alexa The Role of Inflammatory Cytokines and the RANKL-RANK-O
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Review Article

The Role of Inflammatory Cytokines and the RANKL-RANK-OPG Molecular Triad in Periodontal Bone Loss-A Review

Prathiba Chichurakanahalli Srinivasan*
SV Dental Collge, Bangalore, Karnataka, India
Corresponding Author : Prathiba Chichurakanahalli Srinivasan
SV Dental Collge, Bangalore, Karnataka, India
E-mail: [email protected]
Received June 13, 2013; Accepted August 27, 2013; Published August 31, 2013
Citation: Srinivasan PC (2013) The Role of Inflammatory Cytokines and the RANKL-RANK-OPG Molecular Triad in Periodontal Bone Loss-A Review. J Clin Cell Immunol S13:007. doi:10.4172/2155-9899.S13-007
Copyright: © 2013 Srinivasan PC. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Periodontal diseases are chronic inflammatory disorders involving the supporting structures of the teeth. Connective tissue destruction and loss of bone support of the dentition are key features of this disease. Early studies have revealed that biofilm plaque accumulation in the dentogingival area is the primary etiological factor of periodontal diseases. Recent research has not only reinforced the bacterial etiology of periodontal disease, but has also emphasized the role of inflammation in this pathologic process. The host mounts an immune-inflammatory response to combat the bacterial attack. The host response is like a double-edged sword. It eliminates the offending pathogens, but overstimulation and amplification of the same leads to tissue destruction and bone loss. In the mid- 1990s, extensive research in the field of bone biology led to the discovery of the RANKL-RANK-OPG molecular triad. This article explores the mechanisms by which inflammatory host response leads to alveolar bone loss-the role of cytokines, factors that stimulate osteoclastogenesis via the RANKL-RANK-OPG pathway and how inflammation interferes with the uncoupling of bone formation and bone resorption. In addition to the conventional therapeutic modalities aimed at eliminating the microbes, additional therapeutic strategies that interfere with the RANKL-RANKOPG axis may have a protective effect on the bone loss.

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