Tooth is the hardest tissue of the body. It may disintegrate in the oral cavity due to various factors. One of the most important causes for destruction of tooth is dental caries. Dental caries is the microbial disease of the calcified tissues of teeth, characterized by demineralization of the inorganic portion and destruction of organic substance of the tooth. Dental caries is multifactorial, the exact etiology and pathogenesis are not known. Many theories have described the pathogenesis of dental caries but they could not explain all the ramifications of the disease. The theories related to dental caries state that the factors responsible for dental caries are host, parasites, and medium. If any of the above factor is missing then the caries formation does not occur. Dental caries occurs in different individuals at different
progresses at different rates. The dental caries may be incipient, moderate or deep based on extent of the lesion. The incipient caries is asymptomatic, reversible, appears
white opaque region, no major histological changes seen and it can undergo remineralization. A moderate lesion is one in
which caries penetration is easily
observed in the dentin and may involve up to one half of the dentin thickness between
the DEJ and
pulp. It can be treated by placing
therapeutic materials like liner/cement base prior to placement of the permanent restoration. If the dental caries affects more than half the dentin thickness between DEJ and the pulp Or if the lesion is deeper than 2 mm from the DEJ it is called as deep carious lesion. In deep carious lesion an interface of decalcified, softened, but intact dentin is seen on the excavation of carious dentin. It is characterized by sharp 1
pain, lasting for a moment. It is more often brought about by cold than hot beverages. It does not occur spontaneously and disappears on removal of stimulus. Proper diagnosis of the lesion is very important for the management of deep carious lesions. It can be diagnosed by tactile sensation, patient complaints, radiographs, pulp testing, dyes etc. The idea behind treating deep carious lesions are sealing the pulp and to maintain the vitality of the underlying tissue. The various methods used
for treating deep carious lesions are
direct and indirect pulp-capping, pulpotomy and any therapy that minimizes pulpal injury by protecting the pulp from toxic effects of chemical, bacterial, mechanical or thermal affects. In indirect pulp capping, the infected caries is removed and the affected caries is left intact and it is treated with biocompatible materials in order to avoid pulp tissue exposure and to form reparative dentin. When
pin point pulp exposure
without hemorrhage, then it is treated by direct pulp capping. caries affects complete
If the dental
portion of the pulp then pulpotomy
performed. Many materials and drugs have been used for treating deep carious lesions such as calcium hydroxide, zinc oxide eugenol, isobutyl cynoarylates, corticosteroids,
calcium phosphate, collagen fibers, cell inductive agents, bone morphogenic proteins, mineral trioxide aggregate (MTA) etc. Hence in this library dissertation an attempt is made to review and record various treatment aspects of deep carious lesions.
Definitions: Dental caries can be defined as the microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion and destruction of the organic substances of the tooth. (SHAFER) Dental caries is defined as a localized, post eruptive, pathological process of external origin involving softening of the hard tissue and proceeding to the formation of a cavity. (WHO) The meaning of caries in Latin is ‘dry rot ‘. It is the name given to the process of slow disintegration that may affect any of the biological hard tissue as a result of bacterial action. It is the most prevalent chronic disease affecting the human race. It affects persons of both sexes in all races and every age group. it usually begins soon after the teeth erupt in to the oral cavity.
Epidemiology There is evidence from many sources that dental caries is an ancient disease. The difference in caries rates noted in various parts of the world. WHO studies indicate that caries follows a definite pattern according to the region. The caries prevalence is lower in the Asian population and highest in Americans. Generally highly industrialized countries have higher caries indices with DMFT from 4 to 5. The pattern of dental caries is not uniform. Many authors referred
to as ‘civilization dystrophy.’ However from the last
fifteen years it is noted that there is decline in caries prevalence. Preventive measures must be undertaken to improve the oral health.
Etiology Dental caries is a multifactorial disease. The process by which a tooth can be destroyed easily in oral cavity is difficult to understand. There is no universally accepted opinion of the etiology of dental caries. But many theories have tried to explain the etiology of dental caries.
Acidogenic theory: Miller in 1889 explained this theory. According to him the caries is caused by acids produced by microbial enzymatic ingested
action on the inorganic
portion of the tooth. Then the organic portion is disintegrated creating cavities.
Proteolytic theory: It is given by Gottlieb in 1944. He claimed that the organic portion of the tooth is attacked first with certain lytic enzymes. This leaves the inorganic portion without a matrix support causing it to be
Proteolysis chelation theory: Schatz microbiotic
et al described this theory in 1955. He observed secretions
or metabolic products of
the ability to chelate calcium from organic
that have the
be disintegrated. These theories cannot justify all the
aspects of dental caries.
Contributing factors Basically caries occurs when there is interaction of three principle factors. They are 1) host 2) parasites 3) medium.
Host: It encompasses tooth and saliva. The morphological and chemical nature of the tooth is an important factor for initiation of caries. Deep pits
fissures in any tooth make susceptible to caries because of food impaction and bacterial stagnation. Irregularities in the arch form, crowding and overlapping of the teeth favors the development of caries. The caries immune persons exhibit greater ammonia content in saliva. Ammonia
the plaque formation and neutralizes acid formation to
certain extent. The enzymatic activity of saliva in relation to caries is controversial. The critical pH of saliva is 5.5. Below this value the inorganic material of the tooth may dissolve and leads to formation of caries. Lysozyme is an antibacterial agent present in the saliva, can inhibit airborne and waterborne microorganisms in the oral cavity to some extent. The quantity and viscosity of saliva has definite influence on caries incidence. Decrease in flow of saliva or lack of salivary secretions usually experiences increased
rate of dental caries. Prolonged use of certain drugs like anti-depressants, antihistamines may leads to xerostomia and dental caries.
Parasite: The second part of caries triad consists of the microorganisms. The plaque is formed of microorganisms, salivary glycol-proteins and inorganic salts. The plaque adheres to the tooth surface with a sticky polysaccharide carbohydrate called dextrane. The parasite portion of the caries formula is not clearly understood. But some studies proved that the
plays a vital role in
initiation of caries especially
fissure caries. The predominantly present microorganisms in deep dentinal caries are lactobacilli and certain gram positive anaerobes. Filaments are also present such as eubacterium, actinomyces, bacillus etc. In root caries predominantly present organism is actinomyces viscosus. Other species are actinomyces naeslundii and nocardia etc.
Medium: Medium that is diet is the third major factor in the initiation and progress of the decay process. The diet of primitive man consisted of raw food which helps in cleansing the debris, thereby reducing caries. Modern diet includes refined foods, soft drinks and eatables which lead to collection of debris predisposing to more caries. Mechanical rubbing and
definitely has role in caries reduction. Physical and chemical characteristics of a diet determine its relative cariogenecity.
Classification of dental caries There is no universally accepted classification of dental caries. But it can be classified as follows, I) According to location on the tooth a) Pit and fissure caries The caries originating in the pits and fissures of all 6
Teeth are called as pit and fissure caries. b) Smooth surface caries Caries occurring on the smooth surfaces of the teeth are called as smooth surface caries
c) Root caries (senile caries) Caries occurring at the cement enamel junction or cementum seen in gingival recession patients.
d) Linear enamel caries (odontoclasia) Caries occurs at neonatal zones and seen in labial surface of anterior teeth. Itâ€™s because of trauma at birth or metabolic disturbances.
According to the severity and progress of the lesion
a) Incipient caries The incipient caries is asymptomatic, reversible, Appears as opaque region, no
and it can
b) Moderate caries A moderate lesion is
which caries penetration is
observed in the dentin and may involve up to one half of the dentin thickness between the DEJ and the pulp. c) Deep dental caries If the dental caries affects more than half the dentin. Thickness between DEJ and the pulp it is called as deep carious lesion.
d) Acute or rampant caries
It is sudden and rapid onset caries involving at least two teeth and two surfaces. Lesions are soft and light colored and are frequently accompanied by severe pulp reactions. e) Chronic caries Lesions are of variable depth, long standing, dark in color and are hard in consistency f) Arrested caries Lesions are brown to black in color and hard in consistency with smooth surface. This is referred as â€˜Eburnationâ€™ derived from Latin word. g) Recurrent caries It occurs at interface of tooth and restorative material due to many factors like defective cavity preparation, micro leakage etc.
h) Radiation caries It is seen in a patient who has undergone radiotherapy of oral lesions.
of the radiotherapy is
xerostomia, which leads to the development of caries. III) According to age pattern a. Nursing bottle caries The prolonged breast feeding especially at night and bottle fed babies develop caries usually on maxillary incisors. This type of caries is known as nursing bottle caries.
b. Adolescent caries If acute caries attack occurs in adults then it is known as adolescent caries. c. Geriatric caries Caries which occurs in older adults around the age of 50 is referred as geriatric caries. IV) According to pathway of caries a. Forward caries In this decay starts in enamel and then it involves the dentin. (Pit decay). b. Backward caries In this decay attack the enamel from its dentinal side. (Smooth surface caries).
According to number of surface involved a. Simple caries Lesion involves only one surface of a tooth. b. Compound caries Lesion involves two surfaces of a tooth. c. Complex caries Lesion involves three or more surfaces of a tooth. 10
Blackâ€™s classification It is based on the treatment and restoration design.
Cass I: Lesions found on pits, fissures, grooves; occlusal surfaces of molars and premolars, occlusal two thirds of the buccal and lingual surfaces of molars and the lingual surfaces of anterior teeth. Class II: Lesions found on proximal surfaces of bicuspids and molars. Class III: Lesions found on the proximal surfaces of anterior teeth that do not involve or necessitate removal of the incisal angle. Class IV: Lesions found on the proximal surfaces of anterior teeth and involve or require the removal and restoration of the incisal angles. Class V: Lesions found at the gingival third of the facial and lingual surfaces of anterior and posterior teeth. Class VI: Originally are not included in Blackâ€™s classification. Lesions found on incisal edges and cuspid tips and found on molar and premolar cusp tips, axial angles of teeth or any highly self cleansable areas.
Histopathology of caries
Enamel caries: Histologically,
seen as, the loss of
interprismatic or inter-rod substances of the enamel and accentuation of the incremental striae of retzius. Smooth
surface enamel caries
conical in shape with broad base on enamel surface and the tip on the DEJ. Whereas in case of pit and fissure caries, its apex is at the outer surface and itâ€™s base is towards the DEJ. Light microscopic studies of enamel caries revealed four distinct zones starting from the advancing front of the lesion. These zones are classified as: Zone 1: Translucent zone Zone 2: Dark zone Zone 3: Body of the lesion Zone 4: Surface layer Translucent zone: It lies at the advancing front of the enamel lesion. It is not always present. This zone is slightly more porous than sound enamel. Pore volume is 1 percent. Dark zone: It lies adjacent and superficial to the translucent zone. It is usually present. This zone is formed as a result of demineralization Body of the lesion: It lies between the relatively unaffected surface layer and the dark zone. It is the area of greatest demineralization. In polarized light the zone shows a pore volume of 5 percent.
Surface zone: It appears relatively unaffected. The greater resistance of the surface layer may be due to a greater degree of mineralization and / or concentration of fluoride in the surface enamel.
Diagnosis: One of the primary goals of operative dentistry is to provide functional stomatognathic system along with pleasing esthetics. Such goals can be achieved only with sound foundation. The sound foundation in any treatment regime is â€˜proper diagnosisâ€™. Unfortunately, current tools used in dental caries detection are not enough to diagnose the disease process in early stages. Dental caries can be diagnosed by using following diagnostic tools, 1. Explorers A sharp explorer is passed over tooth surface to determine roughness or softness of the tooth. Resistance to removal indicates evidence of demineralization. 2. Radiographs Bite-wing radiographs
are more important to detect incipient
lesions at the contact points. 3. Discoloration This is not true in every case, but discoloration should make one suspicious of decay. 4. Patient complaints Osmotic pressure changes within dentin by having sweets, hot, cold, or any item is an indication of carious lesion. 5. Dental floss or tape The floss is inserted through a contact area and then dragged occlusally in a sawing action against one proximal surface, if it shread then we must suspect a proximal lesion. 14
6. Separation of teeth Tooth is separated using a wood or plastic wedge or mechanical separator to visualize proximal caries. 7. Translumination Light source is focused from ligually and teeth are viewed from facial direction. The shadow of the caries cone is seen through the enamel. 8. Dye penetration method Various dyes have been tried to detect carious enamel such as, procion, calcein, brilliant blue, basic fuchsin, acid red, iodine and methylene blue, etc. 9. Laser auto florescence In this, visible light has been used as the light source for detection of smooth surface and fissure caries at an early stage. The tooth is illuminated with a broad beam of light from argon ion laser and fluorescence observed. Healthy tooth fluoresces differently from that of carious tissue. 10. Ultrasonic imaging This was introduced for detecting early carious lesions in smooth surfaces. It is assessed by ultrasound pulse echo technique. The ultrasonic probe is used which sends longitudinal waves to the surface of the tooth. The sites with visible cavitations produce echoes with higher amplitude.
Deep carious lesions are those in which caries penetration is easily observed in the dentin and may involve more than one half of the dentin thickness between the DEJ and the pulp. A tooth with a deep cavity will reveal upon excavation of the carious and necrotic dentin, an interface of decalcified and softened, but still intact dentin. The deep cavity can destroy the structural components of the tooth, if the rate of the carious process exceeds the speed of the pulpal response. If the lesion is left untreated then it encroaches upon the pulp. It is characterized by sharp pain, lasting for a moment. It is more often brought about by cold than hot beverages. It does not occur spontaneously and disappears on removal of stimulus.
The carious dentin can be divided in to two layers or zones. 1) Infected dentin or outer carious dentin 2) Affected dentin or inner carious dentin Infected dentin is characterized by irreversibly denatured collagen which is infiltrated with bacteria; both organic and inorganic components are deteriorated. It is not remineralizable. It is darker and softer than affected dentin. Whereas, affected dentin is characterized by reversibly denatured collagen, which is not infiltrated with bacteria and is remineralizable. Infected dentin should be removed and affected dentin can be left behind during cavity preparation to avoid pulp exposure. It is believed that affected dentin either remineralizes or becomes sterile once the cavity is thoroughly restored. Clinically, it may be difficult to distinguish between the two layers of carious dentin. The 0.5% solution of basic fuchsin in propylene glycol stains the infected dentin clearly red but not the affected dentin and normal dentin.
Outer carious dentin (1), inner carious dentin (2), and normal dentin (N) distinguished on the section surface of a human carious tooth.
Biochemistry of two layers: Collagen fibers are made of bundles of three molecular chains twisted and assembled by the intermolecular crosslink that fixes periodic structure and develops the cross band structure seen on the electron micrograph. The normal dentin shows prominent peak of inter molecular cross links consisting
(hydroxylisinorleucine) and a moderate peak of precursor consisting of diOHNL (dihydroxylnorleucine) and OH-NL (hydroxylnorleucine). The infected dentin showed both intermolecular cross links and precursors considerably decreased this indicates that the cross links were broken into new materials. It is irreversible. The affected dentin showed significantly decreased intermolecular cross links increased precursors. The cross links shifted to the precursors such a shift is believed to be reversible, because it occurs when the pH shifts to acid and reverses when the pH returns to neutral. The remineralization of dentin occurs on the basis of collagen fibers on the periodic joints on which apatite crystals attach in fringes, it cannot occur in the infected dentin in which collagen fibers are broken, losing intermolecular cross links, but it can occur in the affected dentin in which the intermolecular cross links and cross band structure are reversibly shifting to precursors.
Column chromatograph of collagen intermolecular crosslinks of sound human dentin. The definite peak of crosslinks is observed (one-third in the right)
Column chromatograph of collagen intermolecular crosslinks of the inner carious dentin. The cross-links partly shifted to the precursors (one-third in the left).
Column chromatograph of collagen intermolecular crosslinks of the outer carious dentine. The crosslinks were broken irreversibly.
Carious dentin affected dentin
Normal dentin, Sound layer
Much decreased granular irregularly scattered
Decreased partially dissolved attached to collagen
unchanged slender plate attached to collagen
unclear or lost irreversibly broken
clear shift to precursor
Lost or demineralized Lost Infected
partly demineralized sound uninfected
normal sound uninfected
Characteristics Remineralization Hardness natural discoloration
Not remineralizable Greatly softened discolored
remineralizable intermediate partly discolored
Normal Not discolored
Diagnosis Caries detector stainability
Items compared Between tubules Inorganic crystals Quantity Form Arrangement Collagen fibers cross band structure intermolecular cross links In tubules Peritubular dentin Odontoblastic processes Bacteria
Dentinal carious lesions in vital P-D organ will exhibit five layers or zones, when tooth sections are examined under an optical microscope. All these layers may not be evident in all the carious lesions. There are two types of carious processes acute chronic. The layers differ in their dimensions, contents and activities in the two types of carious processes.
a, Decayed zone. b, Septic zone. c, Demineralized zone. d, Transparent zone. e, Opaque zone.
Zones of decay in dentin. A, Decayed zone. Accumulation of microorganism, plaque, complete loss of structure. B, Septic zone. Invasion by microorganisms, irregular crystal formation, deformed tubules, loss of collagen banding structure and intermolecular connection connection. C, Demineralized zone. D, Transparent zone. E, Opaque zone.
ZONE 1: Decayed zone • The dentin is almost completely devoid of minerals. • It is soft in consistency and seen more in acute carious process. • The collagen fibers if present have completely lost their microstriations and links. • There is high concentration of microorganisms in the destructed dentin. • The maximum thickness is found in closed lesions. ZONE 2: Septic zone • This zone contains highest concentration of microorganisms. • The dentin is very well decalcified, softer in consistency and seen more in acute carious process than chronic. • The collagen fibers have fewer cross-band striations than normal and intermolecular links are lost. • The remaining mineral crystals are deformed, irregularly scattered and show no relation to the collagen fibers. • The dentinal tubules are extremely widened and cavitated. • The color ranges from a light yellow to dark reddish brown depending upon the presence and duration of chromogenic bacterial activity. ZONE 3: Decalcification of dentin • The dentin is demineralized with intact dentinal matrix. • The collagen fibers have their normal structure, cross-band striations. • Dentinal tubules have their normal dimensions. • It is greater in acute process than chronic.
• According to Fusiyama, a maximum width for this layer is 1750 micro meters in acute decay, with a minimum of 50 micrometers width in chronic decay. • Microorganisms will be confined to the superficial 1/3 - 1/2 of this zone in acute decay. But in chronic decay it will be found throughout this layer. • The acute decay has straw yellow color. Whereas chronic decay has yellow brown or dark brown color depending on microbial and environmental staining activity. • Repair activities will be more noticeable at the dentinal caries cone. ZONE 4: Transparent zone •
It is the area of undisturbed mineralization repair.
• It is the zone of dentinal sclerosis and calcific barrier which are impermeable and impenetrable types of dentin. • It is seen as more transparent in ground sections but radio graphically it appears as radiopaque. • It is more pronounced in chronic process and may contain few microorganisms. • Clinically it may be slightly discolored and dentin extremely hard compared to normal dentin.
ZONE 5: Opaque zone • It is found pulpal to the transparent zone. • It is characterized by intratubular fatty degeneration, this type of degeneration predisposes to the sclerosis of dentinal tubules. • It is more pronounced in acute lesions and will appear radiolucent in radiograph. The maximum resistance to pulpal penetration occurs with the arrival of the transparent and demineralized zone. The rate of progress of caries tends to be slower in older adults than young persons because of dentinal sclerosis with aging.
The carious process has three distinct forms of irritants, a) Biologic irritants Microorganisms and metabolites. b) Chemical irritants Acids. c) Physicomechanical irritants The gradual diminution of the effective depth of P-D organ due to the advancing carious lesion. Each of these irritants will precipitate a reaction in the P-D organ at one stage of its progress. Many factors are involved in the type, extent and destructive-protective nature of the P-D organ reaction toward the caries irritation.
The following factors are the guidelines, Type of decay The acute decay process has a greater tendency towards a destructive reaction in the P-D Organ.
Chronic decay is usually slow provides substantial repair.
Duration of the decay process The longer the duration in acute decay, the more massive the destruction of tooth structure. The longer the duration in chronic decay, the greater the chances for repair provided the pulp chamber and root canal system are not directly involved.
Depth of involvement The deeper the caries, the nearer the source of irritation to the pulp. 25
The greater the intensity of irritation, the greater will be the pulp destruction. For peripheral involvements, we can see either no pulpal reaction or a reparative reaction in both acute and chronic lesions. For moderate depth involvement, we can expect same reaction from chronic decay as in peripheral involvement. In case of acute lesions of moderate depth we can see pulpal destruction. For profound depth involvement we can see the some repair and perhaps resolved pulpal destruction in chronic decay, but definite pulpal destruction in acute decay. For perforating lesions we can expect pulpal destruction in both types of decay.
Depth of involvement. A, Peripheral involvement-outer one third, or less of dentin. B, Moderate involvement-outer two thirds, or less, of dentin. C, Profound involvement-more than two thirds of dentin short of perforation. D, Perforating involvement
Number and pathogenecity of micro organisms The greater the virulence and population of microorganisms, the greater will be the likelihood of the pulpal reaction.
Tooth resistance This involves an infinite number of factors such as, Thickness of dentin through which the decay must pass to initiate a recognizable effect. Permeability of the involved dentin. Solubility of the involved dentin. The susceptibility of the tooth.
Individual reaction of the P-D organ It depends on many factors i.e. tooth age, patients age, cellularity, vascularity of the pulpal and root canal system tissues, etc.
Effective depth The effective depth is the area of minimum thickness of sound dentin separating the pulpal tissue from the carious lesion. Three types of pulpal reactions are seen, 1) Healthy reparative reaction: When effective depth is 2 mm or more, healthy reparative reaction occurs. This is the most favorable response. It consists of stimulating P-D organ to form sclerotic dentin and/ or calcific barrier. This is followed by formation of normal secondary dentin. The secondary dentin is different from primary dentin in that secondary dentin tubules are slightly misangulated. 27
It occurs without any disturbance in the pulp tissues. 2) Unhealthy reparative reaction: When effective depth is from 0.8 to 2 mm unhealthy reparative reaction occurs. This may be fairly favorable. It begins with degeneration of the odontoblasts either by poisoned or by being spirated into the dentinal tubules. This is followed by the formation of the dead tract in the dentin and complete cessation in the formation of secondary dentin. This is accompanied by mild pathological and clinical changes of a reversible nature in the pulp tissue resulting in the formation of an irregular type of tertiary dentin replacing the degenerated odontoblasts. Tertiary dentin is formed by the undifferentiated mesenchymal cells and fibroblasts and its deposition continues until they seal the dead tracts. Eventually the odontoblasts will pave over this reparative dentin and start formation of normal secondary dentin. The tertiary dentin is considered to be the function of the pulp tissue proper. Tertiary dentin has certain limitation, 1) It is not completely impervious like the calcific barrier. 2) Its rapid formation will lead to the occupation of part of the pulp chamber with tissues other than those normally responsible for the further repair, metabolism and innervations therefore tertiary dentin may be said to be “age the pulp”. 3) Reduces its capacity for further defensive action against future irritation. 28
4) Tertiary dentin is less elastic than the primary dentin. 3) Destructive reaction When effective depth is less than 0.3-0.8 mm, pulpal destruction occurs. This is the most unfavorable pulpal response to irritation. It begins with the loss of odonoblasts and outer protective layer of the pulp. The insult involves the pulp tissue proper, exceeding its reparative capacity. The resulting tissue reaction will be inflammation, which may progress to abscess formation, phlegmonous or chronic inflammation or finally complete necrosis of the pulp. In any event pulp tissues cannot recuperate from these pathologic changes.
Proper diagnosis of the lesion is vital for planning the method of treatment. Unfortunately there is no particular diagnostic tool for the diagnosis of deep carious lesions. However, by combining the results of the clinical tests and observations, we can make a good diagnostic perspective. Essential factors for adequate and detail diagnoses of deep carious lesions are: Reparative capacity of the P-D organ. Soundness of the dentin in the preparation floors and walls. Reparative capacity of unsound attacked dentin. Type and extent of any degeneration in the P-D organ. Seal ability of the restorative materials to be used. Potential
instrumentation, restorative materials and restorative procedures.
Clinical tests 1. Pain: • The presence of pain may serve as guiding criteria for the status of the P-D organ. • Any symptoms of pain should be recorded. • In deep carious lesions, the pain is of short duration, initiated by thermal or chemical stimulation of the P-D organ that disappears immediately after the removal of the stimulus; it indicates lesser degenerative changes in the P-D organ. • If the pain occurs at night or if it is continuous and it is not initiated by thermal or chemical stimulation of the P-D organ is an indication of destructive /degenerating changes in the P-D organ. 30
2. Radiographs: Radiographs give a two dimensional image of three dimensional structures. Radiographs especially periapical radiographs can be a supporting tool for the diagnosis of deep carious lesions. A radiograph indicates: a) The proximity of the carious lesion to the pulp chamber and root canal system. From this effective depth can be estimated. The extent of lesion as shown in the radiograph will always be less than the actual size of the lesion. b) Any pulpal changes in the form of intrapulpal and peripulpal calcification. c) The thickening of the periodontal ligament space with an intact lamina-dura will indicate increased vascularity and consequently increased activities of the P-D organ. Discontinuity in the laminadura may indicate more advanced activities of the P-D organ. d) The size of the pulp chamber compared to the size of the tooth. The higher the pulp size /tooth size ratio, the better will be the reparative capacity of the P-D organ. Unusually high ratio in comparison to the adjacent, opposing and contra-lateral teeth may indicate complete cessation of the reparative capacities of the pulpal tissues of the involved teeth. e) The location of the caries cone tip relative to the anatomy of the pulp chamber and root canal system. f) The relative size of the apical foramen to that of the pulp chamber and root canal system. g) The dimension of a pulp exposure relative to the dimensions of the pulp chamber and root canal system. This is a major factor in determining the repairability via dentinal bridging of the exposure. 31
h) The gross evaluation of mineralization, permeability of the involved dentin. In radiograph the sclerotic dentin and calcific barrier appears as radiopaque, Tertiary dentin appears as a localized thickening of the dentinal bridge, pulpal to the lesion creating irregularities in the pulp chamber or root canal walls and /or roof. This is very important in determining the reparative capacity of the P-D organ.
3. Pulp testing a. Thermal pulp testing This test helps to determine the status of the pulp tissue. Application of a thermal stimulus, either hot or cold cause rapid movement of the fluid in the dentinal tubules which stimulates the AÎ´ nerve fibers present in the pulp to elicit the symptom of pain. An abnormal response to hot/cold indicates the pulpal disorder. When several teeth in a quadrant are tested thermal tests are helpful in pinpointing the culprit tooth. The thermal tests are broadly categorized in to two: â€˘ Heat tests and â€˘ Cold tests
• Before undergoing the tests, the patient should be told about the type of tests to be performed. • The teeth in the quadrant should be isolated and dried using a 2"x 2"guaze. • The patient should be instructed to raise his hand or a finger when hot or cold sensation or pain is felt on the application of the stimulus.
Heat test: • This test is done by different techniques that deliver different degrees of temperature. • The most common method employed for this test is by heating a temporary gutta-percha stick over an alcohol flame till it becomes shiny and sags. • The tooth is lubricated with a thin layer of coca butter or petroleum jelly to prevent the hot gutta-percha material from adhering to the tooth surface. • The heated gutta-percha is then applied at the junction of the cervical and middle third of the facial surface of the tooth to elicit a response. • Other ways of applying heat to the tooth surface may employ the use of hot compound, hot burnisher, plastic instruments, coffee test or the use of frictional heat produced by rotating polishing rubber disc against the tooth surface. • The most effective thermal test for tooth with porcelain or metal full coverage involves isolating the tooth and bathing it in warm water delivered from a syringe. The preferred temperature for a heat test is approximately 65.50C (1500 F).
Observation: 1. No response – Necrosis, Gangrene, Chronic abscess. 2. Mild to Moderate response – Normal pulp 3. Painful response which subsides immediately after the stimulus is removed – Reversible pulpitis. 33
4. Painful response which may remain even after removal of stimulus â€“ Irreversible pulpitis, acute alveolar abscess, acute pulpitis.
Cold tests: This test is done by applying cold to the tooth surface. Cold tests can be performed in several different ways, i.
By using a stream of cold air directed against the crown of the previously dried tooth.
A simple means of applying cold to the tooth is to wrap ice in wet gauze and place it against the facial surface of the tooth and to compare the reaction to a control tooth.
Pencils of ice can be produced by filling discarded anesthetic carpules with water and freezing them in an upright position in a refrigerator. A quarterâ€“inch diameter cone of ice is usually placed against the tooth for 5 sec.
The use of carbon dioxide snow (dry ice) as a cold test was first described by Ehrmann (1973). The temperature of dry ice is -77.7 0 C/1080F. It is able to penetrate full coverage restorations and elicit a response from the underlying tooth.
Use of Dichloro-Difluoro methane (DDM or FREON 12) and 1,1,1,2 Tetrafluoroethane available as Green Endo-Ice.
Use of ethyl chloride is the easiest of all. It is sprayed liberally on a cotton pellet and the cotton pliers holding the pellet are tapped once or twice to shake out the excess liquid. The cotton pellet is then placed on the area and the patient response is noted. The ethyl chloride technique is effective even on teeth covered with cast metal crowns. A painful response that subsides quickly after the stimulus is removed is characteristic of reversible pulpitis.
Carbon dioxide dry ice “pencil” for thermal testing developed by H. Obwegeser. A, Metal arm and plastic ice former attached to tank of siphoned CO 2 (siphoned type of CO2 should be used). B, Loaded ice former is removed and plunger inserted to extrude the CO 2 ice pencil. C, Ice pencil held in gauze to prevent CO2 “burns.”
5. No response - Non vital or false negative response Ex: - Excessive calcification - Recent trauma to the tooth - Patient is premedicated 6. Moderate response – Normal pulp 7. Painful response which subsides immediately after the stimulus is removed – Reversible pulpitis. 8. Painful response which may remain even after removal of stimulus – Irreversible pulpitis - In case of hyperemia, there may be a quick response and in Chronic pulpitis may be a delayed response. - However thermal tests are not as accurate as an electric pulp test.
b. Electric pulp testing: These are designed to elicit response by stimulating Aδ sensory fibers within the pulp. This is performed with the instruments having either battery or alternating current powered electrodes. They only suggest whether a tooth is vital or non vital.
Procedure: • Before performing the test, the procedure of test should be explained to the patient and asked the patient to raise the hand when he/she experiences pain or tingling sensation. •
The teeth are isolated and dried using a 2" x 2" gauze piece.
• If the tooth has a proximal metallic restoration a rubber dam (or) celluloid strips should be placed interproximally to prevent electrical conduction to the adjacent tooth. • The conducting medium (tooth paste) is applied at the site. 36
• The electric current must complete a circuit from the electrode through the tooth to the body of the patient and then back to the electrode. When gloves are not used, the circuit is completed by the contact of the dentist’s finger with the electrode and the patient’s lips or cheeks. • The current flow should be increased slowly till the patient feels a tingling sensation or a sensation of pain. • Each tooth should be tested for two or three times and average reading should be noted. • When a positive response is obtained, comparisons should be made with the adjacent, opposing and contra-lateral teeth. If required energy is higher in the control teeth, this is an indication of possible acute changes in the PDorgan of the affected tooth. If required energy is lower in the control teeth, this may indicate possible progressive chronic changes, advance repair, or walling off the P-D organ from the offending lesion.
Use of an electric pulp tester. A, Posterior teeth should be isolated and dried. Mylar strips can be used to separate connecting metallic fillings. Using toothpaste as a conductor, contact should be made on the occlusal third. B, Isolated and dried anterior teeth are contacted on the incisal third to avoid false stimulation of gingival tissue. C,Vitality Scanner pulp tester. To complete the circuit, the patient may touch the metal handle. D, Digitest pulp tester with lip contact to complete circuit. Both pulp testers have a digital readout. The difference lies in size and price.
• In case of periapical radiolucency, EPT will help the clinician to determine whether the pulp is vital. • It helps to differentiate pulpal disease from periodontal disease or nonodontogenic causes.
Disadvantages: • The electric pulp test does not provide any information about the vascular supply of the tooth. • Readings taken from posterior teeth may be misleading since some combinations of vital and nonvital root canal pulps may be present. • Teeth with full-coverage restorations because electrical stimulus cannot pass through acrylic, ceramic or metallic portions of crown. • The test may give false positive/ false negative response. Reasons for false positive response: Electrode contacts the gingival tissue. Anxious patient. In case of liquefaction necrosis. Failure to isolate and dry the teeth properly. Multirooted teeth –the pulp may be vital in one or more root canals. Reasons for false negative response: Patients who are premedicated with analgesics, narcotics, alcohol or tranquilizers. Inadequate contact of electrode with the tooth structure. Recently traumatized tooth. Recently erupted teeth with an immature apex. Excessive calcification in the canal. Dead batteries or forgetting to turn on the pulp tester. 38
Presence of pulp protecting bases under restoration Patients with high pain threshold. Partial necrosis.
Contraindication: • In patients with a history of a cardiac pacemaker because it may interfere with the electrical activity of the pacemaker. Therefore electric pulp test should not be the sole diagnostic tool in recording or verifying the vitality or the degenerating status of the P-D organ.
4. Test cavity preparation: •
It is performed when other methods of diagnosis have failed.
• The test cavity is made by drilling through the enamel dentin junction of an unanesthetized tooth. • The drilling should be done at slow speed and without a water coolant. • Sensitivity or pain felt by the patient is an indication of vital pulp. • Sedative cement is then placed in the cavity and the search for the pain continues. • If no pain is felt, cavity preparation may be continued until the pulp chamber is reached. • If the pulp is completely necrotic endodontic treatment can be continued.
5. Anesthetic testing: This test is restricted to patients who are in pain at the time of the test, when the usual tests have failed to enable one to identify the tooth. The main objective is to anesthetize a single tooth at a time until the pain disappears and is localized to a specific tooth.
• Using either infiltration or intraligamentary injection, inject the most posterior tooth in the area suspected of being the cause of pain. • If pain persists when the tooth has been fully anesthetized, anesthetize the next tooth mesial to it and continue to do so until the pain disappears. • If the source of pain cannot be determined, whether in maxillary or mandibular teeth, an inferior alveolar injection should be given. • Cessation of pain naturally indicates involvement of a mandibular tooth and localization of the specific tooth is done by the intraligamentary injection when the anesthetic has spent itself. • This test is a last resort and has an advantage over the test cavity during which iatrogenic damage is possible.
6. Direct pulp exposure: The following are the data that can be collected from observation of a direct pulp exposure and its clinical significance. a) A pin- point exposure having sound dentin at the periphery of the exposure with no hemorrhage in a vital P-D organ is an indication of either no pulpal inflammation or a mild degree of pulpal inflammation restricted to the exposure site. This can be repaired, if properly treated. b) A pin point exposure having sound dentin at its periphery, but accompanied by a drop of blood that coagulates immediately on the cavity floor in the form of a button is also an indication of a healthy, reparable P-D organ. c) An exposure having decayed or infected carious dentin at its periphery would indicate considerable inflammation in the pulpal or root canal tissues for beyond exposure site. The reparability of this type of exposure is doubtful.
d) An exposure accompanied by profuse hemorrhage could be an indication of great involvement of the pulpal and root canal tissues. This type of exposure is beyond repair. e) An exposure accompanied by inflammatory fluids or pus is evidence of extensive inflammation and destruction of the pulpal and root canal tissues. This type of exposure is beyond the repair. f) The lower the ratio of exposure diameter relative to the dimensions of the pulpal and root canal tissues, the greater will be the possibility of repair and healing of the P-D organ. g) If the exposure is very close to anatomical constrictions in the pulp chamber or root canals, the chances of repair is very less.
7. Percussion sensitivity: • Tenderness to percussion is of little value in determining the degree of inflammation in the pulpal and root canal tissues. • A tooth with extensive inflammation often exhibits tenderness to percussion and it indicates some type of pathology in the P-D organ.
8. Type of dentin: • The visual and tactile evaluation by use of an explorer can give an idea of the type of dentin present in the preparation walls and floors. • The presence of a calcific barrier or sclerotic dentin close to the pulp chamber indicates reparative activity. • Generalized discoloration of the dentin not arising from previous amalgam restoration which ranges from grayish to grayish-pink or grayish-brown may indicate devitalized or dying P-D organ that has lost all reparative capacity.
9. Use of dyes to differentiate between reparable and irreparable dentin:
• The use of dyes, guide an operator as to where to stop excavating dentin from cavity walls and floors.
Basic fuchsin: • 0.5% Basic fuchsin in propylene glycol is used to differentiate reparable `and irreparable dentin. •
One drop of 0.5% basic fuchsin is applied to the dentin for 10 second and then thoroughly washes the preparation with the water.
• The irreparable areas of dentin will distinctly stain red. • Fusiyama and his co-workers have shown that the banding between the reparable and irreparable areas will be very clear. • They claim that the nature of the collagen fibers constitute the difference in the stainability of the two layers of dentin. • The reparable dentin will have intact collagen fibers oriented for remineralization and will not stain with the fuchsin solution. • Whereas, irreparable dentin will have its collagen fibers denatured, unremineralizable and can be stained red by the fuchsin solution. • Basic fuchsin (magenta) C20H20N3Cl is a dye of the phenylmethane group. • However carcinogenicity of fuchsin was suspected.
Section surface of a human carious tooth before staining. Two layers of carious dentin cannot be distinguished.
Section surface stained by basic-fuchsin-propylene glycol solution. Two layers of carious dentin are clearly differentiated.
Acid red: • It has same effect as basic fuchsin. • 1% acid red solution in propylene glycol is capable of differentiating two layers of carious dentin. • The acid red C20H29O7N2S2Na (mol.wt 580.67) and chemically called 9-(2'-sulfonium-4'-sulfophenyl)-6-diethylamino-3-(N,N-diethylimino)-3isoxanthene sodium salt.
One drop of caries detector is applied to a cavity and spry washed after 10 seconds
10. To differentiate the pain coming from upper teeth or from maxillary sinus: A swab soaked in topical anesthesia ointment or gel is introduced through the nostrils in to the middle Conchae upwards, medially and backwards for about 他 of an inch applying the topical anesthesia to the mucous membrane to the walls of the conchae. If pain is of a sinus origin, it will disappear momentarily if it is from dental cause it will not.
There is no international consensus on the treatment of deep carious lesions. This can be confirmed when textbooks on cariology and restorative dentistry are compared with the endodontic literature. The cariology opinion aims to prevent pulpal exposure, whereas the endodontic opinion pays little attention to the possibility that a deep carious lesion might be process that can be arrested. The various methods used for management of deep carious lesions are management of acute caries and chronic caries, indirect pulp capping, direct pulp capping and Pulpotomy etc. The ultimate goals in managing deep carious lesions are preservation of pulp vitality before arbitrarily instituting endodontic therapy and reparative dentin formation.
MANAGEMENT OF ACUTE DECAY Deep lesions i.e. deeper than 2mm from the DEJ confirmed as acute decay. It can be treated in the following sequence. The physiologic status of the P-D organ should be evaluated using diagnostic tools. All undermined or unwanted enamel in the preparation should be removed. All softened dentin should be removed if it is safe without creating an exposure. This should be done by using a spoon excavator. The reparability of the remaining dentin should be verified using basic fuchsin or red dye solutions. Any infected dentin should be removed. If There is more chances pulp exposure by removing all softened dentin the deepest layer should be left intact, provided: 1. The P-D organ should be healthy. 2. The remaining dentin should be reparable. 3. The softened dentin that is to remain should be located in the deepest part of the pulpal and/ or axial wall. The surrounding walls and at least a portion of the pulpal and axial walls should be in hard sound dentin. If there is no pulp exposure appropriate intermediary base should be given.
MANAGEMENT OF CHRONIC DECAY 46
Chronic decay can be treated in following sequence: The physiologic status of the P-D organ should be evaluated using diagnostic tools. All undermined or unwanted enamel in the preparation should be removed. All softened dentin should be removed, using either spoon excavators or large round stainless steel burs in a slow speed hand piece. The reparability of the remaining dentin should be verified using basic fuchsin or red dye solutions. Any infected dentin /non reparable dentin should be removed. If removal of softened dentin leads an exposure of the pulpal tissues, proceed with the appropriate pulp capping procedure or with endodontic therapy. If there is no pulp exposure appropriate intermediary base should be given.
INDIRECT PULP CAPPING 47
Pulp capping refers to the treatment of an area of vital pulp tissue with the hope that the recuperative power of the remaining pulp is sufficient to restore it to health.
Definition: Indirect pulp capping is defined as incomplete excavation leaving a thin layer of residual carious dentin (King et al. 1965) Indirect pulp capping is defined as the application of a medicament over a thin layer of remaining carious dentin, after deep excavation, with no exposure of the pulp.
Objective: • To avoid pulp exposure • To stimulate the pulp to generate reparative dentin beneath the carious lesion. This results in the arrest of caries progression and preservation of the vitality of the non exposed pulp.
Historical review: The concept of indirect pulp capping was first described by Pierre Fauchard as reported by John Tomes in the mid-18 th century. He recommended that all caries should not be removed in deep sensitive cavities. In 19th century John Tomes stated that, “it is better that a layer of discolored dentin should be allowed to remain for the protection of the pulp rather than run the risk of sacrificing the tooth”. But they did not mention any medication to softened dentin. In 1891 W.D Miller discussed various “antiseptic” that should be used for sterilizing dentin. G. V. Black stated that, “no decayed or softened material should be left in a cavity preparation, whether or not the pulp was exposed.
Rationale: • Indirect pulp capping is based on the knowledge that decalcification of the dentin precedes bacterial invasion within dentin. • The outer layer of the carious dentin that contains the majority of the microorganisms and reduces the continued demineralization of the deeper dentin layers from bacterial toxins and sealing the lesion to allow the pulp to generate reparative dentin. • Fusiyama and colleagues demonstrated that the dentinal caries actually consists of two distinct layers having different ultramicroscopic and chemical structures. • The outer carious layer is irreversibly denatured, infected and incapable of being remineralized and it should be removed. • The inner carious layer is reversibly denatured, not infected and capable of being remineralized and should be preserved.
Dynamics of indirect pulp capping: • The caries formula consists of three factors which are essential for the caries process to be active and progressive. • The three contributing factors are tooth structure, microorganisms and substrates. • If any of these factors are missing the caries process will not occur. • In indirect pulp capping procedure, we are removing two factors namely, microorganisms and substrates. • In acute decay, the excavation of softened dentin will remove all microorganisms. • In chronic decay, minimal numbers of microorganisms will remain but they will be reduced by effectively sealing cavity with an appropriate therapeutic restorative material. 49
• A favorable environment will have been created for the repair of the damaged structure. • This will proceed in two dimensions 1. Remineralization of the part or all of the remaining decalcified dentin in the cavity floor will occur. 2. Deposition of secondary and/or tertiary dentin pulpal to the carious lesion. • Indirect pulp capping should be limited to those teeth that have been evaluated to be free from any form of pulpal degeneration. • The success of the treatment is dependent upon the reparative capacity of the P-D organ.
Materials used in indirect pulp capping: Most commonly used materials for indirect pulp capping are calcium hydroxide (Ca [OH] 2), Zinc oxide eugenol (ZOE), Acid-etched and bonded composites.
Procedures: Case selection is based on clinical and radiographic assessment. Only those teeth free from irreversible signs and symptoms should be considered for indirect pulp capping.
Indications: The decision to undertake the indirect pulp capping procedure should be based on the following findings: 1. History a. Mild discomfort from chemical and stimuli b. Absence of spontaneous pain 2. Clinical examination a. Large carious lesion b. Absence of lymphadenopathy c. Normal appearance of adjacent gingival d. Normal color of the tooth 3. Radiographic examination a. Large carious lesion in close proximity to the pulp b. Normal lamina dura c. Normal periodontal ligamental space d. No interradicular or periapical radiolucency
Contraindications: Findings that contraindicate this procedure are listed below: 1. History a. Sharp, penetrating pain that persists after withdrawing stimulus b. Prolonged spontaneous pain, particularly at night
2. Clinical examination a. Excessive tooth mobility b. Tooth discoloration c. Nonresponsiveness to pulp testing techniques 3. Radiographic examination a. Large carious lesion with apparent pulp exposure b. Interrupted or broken lamina dura c. Widened periodontal ligament space d. Radiolucency at the root apices or furcation areas If the indications are appropriate for indirect pulp capping, such treatment may be preformed as a one-appointment, a two-appointment or modified stepwise excavation procedure.
One-appointment technique/one step procedure In this procedure, complete demineralized and discolored dentine is removed leaving a thin layer of residual caries and re-entry is not undertaken. The value of re-entry and re-excavation has been questioned by some clinicians. Leung et al. suggested that re-entry to remove the residual minimal carious dentin after capping with calcium hydroxide may not be necessary if the final restoration maintains a seal and the tooth is asymptomatic. Numerous studies reported that, the success rate of indirect pulp capping with calcium hydroxide ranges from 73% to 98% and the second entry subjects the pulp to potential risk of exposure owing to overzealous re-excavation. Tooth selection for one-appointment indirect pulp capping must be based on clinical judgment and experience with many cases.
Technique: Administer local anesthesia and isolate with a rubber dam. Establish cavity outline with a high-speed hand piece. Remove the majority of soft, necrotic, infected dentin with a large round bur in a slow-speed hand piece without exposing the pulp. The bur size should be large and should harmonize with the size of the tooth and the amount of remaining carious dentin (i.e. No. 4, 6, or 8) When removing carious dentin, both the color and texture of the remaining dentin may be used as a guide to indicate proper removal. The hardness and texture of the dentin at the base of the cavity serve as indicators of caries penetration. Remove all peripheral carious dentin with sharp spoon excavators. The use of a large round bur can provide better results than the use of a spoon excavator. Caries indicators can help in determining the extent of
the outer infected layers of caries. Irrigate the cavity and dry with cotton pellets. Cover the remaining affected dentin with a suitable therapeutic restorative material Fill or base the remainder of the cavity with provisional restoration to achieve a good seal. If the tooth is badly broken-down an aluminum crown is often advised to provide temporary protection for the sedative cement. If patient gets symptoms, re-entry would be advised to confirm reparative dentin and pulp exposure status. If pulp exposure occurs during re-entry, either direct pulp capping or pulpotomy would be indicated.
(a) Before treatment (b) after excavation with focus on pulp close excavation (residual caries), (c) No re-entry and permanent restoration are made (d) Iatrogenic pulp exposures might be a potential risk.
Two-appointment technique/ step excavation
Procedure In this procedure dental caries is removed a step - by - step procedure. The first step has focused on excavation close to the residual level of caries, leaving dentin behind to facilitate a biological response from a vital pulp, whereby tertiary dentin can be produced. At re-entry the retained carious tissue is removed, with avoiding a perforation of the pulp because of the extra tertiary dentinal matrix laid down.
Technique: First sitting: Administer local anesthesia and isolate with a rubber dam. Establish cavity outline with a high-speed hand piece. Remove all peripheral carious dentin with large round bur in a slowspeed hand piece and sharp spoon excavators. Remove the majority of soft, necrotic, infected dentin with a large round bur in a slow-speed hand piece without exposing the pulp. Although there are no precise methods to determine how much decayed dentin is to be removed, clinical judgment alerts an experienced practitioner to remove dentin that is necrotic. Irrigate the cavity and dry with cotton pellets. Apply fluoride to semi-carious dentin and Wait for five minutes Cover the remaining affected dentin with a suitable therapeutic restorative material Fill or base the remainder of the cavity with reinforced ZOE cement or a glass-ionomer cement to achieve a good seal. 55
ď ś Do not disturb this sealed cavity for 6 to 8 weeks. It may be necessary to use amalgam, Composite resin or a stainless steel crown as a final restoration to maintain this seal.
The traditional stepwise excavation procedure (a) after excavation to the residual level calcium hydroxide-containing base material and a provisional restoration is made; (b) after a treatment interval extra-dentinal matrix is laid down, (c) Reentry and final excavation can be performed with the likelihood of avoiding perforation, (d) permanent restoration.
Second sitting, 6 to 8 weeks later: If the tooth is asymptomatic, the surrounding soft tissues are free from swelling and the temporary filling is intact, the second step can be performed:
Radiographs of the treated tooth should be assessed for presence of reparative dentin. Again use local anesthesia and rubber dam isolation. Carefully remove all temporary filling material, especially the calcium hydroxide dressing over the deep portions of the cavity floor. The remaining affected carious dentin should appear dehydrated and “flaky” and should be easily removed. The area around the potential exposure should appear whitish and may be soft; this is “predentin”. It should not be disturbed. The cavity preparation should be irrigated and gently dried. Cover the entire floor with a suitable therapeutic restorative material A base should be placed with reinforced ZOE or glass ionomer cement and the tooth should receive a final restoration.
The modified stepwise excavation approach • The concept of a modified and less invasive stepwise excavation technique proposed by Bjorndal et al. with focus on the conversion of lesion activity. • The aim of the first excavation is primarily to make a change within the cariogenic environment by removing only superficial layer of infected, necrotic dentine in the central part and not to attempt to remove carious dentine to the level of residual caries and complete excavation of peripheral part of the lesion. • The final excavation has performed after 6-12 months duration with two aims, 1 To verify that arrest has taken place, i.e. to perform clinical control of the tooth reaction and 2 To remove the slowly progressing caries before carrying out the permanent and final restoration. • Microbiological and clinical studies have shown that the number of bacteria decreases during a treatment interval (6-12 months) and the lesion clinically arrests. The active, soft-yellowish, demineralized dentine turns into inactive darker, harder and drier demineralized dentine, resembling a slowly progressing lesion. (Bjorndal et al 1997) • The advantage of this technique is to reduce the number of iatrogenic pulp perforations performed during the first excavation step. Any attempt to remove ‘most’ of the infected dentine is in danger of pulp exposure. •
The dentist does not know the distance of the base of the lesion from the pulp. Currently there is no particular diagnostic tool to measure this accurately.
Technique: Administer local anesthesia and isolate with a rubber dam. Establish cavity outline with a high-speed hand piece. Remove all peripheral carious dentin with large round bur in a slowspeed hand piece and sharp spoon excavators. Central excavation is done by removing only the outermost necrotic and infected demineralized dentin with a large round bur in slow-speed hand piece Avoid excavating close to the pulp during the first step, in order to reduce the risk of pulp exposure. Choose the provisional restorative material in relation to the length of the treatment interval, which may range between 6 and 8 months. After this treatment interval the retained carious dentine has become darker, harder and shows signs of a slow-progressing lesion and final excavation completed. The cavity preparation should be irrigated and gently dried. Cover the entire floor with a suitable therapeutic restorative material A base should be placed with reinforced ZOE or glass ionomer cement and the tooth should receive a final restoration.
The modified stepwise excavation approach. (a) Closed lesion environment, (b) first and less invasive excavation with no focus on pulp close excavation, (c) A calcium hydroxide-containing base material and a provisional restoration. (d) After the treatment interval the carious dentine has clinically changed into signs of slow lesion progress, (e) after final excavation, (f) permanent restoration.
Evaluation of therapy Sayegh found three distinct types of new dentin in response to indirect pulp capping. 1. Cellular fibrillar dentin at two months post treatment. 2. Globular dentin during the first three months. 3. Tubular dentin in a more uniformly mineralized pattern. In the histological sections, four layers could be demonstrated 1 Carious decalcified dentin 2 Rhythmic layers of irregular dentin 3 Regular tubular dentin 4 Normal pulp with a slight increase in fibrous elements
• Diagnosis of the type of caries influences the treatment planning for indirect pulp capping. • In active lesion, most of the caries related organisms are found in the outer layers of decay; where as deeper decalcified layers are fairly free of bacteria. • In arrested lesion, the surface layers are not always continuated and the surface is hard and leathery.
• The deepest layers are quite sclerotic and free of microorganisms and it is more resistant to decomposition by acids and proteolysis than normal dentin. • Law and lewis reported, - Irritational dentin formation - An active odontoblastic layer - An intact zone of weil and slightly hyperactive pulp with the presence of some inflammatory cells • Held- wydler demonstrated irritational dentin in young molars in which the carious dentin was covered with ZOE cement • Clinical studies have shown no significant differences in the ultimate success of this technique regardless of whether Ca (OH) 2 or ZOE cement is used over residual carious dentin • King and associates, as well as Aponate et al and Parikh et al determined that the residual layer of carious dentin left in the indirect pulp capping technique can be sterilized with either ZOE cement or calcium hydroxide. However it cannot be presumed that all of the remaining infected or affected dentin becomes remineralized. • Nirschl and Avery reported greater than 90% success rates for both Dycal and LIFE • The medicament choice for indirect pulp capping can be based on the clinical history of the carious tooth. •
Some investigators recommend ZOE because of its sealing and obtundant
recommended Ca(OH)2 because of its ability to stimulate a more rapid formation of reparative dentin
• Lado and Stanely demonstrated that light-cured Ca(OH)2 compounds were equally effective in inhibiting growth of organisms commonly found at the base of the cavity preparations • Recently, some investigators have recommended the use of fluoride may cause a more rapid or intense remineralization of affected dentin. • A minimum indirect post-treatment time period of 6 to 8 weeks should be allowed to produce adequate remineralization of the cavity floor. • Present experience from a dental practice environment has shown the effectiveness of treating deep carious lesions using the modified stepwise excavation, and long term recall has shown a high success rate
DIRECT PULP CAPPING Definition Direct pulp capping involves the placement of a biocompatible agent on healthy pulp tissue that has been inadvertently exposed from caries excavation or traumatic injury. The procedure in which the small exposure of the pulp encountered during cavity preparation or following a traumatic injury or due to caries, with a sound surrounding dentin, is dressed with an appropriate biocompatible radiopaque base in contact with the exposed pulp tissue prior to placing a restoration is termed as a direct pulp capping.
Objectives: - To seal the pulp against bacterial leakage - Encourage the pulp to wall off the exposure site by formation of tertiary dentin - There should be no pathologic changes. - No prolonged post-treatment signs or symptoms of sensitivity, pain, or swelling should be evident. - Maintain the vitality of the underlying pulp tissue regions.
Case selection: Success with direct pulp capping is dependent on the coronal and radicular pulp being healthy and free from bacterial invasion. The clinician must rely on the physical appearance of the exposed pulp tissue, radiographic assessment, and diagnostic tests to determine pulpal status.
Indications • The classic indication for direct pulp capping has been for “pinpoint” mechanical exposures that are surrounded with sound dentin. The term “pinpoint” conveys the concept of smallness to the exposed tissue, which should have the lowest possibility of bacterial access. An empirical guideline has been to limit the technique to exposure diameters of less than 1 mm. • The exposed pulp tissue should be bright red in color and have a slight hemorrhage that is easily controlled with dry cotton pellets applied with minimal pressure. • Frigoletto noted that small exposure and a good blood supply have the best healing potential. • Traumatic exposures in a dry, clean field, which report to the dental office within twenty four hours.
Contraindications 1. Spontaneous and nocturnal toothaches 2. Excessive tooth mobility 3. Thickening of the periodontal ligament 4. Radiographic evidence of furcal or periradicular degeneration 5. Uncontrollable hemorrhage at the time of exposure 6. Purulent or serous exudates from the exposure.
Medications and materials used in direct pulp capping Many medicaments and materials have been suggested to cover pulp exposures and initiate tissue healing and /or hard structure repair. They are as follows, • Antibiotics & Corticosteroids
• Calcium hydroxide • Zinc oxide eugenol • Dentin chips • Collagen • Polycarboxylate cements • Cyanoacrylate • Tricalcium phosphate • Hybridizing bonding agents • Cell-inductive agents
Treatment considerations Debridement Necrotic and infected dentin chips are invariably pushed into the exposed pulp during the last stages of caries removal. This debris can impede healing in the area by causing further pulpal inflammation and encapsulation of the dentin chips. Therefore, it is prudent to remove peripheral masses of carious dentin before beginning the excavation where an exposure may occur. When an exposure occurs, The exposure has the following characteristics: The exposure is pin-point in size or has a small diameter relative to the pulp size. There is either no observable hemorrhage from the exposure site, or, if there is hemorrhage, the blood immediately coagulates in the form of a small button at the exposure site.
The dentin at the periphery is reparable as verified by different visual and tactile tests.
The exposure site is not at a constricted or potentially constricting area in the pulp chamber or root canal system. The field of operation is completely aseptic. The exposed area should be appropriately irrigated with nonirritating solutions such as normal saline to keep the pulp moist.
Hemorrhage and clotting The degree and kind of hemorrhage experienced during the exposure of the pulp is a valuable diagnostic aid for prognosis. Generally, if the blood is red, if it flows freely, and if clotting time is normal, the prognosis is good. If the blood is pale and is associated with serum exudates, the prognosis is poor. Hemorrhage at the exposure site can be controlled with cotton pellet pressure. A blood clot must not be allowed to form after the cessation of hemorrhage from the exposure site as it will impede pulpal healing. The capping material must directly contact pulp tissue to exert a reparative dentin bridge response. Maginal seal over the pulp-capping procedure is of prime importance since it prevents ingress of bacteria and reinfection.
Exposure enlargement There have been recommendations that the exposure site be enlarged by a modification of the direct capping technique known as pulp curettage or partial pulpotomy prior to the placement of the capping material. Enlarging this opening into the pulp itself serves three purposes: 1. It removes inflamed and /or infected tissue in the exposed area; 2. It facilitates removal of carious and noncarious debris, particularly dentin chips; and
It ensures intimate contact of the capping medicament with healthy pulp tissue below the exposure site.
Cvek and zilberman et al. have described highly favorable results with a partial pulpotomy technique for pulp exposed, traumatized, anterior teeth and carious molars.
Bacterial contamination It has been emphasized that bacterial micro leakages under various restorations cause pulpal damage in deep lesions, not the toxic properties of the cavity liners and / or restorative materials. The success of pulp-capping procedure is dependent on prevention of micro leakage by an adequate seal. Cox et al. have shown that pulp healing is more dependent on the capacity of the capping material to prevent bacterial microleakage rather than the specific properties of the material itself. Factors promoting healing are conditions of the pulp at the time of amputation, removal of irritants and proper postoperative care such as proper sealing of the margins.
Procedure: All previously described data regarding the physiologic status of the P-D organ should be collected and recorded. Administer local anesthesia and isolate with a rubber dam. Establish cavity outline with a high-speed hand piece. All undesirable and/or undermined enamel and unsound dentin should be removed. Remove the majority of soft, necrotic, infected dentin with a large round bur in a slow-speed hand piece. The bur size should be large should harmonize with the size of the tooth and the amount of remaining carious dentin (i.e. No. 4, 6, or 8) 68
The cavity floor and exposure site should be gently washed and irrigated with sterile water. Drying should be done with sterile cotton pellets, not an air spray. Suitable therapeutic pulp capping material is used, depending on the health of the P-D organ and the location of the exposure site. If the bleeding at the exposure site is arrested and the area is dry, calcium hydroxide paste is the capping material of choice. If the bleeding is stubborn, calcium hydroxide powder is preferred to a paste because of its blotting and coagulating effects upon blood. After cleansing the area to eliminate as much blood and debris as possible, the cavity is dried with cotton pellets. A small pellet of cotton is moistened, blotted free of excess water, dipped in to the dry calcium hydroxide powder to pick up a tuft of calcium hydroxide powder. This is carried to the cavity and placed over the exposed area. A second larger pellet of dry cotton is then pressed over the area to blot the powder dry and to stabilize it over the exposure site When using ZOË, sound dentin shavings are cut from surrounding walls and deposited at the exposure site, and then covered with a creamy mix of unmodified ZOE. The permanent restoration should then be placed. However, in the case of cast restorations, the casting should be temporarily cemented until the status of the P-Dorgan is well established. The patient should be informed of the signs and symptoms of pulpal degeneration and advised to report if any are experienced. The patient is recalled after 6-8 weeks if calcium hydroxide is the capping agent, or 8-9 weeks if the capping agent is unmodified ZOE and dentin shavings. The status of the P-D organ and compared with the data that was gathered prior to treatment, and a prognosis for the P-D organ will be
established. If the pulp is degenerated or degenerating, endodontic therapy should be instituted immediately.
Direct pulp capping procedure. A. Depositing powder over the pulp. B, Larger pellet of dry cotton adapts powder to close the orifice and arrest bleeding. C, Excess fragments of powder are flaked away so that the zinc oxide-eugenol cement can adhere to the surface. D, Grooves are prepared well out to the edges of the cavity. They are usually best placed toward the buccal and lingual surfaces and serve as mechanical interlocks to retain the zinc oxideeugenol cement. A No. 2 steel round bur operated at slow speed is best for this purpose. E, The cavity is based with zinc oxide-eugenol cement. The cement forced into the grooves provides a stable and secure covering for the calcium hydroxide.
Direct pulp-capping technique. A, Capping material covers, pulp exposure and floor of cavity. B, Protective base of zinc oxide-eugenol cement. C, Amalgam restoration.
Clinical success The salient features of a clinically successful direct pulp capping treatment are, 1. Maintenance of pulp vitality, 2. Absence of sensitivity or pain, 3. Minimal pulp inflammatory responses, and 4. Absence of radiographic signs of dystrophic changes.
Permanent teeth Several investigators have provided evidence that direct pulp capping cannot be successful in the presence of pulpal inflammation. Cotton observed that when there is minimal pulp inflammation, a bridge may form against the capping material, but when inflammation is more severe, the bridge is apt to form at a distance from the exposure. Weiss and Bjorvatn have demonstrated that a healthy pulp can exist beneath a direct pulp cap even in the absence of a dentinal bridge. Kakehashi et al., in a germ-free animal study, found pulp exposure healing with bridging even when left uncovered.
Seltzer and bender Langeland et al. have shown that a dentin bridge is not as complete as it appears which can ultimately lead to untoward pulp reactions. It is generally considered that pulps inadvertently exposed and asymptomatic in the preoperative period are more apt to survive when capped. The prognosis is far less favorable if an attempt is made to cap an inflamed pulp infected from caries or trauma. Also, the wide-open apices and high vascularity of young permanent teeth enhance the successful outcome of direct pulp capping techniques.
Primary teeth Kennedy and Kapala attributed the high cellular content of pulp tissue to be
Undifferentiated mesenchymal cells may give rise to odontoblastic cells in response to either the caries process or the pulp-capping material, resulting in internal resorption. Because of the cellular content, increased incidence of internal resorption, some pediatricians contraindicate the direct pulp capping procedure. Starkey and others feel that a high degree of success with direct pulp capping in primary teeth can be achieved in carefully selected cases using specific criteria and treatment methods.
PULPOTOMY Definitions: Complete removal of the coronal portion of the dental pulp, followed by placement of a suitable dressing or medicament that will promote healing and preserve the vitality of the tooth (Finn, 1995). Pulpotomy is defined as the amputation of vital pulp from the coronal chamber followed by placement of a medicament over the radicular pulp stumps to stimulate repair, fixation or mummification of the remaining vital radicular pulp. (Braham and Morris, 1985).
Classifications: A. Pulpotomy can be classified according to treatment objectives as: I.
Devitalization pulpotomy (Mummification, Cauterization). a) Formocresol pulpotomy b) Electrosurgical pulpotomy c) Laser pulpotomy
Preservation (Minimal devitalization, non-inductive) a) Gluteraldehyde b) Ferric sulphate
Regeneration (Inductive, Reparative) a) Bone morphogenic protein
B. It can also be classified depending upon the number of visits as: I.
Single visit pulpotomy
Multiple visit pulpotomy
Rationale: When the coronal pulp is exposed by trauma or operative procedures, carious ingress of bacteria, or iatrogenically, it produces inflammatory changes in the tissue. Through the surgical excision of the coronal pulp, the infected and inflamed area is removed leaving vital, unaffected pulpal tissue in the root canal, well preserved. The removal of the inflamed portion of the pulp affords temporary and rapid relief of pulpalgia. Further, the uninfected tissue may undergo repair while completing apexogenesis that is root end development and calcification. Materials used for this procedure either mummify or fix the tissue or persevere uninflammed tissue or promote healing by formation of a bridge. As in cases of formation of a bridge to promote healing undifferentiated cells in the cell rich zone proliferate and differentiate into odontoblasts subjacent to the area of necrosis. These newly differentiated odontoblasts form a one cell layer that produces reparative dentin to form a bridge to cover and protect the pulp. Another theory proposes that new odontoblasts develop from fibroblasts rather than from undifferentiated mesenchymal cells. In contrast to this, there are materials which fix or produce an area of necrosis in the pulp adjacent to it. This effect of fixation diminishes as it progresses apically through the layers of the pulp. Usually, the apical third of the pulp is unaffected and retains its vitality for an extended time. Hence, pulpotomy is a safe and useful operation for maintaining radicular pulp vitality.
Indications: a) Mechanically exposed vital primary teeth are indicated for single visit pulpotomy procedure. A non vital primary tooth is indicated for two visit devitalization pulpotomy technique b) A vital carious exposure in an asymptomatic primary tooth c) An iatrogenic exposure under proper isolation is the appropriate indication for the pulpotomy procedure. 74
d) In the treatment of pulpally involved primary teeth with clinical manifestations of inflammatory responses confined to coronal pulp. e) In the treatment of pulpally involved young permanent teeth with open apices and vital pulp. f) In the treatment of fractured permanent teeth with pulp exposure greater than one square millimeter with time elapsed less than 72 hours.
Contraindications: a) Spontaneous pain b) Root resorption exceeds more than one-third of the root length; c) The tooth crown is nonrestorable; d) Tenderness to percussion e) Swelling and /or fistula and / or sinus. f) Pus or serous exudates at the exposure site. g) Pathologic mobility. h) Uncontrolled hemorrhage from the amputated pulp stumps i) Pathological external root resorption j) Periapical or inter radicular radiolucency k) Internal root resorption l) Pulp calcification / constrictions of pulp chamber m) Abnormal sensitivity to heat or cold / chronic pulpalgia.
Medicaments used in pulpotomy The various medicaments used in pulpotomy procedure are, 1. Formocresol (Buckleyâ€™s formocresol). 2. Glutaraldehyde. 3. Calcium hydroxide. 75
4. Zinc oxide eugenol. 5. Ferric sulfate. 6. Bone morphogenic protein and osteogenic protein. 7. Paraformaldehyde pastes. 8. Mineral trioxide aggregate 9. Tetrandrine. 10. Freeze dried bone. 11. Tricalcium phosphate.
Procedure Pulpotomy technique as advocated by Sweet in 1930 has developed over the years from multiple visits to a single visit approach.
Techniques of Pulpotomy procedure: I.
Single Visit pulpotomy: Anesthetize the tooth to be operated. Isolation with rubber dam: An essential condition for successful pulp treatment is that the pulp cavity should be free of saliva. Rubber dam. Thus, in addition to isolation, can also protect the inadvertent soft tissue injuries during the procedure. Access cavity preparation: Place a No. 330 bur in a high speed hand piece. Gain occlusal access to the pulp chamber by preparing a Class I cavity. Remove all overhanging enamel. Using a sterile No. 4 or 8 round bur (slow speed), remove all carious dentin from the floor and lateral walls of the cavity and the dentino enamel junction before entering the pulp chamber. This procedure is carried out to prevent contamination of the pulp by carious dentin. Remove the roof of the pulp chamber: Use a sterile fissure bur No. 2. (A fissure bur with high speed and water coolant is used to locate the pulp horns. Bur cuts are made between these horns so as to remove the entire roof of the chamber to gain a straight access to the chamber. The coronal pulp can be removed either with a sharp excavator or with a large round bur at low speed. The pulp tissue should be handled carefully to prevent further damage. The selected instrument should be larger in diameter then the root canal orifice to avert radicular pulp insult. The preoperative radiograph accurately gauges the depth of the pulp chamber. Running the bur counter clockwise may deter disengaging pulp from the root canal. The coronal pulp should be extirpated in toto.
The prepared access cavity should be preferably square in shape with all the walls perpendicular to the floor. There should not be any undercut. Non-irritating solutions like saline, distilled water or Chloramine-T solution (4g-ChloramineT, 9mg–sodium chloride, distilled water-100ml) are used to irrigate the cavity. Post amputation bleeding is controlled by moistening the cotton pellet with a non-irritating solution such as saline or water and placing them over amputated stumps for 3 to 5 minutes. It is important that no material or solution like local anesthetic with adrenaline should be placed over the stumps which would alter the stasis. The tooth may be considered for single visit pulpotomy only if hemorrhage is arrested naturally. Application of medicament: Commonly and routinely used medicament in practice is formocresol. Dip a cotton pledget in formocresol solution. Remove the excess by squeezing with the cotton and place it in a cavity covering the radicular pulp for five minutes to fix the radicular pulp. When the cotton pellet of formocresol is removed, pulp stumps at the orifice should appear dark brown or black in color. Pulp stumps are then covered with zinc oxide eugenol paste and the chamber is filled with hard setting zinc oxide eugenol cement. Restore the tooth: Prepare the tooth for a stainless steel crown as it is the restoration of choice for pulpotomized teeth. The stainless steel crown will prevent the ingress of bacteria and oral fluids that may further irritate the pulp.
Step-by-step technique in one-appointment formocresol pulpotomy.
Exposure of pulp by roof removal.
Coronal pulp amputation with a round bur.
Application of formocresol for 1 minute.
Following formocresol removal, zinc oxide eugenol base and stainless steel crowns are placed.
Two visit pulpotomy: Devitalization pulpotomy: Historically, the indications for 2-visit
pulpotomy procedure are: 1) Inability to arrest hemorrhage from the amputated pulp stumps during a single visit formocresol pulpotomy.
2) Non-vital coronal and / or radicular pulp without the presence of an abscess. 3) In case of uncooperative patient. This is a 2-stage procedure involving the use of Para formaldehyde to fix the entire coronal and radicular pulp tissue. The paste is placed over the exposure and sealed in the tooth for 1-2 weeks. Formaldehyde permeates through the coronal and radicular pulp, fixing the tissues. On the second visit, the pulpotomy is carried out (without the need for local analgesia) and an antiseptic paste is placed over the radicular pulp before restoring the tooth. Hobson (1970) reported a success rate of 77% after 3 years. An alternative method is to perform a vital pulpotomy at the first visit, devitalize the radicular pulp with Para formaldehyde paste for 1-2 weeks and at the second visit, replace the paste with an antiseptic paste and restore the tooth.
Electrosurgical pulpotomy: Many pharmacotherapeutic agents have been employed as pulpotomy medicaments for deciduous teeth. Yet, despite their excellent clinical success rate, pulpotomy medicaments have come under close scrutiny because of safety considerations and varied histological and radiographical findings. Thus, electrosurgical pulpotomy, a form of non-chemical devitalization has been proposed. This is another form of non-chemical devitalization which has emerged during the last decade. Electrosurgical pulpotomy varies from other procedures. Whereas mummification eliminates pulp infection and vitality with chemical cross linking and denaturation, electro-cautery carbonizes and heat denatures pulp and bacterial contamination. The rationale of this is the affected tissue of the coronal pulp is removed during pulpal amputation, a layer of coagulation necrosis caused by the electrosurgery application provides a barrier between healthy radicular tissue and any base material placed in the pulp chamber. The odontoblasts are
stimulated to form a dentinal bridge and the tooth is maintained in the arch with vital radicular tissue until it exfoliates. However, Schulman found that electrosurgical technique produces pathologic tooth resorption and periapical furcal involvement. Experimentally, electrosurgery has been shown to initiate pathologic tooth resorption and a spectrum of pulpal effects including acute and chronic inflammation, edema, and fibrosis and diffuse necrosis. Remarkably, Mack and Dean, 1993, documented 90.4%, a very high success rate, clinical and radiographic success rate.
Laser Pulpotomy: Lasers are the latest hi-tech modality applied to the field of pulp therapy. In the near feature, with the rapid advancement in the types of lasers, laser energy might be able to overcome the histologic deficit of electrosurgery. Ideally, laser irradiation should create a superficial zone of coagulation necrosis that remained compatible with the underlying tissue. The laser has many desirable characteristics when used as a surgical cutting instrument. The effect of ruby laser beam irradiation on the dental pulp had been previously reported. The advantage of CO2 lasers over other lasers are that bloodless tissue incisions can be attained at a practical cutting speed and the edge of the laser irradiated tissue is covered by only a thin layer of necrotic material. As the laser beam has no mechanical contact with the tissue, the incision is made without influencing mechanical damage on the remaining pulp tissue. Furthermore, the operation is performed under aseptic conditions. Thus it is possible to sever the dental pulp by CO 2 laser without causing hemorrhage, mechanical damage or bacterial contamination. Changes in the skin and mucosa irradiated by laser beams have been reported by Goldman and Rockwell.
The width of coagulated layer depends on both the wave length of the beam and the amount of energy per unit area. The width of layer produced by Argon laser is about 50 to 100Âľ. While the width of the layer produced by CO 2 laser is about 150Âľ. As the pulp is surrounded by hard tissue, the width of the layer is found to be greater when compared to the experiments regarding the skin and mucosa. As the diffusion of heat produced in the pulp chamber is limited, the rise in temperature is greater than in other tissues thus producing more coagulation necrosis. The focused beam produced a sharp and deep wound but the width of the necrotic area was narrower than that produced by the defocused beam. Thus, the thermal effect of the defocused beam on the pulp was more extensive. The extent of pulpal injury seemed to depend more on the length of irradiation than on output power.
Preservation: This approach involved medicaments and techniques that provide minimal insult to the orifice tissue and maintain the vitality and normal histologic appearance of the entire radicular pulp. According to Ranly, glutaraldehyde and the more recently used ferric sulfate affect only superficial tissue and are proposed as a means to conserve virtually all of radicular pulp. Though the materials differ, the technique basically remains the same as a single visit procedure described earlier. It is preferable to use a base material other than ZOE is ferric sulfate pulpotomies.
Regeneration Ideally, pulpotomy treatment should leave the radicular pulp vital and healthy and completely enclosed within an odontoblast â€“ lined dentin chamber. Hence, the tissue would be isolated from noxious restorative materials and odontoblasts could enter into the exfoliative process at the appropriate time and sustain it in a physiologic manner. Implied in this scenario is the induction of reparative dentin formation by the pulpotomy agent. Forerunners in this
technique are calcium hydroxide and bone morphogenetic protein along with a host of other materials being experimented with. The technique again basically remains the same as described before with only the material used differing and the final restoration should involve a permanent material with a stainless steel crown as the preferred coverage.
Cvekâ€™s pulpotomy: In contrast to the conventional pulpotomy technique, where all the coronal pulp is removed, partial pulpotomy implies the removal of the pulp tissue only to a depth of 1 to 2mm and covering of pulpal wound with a calcium hydroxide dressing. Cvek has demonstrated a high success rate when pulp exposures in crown fractured teeth were treated by partial pulpotomy. He also stated that the size of exposure and time between the accident and treatment are not critical for recovery of a primarily healthy pulp (Anna B. Fuks, Aubrey, Chosock). The major advantage compared with conventional techniques is that it conserves the tooth structure, permits continued formation of dentin coronally and is simpler to perform. Cvek (1975) obtained a success rate of 96% in teeth treated by partial pulpotomy upto 9 days after exposure and followed for an average of 31 months. Baume and Holz (1981) also reported favourable results from a procedure which was essentially partial pulpotomy.
Calcium hydroxide Calcium hydroxide is a material with myriad applications since its introduction into dentistry in the early part of the twentieth century by Hermann in 1930, Foreman and Barnes in 1990. In addition to its bactericidal effects it possesses a high alkaline pH which has offered as prime reason for its effectiveness. In its pure form, the substance has high pH (11 to 12). The high pH is due to the presence of free Ca (OH) 2 in the set cement and its dental use relates chiefly to its ability to stimulate mineralization and also to its antibacterial properties. A range of products have been formulated with different therapeutic actions, the effects of which are partially dependent upon the tissue to which they are applied.
Applications 1. For direct and indirect pulp capping. 2. As low strength bases beneath silicate and composite restorations for pulp protection. 3. Apexification procedure in young permanent teeth where root formation is incomplete
Advantages Initially bactericidal then bacteriostatic Promotes healing and repair High pH stimulates fibroblasts Neutralizes low pH of acids Inexpensive and easy to use Particles may obdurate open tubules
Disadvantages Does not exclusively stimulate dentinogenesis Associated with primary tooth resorption It may dissolve with cavosurface dissolution May degrade during acid etching degrades upon tooth flexure does not adhere to the dentin or resin restoration
Available as: 1. Two paste system containing base and catalyst pastes in collapsible tubes 2. light cured system 3. single paste in syringe form (pulpdent) 4. Powder form (mixed with distilled water).
Commercial names: Self cured –Dycal, life, Care, calcidor Light cured - Prisma VLC dycal
Composition and chemistry: The constituents and the proportions of commercially available calcium hydroxide cements vary from product to product. There are 3 main calcium hydroxide products: Pulpdent – Paste contains 52.5% calcium hydroxide suspended in aqueous methyl cellulose solution. Dycal – First introduced in 1962 by L.D. Caulk Company. It is available in 2 paste system consisting of a base and catalyst. Base – Titanium dioxide in glycol salicylate with a pigment. 85
Catalyst – Calcium hydroxide and zinc oxide in ethyl toluene Sulfonamide. Hydrex (MPC) – It is a 2 paste non essential oil hard setting compound that contains calcium hydroxide, barium sulphate, titanium dioxide and a selected resin.
Base paste Glycol salicylate 40%
- reacts with Ca (OH) 2 & ZnO
Calcium sulphate Titanium dioxide
- inert fillers, pigments
Calcium tungstate or barium sulphate – provides radiopacity.
Catalyst paste Calcium hydroxide
50% -principal reactive ingredient
Ethylene toluene Sulfonamide
39.5%- oily compound, act as carrier
These cements set by an acid base reaction, the phenolic group in the alkyl salicylate ester acting as an acid. Once set, the therapeutic activity of the set material will depend mainly upon the release of calcium and hydroxyl ions which can occur only if the cement is water soluble. It is the nature of the plasticizer that imparts this solubility. Most cement set by some of the available calcium hydroxide reacting with the salicylate ester chelating agent in the presence of toludine sulphonamide plasticizer. It is hydrophilic and water soluble. Calcium hydroxide powder can be mixed with distilled water to form a creamy paste.
Manipulation Equal lengths of two pastes are dispensed on a paper and mixed to a uniform color. The material is carried and applied using a calcium hydroxide carrier or applicator the material is applied to deep areas of the cavity or directly over mildly exposed pulp. The set cement contains a matrix of calcium alkylsalicylate chelate and excess unreacted calcium hydroxide. The fragility of the set cement suggests that the chelates are held together by weak secondary attraction rather than a stronger polymeric structure Most of the commonly used 2-paste systems (Dycal, Life and Alkaliner) utilize the same chemical reactivity. Both Hydrex and MPC have been shown to be relatively insoluble and have poor antibacterial properties. Lim and McCabe, 1982, supported this chemistry of setting reaction. He mentioned that the whole-reaction is based on the interaction between calcium and zinc ions and a salicylate chelating agent and is accelerated by the presence of water.
Light activated calcium hydroxide cement Light activated calcium hydroxide cements have recently become available. It consists of calcium hydroxide and baroum sulphate dispersed in a urethane dimethacrylate. It contains HEMA and polymerization activators. The light activated cement has a long working time and is less brittle than the conventional two paste system.
Biochemical action and mineralization: Calcium hydroxide has the unique potential to induce mineralization. It is also likely that calcium ions present in the applied calcium hydroxide do not become incorporated in the mineralized repair tissue which derives its mineral contents solely from the dental pulp; hence, presumably calcium hydroxide is an initiator rather than a substrate.
Though the high Ph (11 to 12) is in the favor of mineralization, the hydroxyl ions as the sole initiators of the process and do not explain their role satisfactorily because other alkaline compounds fail to initiate mineralization. However, calcium hydroxide may act as a local buffer. An alkaline pH may also neutralize lactic acid secreted by osteoclasts and this may help to prevent further destruction of mineralized tissue. It produces coagulation necrosis at the contact surface of the pulp. The underlying tissue then differentiates in to odontoblasts, which elaborate a matrix in about 4 weeks. This results in the formation of a reparative dentin bridge, caused by the irritating quality of the highly alkaline calcium hydroxide. It has been speculated that the material exerts a mutagenic and osteogenic effect, the high pH combined with the availability of calcium hydroxyl ions having an effect on enzymatic pathways and hence mineralization. The high pH may also activate alkaline phoshatase activity which is postulated to play an important role in hard tissue formation. The optimum pH for alkaline phosphatase activity is 10.2.
Effects of calcium hydroxide and time on the healing of the capped pulp. A, Twentyfour hours after application of calcium hydroxide. B, After 2 or 3 weeks. C, After 4 or 5 weeks, D. After 8 weeks.
Histology: • Teuscher and Zander reported the use of calcium hydroxide paste as a pulp dressing in indirect pulp capping, direct pulp capping and pulpotomy of both primary and permanent teeth. •
Histologic studies showed that in successful cases, the superficial portion of the pulp nearest the calcium hydroxide was first necrotized, a process accompanied by acute inflammatory changes in the immediate tissue beneath.
• Investigators showed three identifiable histologic zones under the calcium hydroxide in 4 to 5 days: 1. coagulation necrosis 2. Deep - staining basophilic areas with varied osteodentin and 3. Relatively normal pulp tissue, slightly hyperemic, is underlying an odontoblastic layer. • The original proteinate zone is still present. However, against this zone is a new area of coarse fibrous tissue like primitive type of bone. • After four weeks, the acute inflammation subsided and was followed by development of a new odontoblastic layer at the wound site and eventually by a bridge of dentin. • This bridge continues to increase in thickness during the next 12 month period. The pulp tissue beneath the calcified bridge remains vital and is essentially free of inflammatory cells. Calcium hydroxide sometimes appears to stimulate resorption. • Internal resorption is the common finding after calcium hydroxide pulpotomy of deciduous teeth. This occurs near the junction of coronal and radicular pulp (Hannah and Rowe, 1971). • Because of calcium hydroxide’s irritant nature, it produces some degree of inflammation. Inflammatory cells attracted in the area as a result of 89
placement of calcium hydroxide might well attract the osteoclastic cells and initiate the internal resorption. • This may explain the occurrence of internal resorption even though the pulp is normal at the time of treatment. Also, because the roots of primary teeth are undergoing normal physiologic resorption, vascularity of the apical region is increased and there is osteoclastic activity in the area. • This may predispose the tooth to internal resorption when an irritant (calcium hydroxide) is placed on the pulp. Internal resorption can be due to 3 factors: 1. Over stimulation of undifferentiated cells of the pulp. 2. Alkalinity of calcium hydroxide produces severe pulp inflammation and subsequent metaplasia. 3. Calcium hydroxide may attract, provoke or stimulate osteoclastic activity. • Although it is possible that the high pH of the material may cause further irritation to already damaged tissue, resorption is not considered to be sustained by bacterial infection in the dentinal tubules which communicate between necrotic and vital areas of the pulp. • Thus, though this material was the first one to be used in the regeneration modality, its use is not recommended as a pulpotomy medicament for the deciduous teeth (Ranly D.M. 1994).
Zinc oxide eugenol These cements have been used extensively in dentistry since the 1890’s. When ZOE is applied to dentin, pain and sensitivity are often reduced and the material is therefore termed therapeutic, sedative, anodyne or obtundant. However, when it is applied directly to dental pulp, nerve tissue or particularly cells in culture, the same medicament is reported to be toxic. This cement can be used as a pulp capping medicament, base, temporary dressing, endodontic root filling paste, impression material in periodontal packs. However, they share common chemistry and pharmacology. These cements are usually dispersed in the form of powder and liquid and sometimes as two pastes. The pH is approximately seven at the time they are inserted into the tooth. Thus, they are one of the least irritating of all dental materials. The various formulations and uses are reflected in ADA specification No. 30 for ZOE restorative materials which lists 4 types: Type I
– For temporary cementations.
– For permanent cementation of restorations / appliances fabricated outside the mouth.
– Temporary filling materials, thermal insulating base.
– Cavity liners.
Commercial names I. Unmodified Tempac
- Type III
- Type IV
- Type I
II. EBAalumina modified Opotow Alumina EBA
- Type II
III. Polymer modified Fynal
- Type II
- Type III
IV. Non-eugenol Nogenol
- Type I
- Type I
The main constituents are zinc oxide in the form of powder and eugenol (clove oil) in liquid form.
Composition: Powder Zinc oxide
– 69% - principal ingredient
White rosin – 29.3%
- to reduce brittleness of set cement
Zinc stearate – 1%
- accelerator, plasticizer
Zinc acetate – 0.7%
- accelerator, improves strength
- is added in some powders, acts with eugenol in a manner as zinc oxide
The first reaction consists of hydrolysis of zinc oxide to its hydroxide. Thus indicating that water is essential for the reaction. ZnO + H2O Zn (OH)2 92
Dehydrated zinc oxide will not react with eugenol. Water is probably one of the products of the reaction. Consequently the reaction is autocatalytic. The final setting action is a typical acid base reaction to form a chelate. Zn (OH)2 (base)
The chelate is thought to form an amorphous gel that tends to crystallize imparting increased strength to the set mass. Formation of the crystalline zinc eugenolate is greatly enhanced when the setting reaction is accelerated by zinc acetate dehydrate which is more soluble than zinc hydroxide and can supply zinc ions more rapidly. An acid, such as acetic acid is a more active accelerator for the setting reaction than is water, since it increases the speed of formation of zinc hydroxide. High atmospheric temperature and humidity are also very effective accelerators for the setting reaction. The water that is formed in the setting reaction probably acts in binding the individual chelate units together. They are relatively weak cements. The strength depends on what it is used for. Their thermal insulating properties are excellent and are approximately same as human dentin. The solubility of the set cement is highest among the current cement i.e. 0.4%. The Ph is 6.6 to 8.0. They are the least irritating of all cements. The common powder liquid ratio is 4.2g/ml. The free eugenol content is then low.
Histology: â€˘ Stanley believes that it makes no difference whether Ca(OH) 2 or ZOE is used because neither is in direct contact with pulp tissue in indirect pulp capping and increased dentin thickness was observed to occur beneath deep lesions treated with both agents.
• Glass and Zander reported that zinc oxide eugenol in direct contact with vital pulp tissue produced chronic inflammation, a lack of calcific barrier and an end result of necrosis. ZOE failed to stimulate osteogenesis. • Watts also found mild to moderate inflammation and no calcific bridges in the specimens. • Weiss and Bjorvatn, on the other hand, noted negligible necrosis of the pulp in direct contact with ZOE but stated that any calcific bridging of an exposure site was probably a layer of dentinal chips. They also find no difference in the pulp reactions of primary and permanent teeth. •
James E. Berger observed active inflammatory reactions in all teeth treated with ZOE as a pulpotomy medicament. The reactions varied from simple chronic to acute suppurative pulpitis.
• High power examination of generalized acutely inflamed pulps showed inflammatory exudates at the amputation site. The exudate contained neutrophilic, eosonophilic and basophilic leukocytes, plasma cells, macrophages and erythrocytes. There was complete degeneration of odontoblast layer and disruption of the cell –free zone of Weil. Only the apical third pulp tissue was present and engorged blood vessels with extravasated erythrocytes were observed. The pulp tissue was pale staining in character, granular and revealed necrotic fibrocyte and loss of organized form and cellular detail. Teeth treated with ZOE as a pulp capping medicament showed variable responses of acute or chronic inflammation, internal
destruction and pulpal fibrosis located subjacent to the amputation site. • In spite of lack of success with ZOE cement, Sveen reported 87% success with the capping of teeth with ZOE in ideal situations of pulp exposure.
Corticosteroids and antibiotics Corticosteroids and antibiotics were suggested for direct pulp capping in the pretreatment phase and also mixed with calcium hydroxide with the thought of reducing or preventing pulp inflammation. The agents included are neomycin and hydrocortisone, cleocin, cortisone, ledermix (calcium hydroxide plus prednisolone), penicillin and keflin (cehalothin sodium). Although many of these combinations reduced pain for the most part, they were found only to preserve chronic inflammation and/ or reduce reparative dentin. Also, Watts and Paterson cautioned that anti-inflammatory compounds should not be used in patients at risk from bacteremia. Garderet al. found, however, that vancomycin, in combination with calcium hydroxide, was somewhat more effective than calcium hydroxide used alone and stimulated a more regular reparative dentin bridge.
Polycarboxylate cements These cements have also been suggested as a direct pulp capping material. The material was shown to lack an antibacterial effect and did not stimulate calcific bridging in the pulps of monkey primary and permanent teeth. Negm et al. placed calcium hydroxide and zinc oxide in to a 42% aqueous polyacrylic acid and used this combination for direct pulp exposure in patients from 10 to 45 years of age. This mixture showed faster dentin bridging over the exposures in 88 to 91% of the patients when compared to Dycal as the control.
Calcium phosphate cement It has been developed for repairing cranial defects following brain neurosurgery. The components of this material include tetracalcium phosphate and dicalcium phosphate, which react in an aqueous environment to form hydroxyapatite, the mineral component of hard tissues. Chaung et al. histologically compared calcium phosphate cement with calcium hydroxide as a direct pulp-capping agent although both materials produced similar results with respect to pulp biocompatibility and hard tissue barrier formation, calcium phosphate cement was suggested as available alternative because of, 1) Its more neutral pH resulting in less localized tissue destruction 2) its superior compressive strength and 3) Its transformation in to hydroxyappetite over time. Yoshimine et al. demonstrated the potential benefits of direct pulp capping with tetracalcium phosphate-based cement. As with calcium phosphate cement, this material has the ability to be gradually converted in to hydroxyl apatite over time. In contrast to calcium hydroxide, tetracalcium phosphate cement induced bridge formation with no superficial tissue necrosis and significant absence of pulp inflammation.
Inert materials Inert materials such as isobutyl cyanoacrylate and tricalcium phosphate ceramic have also investigated as direct pulp-capping materials. Although pulpal responses in the form of reduced inflammation and unpredictable dentin bridging were found, none of these materials have been promoted to the dental profession as a viable technique. It has been reported to be an excellent pulp-capping agent because of its haemostatic and bacteriostatic properties. At the same time it causes less inflammation than calcium hydroxide. However, it cannot be regarded as an adequate therapeutic alternative to calcium hydroxide since it does not produce a continuous barrier of a reparative dentin following application to the exposed pulp tissue. At Istaanbul University, dentists capped 44 pulps, half with tricalcium phosphate hydroxyapatite and half with Dycal. At 60 days, none of the hydroxyapatite-capped pulps exhibited hard tissue bridging but instead had mild inflammation. Nearly all of the Dycal-capped pulps, however, were dentin bridged, with little or no inflammation
Hybridizing bonding agents Recent evidence has given us the development of dentin adhesives, comprising a myriad group of composites and chemicals with different generations, the key component is the multi purpose dentin bonding adhesive which forms an impermeable hybrid layer. Several investigations on bonding systems have proposed them for pulp therapy (Cox, Akimoto et al 1998, Inokoshi et al, 1990, Kashiwada T. et al 1991). Kopel strongly advocated their use in pulp therapy. It has shown that elimination of bacterial microleakage is the most significant factor affecting restorative material biocompatibility. A major short coming of calcium hydroxide preparations are their lack of adhesion to hard tissues and resultant inability to provide an adequate seal against microleakage. Furthermore calcium hydroxide materials have been found to dissolve under restorations where microleakage has occurred, resulting in bacterial access to the pulp. Currently, hybridizing dentinal bonding agents (such as AmalgaBond or C and B Metabond, parkell products, farmingdale) represent the state of an art in mechanical adhesion to dentin with resultant microleakage control beneath restorations. Miyakoshi and et al. have shown the effectiveness of 4-META-MMATBB adhesives in obtaining an effective biologic seal. Cox et al. demonstrated that pulps sealed with 4-META â€œshowed reparative dentin deposition without subjacent pulp pathosis A number of investigators have proposed that sealing vital pulp exposures with Hybridizing bonding agents may provide a superior outcome to calcium hydroxide direct pulp-capping techniques. Because of their adhesion to peripheral hard tissues, an effective seal against microleakage can be expected. These proposals have been made in spite of concerns with the effects of acid etchant and resin materials on pulp tissue.
Kashiwada and Takagi demonstrated 60 of 64 teeth to be vital and free of any clinical and radiographic signs of pulp degeneration 12 months after pulp capping with a resin bonding agent and composite resin. Conversely, other investigators provide conflicting evidence that does not support using dentin bonding agents in pulp-capping techniques. Stanley has stated that acid conditioning agents can harm the pulp when placed in direct contact with exposed tissues Gwinnett and Tay, using light microscopic and electron microscopic techniques, identified early and intermediate pulp responses to total-etch followed by a resin bonding agent and composite resin restorations in human teeth. Some specimens demonstrated signs of initial repair with dentin bridge formation along the exposed site and reparative dentin adjacent to the exposed site. Other specimens demonstrated persistence of chronic inflammation with a foreign body in the exposed pulp tissue that was surrounded by pulpal macrophages. Although using dentin bonding agents as a replacement for calcium hydroxide in the direct pulp-capping technique has been advocated, more longterm evidence and histologic evolutions are needed.
Formocresol Formocresol was introduced in 1894. Credit of its origin is given to a list of researchers – Marion (1895), Lepkowski (1895), Schroeder (1896), Prinz (1898), Gysi (1899) and Buckley (1904).
Chemistry and pharmacological action: Formaldehyde is a gas produced by an incomplete combustion of methanol and has the chemical formula O
H–C–H It is readily soluble in water with the concentrated aqueous solution called formalin (38 to 40% formaldehyde by weight). Formocresol is made by combining formalin and cresol with various additives. The major action of formocresol on the pulp tissue has been attributed to the formaldehyde portion of the drug. Glycerin was added to lessen the polymerization to Para formaldehyde which causes “clouding” of the solution. A solution of 10% formalin is utilized widely as a fixative. Its action to prevent autolysis of tissue is believed to be caused by a complex chemical binding of formaldehyde with the protein. This reaction is reversible and bond can be hydrolyzed in human body by enzymatic action. The exact site of the chemical binding is thought to be the peptide groups of certain side chain amino acids, especially those amino acids having dual peptide groups. Furthermore, formaldehyde is believed to link adjacent protein molecules by the formation of methylene bridges between peptide groups and adjacent amino acids. Such cross linkages connect protein molecules without changing their basic overall structure and probably underlying some of the altered chemical reactivity and increased tissue hardness. Because of its chemical binding action 101
formalin is classified as an additive, non-coagulation fixative. This is as opposed to some other fixative solutions or to heat, both of which drastically and irreversibly alter the chemical and physical properties of the protein molecules. The chemical binding with the proteins of microorganisms is thought to be the basis of formaldehyde’s action as a bactericide. The other major constituent of formocresol is tricresol (35%). It is a pungent and caustic organic compound. It is lipophilic and completely destroys the cellular integrity. This is an acqueous suspension of three isomeric forms of methylphenol which are derived from coal tar. Tricresol is a strong antiseptic. Tricresol was added to the formaldehyde solution as it was thought to lessen the irritating properties of the compound. It produces irreversible damage to connective tissue and delays recovery of normal biological activity. The action of formocresol on pulp tissue can be thus summarized as follows, The formaldehyde of the formocresol undoubtedly fixes the pulp tissue adjacent to it because of the chemical reaction between the drug and the cellular proteins. Formaldehyde alters blood flow by inducing thrombus formation with resulting areas of ischemia. The ischemia thus produced gives rise to autolytic changes and coagulation necrosis of the tissue deprived of their normal nutrition and respiration. Enzymatic hydrolysis of the necrotic tissues could then take place with the replacement of it by granulation tissue. Slight resorption of the dentinal walls in the region of the zone of replacement and the deposition of osteodentin as a repair tissue is observed. The clinical success of the treatment using formocresol has been thus attributed to its germicidal and fixative qualities. 102
Advantages of formocresol: 1. Commonly available medicament. 2. Stable at room temperature. 3. Long shelf life. 4. High clinical and radiographic success of formocresol pulpotomy.
Disadvantages: 1. Reaction with the pulp is reversible. 2. It is a very caustic medicament. 3. In high doses it is toxic. 4. Potential systemic absorption and distribution throughout the body. 5. It has a mutagenic and carcinogenic potential.
Composition: Variable compositions of formocresol medicament exist. Most commonly accepted compositions are Buckley’s and Andlaw and Rock formocresol. Buckley’s formocresol: Formalin (375)
To achieve 1:5 concentration of original Buckley’s formocresol: 1. Dilute 3 parts of glycerine with 1 part distilled sterile water, mix well. 2. Add 1 part formocresol to 4 parts diluent.
90 ml glycerine. + 30 ml water =
120 ml diluent
Another composition (Andlaw and Rock): Formalin (37%)
Successful results have been obtained using 1:5 dilution of this solution and this is widely used. This dilution is as effective as original Buckleyâ€™s formula and allows faster recovery of cells and represents a safer medicament as compared to irrecoverable damage caused by full concentration. Clinically, formocresol is delivered to the tooth by twice squeezing out a No. 4 cotton pellet that has been dipped in formocresol. This amount was quantified to 1/5th of a drop or 4.86mg. Wesley reported that smaller amounts are equally effective; concluding that 1/10th of a drop will achieve the same result as 1/5th of a drop. Formocresol application time varies from minutes to days or to even weeks. In experimental animals, Venham (1967) observed identical pulpal reactions to formocresol applications for 15 s and 5 minutes. Emmerson determined significant formocresol action within the first five minutes. When the formocresol application exceeded 3 days, linear calcification manifesting vertically along root canal walls was observed. The
same observation was noted by Willard (1976) relative to vital primary teeth treated by 5 – minute formocresol pulpotomy.
Histological observations: The histological studies of the pulpotomized teeth treated with formocresol revealed various distinct zones apical to the amputation site. Since 1950, much work has been carried out in this aspect. After exposure of the pulp to formocresol, three distinct histological zones were observed. A broad acidophilic zone of fixation in the most coronal part of the radicular pulp. The zone of fixation is bacteria free, inert, and resistant to autolysis and it apparently acts as a deterrent to further microbial infiltration. A broad, pale-staining zone of atrophy in the middle region of the radicular pulp wherein cells and fibers were greatly diminished. A broad zone of inflammatory cells diffusing deeply into the underlying normal pulp in the apical region. No tendency to wall off the inflammatory zone by either fibrous layer or a calcific barrier was seen. No reparative dentin formation was evident laterally, centrally or peripherally. Rather, a progressive fixation of the pulpal tissue with ultimate fibrosis of the entire pulp occurred.
Toxicity: Although the clinical success rate of formocresol pulpotomy is satisfying, the medicament itself gives rise to various problems: -
Postoperative systemic distribution.
Possible effects on the enamel of succedaneums teeth.
Possibility of reversible fixation leading to autoantibody formation.
Mutagenicity and carcinogenicity.
Destruction of cellular integrity due to cresol factor.
Irreversible connective tissue changes. (Kettley 1991 and Mejare, 1978). Toxicity of formocresol has been studied since many years. Black, as
early as 1920, noticed the destructive effects of formocresol. Grossman studied several medicaments and found that formocresol was the only one that caused noticeable irritation and necrosis. According to Sommer, formaldehyde-cresol solutions are too caustic to be sealed in the root canals. The compounds have been reported to act as haptens rendering the pulp tissue antigenic.
Mutagenicity and carcinogenicity: Formaldehyde was identified with mutagenic activity as early as 1946. This was demonstrated in Drosophilia, by Kaplan W.D. in 1948, in Neurospora by Jenson K.A. and Kirk I. In 1951, in E.coli by Nishioka in 1973 and in cultured monkey kidney cells by Noncentini and Mareno in 1980. Mutagenic properties of formaldehyde are usually associated with its ability to form adenine dimers through methylene bridges. Formaldehyde is known to inhibit catalase, an enzyme involved in mutation and chromosome breakage. Formaldehyde can react with nucleosides, nucleotides and nucleic acids, an example of which is the anti tumor activity and production of chromosome aberration by RNA treated formaldehyde.
Glutaraldehyde Glutaraldehyde is a common fixative of electro microscopy, was suggested by ‘s-Gravenmade as an alternative to formocresol for the purpose of various pulp treatment modalities.
Preparation, Storage and Chemistry: As aliquot of 25% stalk solution of commercial glutaraldehyde (pH – 2.9) was vacuum distilled at 80°C to obtain the pure dialdehyde. The distillate was diluted immediately with either distilled water to make 2 to 5% unbuffered solutions or with 0.1M phosphate buffer (pH-7.2) to make 2 to 5% buffered solutions. The initial pH of the freshly made unbuffered preparation was 5.8. An aliquot of each was refrigerated at 4°C and another aliquot was stored at room temperature (Ranly D.M. 1984). Ranly has recommended a pH of 8 for good results with 2% buffered glutaraldehyde as a pulpotomy medicament. Ranly has evaluated the purity, efficacy and stability of glutaraldehyde by spectrophotometric and biochemical methods in order to develop principles concerning the preparation and storage of diluted solution. He concluded that a concentrated stalk solution of glutaraldehyde that typically might be used in the preparation of the pulpotomy agent contained a variety of molecules other than glutaraldehyde monomer. Un buffered solution remained stable regardless of temperature while buffered solutions benefited from cold storage. If refrigeration is not practical, the use of unbuffered preparation at slightly stronger concentration is recommended (Ranly D.M. 1984).
Histology: Martin J. Davis, Myers and Switkase 1982 studied the histologic changes following glutaraldehyde pulpotomy. They used 5% buffered glutaraldehyde pH of 8.5 for the procedure.
After 1 week, all the specimens presented a histologic picture similar to that of formocresol with identifiable zones with less distinction than in the case of formocresol. Specifically, the coronal third of the radicular tissue was fixed and found to be non-vital. The cells in this area were somewhat compressed and darkly stained, but not as darkly as with formocresol. The middle one third of the radicular tissue appeared vital with good cellular details and evidence of moderate inflammation. The apical third remained vital with scattered inflammatory cells. At the four weeks interval, the coronal third of the radicular tissue remained as before. The middle portion demonstrated clear cellular details with unchanged degree of inflammation. There was limited dystrophic calcification apparent on the lateral canal walls. Apical third appeared unchanged from one week specimen and was apparently vital with occasionally observed inflammatory cells. The 8th week specimen demonstrated no change in the coronal third of the radicular tissue. The middle third of the canal appeared similar to the 4week specimen. The apical third appeared vital and demonstrated good cellular details with scattered inflammatory cells. An interesting observation was the appearance of multinucleated giant cells and fibroblasts immediately apical to the glutaraldehyde fixed coronal tissue. Such cells are indicative of replacement repair. The absence of multizones in the root pulp following glutaraldehyde pulpotomy was the striking finding observed by Kopel in 1980. One month following the pulpotomy, there was a deep red, cellular zone adjacent to the amputation surface and few lymphocyte and plasma cells were present in the pulp tissue below the red staining zone. Blood vessels below this zone appeared dilated. The remaining pulp was free of inflammatory cells and the root canal was lined with a layer of reparative dentin.
After 3 months, the coronal region still stained red with PAS reaction. The remaining pulp tissue showed no layering or signs of inflammation. With high magnification, macrophages were visible in and adjacent to the red zone. Lysed material was also present. No pathosis was noted at the apical end. By six months, following the pulpotomy, there was decrease in the width and staining intensity of the cellular coronal zone. No pathosis was present in the tissue of the pulp. Furthermore, there was no invasion of fibroblasts from the apical periodontal ligament into the pulp. Kopel concluded the study as follows: 1. 2% glutaraldehyde is biologically acceptable as a dressing medicament for maintaining vitality of the remaining pulp tissue following the pulpotomy. 2. Histologically, the pulp tissue in the root does not resemble formocresol pulpotomized pulp. 3. There is an initial zone of fixation adjacent to the applied glutaraldehyde dressing which does not proceed apically. The tissue which adjoins the fixed zone has the cellular detail found in normal pulp and is considered to be vital. 4. In time, the fixed zone is replaced through macrophagic action with dense collagenous tissue demonstrating the vitality of the entire pulp tissue. 5. Because of its established biochemical properties and effects on the vital pulp tissue, 2% glutaraldehyde can confidently be suggested for use in pulpotomies.
Advantages: 1. Reaction with pulp is irreversible. 2. It does not diffuse out of the apical foramen. 3. It fixes tissue instantly and excess solution is unnecessary. 109
4. It is not known to be cytotoxic, mutagenic or carcinogenic. 5. It has no known systemic toxic effects.
Disadvantages: 1. Short shelf life. 2. It has to be freshly prepared. 3. Buffered solution has to be refrigerated.
Glutaraldehyde v/s Formocresol: Glutaraldehyde presents various advantages over formocresol: 1. It is a better bactericidal than formocresol. 2. It does not diffuse apically or laterally from the canals because of large molecule size whereas formocresol does. 3. It is not known to be carcinogenic or mutagenic. 4. It does not induce toxic effects and demonstrates less systemic distribution. 5. It fixes tissue instantly unlike formocresol which fixes tissue slowly. 6. It is not known to be caustic. 7. It is a better fixative at lower concentration than formocresol. 8. The action is irreversible. 9. It causes less dystrophic calcification in pulp canals and less necrosis of pulpal tissue. 10. it is a bifunctional reagent, which allows it to form strong intra- and intermolecular protein bonds, leading to superior fixation by crosslinkage;
While glutaraldehyde may prove to be a better pulpotomy medicament based on its local tissue effect, its use will also have to be judged on wider issues of success and safety. The effect of glutaraldehyde appears to be localized and gentle (Kopel 1980, Garcia-Godoy 1983). On the other hand, formocresol appears extensively destructive (Rolling 1976, Magnassion 1976, Garcia-Godoy 1981). Ranly data agrees that glutaraldehyde is safer than formocresol.
Astringents Kouri et al. compared formacresol pulpotomies in primary teeth using epinephrine versus sterile water and cotton pellets for hemorrhage control. After 6 week to 3- month post-treatment periods, histologic and electron microscopic evidence of healing was similar for both groups. Bleeding times for the epinephrine-treated pulps were 50 seconds versus 251 seconds for the sterile water-treated pulps. Helig et al. compared aluminum chloride versus sterile water in achieving homeostasis prior to medicament in calcium hydroxide pulpotomies for primary teeth in humans. They found a 25% radiographic failure rate in the sterile water group versus no radiographic failures with the aluminum chloride group after 9 months.
Paraformaldehyde The use of paraformaldehyde depends on the acceptance and concepts and therapies related to early attempts at mummifying or fixing pulp tissues. The basic technique introduced by Witlzel, used a true paraformaldehyde paste. The early Gysi Triopaste was followed by Robin’s paste in France. Other variations
Corticosonol, Riebler’s and Oxpara. In 1959, Sargenti and Richter introduced a material for endodontic therapy. They reported that the success of this treatment is dependent on the presence of paraformaldehyde. N2, the term they gave it, is a slow setting cement prepared by mixing a powder which is essentially zinc oxide with 5% paraformaldehyde with a liquid which is chiefly eugenol.
Eugenol – 92%
Rose oil – 8%
Paraformaldehyde – 4.7% Calcium hydroxide – 0.94% Phenyl mercuric borate – 0.16% Hannah and Rowe, 1971 found a high clinical success rate with the medicament. The fixation of the pulp prevented its autolysis and was the essential therapeutic action of N2 and other paraformaldehyde containing drugs. Langerland and others have condemned the terminology and philosophy of N2 as non biologic. The method of delivery and the deleterious effects of paste systems have been areas of concern. There is little doubt about the medicaments toxicity. Necrosis of tissue in contact with paraformaldehyde has been reported.
Tetrandrine A novel anti-inflammatory agent â€“ Tetrandrine with a molecular weight of 622.73 Daltons used as a powder of 98% purity was dissolved in phosphate buffered saline and 20%. 0.1N HCl with pH of 7.2. Pulpotomies with this medicament show significantly less inflammatory changes as compared to formocresol and Ledermix. It is a naturally occurring analog, Berbamine, while not as potent as Tetrandrine, is also significantly better than formocresol. However, only exploratory research exists regarding this medicament.
Collagen Another pulpotomy medicament used is Enriched collagen solution. Anna B. Fuks, Y. Michaeli et al (1984) studied pulp healing in baboons after pulpotomy using enriched collagen solution. The result indicated 80% of teeth with vital pulps and dentin bridges were present in 73% of the teeth and cells were seen proliferating through the incomplete dentin bridge into the pulp chamber. Because collagen fibers are known to influence mineralization, Dick and Carmichael placed modified wet collagen sponges with reduced antigenecity in the pulp-exposed teeth of young dogs. Although the material was found to be relatively less irritating than calcium hydroxide, and with minimal dentin bridging in 8 weeks, it was concluded that collagen was not as effective in promoting a dentin bridge as was calcium hydroxide.
Ferric sulfate pulpotomy Ferric sulfate has been suggested as a substitute for formocresol (Fei et al 1991). In search for alternate medicaments, Landau and Johnson found a favorable pulpal response in monkeys to ferric sulfate as a promising medicament for pulpotomies. A non-aldehyde, ferric sulfate has received some attention recently as a pulpotomy agent. This haemostatic agent was proposed on the theory that it might prevent problems encountered with clot formation and thereby minimize the chances for inflammation and internal resorption. It has not been explained how clotting itself could curtail these activities. Possibly, the metal protein clot acts as a barrier to the irritative components of the sub base. The ferric surface may function solely in a passive manner. Despite the promising findings regarding the use of ferric sulfate, there is need for longer follow-ups and greater teeth evaluation. Different base materials other than ZOE can be used as ferric sub base is not a mummifying / fixative agent and ZOE leads to severe inflammation. Thus various different base materials should be used to determine pulpal response to this material. Studies should determine the potential effects on underlying permanent teeth and the nature of any absorption and systemic distribution of ferric sulfate from pulpal tissue. The results documented by Fei and Johnson, 1991 and by Fuks, 1994 showed great variations. The 1 year success rate for formocresol pulpotomies was 78% while the success rate for those primary molars treated with ferric sulfate was 96%. Additional evaluation was suggested.
Lasers Application of laser irradiation in vital pulp therapy has been proposed as another alternative to pharmacotherapeutic techniques. Adrian reported that irradiation of the buccal tooth surface with the neodymium: yttrium-aluminumgarnet (Nd: YAG) laser produced less pulp damage than the ruby laser with less histological evidence of coagulation and focal necrosis. Shoji et al. histologically studied the carbon-dioxide laser in the pulpotomy procedure. They noted that the least amount of pulp tissue injury occurred with defocused irradiation with lower power settings and shorter application. McGuire et al. compared the Nd:YAG laser with formocresol in permanent tooth pulpotomies in dogs at 6-week post-treatment periods. Histologically, the frequency of pulpal inflammation was higher for the laser group (29%) at 12 weeks than for the formocresol group (0%). Although clinical and histological investigations are needed to address the variables of power settings, application times, continuous versus pulsed modes of application and degree of heat dissipation in the radicular pulp and surrounding hard tissues. Andreas moritz evaluated the effect of CO2 laser on direct pulp capping and reported a success rate of 89%.
Freeze Dried Bone Clinically freeze dried bone has been used in a variety of orthopedic and oral surgical procedures. Its compatibility with host bone and effectiveness as a successful graft material has been shown. Also, it induces new bone and stimulates osteogenesis along with cementogenesis. Since pulp and dentin are mesodermal tissues â€“ as are bone and cementum, it seems reasonable to suggest that Freeze Dried Bone may serve as an inducer of a calcific barrier. Additionally, it has been shown that dentin chips in contact with pulp tissue may serve as a nidus for calcific barrier formation. Further more, observation by McLean and Urist (1968) showed that proteins of matrix of bone and dentin contain precursors of the inducing substance. It is the interaction of the mesodermal cells and mesodermal derivatives during bone resorption that induces differentiation of preosteoblasts, osteoblast and new bone formation. Thus Freeze Dried Bone may be useful as an alternative to formocresol pulpotomy. Shahrbanoo Fadavi et al (1996) conducted a study to compare the pulpal response to Freeze Dried Bone, calcium hydroxide and zinc oxide eugenol in cynomolgus monkeys and found that Freeze Dried Bone was superior to calcium hydroxide.
Bone Morphogenetic Protein and Osteogenic Protein: Bone Morphogenetic Protein and Osteogenic Protein are members of a family of signaling proteins that regulate cell differentiation. Their discovery primarily came about by observations of Huggins and Urist. The family includes BMP 2 through 7 and OP 1 and 2. Most of the proteins were evaluated for osteogenic potential in vivo in rats. Pulp responses were determined in dog and primate teeth. They, along with inducing bone and dentin, seem to have other functions during embryogenesis. Their ability to promote bone healing is being used to advantage. They are part of genetic molecular biology and research. An implant of HCl-demineralized dentin matrix invariably induces differentiation of perivascular connective tissue cells into cartilage and bone. The response is as consistent with bone matrix. The sequence of developmental events is same as with bone matrix or BMP. Conover and Urist separated dentin BMP and this induced bone formation. Importantly for dentistry, OPs and BMPs hold promise for pulp therapy. Capitalizing on the early knowledge that demineralized bone and dentin are inductive, Fadavi et al dressed pulpotomized monkey teeth with freeze dried bone and Nakashima used dentin matrix to treat amputated pulps of dogs. More recently, crude BMP from bovine bone was used to treat pulpotomized dog teeth. They reported sequential induction of osteo and tubular dentin.
Mineral Trioxide Aggregate (MTA) Mineral trioxide aggregate or MTA was developed in the Loma Linda University by Torbenijed.
Properties of MTA: • Mineral trioxide aggregate is a powder that consists of fine hydrophilic particles that sets in the presence of moisture. Hydration of the powder results in a colloidal gel. • MTA has the pH of 10.2 initially which rises to 12.5 after three hours of mixing. • The setting time for the cement is 2 hours 45 minutes.
Uses of MTA: 1. In vital pulp therapy as pulp capping agent 2. Apical plug formation 3. Repair of root perforation 4. Root end filling 5. It can be used as a coronal plug after obturation and before non vital bleaching 6. To repair a vertical root fracture. 7. Root canal filing material.
Advantages of MTA 1. Least toxic of all the filling materials 2. Excellent biocompatibility 3. Hydrophilic in nature 4. Reasonably radio opaque 5. Non- resorbable 120
6. Good marginal seal 7. Stimulates hare tissue formation (cementum)
Disadvantages 1. Difficult to manipulate 2. Long setting time 3. Expensive 4. no antimicrobial property 5. dissolves in an acidic pH
Composition Tricalcium Silicate. Tricalcium aluminate. Tricalcium oxide Silicate oxide Mineral oxide in traces Bismuth oxide
Mixing MTA Mineral trioxide aggregate should be prepared just before its use. Mineral trioxide aggregate powder must be kept in containers with tight lids and away room moisture. The powder should be mixed with sterile water at a ratio of 3:1 on a glass slab or paper pads with the aid of plastic or metal spatulas. The mixture can be carried in a plastic or metal carrier to its intended site of the operation. If the area of application is very wet the extra moisture can be removed with a dry piece of gauze or foam. In cases where the mixture is very dry, more water can be added to the dry mix, because mineral trioxide aggregate requires the moisture to set. Leaving the mixture on a glass slab or a
paper will result in dehydration of the material and a dry sandy mixture. After its use the mixture can be washed off the slab with running water. Several in vitro and in vivo studies have shown that mineral trioxide aggregate prevents microleakage, is biocompatible and promote regeneration of the original tissues when it is placed in contact with the dental pulp or periradicular tissue. MTA has the ability to encourage hard-tissue deposition and the mechanism of action may have some similarity to that of calcium hydroxide. Although hard-tissue formation occurs early with MTA, there was no significant difference in the quantity of cementum or osseous healing associated with freshly placed or set MTA. It has been demonstrated that, MTA actively promotes hard tissue formation through cytokine stimulation and formation of thick definite dentinal bridges (Pitt Ford, Torabinejad et al 1996). It has low tissue toxicity and no mutagenicity (Torabinejad et al 1995).
T. R. Pitt ford et al (1991) investigated the pulpal response to mechanical exposure and capping either immediately or after 24 hours using visible lightcured calcium hydroxide preparation. The success rate of pulp capping delayed for 24 hours was as high as that for immediate capping. A. A. Chohayeb et al (1991) evaluated tricalcium phosphate as a pulp capping agent. 39 teeth were taken class I and V cavities prepared with minimal pulp exposure. Then in 5 teeth coated with Ca(OH) 2 (control) and tricalcium phosphate in others. It was found that tricalcium phosphate as a capping agent precipited the highest mean inflammatory response and demonstrated the highest percentage of reparative dentin formation. Yoshimine Y, Maeda K (1995) evaluated Tetracalcium phosphate-based cement as a direct pulp-capping agent. Tetracalcium phosphate cement elicited a dentine bridge formation with no evidence of either intervening tissue necrosis or marked inflammation. This study suggests that Tetracalcium phosphate cement possesses a biocompatible property, which indicates its potential for use as a direct pulp-capping agent. Leksell E, Ridell K, Cvek M, Mejare I. (1996) assessed pulp exposure after stepwise versus direct complete excavation of deep carious lesions in young posterior permanent teeth. direct complete excavation of caries revealed pulp exposure and stepwise excavation showed normal clinical and radiographic conditions. Fishman SA, Udin RD, Good DL, Rodef F. (1996) compared Success of electrofulguration pulpotomies covered by zinc oxide eugenol or calcium hydroxide. Electrofulguration pulpotomies were completed on 47 primary molars in 38 patients, In group 1, a zinc oxide and eugenol (ZOE) base was placed over the pulpal stumps and, in group 2, a calcium hydroxide Ca(OH) 2 base was placed. There were no statistical differences between the two groups, either clinically or radiographically.
Bjorndal L, Larsen T, Thylstrup A. (1997) examined the clinical and microbiological alterations during the final excavation performed during long intervals (6-12 months) after the initial treatment that included peripheral dentine excavation and removal of the central cariogenic biomass and the superficial necrotic dentine. . Reassessments were performed before and after final excavation. The clinical dentine changes occurring during stepwise excavation were characterized by enhanced hardness of the dentine which was associated with a marked reduction in bacterial growth after the final excavation. Anna b. fuks et al (1997) performed a long term follow up on ferric sulfate and dilutes formacresol in pulpotomized primary molars. Ferric sulfate and 20% dilute formocresol with ZOE, IRM and stainless steel crown restoration were used. High success rates of 92 and 83% respectively with no statistically significant difference indicated both modalities as acceptable pulpotomy therapies. Bjorndal L, Thylstrup A (1998) reported the results from a practice-based study in which deep carious lesions were treated by general dental practitioners using stepwise excavation in 94 carious lesions. At the first visit excavation of the peripheral dentine was completed. The final excavation was completed after a treatment interval ranging from 2 to 19 months. Only five cases resulted in pulp perforation during the final excavation. After 1 year of observation shows that it was possible for dentists in general practice to administer and manage the treatment of deep carious lesions, a process which may prolong tooth survival compared with conventional endodontic techniques. Moritz A, Schoop U, Goharkhay K, Sperr W. (1998) used The CO2 laser as an aid in direct pulp capping. Two hundred direct pulp capping procedures were conducted in the present study. One hundred of them were performed with the CO2 laser, and 100 were conducted conventionally as a control by using a calcium hydroxide preparation. The CO2 laser seems to be a valuable aid in direct pulp capping. 124
Weerheijm KL et al (1999) investigated the 2-year influence of resinmodified glass ionomer cement (RM-GIC) and amalgam on the bacteriological counts of carious dentine that remained under class I restorations. Both materials showed a substantial decrease in numbers of TVC and LB of the carious dentine after the 2-year period. This study suggested that complete removal of carious dentine is still the best conservative treatment, irrespective of the restorative material used. Dimitrios Tziafas et al. (1999) examined the surface of calcium hydroxidecontaining materials when treated in different in vitro conditions. Five calcium hydroxide-containing materials and two control calcium hydroxide-free materials were tested. The results demonstrated organized crystalline structures in the calcium hydroxide containing specimens treated in all experimental conditions. Shumayrikh NM, Adenubi JO (1999) evaluated glutaraldehyde with calcium hydroxide and glutaraldehyde with zinc oxide eugenol in pulpotomy of primary molars. There was no statistically significant difference between the two groups either clinically or radiographically. The overall clinical success rate suggested that 2% buffered glutaraldehyde was an effective agent in the pulpotomy of human primary molars. Bjorndal L, Larsen T (2000) examined Changes in the cultivable flora in deep carious lesions following a stepwise excavation procedure in 9 permanent teeth, The final excavation was performed 4-6 months after the initial treatment, which included peripheral dentine excavation and removal of the central cariogenic biomass and the superficial necrotic dentine. Reassessments were performed before and after the final excavation. In conclusion, the cultivable flora detected following the treatment interval had declined substantially, and the distribution of bacterial species did not represent typical cariogenic microbes of deep lesions. Waterhouse PJ, Nunn JH, Whitworth JM. (2000) investigated the relative efficacy of Buckley's Formocresol and calcium hydroxide in primary molar 125
vital pulp therapy. This investigation confirms the clinical efficacy of a onefifth dilution of Buckley's Formocresol as an agent in pulp treatment of cariously exposed, vital primary molar teeth. However, calcium hydroxide in its pure, powder form is a clinically acceptable alternative when combined with strict selection criteria for this method of restorative care. do Nascimento AB, Fontana UF, Teixeira HM, Costa CA (2000) evaluated the human pulp response following pulp capping with calcium hydroxide (CH, Group 1), and the resin-modified glass-ionomer Vitrebond (VIT, Group 2). Buccal Class V cavities were prepared in 34 sound human premolars and cavities were filled using Clearfil Liner Bond 2 bonding agent and Z100 resinbased composite. CH caused a large zone of coagulation necrosis. The mononuclear inflammatory reaction underneath the necrotic zone was slight to moderate. VIT caused a moderate to intense inflammatory pulp response with a large necrotic zone. A number of congested venules associated with plasma extravasation and neutrophilic infiltration was observed. Over time, only CH allowed pulp repair and complete dentin bridging around the pulp exposure site. VIT components displaced into the pulp tissue triggered a persistent inflammatory reaction which appeared to be associated with a lack of dentin bridge formation. Maltz M, de Oliveira EF, Fontanella V, Bianchi R. (2002) assessed the clinical, radiographic, and microbiologic changes in deep caries lesions, after incomplete carious dentin removal and tooth sealing. Treatment consisted of incomplete excavation of the demineralized dentin, application of calcium hydroxide, and sealing for a 6 to 7 month period in 32 teeth. Incomplete removal of carious dentin and subsequent tooth sealing resulted in the arrest of the lesions, suggesting that complete dentinal caries lesion removal is not essential to the control of caries lesions. Falster CA, Araujo FB, Straffon LH, Nor JE. (2002) compared the clinical and radiographic outcomes of adhesive resin system vs a calcium hydroxide liner for protection of the dentin-pulp complex of primary molars treated with 126
indirect pulp treatment. This study demonstrates that protection of the dentinpulp complex of primary molars with an adhesive resin system results in similar clinical and radiographic 2-year outcomes as compared to calcium hydroxide when indirect pulp treatment is performed in Class I composite restorations. D. Tziafas et al (2002) studied the dentogenic effect of mineral trioxide aggregate (MTA) after direct pulp capping. 33 teeth were mechanically exposed via class V cavities. MTA was placed at the exposure site. The cavities were restored with amalgam. Experiments indicate that MTA is an effective pulp capping material, able to stimulate reparative dentine formation. Wicht MJ ET AL (2004) investigated the efficiency of a chlorhexidine varnish and an antibiotic paste in suppressing the cultivable microflora of deep dentine cavities in a stepwise excavation procedure. Ten cavities each were either covered with the 1% chlorhexidine- and 1% thymol-containing varnish Cervitec (CE), the demeclocycline hydrocortisone-containing ointment Ledermix (LE) or received no treatment as control (CO) Although none of the materials completely eliminated the viable microorganisms, the use of LE was more effective than CE in reducing the total anaerobic microorganisms associated with carious dentine. S.E. Jabbarifar et al. (2004) studied the Success Rate of Formocresol Pulpotomy versus Mineral Trioxide Aggregate. 64 molars were pulpotomized equally and randomly with mineral trioxide Aggregate and Formocresol. : Findings of this study show that mineral trioxide aggregate can be an alternative procedure for FC pulpotomy. M. Ghavamnasiri et al. (2004) evaluated histological pulp response of 90 mechanically exposed pulps to two adhesive resins (scotch bond and single bond 3M) were compared with Ca(OH) 2. There was no significant difference in inflammatory reaction of pulp between dycal and 2 adhesive systems after 7 days and 60 days.
Agamy HA, Bakry NS, Mounir MM, Avery DR.(2004) Compared the mineral trioxide aggregate and Formocresol as pulp-capping agents in pulpotomized primary teeth. All selected teeth were evenly divided into 3 test groups and treated with pulpotomies. Gray MTA was used as the pulp dressing for one third of the teeth, white MTA was the dressing for one third, and the remaining one third were treated with formocresol. Gray MTA appears to be superior to white MTA and formocresol as a pulp dressing for pulpotomized primary teeth. O. Bodem, S. Blumenshine, D Zeh and M. J. Koch (2004) studied the direct pulp capping with mineral trioxide aggregate in a mandibular primary molar. There was no pathological finding on a radiograph taken after one year and it remained vital after capping with MTA. Carlos Alberto Conrado (2004) evaluated a possible remineralization of human carious dentin by calcium hydroxide. Thirty-nine freshly extracted human permanent and deciduous carious teeth were split into two halves. One half was used as control and the other as experimental. In the latter, a cavity was prepared and the remaining bottom layer of demineralized dentin capped with chemically pure calcium hydroxide. The results indicate that remineralization of carious dentin by calcium hydroxide Cavalcanti BN, Rode SM, Marques MM (2005) evaluated the cytotoxic effects of substances leached or dissolved from pulp capping materials on human pulp fibroblasts. The experimental groups were: GI (control; n = 24)cultures treated with fresh medium; GII (n = 24)--cultures treated with calcium hydroxide cement; GIII (n = 24)--cultures treated with adhesive resin and GIV (n = 24)--cultures treated with 37% orthophosphoric acid. Substances dissolved from the adhesive system tested were cytotoxic for human dental pulp fibroblasts in culture, whilst substances leached from calcium hydroxide were biocompatible. Ngo HC, Mount G Mc Intyre J, Tuisuva J, Von Doussa RJ. (2006) evaluate the remineralization of carious dentine following the restoration of an extensive 128
lesion in a permanent molar with a high strength glass-ionomer cement demonstrated that both fluorine and strontium ions had penetrated deep into the underlying demineralized dentine. The pattern of penetration of the fluorine and strontium ions into the dentine was consistent with a remineralization process.
Many materials and methods are used for treating deep carious lesions. The success rate of vital pulp therapy depends upon the proper case selection and type of investigation. Present experience from a dental practice has shown that effectiveness of treating deep carious lesions using the modified stepwise excavation and long term recall has shown a high success rate. Direct pulp capping and pulpotomy are well established methods of treatment that protects the pulp from additional injury and permits healing and repair. Pulp capping with calcium hydroxide remains a method of treatment for mature teeth since ages. Calcium hydroxide based materials have found wide spread use in traditional vital pulp therapy over a number of decades. A number of new agents such as lasers, bone morphogenic proteins, mineral trioxide aggregate and bonding agents etc. have been tested during the last two decades as potential materials of choice. However continued research and clinical trials are needed to develop the appropriate case selection guidelines, treatment approaches and materials to maximize clinical success.
Boston DW, Graver HT. Histological study of an acid red cariesdisclosing dye. Oper Dent. 1989 Autumn; 14(4):186-92.
Bjorndal L, Larsen T, A clinical and microbiological study of deep carious lesions during stepwise excavation using long treatment intervals. Caries Res. 1997; 31(6):411-7.
Bjorndal L, Thylstrup A. A practice-based study on stepwise excavation of deep carious lesions in permanent teeth: a 1-year followup study. Community Dent Oral Epidemiol. 1998 Apr; 26(2):122-8.
Bjorndal L, Darvann T. A light microscopic study of odontoblastic and non-odontoblastic cells involved in tertiary dentinogenesis in welldefined cavitated carious lesions. Caries Res. 1999; 33(1):50-60.
Bjorndal L, Larsen T Changes in the cultivable flora in deep carious lesions following a stepwise excavation procedure. Caries Res. 2000 Nov-Dec; 34(6):502-8.
Bjorndal L. Buonocore Memorial Lecture. Dentin caries: progression and clinical management. Oper Dent. 2002 May-Jun; 27(3):211-7.
Bjornal L, Kidd EA. The treatment of deep dentine caries lesions. : Dent Update. 2005 Sep; 32(7):402-4, 407-10, 413.
Baum Phillips lund text book of operative dentistry third edition
Chandler NP, Pitt Ford TR, Watson TF Pattern of transmission of laser light through carious molar teeth. Int Endod J. 2001 Oct; 34(7):526-32.
10. Dorothy McComb, BDS, M.Sc.D., FRCD(C) Caries-Detector Dyes How Accurate and Useful Are They? April 2000, Vol. 66, No. 4 195 Journal of the Canadian Dental Association 11. Dorothy McComb, BDS, MScD, FRCD(C) â€˘ Laura E. Tam, DDS, M.Sc. Diagnosis of Occlusal Caries: Part I. Conventional Methods 131
Journal of the Canadian Dental Association 454 September 2001, Vol. 67, No. 8 12. D. Tziafas The Future Role of a Molecular Approach to Pulp-Dentinal Regeneration Caries Res 2004;38:314â€“320 13. El-Mowafy O. Management of extensive carious lesions in permanent molars of a child with nonmetallic bonded restorations--a case report. J Can Dent Assoc. 2000 Jun; 66(6):302-7. 14. Hebling J, Giro EM, Costa CA Human pulp response after an adhesive system application in deep cavities. J Dent. 1999 Nov; 27(8):557-64. 15. John I. Ingle, DDS, MSD Endodontics fifth edition 16. Kreulen CM, de Soet JJ, Weerheijm KL, van Amerongen WE. In vivo cariostatic effect of resin modified glass ionomer cement and amalgam on dentine. Caries Res. 1997; 31(5):384-9. 17. Langeland K, Langeland LK, Anderson DM. Corticosteroids in dentistry. : Int Dent J. 1977 Sep; 27(3):217-51. 18. Lado EA, Pappas J, Tyler K, Stanley HR, Walker C. In vitro antimicrobial activity of six pulp-capping agents. Oral Surg Oral Med Oral Pathol. 1986 Feb;61(2):197-200. 19. Leksell E, Ridell K, Cvek M, Mejare I. Pulp exposure after stepwise versus direct complete excavation of deep carious lesions in young posterior permanent teeth. Endod Dent Traumatol. 1996 Aug; 12(4):192-6. 20. Lawrence W. Stockton, DMD Vital Pulp Capping: A Worthwhile Procedure Journal of the Canadian Dental Association 328 June 1999, Vol. 65, No. 6 21. Laura E. Tam, DDS, M.Sc â€˘ Dorothy McComb, BDS, MScD, FRCD(C) Diagnosis of Occlusal Caries: Part II. Recent Diagnostic
Technologies September 2001, Vol. 67, No. 8 459 Journal of the Canadian Dental Association 22. Louis I. Grossman Seymour Oliet, Carlos E. Del Rio Endodontic practice eleventh edition 23. Murray PE, Hafez AA, Windsor LJ, Smith AJ, Cox CF Comparison of pulp responses following restoration of exposed and non-exposed cavities. J Dent. 2002 Jul-Aug; 30(5-6):213-22. 24. Maltz M, de Oliveira EF, Fontanella V, Bianchi R
microbiologic, and radiographic study of deep caries lesions after incomplete caries removal. Quintessence Int. 2002 Feb; 33(2):151-9. 25. Murray PE, Lumley PJ, Smith AJ
Preserving the vital pulp in
operative dentistry: 3. Thickness of remaining cavity dentine as a key mediator of pulpal injury and repair responses. Dent Update. 2002 May; 29(4):172-8. 26. Misako Nakashima et al the application of bone morphogenic protein to dental tissue engineering nature biotechnology vol 21no. 9, 2003. 27. M. Ghavamnasiri et al. A histopathological study of direct pulp capping with adhesive resin. J Dent TUMS 2004 vol 1, 4. 28. Ngo HC, Mount G, Mc Intyre J, Tuisuva J, Von Doussa RJ. Chemical exchange between glass-ionomer restorations and residual carious dentine in permanent molars: An in vivo study. J Dent. 2006 Mar 13 29. M.A. Marzouk, A.L.Simonton, R.D. Gross Modern theory and practice operative dentistry. 30. Papagiannoulis L, Kakaboura A, Eliades G. In vivo vs in vitro anticariogenic behavior of glass-ionomer and resin composite restorative materials. Dent Mater. 2002 Dec;18(8):561-9
31. Ricketts D Management of the deep carious lesion and the vital pulp dentine complex. Br Dent J. 2001 Dec 8; 191(11):606-10. 32. Samraj RV et al recent advances in pulp vitality test endodontology vol 15, 2003 33. Tveit AB, Espelid I, Fjelltveit A Clinical diagnosis of occlusal dentin caries. Caries Res. 1994; 28(5):368-72. 34. Torstenson B. Pulpal reaction to a dental adhesive in deep human cavities. Endod Dent Traumatol. 1995 Aug; 11(4):172-6. 35. Takao Fusayama differentiating two layers of carious dentin and using an adhesive resin. New concepts in operative dentistry. 36. Weerheijm KL, Groen HJ The residual caries dilemma. Community Dent Oral Epidemiol. 1999 Dec;27(6):436-41 37. Wicht MJ, Haak R, Schutt-Gerowitt H, Kneist S, Noack MJ Suppression of caries-related microorganisms in dentine lesions after short-term chlorhexidine or antibiotic treatment. Caries Res. 2004 SepOct; 38(5):436-41. 38. Wicht MJ, Haak R, Schutt-Gerowitt H, Kneist S, Noack MJ Suppression of caries-related microorganisms in dentine lesions after short-term chlorhexidine or antibiotic treatment. Caries Res. 2004 SepOct; 38(5):436-41. 39. Yazici AR, Baseren M, Gokalp S. The in vitro performance of laser fluorescence and caries-detector dye for detecting residual carious dentin during tooth preparation. Quintessence Int. 2005 Jun;36(6):41722 40. Zero DT. Dental caries process. Dent Clin North Am. 1999 Oct; 43(4):635-64.
Published on Apr 28, 2014
Published on Apr 28, 2014
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide r...