期刊
JOURNAL OF DENTAL RESEARCH
卷 90, 期 11, 页码 1339-1345出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0022034511420430
关键词
bisphosphonate-induced osteonecrosis of the jaw; pamidronate; gingival fibroblast; KGF; wound healing; Fusobacterium nucleatum
资金
- NIH from the NIDCR [DE-18499, DE-19917]
No consensus has yet been reached to associate oral bacteria conclusively with the etio-pathogenesis of bisphosphonate-induced osteonecrosis of the jaw (BONJ). Therefore, the present study examined the effects of oral bacteria on the development of BONJ-like lesions in a mouse model. In the pamidronate (Pam)-treated mice, but not control non-drug-treated mice, tooth extraction followed by oral infection with Fusobacterium nucleatum caused BONJ-like lesions and delayed epithelial healing, both of which were completely suppressed by a broad-spectrum antibiotic cocktail. Furthermore, in both in vitro and in vivo experiments, the combination of Pam and Fusobacterium nucleatum caused the death of gingival fibroblasts (GFs) and down-regulated their production of keratinocyte growth factor (KGF), which induces epithelial cell growth and migration. Therefore, in periodontal tissues pre-exposed to bisphosphonate, bacterial infection at tooth extraction sites caused diminished KGF expression in GFs, leading to a delay in the epithelial wound-healing process that was mitigated by antibiotics.
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