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,

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

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, fibronectindegrading 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 lymphocytes

T-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 cytokin

production.
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 osteoclastic

destruction 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 osteoclasts
that 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 GF
endothelial 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..!