DEFENCE MECHANISM OF ORAL CAVITY

INTRODUCTION The oral cavity is loaded with acrobes and anaerobes which are normal commensals of the oral cavity. Any breach of the integrity of the oral mucosa may lead to rapid attack by various other microorganisms present in the environment. Hence, an effective defence mechanism is necessary within the oral cavity to safeguard it from these attacks. These defence mechanisms can be broadly divided into a. Integrity of oral mucosa and role of lymphoid system. b. Role of Gingival crevicular fluid c. Role of saliva d. ascular component of most defence mechanism

1. Integrity of oral mucosa and role of lymphoid system The health of oral cavity primarily depends on the integrity of the oral mucosa. !rovided this mucosa remains intact, few microorganisms can penetrate the underlying tissues. This partly reflects the functions of the "eratin barrier. The oral mucosa can be broadly # into

a. Masticatory mucosa % which covers the crest of the RR and the hard palate. b. Lining mucosa % which covers the lips and cheeks, the vestibular spaces, the alveolingual sulcus, the soft palate the ventral surface of the tongue and the unattached gingiva found of the slopes of RR. c. The specialized mucosa% which covers the dorsum of the tongue. The oral cavity is lined by a stratified s&uamous epithelium whose functions include% $. 'orming a primary structure barrier between the internal and e(ternal environment. ). !rotection against mechanical damage, entry of no(ious substances or organi*ing and loss of fluids. +ike the skin, the oral mucosa comprises a surface epithelium, overlying the layer of basement membrane. This string s& epithelium undergoes mitosis, synthetic activity and disintegration leaving the underlying cells as a cohesive tissue. The epithelial cells undertake a member of speciali*ed synthetic activities associated with the maintenance of a surface barrier including. $. The synthesis of "eratin

). ,efradation of other intracellular organelles -. .ynthesis of cell membrane and e(tra cellular components associated with cell adhesion and barrier function. /. 0asement membrane synthesis to provide attachment to the underlying 1T. In the lamina propia ad2acent to the basement membrane there are a few lymphoid cells which may combat microorganisms that penetrate to this depth. These intraoral lymphoid aggregations, function together with the e(tra oral lymph nodes for the protection of the oral cavity as a whole. There are in fact several intra oral lymphosis aggregations. $. The palatine Tonsils comprise paired lymphoid masses, between the glossopalatine and pharyngo palatine arches. The component lymphoid tissue contains both 0 and T cells, IgG producing cells being the most prominent. ). The lingual Tonsils are much less prominent lying on each side of the tongue 2ust distal to the circum vallate papillae. They contain lymphoid modules some of which have germinal centers in addition to perifellicular diffuse lymphoid cells.

-. The pharyngeal tonsil comparison of simple mass of lymphoid tissue under the nasopharangeal mucosa. There are also scattered collections of lymphoid tissue in other regions of the oral cavity. +ymphocytes and plasma cells are found in small clusters in both ma2or or minor .G. 3ost of the plasma cells secrete Ig A. ROLE OF GINGIVAL CREVICULAR FLUID 4ith continued pla&ue accumulation at the cervical surface of the tooth, there is a corresponding increase in crevicular fluid formation. This fluid contains immunoglobulins Ig G, A, 3 in adition to complement components namely 1-, 1/ and 15 and 1- !ro activator. Thus the crevicular fluid contains most of the humoral and cellular immune components found in the blood, altering salivary Ig A is the predominant component. There are abo, a number of other components of the crevicular fluids including% a6 Albumin b6 Transferring c6 traptaglobulin d6 Glycoproteins e6 +ipoproteins Tube en*ymes not only affect specific tissues e.g. collagen, but also selective Ig A in activation results from specific protease activity. f6 lysosomal en*ymes g6 lyso*yme h6 Tryaluronidase I6 1ollagenase

1revicular fluid also contains macrophages and T and 0 cells which migrate from the underlying blood vessels. ROLE OF SALIVA In addition to mechanical lavage the saliva function as a component of the oral immune system saliva combines both specific and non specific immune components. A) NON SPECIFIC COMPONENTS i) Lysozyme (Meramidase) This is bactericidal en*yme that splits the bond between 7 acetyl glucosomine and 7 acetyl inuramic acid in the micopeptide components of bacterial cell wall. Apart from .tr. 3utans, the oral flora is generally resistant to lyso*yme. ii) Peroxidase In the p8o thiocyanate ions and hydrogen pero(ide, pero(idase kills acidophilus by inhibiting lysin uptake and may inhibit some streptococci by limiting the action of their glycolytic en*ymes. iii) Lactoferrin

This has a bacteriostatic effect on a whole microbial spectrum, possibly by depleting local environmental iron re&uired for microbial growth. B) SPECIFIC COMPONENTS SE !E"#!$ Ig % IgA is &uantitatively the most important Ig present in saliva, mainly derived locally from plasma cells. It is then trasported to the distal human and e(erted into the oral cavity . IG A is more resistant to microbial and particularly suited for saliva, which then functions as an antisept paint for various oral surfaces. .igA also appears to limit microbial adherence to the mucosal surface. PE!I#&#'"%L &ISE%SE The effect of dental pla&ue on the immune response are both comple( and varied. It results $. In the activation of complement pathways. ). +ymphocytic stimulation -. +ymphokine release /. 3acrophages activation

The potent reactions are probably modulated by effects of the dental pla&ue components resulting primarily in a locali*ed chronic inflammatory response in the gingiva. :nless meticulous oral hygiene is maintained chronic periodontic diseases. 'or ease, it has been subdivided into four stages. ;ach stage in associated with certain immune treatment. $. In the initial lesion, there is a locali*ed inflammatory reaction at the fase of gingival sulcus. This correlates with a locali*ed inflammatory response of !3+s reflecting chemotactic action of pla&ue antigen and complement activation. ). The subse&uent early lesion involves the local gingival tissue infiltration of predominantly T cells and a few 0< cells. In the circulation, lymphocytes are sensiti*ed as shown by their ability to release lymphokines. -. In the established lesion, there is a characteristic locali*ed plasma cell infiltration of the gingival tissues. /. The advanced lesion marks the trasition to an advanced irreversible destructive process readily and alveolar bone loss. This phase is characteri*ed by Types I, II, III, I hypersensitivity treatment

associated with the protective destructive mechanism of lyphocytic and macnophagic function coupled with complement activation. The role of specific G # ve microorganisms in the aetiology and pathogenesis of destructive forms of !, diseases is well established. a. 0. gingivalis # severe aduct periodontitis b. Actinobacillus actinomycetem comitans # +T! c. 0. intermidus # A7:G d. 0. Intermidus # !regnancy gingivitis. There are potective mechanisms operating to prevent the spread of pathogenic microorganism e(tra oral sites in most individuals. These protective mechanisms effectively locali*e the infection to the !, tissues. ;ither secretory or scrum derived antibacillus may impede microbial adherence and so coloni*ation in the initial stages of dental pla&ue accumulation. Also in the initial stages of microbial tissue invasion, phagocytosis especially !37+s acting in concert with opsonic antibodies and complements, may play a role in limiting their pathological effects.

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HOST DEFENCE MECHANISM IN PERIODONTAL DISEASES ?ne of the ma2or components of the host defence mechanisms in periodontal diseases centres on the immune system. In fact the following components of the immune system are implicted. SECRETORY IMMUNE SYSTEM The secretary immune system comprises mucosal associated lymphoid tissues @eg. +ocal Ig A containing tissue, peyerAs patches6 with the Ig A antibodies comprising prominent antibodies in the secretion which both the mucosal surface. In the microbial coloni*ation stage, antibody mediate inhibition of adherence may play a role in influencing the microbial play a role in influencing the microbial content of both dental pla&ue and the subgingival microflora. Initially, such defence mechanisms may enter around .igA antibodies from saliva, although serum derived and gingival crevicular fluid antibodies may subse&uently activity may include disruption of coloni*ation, microbial aggregation or enhancement of microbial phagocytosis. NEUTROPHIL ANTIBODY COMPLEMENT SYSTEM The 7eutrophil # antibody # complement system comprises phagocytic blood and tissue !37s +eucocytes whichare not only highly B

motile but also migrate in large numbers from the gingival 0 v, through the gingival 1T and epithelium into the gingival crevice or the periodontal pocket. They serve as a powerful host reference mechanism to combat the coloni*ation and invasion by oral microbial flora. The !37s do met work in isolation but in concert with Ig G and Ig 3 antibodies and complement. The Ig G antibody coats the microorganism and the Ig G coated microorganism then binds to !37s surface receptors for the 'c portion of the Ig G to enhance phagocytosis. Once the microorganism has been phagocytosed by the PMN, it can be killed by: A) OXIDATIVE MECHANISMS These involve reactive o(ygen specie, is H)?), supero(ide ion and H the catalase produced by either !37s or micro effect inhibit pero(idase effects whereas myelopero(idase may enhance H)?) microbial lysis in the p8o chloride. B) NON OXIDATIVE MECHANISM These important mechanisms result from !37 derived lyso*yme, lactoferrin and cathepsins which kill microorganisms directly in the absence of ?) i.e. under anaerobic conditions which typify the gingival crevice and particularly periodontal pocket.

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LYMPHOCYTE MACROPHAGE LYMPHOKINE SYSTEM The lymphocyte macrophage lymphokine a(is mainly comprises effector T lymphocytes, whose function include the following% a. T< helper and T< suppressor lymphocytes regulate T effector cell activity and antibody production by 0 lymphocytes. b. T lymphocyte modulations of macrophage activity. c. .pecific lymphocyte stimulation by antigens which results in lymphokine production which includes ?steoblast activating factor @?A'6 +ymphoto(in @+T6 3acrophage activation factor @3A'6 3igration inhibition factor @3I'6 +ymphocyte inhibitory factor @+I'6 Interference.

The lymphocyte macrophage lymphokenes a(is has a potential to e(ert marked pathological effects on the host tissues. It releases lymphoto(in to kill fibroblasts and ?A' to result in alveolar bone resorption. The healing stage of !, disease may be associated with macrophagic phagocytosis of microorganisms and tissue debris whereas

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there are also lymphokines e.g. 'ibroblast activity factor that stimulate both fibroblastic proliferation and collagen formation. 5) VASCULAR COMPONENTS 4hen the vessel is damaged or cut, there is an immediate transient arteriolar vasoconstriction that serves to reduce the blood flow. In2uries to the enodothelial cells e(poses highly thrombogenic sub endothelial 1T to which the platelets adhere and undergo contact activation involving shape change, a release treatment and further aggregation of more platelets. .imultaneously, tissue factors released at the site of in2ury in combination with platelet factors activate the plasma coagulation system. :litmately, a permanent hemostatic plug is produced by the combined activitis of endothelial cells, platelets and the coagulation se&uence, primarily as the result of the platelet serotinin release. The initial platelet plug in therefore subse&uently replacement by a blood clot and fibrin plug formation. The coagulation se&uence essentially involves a cascade which begins as two separate pathways that ultimately converge. ?ne is the intrinsic to the blood and probably plays a ma2or role in hmostasis following an in2ury. The other is instrinsic and triggered by the introduction into the blood of tissue factors containing thromboplastin.

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INFLAMMATION AS A DEFENCE MECHANISM It may be defined as the reaction of living tissues to the in2ury in essence, it is a defence mechanism in itself. This reaction is a beneficial one, for without inflammation, life would be impossible. It is evidently on evolutionary adaptive response having several beneficial values or the species. The character and outcome of this reaction varies depending on the nature of stimuli and the defence capacity of the host. ,uring inflammation, there is an increased dilatation of blood vessels # healing in that area. The main cells of inflammatory e(udates are !37s leucocytes, plasma cells and macrophages. The inflammation reaction tends to present the dissemination of infection. .peaking generally, the more intense the reaction, the more likely the infection is locali*ed. 7) A REFLEX MECHANISM AS A DEFENCE MECH. A refle( is an involuntary, impremeidated unlearned Dbuilt in response to a stimulus in general, most refle(es, no matter how basic they may appear to be, are sub2ect to alteration by learning , that is there is no clear distinction between a basic refle( and a learned component.

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I7T;GRATI7G 1;7TR; A'';R;7T !ATH4AE. R;1;!T?R .TI3:+:. ';;,0A1" ;'';R;7T !ATH4AE. ;'';1T?R R;.!?7.;

8) PAIN AS A PROTECIVE MECH !ain is definitely regarded as a defence mechanism because whenever there is an offending stimulus to the oral cavity, it is the pain which is the primary sign and symptom of the patient. As soon as the patient e(perience pain, the normal tendency is to withdraw the oral tissues from the offending stimulus. This procedure, in turn, helps to prevent further damage by the offending stimulus to the oral cavity. 9) GAGGING AS A DEFENCE MECH The gagging reaction ranges from mild choking when the palate is inadvantantly touched by the mouth mirror, to violent, uncontroled retching during impression taking.

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Gag refle( is a normal, healthy, defence mechanism. It function is to prevent foreign bodies from entering the trachea by altering the shape of thepharyn( and its various openings to e2ect out foreign bodies. 'ive regions in the oral cavity are identified as regions of ma(imum sensitivity and are named DTriggen *onesF. They are $. The forces ). 0ase of the tongue -. !alate /. :vula 5. !ost pharyngeal wall 8) MISC. FACTORS arious other factors may also play a role in defence mechanisms of the oral cavity these includes a. Adaptive capacity of muscles to protect T3G. b. T3G remodality c. !rotective @1leansing6 function of tongue d. !repodentinal factors like ,entinal pain Tubular sclerosin .mear layer Irritation @reparetive6 dentin Information of sub2acent 1T

e. 1ough refle( f. Taste sensation, Temperature g. 3utality protected occlusionH

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