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REPAIR INDIAN DENTAL ACADEMY Leader in continuing dental education

Clinical dentistry will be able to adapt to a rapidly changing world only if it is based upon a sound understanding of the structure, metabolism and function of the oral tissues. Such understanding should not only be of the healthy and normal tissues but also include a knowledge of effects of microbiological and pathological interactions with the tissues so that proper treatment plan can be done.

Contents Of The Seminar. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

Introduction. Definition. Types of inflammation. Causes of inflammation. Cardinal signs of inflammation. Microscopic features of inflammation. Mediators of inflammation. Regulation of inflammation. The inflammatory cells. Morphology of inflammation. Systemic effects of inflammation. Fate of acute inflammation.

13. Chronic inflammation. a) General features. b) Granulomatous inflammation. 14. Healing. a) Regeneration. b) Repair. 15. Wound healing. 16. Healing of specialized tissues. 17.Inflammatory conditions of the oral cavity. 18. Prosthodontic considerations. 19. References from Journals. 20. Bibliography.


Definitioninflammation can be defined as the local response of a living tissue to any injury due to any agent. or Inflammation can also be defined as a dynamic process by which living tissues react to injury. or It is a body defense reaction in order to eliminate or limit the spread of injurious agent as well as to remove the consequent necrosed cells and tissues

Types of inflammation. Depending upon the defense capacity of the host & duration of response, inflammation can be classified as 1.Acute inflammationis of short duration & represents the early body reaction & is usually followed by repair . 2. Chronic inflammationis of longer duration & occurs after the causative agent of acute inflammation persists for a long time.

Causes of inflammation. Physical


Trauma Heat or cold Radiation


Infective Bacteria


organic poisons

Immunological Parasites Antigen-antibody cell-mediated

Cardinal signs of inflammation. 1.Calor(Heat)

2. Rubor(Redness) 3.Tumour(Swelling) 5.Functio laesa(Loss of function)


Acute inflammation. Vascular events-alteration in the microvasculature is the earliest response to tissue injury. These include haemodynamic changes and changes in the vascular permeability. Transient vasoconstriction Persistent progressive vasodilatation Increase in local hydrostatic pressure Slowing or stasis Leucocytic margination

Altered vascular permeability Mechanisms of altered vascular permeability. 1.Contraction of the endothelial cells. 2.Retraction of the endothelial cells. 3.Direct injury to the endothelial cells. 4.Endothelial injury mediated by leucocytes.

Cellular events.

The cellular events consists of two processes A. Exudation of leucocytes. B.Phagocytosis. A. Exudation of leucocytes-the escape of leucocytes from the lumen of microvasculature to the interstitial tissue. Changes leading to migration of leucocytes are1.

Changes in the formed elements of the bloodin the early stages of inflammation the rate of flow of blood is increased due to vasodilatation. But subsequently there is stasis of blood stream. The central stream of cells widens & the peripheral plasma zone becomes narrow due to exudation. This is known as margination.As a result of this redistribution the neutrophils of the central column come close to the vessel wall which is known as pavementing.

2.Adhesion or rollingthe peripherally marginated neutrophils stick briefly to the endothelial cells lining the vessel wall or roll over it. Injury leads to neutralization of the normal negative charge of the leucocytes and endothelial cells so as to cause adhesion. 3.EmigrationNeutrophils move along the endothelial surface till a suitable site between the cells is found where neutrophils throw out cytoplasmic pseudopods. Subsequently, cross the basement membrane by damaging it locally with secreted collagenases & escape into the extra vascular space, this is known as emigration. Escape of red cells through the gaps takes place which is called as diapedesis responsible for the hemorrhagic appearance of the inflammatory exudate.

4.chemotaxisthe chemotactic factor mediated emigration of leucocytes after crossing the several barriers to reach the interstitial tissues is called as chemotaxis. the agents acting as potent chemotactic substances for leucocytes are 1.Leukotriene B4 2.Platelet factor 4 3.Components of the complement system(c5a in particular) 4.Cytokines-IL8 5.Soluble bacterial products. 6.Chemotactic factor for CD4 cells.


Phagocytosis is defined as the process of engulfment of a solid particulate matter by the cells. The cells are called phagocytes. There are two main types of phagocytic cells 1. Polymorphonuclear neutrophils which appear in acute inflammatory response and are also called as microphages. 2. Circulating monocytes & fixed mononuclear phagocytes called as macrophages. Phagocytosis involves 4 steps 1.Attachment stage(Opsonisation) 2.Engulfment stage 3.Secretion or degranulation stage 4.Killing or Degradation stage

1.Attachment stage or Opsonisation To bond the bacteria & the cell membrane of the phagocytic cell, the microorganisms get coated with opsonins which are naturally occurring factors in the serum. The opsonins present in the serum are IgG opsonin & C3b opsonin.

2.Engulfment stageBy formation of pseudopods around the particle, enveloping it in a phagocytic vacuole. Eventually the plasma membrane enclosing the phagocytic vacuole breaks the cell surface and the lysosomes of the cell fuse with the vacuole and form phagolysosome or phagosome.

3.Degranulation stage-The preformed granule products of PMN’s are discharged. Specific or secondary granules of PMN’s are released with interlukin2,TNF,superoxide oxygen, hydrogen peroxide,hypochlorous acid. 4.Killing or degradation stage-This stage of killing & digestion of the microorganisms by the phagocytes as scavenger cells is done. The microorganisms are degraded by the hydrolytic enzymes. The antimicrobial agents act by either of the following mechanisms A) Oxygen dependant mechanism B) Oxygen independent mechanism C) Nitric oxide mechanism


Oxygen dependant mechanismin this mechanism the microorganisms are killed by the production of reactive oxygen metabolites such as O 2’,H2O2, HOCL,HOI,HOBR.In this mechanism there is production of Hypohalous acid which is a more potent antibacterial agent than H2O2.


Oxygen independent mechanismSome agents released from the granules of the phagocytic cells do not require oxygen for bactericidal activity. These include lysosomal hydrolases,defensins and cationic proteins.


Nitric oxide mechanismNitric oxide is produced by the endothelial cells as well as by activated macrophages and has potent fungicidal and antiparasitic action.


Plasma derived




Mastcells,Basophil Platelets






Inflammatory cells

Lysosomal enzymes, PAF Prostaglandins Cytokines NO & O2 metabolites

Tissue damage Permeability Fever Antibacterial Tissue damage

Clotting & Fibrinolytic system

Fibrin split products


Kinin system





Complement system

REGULATION OF INFLAMMATION Damaging effects are kept in check by the host mechanisms so as to resolve inflammation as seen in hypersensitivity reactions. These include

1.Acute phase proteinsthese are α1−antitrypsin,protease inibitor,haptoglobin, C-reactive protein, serum amyloid A & P component. These are synthesized in the liver & they are released in response to inflammation.APP combined with systemic features of fever & leucocytosis is termed as ‘acute phase response'. Deficiency of these APP leads to severe form of disease in chronic & repeated inflammatory response.

2. CorticosteroidsThe endogenous glucocorticoids act as anti-inflammatory agents. Their levels are raised in infection and trauma by self regulating mechanism.

3.Free cytokine receptorsthe presence of free receptors for cytokines in the serum correlates directly the disease activity.

4. Suppressor T-Cellsthese inhibit the function of T & B cells

5. Anti-inflammatory chemical mediatorsthese are PGE2 and Prostacyclin which have both pro-inflammatory as well as anti-inflammatory actions.

The inflammatory cells Polymorpho nuclear neutrophils Initial phagocytosis, acute inflammatory cell

Monocyte/macrophage Bacterial phagocytosis Chronic inflammatory cell Regulates Lymphocyte response

Lymphocyte Humoral & cell mediated response Chronic inflammatory cell Regulates Macrophage response

Eosinophil Allergic states Parasitic infestations Chronic inflammatory cell

PGE2 synthesis Reactive O2 metabolites

Mast cell Receptor for IgE antibodies

Histamine, leukotreins, PAF

Plasma cell Chronic inflammatory cell

Anti-body synthesis


.Factors involving the organisms I) Type of injury & infection II) Virulence III) Dose IV) Portal of entry V) Product of the organisms


Factors involving the Host I) General health of the host II) Immune state of the host III) Leucopenia IV) Type of tissue involved V) Local host factors

3. Type of exudation I) Serous II) Fibrinous III) Purulent IV) Haemorrhagic V) Catarrhal 4. Necrosis I) Gas Gangrene II) Acute appendicitis

MORPHOLOGY OF ACUTE INFLAMMATION 1.Pseudomembranous inflammationit’s a inflammatory response of the mucous surface to toxins of diphtheria or irritant gases. As a result of denudation of the epithelium, plasma exudes on the surface where it coagulates & together with the necrosed epithelium forms a false membrane. 2.Ulcer-

Ulcers are local defects on the surface of an organ produced by inflammation. Common sites of ulcerations are the stomach, duodenum,intestinal ulcers in typhoid, ulcers of the legs due to varicose veins.

3.Suppuration(Abscess formation)Accompaniment by intense neutrophilic infiltrate in the inflamed tissue results in tissue necrosis. A cavity is formed which is called an abscess & contains a purulent exudate such as a Boil or Furuncle which is an acute inflammation of the hair follicles in the dermal tissues. 4.Cellulititsit’s a diffuse inflammation of soft tissues resulting from spreading effects of substances like hyaluronidase released by some bacteria. 5.Bacterial infection of the blooda) Bacteraemia b) Septicemia c) Pyaemia

SYSTEMIC EFFECTS OF INFLAMMATION The systemic effects of inflammation are 1.feverThis occurs due to bacteraemia mediated by the release of factors like prostaglandins,interleukin-1 and tumour necrosis factor.

2.LeucocytosisIn bacterial infections there is neutrophilia,in viral infections lymphocytosis & in parasitic infestations eosinophilia.

3.Lymphagitis-LymphadenitisThe affected lymph may show hyperplasia of the lymphoid follicles & proliferation of mononuclear phagocytic cells in the sinuses of the lymph nodes.

4.Shockoccurs in severe cases wherein there is massive release of cytokine & TNF-Îą in severe tissue injury or infection resulting in profuse systemic vasodilatation, increased vascular permeability & intravascular volume loss. The net effect of these changes is hypotension & shock. Systemic activation of the coagulation pathway may occur leading to micro thrombi through the body & result in disseminated intravascular coagulation, bleeding and death.

FATE OF ACUTE INFLAMMATION. 1.ResolutionIt means complete return to normal tissue following acute inflammation. This occurs if tissue changes are slight & the cellular changes are reversible e.g.-resolution of lobar pneumonia. 2.Healing by scarringThis takes place when the tissue destruction is extensive so that there is no tissue regeneration but actually there is healing by fibrosis. 3.Progression to suppuration When the pyogenic bacteria cause severe tissue necrosis, inflammation progresses to suppuration. Mixture of neutrophils,bacteria,fragments of necrotic tissue, cell debris & fibrin comprise pus which is contained in a cavity to form abscess. 4.Progression to Chronic inflammation.The acute inflammation may progress to chronic inflammation in which processes of inflammation & healing proceed side by side.

CHRONIC INFLAMMATION Chronic inflammation can be defined as a prolonged process in which tissue destruction and inflammation occur at the same time.

Causes of Chronic inflammation 1.Chronic inflammation following Acute inflammationWhen the tissue destruction is extensive or the bacteria survive & persist in small numbers at the site of inflammation. e.g.Osteomyelitis,Pneumonia terminating in lung abscess. 2.Recurrrent attacks of acute inflammationwhen recurrent bouts of acute inflammation culminate in chronicity of the process. e.g. recurrent urinary tract infection leading to chronic pyelonephritis. 3.Chronic inflammation starting de novowhen the infection of the organisms of low pathogenicity is chronic from the beginning. e.g. infection with Mycobacterium tuberculosis.

GENERAL FEATURES OF CHRONIC INFLAMMATION 1.Mononuclear cell infiltration. Infiltrated by mononuclear inflammatory cells like phagocytes, circulating monocytes, macrophages & giant cells. 2.Tissue destruction or necrosis. Tissue destruction & necrosis are common in many inflammatory lesions & are brought about by activated macrophages by release of a variety of biologically active substances. 3.Proliferative changes. As a result of necrosis, proliferation of small blood vessels & fibroblasts is stimulated resulting in formation of inflammatory granulation tissue eventually leading to healing by fibrosis.

Types Of Chronic Inflammation

1.Nonspecific inflammation-when the irritant substance produces a non-specific chronic inflammatory reaction with formation of granulation tissue and healing by fibrosis e.g. Chronic ostomyelitis,Chronic ulcer.

2.Specific-When the injurious agent causes a characteristic histologic tissue response e.g.Tuberculosis,Leprosy,Syphilis.

According to histological findings these are again classified into 1.Chronic nonspecific inflammation-It is characterized by nonspecific cell infiltration e.g. chronic osteomyelitis,Actinomycois.

2.Chronic Granulomatous inflammation-It is characterized by formation of granulomas e.g.Tuberculosis,Leprosy,Actinomycosis,Sarcoidosis.

Granulomatous Inflammation Granuloma is a circumscribed lesion composed predominantly of modified macrophages called epitheloid cells and rimmed at the periphery by lymphoid cells.

Giant cells- Formed by the fusion of adjacent epitheloid cells & may have 20 or more nuclei. The giant cells are weakly phagocytic but produce secretory products which help in removing the invading agents.

Examples of some Granulomatous inflammations Conditions

Etiologic agent




Tuberculous granulomas with central caseating necrosis.


Treponema pallidum

Gummas composed of histiocytes, plasma cell infiltration, central necrosis

3.Cat scratch disease


Lymphadenitis,reticuloendothelial hyperplasia,granulomas with central necrosis.

4.Actinomycosis Actinomycosis Israeli

Cervicofacial lesions

5.Foreign body granulomas

Non caseating granuloma with foreign body giant cells

Talc,suture,oils, wood splinter etc

Healing and repair

Injury to the tissue may result in cell death & tissue destruction. Healing is the body response to injury in an attempt to restore the normal structure & function. Healing occurs in the following phases REMOVAL OF DEAD TISSUE




Regeneration involves two processes 1.Proliferation of surviving cells to replace lost tissue. 2.Migration of surviving cells into the vacant space. The factors which control healing & repair are complex & they include the production of variety of growth factors Damaged epithelial cells



Growth factors and cytokines

Specialized cell regeneration (epidermal growth factor)

Fibroblast activation (transforming growth factor β) factor)

Angiogenesis (angiogenic


Repair is the replacement of injured tissue by fibrous tissue.The processes involved in repair are

1.Granulation tissue formation 2. Contraction of wounds Takes place by the participation of mesenchymal cells (consisting of connective tissue stem cells,fibrocytes& histiocytes), endothelial cells, macrophages, platelets & parenchymal cells of the injured organ.

Granulation tissue formation Granulation tissue derives its name from the slightly pink appearance of the tissue. Each granule corresponds histologically to proliferation of new blood vessels which are slightly lifted on the surface by a thin covering of fibroblasts and young collagen. Phases involved in formation of granulation tissue. Phase of inflammation Phase of clearance Phase of in growth of granulation tissue angiogenesis(neovascularization) Fibrous tissue formation

Contraction of wounds The wound starts contracting after 2-3 days & the process is completed by 14th day, during this period the wound is reduced by approximately 80% of its original size.Contracted wound results is rapid healing since lesser surface area of the injured tissue has to be replaced.

Mechanism Dehydration as a result of removal of fluid by drying of wound Contraction of collagen proceeds at a stage when the collagen content of the granulation tissue is very small

Myofibroblasts migrate and their active contraction decreases the size of the defect, these cells contain actin & myosin & thereby causing formation of new tissue and contraction takes place.


Regeneration & repair is accomplished in one of the following two ways 1.Healing by first intention (primary union) 2.Healing by secondary intention (secondary union)

HEALING BY FIRST INTENTION This occurs in clean, incised wounds with good opposition of the edges. Immediately blood clot & debris fill in the defect

2-3 hours early inflammation close to the edges with mild hyperemia & few PMN’s

2-3 days macrophagic activity removing the clot. Proliferation of blood vessels & fibroblastic activity

10-14 days scab loose & epithelial covering complete. Fibrous union of the edges

Weeks: scar tissue still hyperemic with good fibrous union but not of full strength

Months-years: Devascularisation & Remodeling of collagen by enzymatic action. Scar is minimal & merges with the surrounding tissues

HEALING BY SECONDARY INTENTION This occurs in open wounds particularly when there has been significant loss of tissue because of necrosis or infection Early stages the cavity is filled with blood & clot. Acute inflammation at the junction of the living tissues. A few days later contraction of the wound takes place with a single sheet of epithelial cells between the surface of the debris & the underlying living tissue. 1 week: granulation tissue formation 2 weeks: Epithelial covering complete with capillaries less prominent. Months: There is a varying depth on the skin surface with thick collagenous scar tissue becoming less vascular

COMPLICATIONS OF WOUND HEALING Contracture is due to the thickening & shortening of the collagen bundles & may cause serious cosmetic & functional disability, particularly in deep & extensive burns & around the joints of the muscles if seriously damaged.

Occasional complications may occur at the edges & base of the wound in which granulation tissue may form in excess and prevent proper healing.

FACTORS INFLUENCING HEALNG These can be divided into local factors & systemic factors A. Local factors i) Infection ii) Poor blood supply iii) Foreign bodies iv) Movement v) Exposure to ionizing radiation delays granulation tissue formation vi) Exposure to ultra violet light facilitates healing vii) Type, size & location of injury B. Systemic factors i) Age ii) Nutrition iii) systemic infections iv) Cortisteroids act as anti-inflammatory agents. v) Uncontrolled diabetics vi) Hematological disturbances

HEALING OF SPECIALIZED TISSUES Healing of Nervous tissue1.Central nervous system-The nerve cells of brain, spinal cord and the ganglia once destroyed cannot be healed. The damaged neuroglial cells however may show proliferation of astrocytes called gliosis. 2.Peripheral nervous system- The peripheral nerves show regeneration, mainly from proliferation of Schwann cells and fibrils from the distal end. The myelin sheath & the axon of the intact distal nerve undergo Wallerian degeneration upto the next node of Ranvier towards the proximal end. Sprouting of fibrils takes place from the viable axon. In 6-7 weeks the peripheral stump consists of tube filled with elongated Schwann cells. Once the fibrils from the proximal stump enter the old neural tube it develops into a new functional axon.

HEALING OF MUSCLE All three types of muscle fibres have a limited capacity to regenerate 1. Skeletal muscle- On injury the cut ends of the fibres are held together by stromal connective tissue. The injured site is filled with fibrinous material,PMN’s & macrophages. If the muscle sheath is intact sarcolemmal tubes containing histiocytes appear along the endomysial tube which in about 3 months time restores properly the oriented muscle fibres If the muscle sheath is damaged it forms a disorganized multinucleate mass & scar composed of fibro vascular tissue. 2. Smooth muscle-Non-striated muscle has limited regenerative capacity e.g. appearance of smooth muscle in the arterioles as granulation tissue. 3. Cardiac muscle-Destruction of the heart muscle is replaced by fibrous tissue & in situations where the endomysium of the individual cardiac fibre is intact regeneration may occur in young patients.

HEALING OF MUCOSAL SURFACES The cells of the mucosal surfaces have a very good regeneration capacity and are replaced continuously as the blood supply is excellent and promotes healing due to rapid differentiation of cells.


Prosthodontic Considerations FIXED PARTIAL DENTURE Factors of specific influence are 1.Ridge contact-Pressure free contact between the pontic & the underlying tissues. If any blanching of the tissues is observed at the try in stage the pressure area should be identified by disclosing medium & the pontic recontoured until contact is entirely passive. This passive contact should be on the keratinized mucosa. Scraping of the cast should be avoided as this may also cause positive ridge pressure. 2. Oral hygiene considerations-Patients must be taught efficient oral hygiene techniques.

PONTIC MATERIAL Glazed porcelain is generally considered the most biocompatible. Well polished gold is smoother, less prone to corrosion & less retentive to plaque than an unpolished or porous casting. Regardless of the choice of the pontic material patients can prevent inflammation around the pontic with meticulous oral hygiene.

OCCLUSAL FORCES Reducing the buccolingual width of the pontic by as much as 30% has been suggested as a way to reduce the occlusal forces on & thus the loading of the abutment teeth. Reducing the pontic width may be desired as it facilitates plaque control measures by lessening the lingual contour.

USE OF SOFT TISSUE MODELS Use of soft tissue models will help the technician to fabricate the prosthesis by the adequate guidance of the soft tissue contours.

COMPLETE DENTURES 1.Soft tissue hyperplasia-it is the response of the soft tissues under or around the complete denture due to fibro epithelial response to complete denture wearing. The causes are a) Trauma from denture wearing b) Gradual residual ridge resorption c) Habits & duration of wear d) Excessive forces on limited segments of the dental arches because of lack of balancing contacts in eccentric jaw positions. 2.Epulis fissuratum- Hyperplasia occurring around the dentures leading to a fibrous growth which occurs due to ill-fitting or over extended dentures. 3. Denture stomatitis -is a chronic inflammation of the denture bearing mucosa caused due to ill-fitting dentures or Para functional habits. Effective management of all these conditions can be done by A) Oral and denture hygiene accompanied by tissue rest. B) Antifungal therapy . C) Surgical excision of papillomatosis.

Subpontic osseous hyperplasia: A literature review J.P.D:1991:66;638-41 The proposed etiologies for this condition are 1.FPD acting as a stimulus to osseous proliferation. 2.Chronic irritation produced by the pontic initiates the subperiosteal growth. 3.Functional stresses on bone during mastication. 4.Stress generated electrical potentials of the bone.

CONCLUSION The mouth represents one of the most complex areas of the body with regard to the broad range of disorders affecting it. By virtue of its partial Ectodermal and Endodermal origin, the oral mucosa may show manifestations of the systemic diseases. Oral mucosa is extremely sensitive to metabolic disturbances perhaps only paralleled by the bone marrow and thus serves as an excellent marker for such disorders. The modern concept of practicing dentistry is to recognize these basic etiological factors & pathological changes occurring in the oral tissues as it is a significant diagnostic aid representing the patient’s general medical status. “


BIBLIOGRAPHY 1.Text of Pathology-Harshmohan 4th edition 2. Pathology illustrated-Peter.S.Macfarlene 5th edition 3. Text of Pathology –Robbins 4. Pathology in dentistry-Shefield 5. Gen. & systemic Pathology-Underwood 2nd edition 6. Colour atlas of Oral pathology-Robinson & miller 4 th edition 7. Colour atlas of common oral diseases- Robert.P.Langlais 8. Oral bio-science-Fergusson 9. Oral medicine – Tyldessly & Field 4th edition 10.Essentials of Oral pathology & Oral Medicine- R.A.Cawson 11.Contemporary Fixed Prosthodontics-Rosenstiel 3rd edition 12.Prosthodontic treatment for edentulous Patients-Bouchers 10th edition

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