Mawardi, H.Giro, G. [UNESP]Kajiya, M.Ohta, K.Almazrooa, S.Alshwaimi, E.Woo, S-B.Nishimura, I.Kawai, T.2013-09-302014-05-202013-09-302014-05-202011-11-01Journal of Dental Research. Thousand Oaks: Sage Publications Inc, v. 90, n. 11, p. 1339-1345, 2011.0022-0345http://hdl.handle.net/11449/15998No 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.1339-1345engbisphosphonate-induced osteonecrosis of the jawpamidronategingival fibroblastKGFwound healingFusobacterium nucleatumArtigo10.1177/0022034511420430WOS:000295692600013Acesso restrito