期刊
ARCHIVES OF ORAL BIOLOGY
卷 56, 期 5, 页码 491-498出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.archoralbio.2010.11.003
关键词
Bisphosphonates (BPs); Osteonecrosis of the jaw (ONJ); Fibroblasts; Epithelium; Oral cavity; Wound healing; Proliferation; Apoptosis; Migration; Collagen
资金
- University of Missouri Research Board, Department of Pathology and Anatomical Sciences, University of Missouri School of Medicine
- Department of Pathology and Anatomical Sciences at the University of Missouri School of Medicine
- University of Missouri Research Board
Objective: Bisphosphonates (BPs) like Zometa (ZA) are widely used to treat complications of bony metastases in cancer patients. A serious adverse event occurs in 1-12% of patients on BP therapy, osteonecrosis of the jaw (BPONJ). BPONJ develops after oral trauma and is manifested by poor wound healing and soft-tissue breakdown followed by exposure and necrosis of intra-oral bone. Currently, there is no effective clinical treatment for BPONJ. Design: We evaluated the effect of ZA on the proliferation, apoptosis and migratory capacity of the cell lines CRL-7408, an oral fibroblast culture and OKF/6, an oral epithelial cell line. Results: In both oral epithelium and fibroblasts, ZA exposure inhibited proliferation and elevated apoptosis; however oral fibroblasts were differentially influenced versus oral epithelial cells. In oral fibroblasts, ZA treatment significantly inhibited motility. Further, quantitative real-time PCR demonstrated that ZA treatment of oral fibroblasts inhibits expression of both the COL1A1 and COL1A2 chains of type-I collagen, consistent with a loss of collagen immunofluorescent staining. Conclusions: These data support a model wherein ZA treatment impedes oral wound healing by blocking the growth and migratory capacity of oral fibroblasts as well as downregulating the transcription of type-I collagen, functions necessary to deposit the granulation tissue needed for re-epithelization. Therefore, BP released from bone following tooth extraction may delay wound healing of the oral mucosal barrier and contribute to BPONJ pathogenesis. (C) 2010 Elsevier Ltd. All rights reserved.
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