Dual Regulation of Osteoclast Differentiation by Periodontal Ligament Cells through RANKL Stimulation and OPG Inhibition

Abstract

Periodontal ligament (PDL) cells play an important role in maintaining the homeostasis of periodontal tissues. However, it is not known how PDL cells contribute to osteoclastogenesis. In this study, we examined the consequences of cell-to-cell interactions between peripheral blood mononuclear cells (PBMCs) and PDL cells during osteoclastogenesis. PBMCs were co-cultured directly or indirectly with PDL cells for two to four weeks. PBMCs that were directly co-cultured with PDL cells formed significantly more resorption pits on dentin slices than did PBMCs that were cultured alone. However, soluble factor(s) produced from PDL cells inhibited the formation of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. Furthermore, PDL cells expressed both receptor activator nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG) mRNA. In conclusion, PDL cells support osteoclastogenesis through cell-to-cell contact. PDL cells might regulate osteoclastogenesis by opposing mechanisms-stimulation of resorptive activity by RANKL and inhibition by OPG-thus affecting processes such as periodontitis and orthodontic tooth movement.

Keywords

osteoclastogenesis periodontal ligament fibroblast-like cells RANKL OPG peripheral blood mononuclear cells

Get full access to this article

View all access options for this article.

References

Davidovitch Z. (1991). Tooth movement. Crit Rev Oral Biol Med 2:411-450.

Fujikawa Y. , Quinn JM , Sabokbar A. , McGee JO , Athanasou NA (1996a). The human osteoclast precursor circulates in the monocyte fraction. Endocrinology 137:4058-4060.

Fujikawa Y. , Sabokbar A. , Neale S. , Athanasou NA (1996b). Human osteoclast formation and bone resorption by monocytes and synovial macrophages in rheumatoid arthritis. Ann Rheum Dis 55:816-822.

Lekic P. , McCulloch CA (1996). Periodontal ligament cell population: the central role of fibroblasts in creating a unique tissue. Anat Rec 245:327-341.

Mitchell DL , West JD ( 1975). Attempted orthodontic movement in the presence of suspected ankylosis. Am J Orthod 68:404-411.

Roberts WE , Goodwin WC Jr , Heiner SR (1981). Cellular response to orthodontic force. Dent Clin North Am 25:3-17.

Shimizu Y. , Inomata Y. , Tagami A. (1996). Suppression of osteoclast-like cell formation by periodontal ligament cells. J Bone Miner Metab 14:65-72.

Simonet WS , Lacey DL , Dunstan CR , Kelley M. , Chang MS , Luthy R. , et al. (1997). Osteoprotegerin: a novel secreted protein involved in the regulation of bone density. Cell 89:309-319.

Suda T. , Udagawa N. , Nakamura I. , Miyaura C. , Takahashi N. (1995). Modulation of osteoclast differentiation by local factors. Bone 17:87S-91S.

10.

Wu YM , Richards DW , Rowe DJ ( 1999). Production of matrix-degrading enzymes and inhibition of osteoclast-like cell differentiation by fibroblast-like cells from the periodontal ligament of human primary teeth. J Dent Res 78:681-689.

11.

Yasuda H. , Shima N. , Nakagawa N. , Yamaguchi K. , Kinosaki M. , Mochizuki S. , et al. (1998). Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL. Proc Natl Acad Sci USA 95:3597-3602.

12.

Yasuda H. , Shima N. , Nakagawa N. , Yamaguchi K. , Kinosaki M. , Goto M. , et al. (1999). A novel molecular mechanism modulating osteoclast differentiation and function. Bone 25:109-113.