Effect of Treponema lecithinolyticum lipopolysaccharide on matrix metalloproteinase-9 expression.
10.5051/jkape.2005.35.3.675
- Author:
Jeong Ah NAM
1
;
Sun Young MOON
;
Jin Wook LEE
;
Jeong Heon CHA
;
Bong Kyu CHOI
;
Yun Jung YOO
Author Information
1. Department of Oral Biology, College of Dentistry, Yonsei University, Seoul, Korea. yu618@yumc.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Treponema lecithinolyticum;
lipopolysaccharide;
MMP-9
- MeSH:
Mice;
Animals
- From:The Journal of the Korean Academy of Periodontology
2005;35(3):675-685
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Bone resorption involves sequential stages of osteoclast precursor migration and differen-tiation of osteoclast precursors into multinucleated osteoclasts. Stromal cell derived factor (SDF)-1 is a chemotactic factor for osteoclast precursor migration. Matrix metalloproteinase (MMP)-9 is involved in migration of osteoclast precursors and activation of interleukin(IL)-1beta. Alveolar bone destruction is a characteristic feature of periodontal disease. Treponema lecithinolyticum is a oral spirochete isolated from the periodontal lesions. The effect of lipopolysaccharide(LPS) from T. lecithinolyticum on expression of SDF-1 and MMP-9 was examined in cocultures of bone marrow cells and osteblasts derived from mouse calvariae. T. lecithinolyticum LPS increased expression of MMP-9 in the coculture. Polymyxin B, an inhibitor of LPS, abolished the increase of MMP-9 mRNA expression by LPS. LPS did not increase the expression of SDF-1, IL-1beta and tumor necrosis factor(TNF)-alpha mRNA in cocultures. Prostaglandin E2(PGE2) up-regulated the expression of MMP-9 and NS398, an inhibitor of PGE2 synthesis, down-regulated the induction of MMP-9 expression by T. lecithinolyticm LPS. These results suggest that T. lecithinolytium LPS increases MMP-9 expression in bone cells via PGE2 and that the induction of MMP-9 expression by T. lecithinolyticum LPS is involved in alveolar bone destruction of periodontitis patients by the increase of osteoclast precursor migration and the activation of bone resorption-inducing cytokine.
