Compressive mechanical stress promotes osteoclast formation through RANKL expression on synovial cells

被引:37
作者
Ichimiya, Hisashi
Takahashi, Tetsu
Ariyoshi, Wataru
Takano, Hiroshi
Matayoshi, Takaaki
Nishihara, Tatsuji
机构
[1] Kyushu Dent Coll, Dept Hlth Promot, Div Infect & Mol Biol, Kokurakita Ku, Kitakyushu, Fukuoka 8038580, Japan
[2] Kyushu Dent Coll, Dept Oral & Maxillofacial Surg, Div Oral & Maxillofacial Reconstruct Surg, Kitakyushu, Fukuoka 8038580, Japan
来源
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTOLOGY | 2007年 / 103卷 / 03期
关键词
D O I
10.1016/j.tripleo.2006.05.026
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Objectives. We investigated the effects of compressive mechanical stress on osteoclastogenesis of synovial cells to clarify the mechanism of osteoclast formation by those cells in temporomandibular joint (TMJ) disorders. Study design. Synovial cells were isolated from rat knee joints and continuously compressed using a conventional method. The expression of receptor activator nuclear factor kappa B ligand (RANKL) mRNA and protein in synovial cells was analyzed by reverse transcriptase-polymerase chain reaction, immunoblotting, and immunofluorescence staining. Mouse bone marrow cells were cultured with synovial cells for 7 days to detect osteoclasts. Results. The expressions of RANKL mRNA and protein in synovial cells were increased with compressive force. When mouse bone marrow cells were cultured with continuously compressed synovial cells, tartrate-resistant acid phosphatase-positive multinucleated cells were formed. Osteoprotegerin completely inhibited osteoclast formation induced by culturing with compressed synovial cells. Conclusion. Our results indicated that the expression of RANKL in compressed synovial cells enhanced osteoclast formation, whereas continuous compressive force may induce osteoclastic bone destruction in the TMJ.
引用
收藏
页码:334 / 341
页数:8
相关论文
共 41 条
[31]   Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families [J].
Suda, T ;
Takahashi, N ;
Udagawa, N ;
Jimi, E ;
Gillespie, MT ;
Martin, TJ .
ENDOCRINE REVIEWS, 1999, 20 (03) :345-357
[32]   Association between arthroscopic diagnosis of temporomandibular joint osteoarthritis and synovial fluid nitric oxide levels [J].
Takahashi, T ;
Kondoh, T ;
Ohtani, M ;
Homma, H ;
Fukuda, M .
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTICS, 1999, 88 (02) :129-136
[33]  
Takayanagi H, 2000, ARTHRITIS RHEUM-US, V43, P259, DOI 10.1002/1529-0131(200002)43:2<259::AID-ANR4>3.0.CO
[34]  
2-W
[35]   A new mechanism of bone destruction in rheumatoid arthritis: Synovial fibroblasts induce osteoclastogenesis [J].
Takayanagi, H ;
Oda, H ;
Yamamoto, S ;
Kawaguchi, H ;
Tanaka, S ;
Nishikawa, T ;
Koshihara, Y .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 240 (02) :279-286
[36]   Bone resorption by osteoclasts [J].
Teitelbaum, SL .
SCIENCE, 2000, 289 (5484) :1504-1508
[37]   Functional human T-cell immunity and osteoprotegerin ligand control alveolar bone destruction in periodontal infection [J].
Teng, YTA ;
Nguyen, H ;
Gao, XJ ;
Kong, YY ;
Gorczynski, RM ;
Singh, B ;
Ellen, RP ;
Penninger, JM .
JOURNAL OF CLINICAL INVESTIGATION, 2000, 106 (06) :R59-R67
[38]   Isolation of a novel cytokine from human fibroblasts that specifically inhibits osteoclastogenesis [J].
Tsuda, E ;
Goto, M ;
Mochizuki, S ;
Yano, K ;
Kobayashi, F ;
Morinaga, T ;
Higashio, K .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 234 (01) :137-142
[39]   Osteoblasts/stromal cells stimulate osteoclast activation through expression of osteoclast differentiation factor/RANKL but not macrophage colony-stimulating factor [J].
Udagawa, N ;
Takahashi, N ;
Jimi, E ;
Matsuzaki, K ;
Tsurukai, T ;
Itoh, K ;
Nakagawa, N ;
Yasuda, H ;
Goto, M ;
Tsuda, E ;
Higashio, K ;
Gillespie, MT ;
Martin, TJ ;
Suda, T .
BONE, 1999, 25 (05) :517-523
[40]   The molecular mechanism of osteoclastogenesis in rheumatoid arthritis [J].
Udagawa, N ;
Kotake, S ;
Kamatani, N ;
Takahashi, N ;
Suda, T .
ARTHRITIS RESEARCH, 2002, 4 (05) :281-289