Periodontal

Immunology Yenny Yustisia

Dept. of Oral Biology

FKG Unej

Introduction

Mouth & nose are the principal portals of

entry of infectious agents & allergens into

the human body.

Complexity of oral immunology is due to

the changing oral environment and

different surfaces

it involves a dynamic equilibrium exists

between resident oral microbial & host

immune response in healthy situation

Oral environment consists of three

Hard tissue, which includes teeth

Soft tissues, which includes Oral

mucosa Tongue Gingiva

Oral fluids, which includes Saliva &

Gingival crevicular fluid

ORAL CAVITY AS AN

IMMUNOLOGICAL ENTITY

Immunologic defense in the mouth is mediated

by a complex system of cells & molecules.

The Cells includes Mucosal barrier epithelium &

phagocytes, lymphocytes & leukocytes.

The Molecules includes Antibodies &

nonimmunoglobulin proteins, glycoproteins &

lipoproteins derived from GCF & saliva.

Oral cavity has several unique environment for

bacterial colonization.

Distinct immune mechanisms are encountered

in different oral environments or different stages

of disease.

Oral Soft tissues Protective barriers includes:

Salivary barrier,

Membrane coating granules from nonkeratinized

epithelium

Epithelial basement membrane,

Cellular & free Ig components of the lymphoid

system block penetrating microorganisms.

Microbial-host interaction

Host responses play an important role in the pathogenesis of periodontal diseases.

Several components of the immune system are active in periodontal disease

These functions influence:

Bacterial colonization

Bacterial invasion

Tissue destruction

Healing and fibrosis

BACTERIAL COLONIZATION

In periodontal disease, the sub gingival area is

the major environment of concern.

In contrast to the supra gingival sites were

secretory IgA from saliva can reduce or inhibit

specific bacteria with in plaque there is little if

any sub gingival s-IgA.

Sub gingivally the major source of

immunoglobulins and complement is gingival or

crevicular fluid, which contains systemically and

locally produced antibodies

These antibodies could

potentially modulate

the types and numbers

of micro organisms

through inhibition of

colonization or lysis or

both.

In bacterial associated

periodontal disease,

there is an explosion in

BACTERIAL INVASION

Invasion of the tissues

occurs by whole bacterial

cells and products in

bacterial associated

periodontal diseases.

In comparison to the large

number of bacteria with in

the gingival crevice or

pocket, relatively few reach

beneath the basal lamina of

This reduction is probably is a combination of

the physical barrier provided by the junctional

epithelium and the host protective responses.

The gingival tissues are bathed with antibodies

to the oral bacteria complement which could

lead to bacterial lysis

Bacteria can enter host tissue

through:

Ulceration in epithelium of gingival

sulcus or periodontal pocket

Intercellular space of gingival tissues

Direct penetration on epithelial or

connective cells

Toxic molecule & enzymes: collagenase, trypsin like enzymes, aryl sulfatasem neuraminidase, fibronectin-

degrading enzymes, phospholipase-A

Immunological aspects of

periodontal diseases

Innate factors such as complement, resident

leukocyte and especially mast cell play significant

role in signalling endothelium inflammation

Acute inflammatory cells (neutrophils) protect

local tissue by controlling the periodontal

microbiota

Chronic inflammatory cells, macrophages and

lymphocytes protect the entire host to prevent a

local infection from becoming systemic and life

threatening

Cellular elements

PMN

Lymphocytes

Macrophages

osteoclasts

Epithelial cells

PMN

The interaction of PMN with microorganisms is of particular importance in the progression of periodontitis.

The polymorphonuclear leukocytes have a protective and destructive function in nonspecific inflammatory reactions.

The protective function is expressed in their ability to

phagocytose.

They contain lysosomal granules, in which there are

numerous hydrolytic enzymes, whose release is

responsible for the tissue damage.

The enzymes in the lysosomal granules are collagenase,

alkaline phosphatase, elastase, proteinase, lysosomes,

which have a destructive effect on the extracellular

constituents of connective tissue.

Because they are short lived cells, PMN die in great

numbers at acute inflammatory sites.

The accumulation and massive death of neutrophils are a major cause for tissue breakdown in acute phases of apical periodontitis

lymphocytes

Among the three major classes of lymphocytesT-lymphocytes, B-lymphocytes, and the natural killer (NK) cells.

The T- and B-lymphocytes are of importance in apical periodontitis.

macrophages

Macrophages are very important in the development of the periapical lesion.

Their two basic functions are phagocytosis and cytokinproduction.

Macrophages are activated by microorganisms, their products (LPS), chemical mediators, or foreign particles.

Produce cytokines IL-1, TNF-a, interferons (IFN), and growth factors

They also contribute serum components and metabolites, such as prostaglandins and leukotrienes, that are important in inflammation.

TISSUE DESTRUCTION

The fundamental event in the transition from

gingivitis to periodontitis is the loss of the soft

tissue attachment to the tooth and subsequent

loss of bone

Mediators produced (proteinase, cytokines,

prostaglandins) as part of host response

contribute to tissue destruction

A major pathological event of apical periodontitis is the osteoclasticdestruction of bone and dental hard tissues.

The pro-osteoclasts migrate through blood as monocytes to the periradicular tissues and attach themselves to the surface of bone.

They remain dormant until stimulated by IL-1, PGE and TNF to proliferate and differentiate

Several daughter cells fuse to form multinucleated osteoclaststhat spread over injured and exposed bone surfaces.

Root cementum and dentin are also resorbed in apical periodontitis by fusion macrophages designated as 'odontoclasts'.

HEALING AND FIBROSIS

Periodontal repair occurs in overlapping phases

of:

Inflammation shutdown

Angiogenesis

fibrogenesis

Shutdown of inflammatory processes and

initiation of post healing are orchestrated by

leukocytes

Anti inflammatory signals: IL-1 receptor

antagonis {macrophages} and TGF-

{neutrophils, macrophages, mast cell,

lymphocytes}

also IL-4, IL-10, IL-11

Macrophage influences fibroblastic activity.

They play a role in healing through their release

of fibronectin which is chemo tactic for

fibroblasts and other factors that influence

fibroblast function and lead to fibroblast

activation.

Lymphocytes also release lymphokines capable

of activating recruiting fibroblasts.

IL-1 , TNF-, IL-

Release of Platelet derived growth factor

(PDGF) ~ Vascular endothelial GFendothelial proliferation

PDGF activates fibroblast and osteoblast protein synthesis

TGF- inhibit osteoclast formation

INF- {NK cells, Th cells, Macrophages) inhibit

osteoclast diff and activation

Thank you..!