Role of TNF-α in Periodontal Disease &amp; Its Implication on Systemic Health

,Dr Kalpana Gokul

doi:10.47191/ijcsrr/v4-i10-31

Abstract

Periodontal disease is a polymicrobial infection, characterized by gingival inflammation, pocket formation, loss of connective tissue attachment and supporting alveolar bone. Though the etiology of periodontal disease has been established and micro-organisms have been implicated, pathology of these inflammatory lesions have been attributed not only to bacterial products, that have adverse effects on the tissues, but also to chemical mediators released by the host cells, as a result of inflammatory and immune reactions. Oral micro- organisms trigger the endogenous pathways of tissue degradation by activating host cells to produce and release inflammatory mediators and cytokines. These inflammatory mediators and cytokines manifest potent pro-inflammatory and catabolic activity and may play a key role in local amplification of the immune response as well as in periodontal tissue breakdown Apart from playing an important role in periodontal destruction, systemic elevation of TNF –  levels is extremely toxic to the host and hence has been termed as the “Suicide hormone”. TNF – , has been postulated to mediate wasting during chronic infections. This review aims to explore the role of TNF –  in periodontal disease & its implication on systemic health.

Highlights

Periodontal disease is a polymicrobial infection, characterized by gingival inflammation, pocket formation, loss of connective tissue attachment and supporting alveolar bone[1]
Though the etiology of periodontal disease has been established and microorganisms have been implicated, pathology of these inflammatory lesions have been attributed to bacterial products, that have adverse effects on the tissues, and to chemical mediators released by the host cells, as a result of inflammatory and immune reactions[2]
Oral micro- organisms trigger the endogenous pathways of tissue degradation by activating host cells to produce and release inflammatory mediators and cytokines

Summary

INTRODUCTION

Periodontal disease is a polymicrobial infection, characterized by gingival inflammation, pocket formation, loss of connective tissue attachment and supporting alveolar bone[1]. TNF - IN PERIODONTAL DISEASE TNF - is a proinflammatory cytokine that is secreted mainly by monocytes and macrophages It induces the secretion of collagenase by fibroblasts, resorption of cartilage and bone, and has been implicated in the destruction of periodontal tissues in periodontitis[14]. Lipopolysaccharide obtained from periodontal Gram negative bacteria can initiate the production of TNF - peripheral blood monocytes, which in turn leads to alveolar bone resorption and to enhanced synthesis of collagenase by human gingival fibroblasts to degrade collagen. TNF - has been shown to induce the secretion of collagenase, PGE2 and interleukin – 6 by human fibroblasts and bone culture cells[10] Both IL -1 and TNF - have been demonstrated in increased amounts in GCF at periodontal disease sites and in periodontal tissues of patients with different forms of disease[10]. These findings support the hypothesis that TNF - could provide a mechanistic bridge between the inflammatory process and tissue destruction

DISCUSSION

CONCLUSION