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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.