Iatrogenic Effects of Bonding in Orthodontics - A Narrative Review

which is unesthetic. Moreover, the left over adhesives can discolour inside the oral cavity. The clinician should also instruct the patient to do proper brushing and can encourage fluoride mouth rinses (0.05% NaF) on a daily basis1.

Debonding The goals of debonding involve the removal of brackets and the residual adhesives from the tooth and bring back the enamel surface nearly to its previous state without asserting any iatrogenic effects5. There are 4 debonding techniques: mechanical debonding, electrothermal debonding7, laser debonding 8and ultrasonic debonding. Mechanical debonding is the disengagement at the enamel–adhesive interface with debonding pliers by appling force at a controlled level6. The other means of debonding such as electrothermal and laser debonding work by dissolving the adhesive used for bonding by generating heat. Mucosal burns and pulpal damage are the possible risks of electrothermal debonding. Ultrasonic vibrations are used for facilitating bond failure in ultrasonic debonding7, 9. The various features under debonding procedures include: • Clinical procedures • Impact of various debonding instruments on the enamel • Enamel loss during debonding • Enamel tearouts • Enamel cracks (fracture lines) • Wear of the residual adhesives • Removal of decalcifications

Clinical Procedures Debonding can be considered as a two step procedure which involves:

1. Removal of brackets 2. Elimination of residual adhesives

Helen Rachel Xavier et al

Removal of bracket The usage of debonding pliers are considered to be the most convenient and simple method of debonding11. When debonding metal brackets, forces are applied to peel the bracket base away from the enamel surface. This leads to a bond failure at bracket-adhesive interface12. Another debonding technique which involves the application of squeezing force at the bracket base is considered to be a better method. This dislodges the bracket and leave some amount of residual adhesives, which can be cleared off later.11 Debonding of ceramic brackets can pose a risk to the patient in the form of enamel fractures due to the greater bond strength.13 Chemically retained ceramic brackets bring about a greater degree of iatrogenic effects than mechanically retained ceramic brackets. Dislodging the brackets with the application of peripheral force is the preferred method of debonding for ceramic brackets14. Cutting the brackets off with gradual pressure using the tips of twin-beaked pliers, directed close to the bracketadhesive interface is not advised due to the chance of horizontal enamel cracks. Grinding of ceramic brackets (when tie wing fractures) without water spray may result in irreversible damage or necrosis of the pulp.

Removal of remnant adhesive Nowadays the color resemblance between the adhesives and enamel makes the complete removal of residual adhesive difficult and this can result in discoloration of the adhesives in the long run, which is undoubtedly unaesthetic. Residual adhesives can be dislodged by bracket removing pliers or with a scaler or by the use of tapered shaped tungsten carbide bur (#1171 or #1172) in a contraangled handpiece15. Previous studies suggested 30,000 rpm as the ideal for the fast adhesive removal without iatrogenic damage. Water cooling should not be used during removal as water lessens the contradiction with enamel. High speed more than 30,000 rpm can pose the risk of marring the enamel surface. Ultrafine highspeed diamond burs are also not advisable as it can result in enamel surface scratches16.

Effect of various debonding instruments on the enamel On comparing various debonding instruments and grading their degrees of surface marring on the enamel, it was found that diamond instruments were unsatisfactory as they produced coarse scratches. The plain cut and spiral fluted tungsten carbide burs regulated at about 25,000 rpm were found to be showing acceptable enamel surface Journal of Scientific Dentistry, 8(2), 2018

Iatrogenic Effects of Bonding in Orthodontics - A Narrative Review

Helen Rachel Xavier et al

representation. Previous studies advocated the use of oval shaped tungsten carbide bur for removing residual adhesives after removing attachments on the lingual surfaces of teeth16.

bite correction should be done before bonding ceramic brackets and the ceramic brackets bonded on mandibular teeth must be relieved from occlusion for preventing enamel abrasion10.

Adhesive Remnant Wear

Tearouts

Usually leftovers of adhesive can be observed on the enamel surface even after mechanical instrumentations.

Tearouts on the surface of enamel were described in literature following bonding and debonding of metal and ceramic brackets. Tearouts can be related to many factors such as bond failure location and the type of filler particles in the adhesives. The enamel surface appearance followed by debonding metal brackets which are bonded with macrofilled (10 to 30 µm) adhesives when compared with microfilled (0.2 to 0.3 µm) adhesives, a difference was found when pliers were used for scraping off the resin. Macrofilled particles can penetrate less into the etched enamel than microfilled particles. The voids correspondent to the dissolved enamel prism cores in the central etch type are 3 to 5 µm in diameter. During debonding adhesive tags were reinforced by the small fillers. The macrofillers, however, create a more natural break point in the interface between enamel and adhesive. The precautions to be followed are:

Gwinnett and Ceen proclaimed that leftover adhesives will not cause any plaque deposition and they will get removed with time24. In contrast to this, Brobakken and Zachrisson’s found that residual adhesive will not get cleared by itself following debonding26.

Amount of Enamel Lost in Debonding Previous studies shows informations regarding the enamel loss following bonding procedures. Various factors like prophylactic and debonding instruments or even adhesive resins used can be responsible for this. The enamel surface generally have a thickness of 1500 to 2000 µm. The primary prophylaxis with bristle brush for about 10 to 15 seconds for each teeth may scrape off approximately 10 µm of enamel. The usage of rubber cups can remove about 5 µm of enamel. Removal of adhesive remnants using hand instruments can result in an enamel loss of 5 to 8 µm. Depending upon the prophylactic instruments, the approximate enamel loss for unfilled resins can be upto 2 to 40 µm. Proper removal of filled resin usually needs rotary instruments. The enamel loss then may be 10 to 25 µm. A high-speed bur or a green rubber wheel can remove about 20 µm and a low speed tungsten carbide bur reduces about 10 µm of enamel. Generally the enamel loss for filled resins was calculated to be around 30 to 60 µm, depending on the instruments used for prophylaxis and debonding. Additional deep-reaching enamel tearouts down to a depth of 100 µm and localized enamel loss of 150 to 160 µm also have been reported. However, Van Waes et al. reported lesser enamel loss with the usage of tungsten carbide burs. It was found that an average enamel loss is of only 7.4 µm and concluded that lesser damage to enamel is observed with cautious usage of tungsten carbide bur17.

Iatrogenic Factors Affecting Enamel Abrasion Ceramic brackets generate more enamel abrasions than metal brackets. Polycrystalline ceramic brackets causes less enamel abrasions than monocrystalline ones. Cross

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1. Use brackets that have mechanical retention 2. Use debonding instruments and procedures that leaves most of the adhesives on the tooth and 3. Avoid scraping the left over adhesive with hand instruments. Cracks Cracksoccurs as split lines in the enamel [Figure 2]. They are common but usually unnoticed at clinical examination. Most of the cracks seems to be very difficult to differentiate properly without special techniques. Usually pinpointing them on routine intraoral photographs is challenging. Fiberoptic transillumination is essential for a proper visualization of cracks. Cracks can occur due to many causes. Mechanical and thermal insults can cause fracture to the enamel following eruption.Sometimes the sharp sound heard on removal of orthodontic brackets with debonding pliers can be associated with the generation of enamel cracks. A study by Zachrisson et al discussed the occurance of cracks in debonded, debanded and orthodontically untreated teeth.16 The most important findings were that vertical cracks are common and the most notable cracks (i.e., those invisible under normal office illumination) are on the maxillary central incisors and canines. 71

Iatrogenic Effects of Bonding in Orthodontics - A Narrative Review

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Figure 2: Enamel cracks

Figure 3: Decalcification

The clinical relevance of these observations is that if an orthodontist observes several distinct enamel cracks on the patientâ&#x20AC;&#x2122;s teeth after debonding or detects cracks in a horizontal direction, it suggests that the bonding or debonding technique has to be improvised.

patient 18. An increase in counts of Streptococcus mutans, reduction in the salivary pH and high food debris retention predispose patients undergoing orthodontic treatment to decalcification 19. Fluoride being an anticariogenic agent has been quite effective in remineralization of white spot lesions20. Administration of topical fluoride or the use of fluoride containing toothpastes and mouth rinses offer powerful protection in opposition to white spot formation by blocking the bacterial enzymes. Agents such as Xylitol, argon laser irradiation and topical fluoride have helped in decreasing enamel demineralization 21, 22.

Another clinical implication may be the need for pretreatment examination of cracks, notifying the patient and the parents if pronounced cracks are present. The reason for this examination is that if the patient notices this only after debonding of the appliance, they might question the orthodontist regarding the cause of the cracks.

Allergic reactions to bonding agents The unpolymerized methyl methacrylate in composite or acrylic has the tendency to cause allergic reactions such as tissue inflammation and necrosis in some patients. The cytotoxic effects may still be evident 2 years after polymerization4. Excess adhesive should be removed by scaling particularly in areas close to the gingival margin.

Decalcification Orthodontic patients are found to be the sufferers of decalcification but the orthodontic appliance cannot be the cause of caries [Figure 3]. However, fixed appliances interfere with the normal oral hygiene practice of the 72

Reversal in enamel decalcification White spot lesions are subsurface porosities in enamel resulting from carious demineralization. There have been several studies in literature which have evaluated the frequency of white spot lesions post orthodontic treatment. The incidence of white spot lesions were found to be increased in teeth which had undergone fixed appliance therapy as compared to the teeth that are untreated. Remineralization is a phenomenon of healing of small carious lesions. Fluoride ions can improve the extend of remineralization in a short period of time by absorbing calcium and phosphate from the saliva. Ă&#x2026;rtun and Thylstrup suggested that removal of the cariogenic factors following debonding can eliminate the progression of demineralization with the initiation of some amount Journal of Scientific Dentistry, 8(2), 2018

Iatrogenic Effects of Bonding in Orthodontics - A Narrative Review

of remineralization. However, Øgaard et al observed that the surface-softened lesions can remineralize rapidly and totally than subsurface lesions23. White spots that have evolved in the duration of orthodontic therapy therefore should not be dealt with fluoride agents immediately after debonding because this method will arrest the white spot lesions and prevent complete repair. It is better to recommend 2 to 3 months of good oral hygiene maintenance without fluoride supplementation after debonding. Microabrasion Once the white spots are established, microabrasion is the recommended way of removal of superficial enamel opacities. This technique removes enamel stains with minimal enamel loss. This involves the use of abrasive gel with 18% hydrochloric acid, finely powdered pumice, and glycerin applied using electric toothbrush. Microabrasion procedure can be repeated 2 to 3 times per month based on the nature and severity of the lesions for a better outcome. The microabrasion method is effective in getting rid of white spots and streaks and brown or yellow discolorations of the enamel. In cases of huge mineral loss, however, grinding with diamond burs under water cooling or composite restorations are inevitable.

Conclusion Various iatrogenic effects might occur during orthodontic treatment. Hence, proper care and caution should be implemented by the orthodontist during each step in bonding and removal of orthodontic appliance. The orthodontist should also motivate the patient regarding the importance of maintaining good oral hygiene and dietary regime. The ideal oral hygiene regime during fixed orthodontic treatment involves the use of topical fluoride agents such as fluoridated toothpaste and mouth rinse, gels and varnishes. The proper implementation of this protocol followed by the clinician and the patient might prove successful in prevention of occurrence of the mentioned iatrogenic effects.

Abbreviations NaF

Sodium Fluoride

WSL

White Spot Lesions

Journal of Scientific Dentistry, 8(2), 2018

Helen Rachel Xavier et al

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Iatrogenic Effects of Bonding in Orthodontics - A Narrative Review

Helen Rachel Xavier et al

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Address of Correspondence

Helen Rachel Xavier, Post Graduate Student, Department of Orthodontics and Dentofacial Orthopaedics, Indira Gandhi Institute of Dental Sciences, Sri Balaji Vidyapeeth Deemed University Email id: helenrachelxavier@gmail.com Phone no: +91 9961750082

Authors Post Graduate Student, Department of Orthodontics and Dentofacial Orthopaedics. Indira Gandhi Institute of Dental Sciences, Sri Balaji Vidyapeeth Deemed University. 1,5,6

Professor and Head, Department Of Orthodontics and Dentofacial Orthopaedics. Indira Gandhi Institute of Dental Sciences, Sri Balaji Vidyapeeth Deemed University.

3,4 Senior Lecturer, Department Of Orthodontics and Dentofacial Orthopaedics. Indira Gandhi Institute of Dental Sciences, Sri Balaji Vidyapeeth Deemed University.

How to cite this article : H elen Rachel Xavier, U B Rajasekaran, Aniruddh V Yashwant, Vijay Kumar V, Lijin James, Basil Joseph. Iatrogenic Effects of Bonding in Orthodontics - A Narrative Review. Journal of Scientific Dentistry 2018;8(2):69-74 Source of support : Nil, Conflicts of Interest : None declared

Journal of Scientific Dentistry, 8(2), 2018