APOPTOSIS OF OSTEOCLASTS AND INFLAMMATORY BONE

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Periodontitis often results in tooth loss due to inflammatory bone resorption. Bone resorption is mediated by osteoclasts. Although the differentiation pathway of osteoclasts is not well known at present, various inflammatory mediators are known to trigger the production of osteoclasts. We have found that lipopolysaccharides (LPS) of various periodontophatic bacteria mediate osteoclast formation and stimulate bone resorption in vitro. In this project, we investigate the mechanism of osteoclast differentiation mediated by LPS from a periodontophatic bacteria Actinobacillus actinomycetemcomitans.In mouse bone marrow cultures, LPS of A. actinomycetemocomitans induced osteoclast formation. Indomethacin and anti-IL-1 antibodies significantly inhibited the osteoclast formation, suggesting that prostaglandin E2 (PGE2) and IL-1 were involved in LPS-mediated osteoclast formation. We also found that LPS from A. actinomycetemcomitans induced expression of osteoclast differentiation factor (ODF) on cells of osteoblastic lineage. These results indicated that LPS of A. actinomycetemcomitans mediated osteoclast formation through upregulation of PGE2, IL-1 and ODF in periodontal tissues. Furthermore, we found that taurine, a sulfer containing amino acid, inhibited the osteoclast formation mediated by LPS from A. actinomycetemcomitans. Taurine was also found to inhibit the experimental bone resorption in ligature-mediated periodontitis in hamsters.