Roles of osteoclast inhibitory and differentiation factors in periodontal tissue.

2006 Fiscal Year Final Research Report Summary

• Project/Area Number: 17592181
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Social dentistry
• Research Institution: HIROSHIMA UNIVERSITY
• Principal Investigator: SHIMAZU Atsushi Hiroshima University, Graduate School of Biomedical Science, Research Associate, 大学院医歯薬学総合研究科, 助手 (10274094)
• Co-Investigator(Kenkyū-buntansha): KAWAMOTO Takeshi Hiroshima University, Graduate School of Biomedical Science, Lecturer, 大学院医歯薬学総合研究科, 講師 (50224861)
• Project Period (FY): 2005 – 2006
• Keywords: periodontal tissue / osteoclasts / periodontal disease

Research Abstract

Many people were lost their tooth by periodontal disease. However preventive method for periodontal disease is not currently established. In order to prevent the lost of tooth in their life, we have to develop the preventive method for periodontal disease.
Osteoclast differentiation factor; (ODF or RANKL) is essential for osteoclastogenesis, and its decoy receptor osteoprotegerin (OPG) negatively regulates this process. Both genes are expressed in cells of the osteoblast lineage, but the precise relationship between the state of osteoblast differentiation and RANKL and OPG expression is not clearly defined.
It is believed that periodontal ligament cells play a vital role in maintaining the homeostasis of periodontal tissues and release cytokines to affect alveolar bone metabolism. We found that periodontal ligament fibroblasts produced the OPG. Furthermore, RANKL induced osteoclast development in preosteoclasts cell lines, RAW264.7 cells. These cells expressed osteoclast differentiation markers analyzed by RT-PCR. RANKL increased TRAP, cathepsin K, calcitonin receptor and NFATc1 mRNAs dose-dependent manner. Among co-stimulatory molecules, RANKL increased OSCAR mRNA in these cells, although PIR-A, PIR-B, TREM2, TREM3 and DAP12 were not changed. In addition, we found the stress-inducible molecules such as MICA were expressed in gingival fibroblasts. These evidences might indicate that the periodontal bacterial infection in gingival tissue causes the induction of MICA, and the induced MICA may be the marker of the beginning of process in osteoclastogenesis in periodontal tissue.