Mice lacking pten in osteoblasts have improved intramembranous and late endochondral fracture healing.

摘要: The failure of an osseous fracture to heal (development a non-union) is common and debilitating clinical problem. Mice lacking the tumor suppressor Pten in osteoblasts have dramatic progressive increases bone volume density throughout life. Since healing recapitulation development, we investigated process mice (Ocn-cretg/+;Ptenflox/flox). Mid-diaphyseal femoral fractures induced wild-type Ocn-cretg/+;Ptenflox/flox were studied via micro-computed tomography (µCT) scans, biomechanical testing, histological histomorphometric analysis, protein expression analysis. had significantly stiffer stronger intact bones relative controls all cohorts. They also at day 28 post-fracture (PF) days 14, 21, PF. At 7 PF, proximal distal ends mutant calluses more ossified. By mutants larger mineralized calluses. improved intramembranous formation during originating from periosteum. endochondral later process, after mature are present callus. Our results indicate that inhibition can improve local or short-term use commercially available Pten-inhibiting agents may application for enhancing healing.