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. Vascular 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. Provided this mucosa remains intact, few microorganisms can

penetrate the underlying tissues. This partly reflects the functions of the

Keratin barrier.

The oral mucosa can be broadly – into

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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 squamous epithelium whose

functions include:

1. Forming a primary structure barrier between the internal and external

environment.

2. Protection against mechanical damage, entry of noxious substances or

organizing and loss of fluids.

Like the skin, the oral mucosa comprises a surface epithelium,

overlying the layer of basement membrane. This string sq epithelium

undergoes mitosis, synthetic activity and disintegration leaving the

underlying cells as a cohesive tissue.

The epithelial cells undertake a member of specialized synthetic

activities associated with the maintenance of a surface barrier including.

1. The synthesis of Keratin

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2. Defradation of other intracellular organelles

3. Synthesis of cell membrane and extra cellular components associated

with cell adhesion and barrier function.

4. Basement membrane synthesis to provide attachment to the underlying

CT.

In the lamina propia adjacent 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 extra oral lymph nodes for the protection of the oral cavity as a whole.

There are in fact several intra oral lymphosis aggregations.

1. The palatine Tonsils comprise paired lymphoid masses, between the

glossopalatine and pharyngo palatine arches. The component lymphoid

tissue contains both B and T cells, IgG producing cells being the most

prominent.

2. The lingual Tonsils are much less prominent lying on each side of the

tongue just distal to the circum vallate papillae. They contain lymphoid

modules some of which have germinal centers in addition to

perifellicular diffuse lymphoid cells.

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3. 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. Lymphocytes and plasma cells are found in

small clusters in both major or minor SG. Most of the plasma cells secrete

Ig A.

ROLE OF GINGIVAL CREVICULAR FLUID

With continued plaque accumulation at the cervical surface of the

tooth, there is a corresponding increase in crevicular fluid formation. This

fluid contains immunoglobulins Ig G, A, M in adition to complement

components namely C3, C4 and C5 and C3 Pro 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:

a) Albumin f) lysosomal enzymes

b) Transferring g) lysozyme

c) traptaglobulin h) Tryaluronidase

d) Glycoproteins I) Collagenase

e) Lipoproteins

Tube enzymes not only affect specific tissues e.g. collagen, but also

selective Ig A in activation results from specific protease activity.

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Crevicular fluid also contains macrophages and T and B 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 enzyme that splits the bond between N acetyl

glucosomine and N acetyl inuramic acid in the micopeptide components of

bacterial cell wall. Apart from Str. Mutans, the oral flora is generally

resistant to lysozyme.

ii) Peroxidase

In the p/o thiocyanate ions and hydrogen peroxide, peroxidase kills

acidophilus by inhibiting lysin uptake and may inhibit some streptococci

by limiting the action of their glycolytic enzymes.

iii) Lactoferrin

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This has a bacteriostatic effect on a whole microbial spectrum,

possibly by depleting local environmental iron required for microbial

growth.

B) SPECIFIC COMPONENTS

SECRETORY Ig A

IgA is quantitatively the most important Ig present in saliva, mainly

derived locally from plasma cells. It is then trasported to the distal human

and exerted into the oral cavity S IG A is more resistant to microbial and

particularly suited for saliva, which then functions as an antisept paint for

various oral surfaces. SigA also appears to limit microbial adherence to the

mucosal surface.

PERIODONTAL DISEASE

The effect of dental plaque on the immune response are both

complex and varied. It results

1. In the activation of complement pathways.

2. Lymphocytic stimulation

3. Lymphokine release

4. Macrophages activation

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The potent reactions are probably modulated by effects of the dental

plaque components resulting primarily in a localized chronic inflammatory

response in the gingiva.

Unless meticulous oral hygiene is maintained chronic periodontic

diseases. For ease, it has been subdivided into four stages. Each stage in

associated with certain immune treatment.

1. In the initial lesion, there is a localized inflammatory reaction at the

fase of gingival sulcus. This correlates with a localized inflammatory

response of PMLs reflecting chemotactic action of plaque antigen and

complement activation.

2. The subsequent early lesion involves the local gingival tissue

infiltration of predominantly T cells and a few B- cells. In the

circulation, lymphocytes are sensitized as shown by their ability to

release lymphokines.

3. In the established lesion, there is a characteristic localized plasma cell

infiltration of the gingival tissues.

4. The advanced lesion marks the trasition to an advanced irreversible

destructive process readily and alveolar bone loss. This phase is

characterized by Types I, II, III, IV hypersensitivity treatment

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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 PD diseases is well established.

a. B. gingivalis – severe aduct periodontitis

b. Actinobacillus actinomycetem comitans – LTP

c. B. intermidus – ANUG

d. B. Intermidus – Pregnancy gingivitis.

There are potective mechanisms operating to prevent the spread of

pathogenic microorganism extra oral sites in most individuals. These

protective mechanisms effectively localize the infection to the PD tissues.

Either secretory or scrum derived antibacillus may impede microbial

adherence and so colonization in the initial stages of dental plaque

accumulation. Also in the initial stages of microbial tissue invasion,

phagocytosis especially PMNLs 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

One of the major 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. Local Ig A containing tissue, peyer’s patches) with

the Ig A antibodies comprising prominent antibodies in the secretion which

both the mucosal surface.

In the microbial colonization 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 plaque and the subgingival

microflora. Initially, such defence mechanisms may enter around SigA

antibodies from saliva, although serum derived and gingival crevicular

fluid antibodies may subsequently activity may include disruption of

colonization, microbial aggregation or enhancement of microbial

phagocytosis.

NEUTROPHIL – ANTIBODY – COMPLEMENT SYSTEM

The Neutrophil – antibody – complement system comprises

phagocytic blood and tissue PMNs Leucocytes whichare not only highly

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motile but also migrate in large numbers from the gingival B v, through the

gingival CT and epithelium into the gingival crevice or the periodontal

pocket. They serve as a powerful host reference mechanism to combat the

colonization and invasion by oral microbial flora. The PMNs do met work

in isolation but in concert with Ig G and Ig M antibodies and complement.

The Ig G antibody coats the microorganism and the Ig G coated

microorganism then binds to PMNs surface receptors for the Fc 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 oxygen specie, is H2O2, superoxide ion and H

the catalase produced by either PMNs or micro effect inhibit peroxidase

effects whereas myeloperoxidase may enhance H2O2 microbial lysis in the

p/o chloride.

B) NON OXIDATIVE MECHANISM

These important mechanisms result from PMN derived lysozyme,

lactoferrin and cathepsins which kill microorganisms directly in the

absence of O2 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 axis 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 B lymphocytes.

b. T lymphocyte modulations of macrophage activity.

c. Specific lymphocyte stimulation by antigens which results in

lymphokine production which includes

- Osteoblast activating factor (OAF)

- Lymphotoxin (LT)

- Macrophage activation factor (MAF)

- Migration inhibition factor (MIF)

- Lymphocyte inhibitory factor (LIF)

- Interference.

The lymphocyte macrophage lymphokenes axis has a potential to

exert marked pathological effects on the host tissues. It releases

lymphotoxin to kill fibroblasts and OAF to result in alveolar bone

resorption.

The healing stage of PD disease may be associated with

macrophagic phagocytosis of microorganisms and tissue debris whereas

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there are also lymphokines e.g. Fibroblast activity factor that stimulate both

fibroblastic proliferation and collagen formation.

5) VASCULAR COMPONENTS

When the vessel is damaged or cut, there is an immediate transient

arteriolar vasoconstriction that serves to reduce the blood flow. Injuries to

the enodothelial cells exposes highly thrombogenic sub endothelial CT to

which the platelets adhere and undergo contact activation involving shape

change, a release treatment and further aggregation of more platelets.

Simultaneously, tissue factors released at the site of injury in combination

with platelet factors activate the plasma coagulation system.

Ulitmately, a permanent hemostatic plug is produced by the

combined activitis of endothelial cells, platelets and the coagulation

sequence, primarily as the result of the platelet serotinin release.

The initial platelet plug in therefore subsequently replacement by a

blood clot and fibrin plug formation. The coagulation sequence essentially

involves a cascade which begins as two separate pathways that ultimately

converge. One is the intrinsic to the blood and probably plays a major role

in hmostasis following an injury. 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 injury 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.

During inflammation, there is an increased dilatation of blood

vessels – healing in that area. The main cells of inflammatory exudates are

PMNs leucocytes, plasma cells and macrophages.

The inflammation reaction tends to present the dissemination of

infection. Speaking generally, the more intense the reaction, the more

likely the infection is localized.

7) A REFLEX MECHANISM AS A DEFENCE MECH.

A reflex is an involuntary, impremeidated unlearned “built in

response to a stimulus in general, most reflexes, no matter how basic they

may appear to be, are subject to alteration by learning , that is there is no

clear distinction between a basic reflex and a learned component.

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INTEGRATING CENTRE

AFFERENT PATHWAYS EFFERENT PATHWAYS

RECEPTOR EFFECTOR

STIMULUS RESPONSE

FEEDBACK

8) PAIN AS A PROTECIVE MECH

Pain 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 experience 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 reflex is a normal, healthy, defence mechanism. It function is to

prevent foreign bodies from entering the trachea by altering the shape of

thepharynx and its various openings to eject out foreign bodies.

Five regions in the oral cavity are identified as regions of maximum

sensitivity and are named “Triggen zones”. They are

1. The forces

2. Base of the tongue

3. Palate

4. Uvula

5. Post pharyngeal wall

8) MISC. FACTORS

Various other factors may also play a role in defence mechanisms of

the oral cavity these includes

a. Adaptive capacity of muscles to protect TMJ.

b. TMJ remodality

c. Protective (Cleansing) function of tongue

d. Prepodentinal factors like

- Dentinal pain- Tubular sclerosin- Smear layer- Irritation (reparetive) dentin- Information of subjacent CT

e. Cough reflex

f. Taste sensation, Temperature

g. Mutality protected occlusion?

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