A Role of Oral Bacteria in Bisphosphonate-induced Osteonecrosis of the Jaw

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Data

2011-11-01

Autores

Mawardi, H.
Giro, G. [UNESP]
Kajiya, M.
Ohta, K.
Almazrooa, S.
Alshwaimi, E.
Woo, S-B.
Nishimura, I.
Kawai, T.

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Editor

Sage Publications Inc

Resumo

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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bisphosphonate-induced osteonecrosis of the jaw, pamidronate, gingival fibroblast, KGF, wound healing, Fusobacterium nucleatum

Como citar

Journal of Dental Research. Thousand Oaks: Sage Publications Inc, v. 90, n. 11, p. 1339-1345, 2011.