Sclerostin antibody stimulates bone regeneration after experimental periodontitis.

摘要: The reconstruction of large osseous defects due to periodontitis is a challenge in regenerative therapy. Sclerostin, secreted by osteocytes, key physiological inhibitor osteogenesis. Pharmacologic inhibition sclerostin using sclerostin-neutralizing monoclonal antibody (Scl-Ab) thus increases bone formation, mass and strength models osteopenia fracture repair. This study assessed the therapeutic potential Scl-Ab stimulate alveolar regeneration following experimental (EP). Ligature-induced EP was induced rats generate localized defects. Following 4 weeks disease induction, (+EP) or vehicle (+/− EP) were systemically delivered, twice weekly for up 6 wks determine ability regenerate around tooth-supporting 3 after initiation treatment, femur maxillary jawbones harvested histology, histomorphometry, micro-computed tomography (micro-CT) linear loss (ABL) volumetric measures support, including volume fraction (BVF) tissue mineral density (TMD). Serum analyzed examine turnover markers during Vehicle + EP animals exhibited (BVF, TMD ABL) at ligature removal thereafter. significantly improved healing, as measured BVF, ABL, when compared vehicle + EP. After BVF values Scl-Ab + EP group similar those healthy controls. analysis demonstrated higher levels formation osteocalcin PINP treatment groups. restored periodontitis. These findings warrant further exploration therapy this other oral defect scenarios. © 2013 American Society Bone Mineral Research.