Periodontal Immunology

Introduction

ORAL CAVITY AS AN IMMUNOLOGICAL ENTITY

Immunological aspects of periodontal diseases

BACTERIAL COLONIZATION

BACTERIAL INVASION

TISSUE DESTRUCTION

HEALING AND FIBROSIS

Cellular elements

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, protease, 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 neutrophilsare 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 periapicallesion.

Their two basic functions are phagocytosis and cytokin production.

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

Among the various molecular mediators that are secreted by macrophages, the cytokines IL-1, TNF-a, interferons (IFN), and growth factors are of particular importance in apical periodontitis.

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

osteoclasts

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 signaled by osteoblasts to proliferate.

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'.

Epithelial cells

About 30 to 52% of all apical periodontitis lesions contain proliferating epithelium.

During periapical inflammation, the epithelial cell rests are believed to be stimulated by cytokines and growth factors to undergo division and proliferation, a process commonly described as 'inflammatory hyperplasia'.

These cells participate in the pathogenesis of radicularcysts by serving as the source of epithelium.

However, ciliated epithelial cells are also found in periapical lesions, particularly in lesions affecting maxillary molars.

The maxillary sinus epithelium was suggested to be a source of those cells.

LOCALISED JUVENILE PERIDONTITIS [LJP]

GENERALISED JUVENILE PERIODONTITIS [GJP]

RAPID PERIODONTITIS

PREPUBERTY PERIODONTITIS

IMMUNOLOGIC FINDINGS GENERALISED FORM

LOCALISED FORM

ACUTE NECROTISING ULCERATIVE GINGIVITIS [ANUG]