1250 Sclerostin Deletion Rescues Periodontal Bone Loss in Periostin Knock-out Mice

Saturday, March 24, 2012: 9:45 a.m. - 11 a.m.
Presentation Type: Poster Session
Y. REN1, X. HAN1, M. LIU2, J. WANG1, Y. LIU1, H. KE2, and J. FENG1, 1Biomedical Sciences, Baylor College of Dentistry, Dallas, TX, 2Amgen, Thousand Oaks, CA
Objective: Periostin is highly expressed in periodontal ligament (PDL). We previously reported that periostin knock-out (KO) mice display a periodontal disease-like phenotype. Sclerostin (SOST) is mainly expressed in osteocytes. High bone mass phenotype was observed in SOST KO mice. The goal of this study was to examine (1) whether there is a morphologic changes in osteocytes of alveolar bone in periostin KO; and 2) whether blocking SOST via generation of double KO mice (lacking both periostin and SOST genes) could increase alveolar bone mass in periostin KO mice. 

Method: Double KO mice were created by crossing both heterozygous periostin and sclerostin mice. Their phenotypic changes were examined at 3-month of age. These mice were analyzed to study the osteocyte changes and the effect of blocking SOST on alveolar bone and PDL. Radiographs, MicroCT, histology, SEM, and immuno-histochemistry were utilized for phenotypic analyses.

Result: Irregular cell shape and a sharp reduction in mineral content surrounding osteocyte body and dendrites were observed in periostin KO mice. There was a higher bone resorption, leading to alveolar bone loss in the periostin KO mice.  Bone anabolic effects with significant increases in alveolar bone volume was observed in periostin KO mice by knocking out the sclerostin gene. Similarly, blocking SOST greatly improved osteocyte phenotype and decreased bone resorption in periostin KO mice.    

Conclusion: Our data revealed a high bone resorption with abnormal osteocytes in periostin KO mice, and that deleting SOST completely reverse bone loss in periostin KO mice. This study suggests that deletion of sclerostin protects against alveolar bone loss in periostin KO mice.

This abstract is based on research that was funded entirely or partially by an outside source: NIH/NIDCR (DE018486), Amgen Inc. and UCB Inc

Keywords: Bone repair, Periodontal disease and Periostin
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