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Abstract
Introduction: The biological enhancement of fracture healing may prevent complications such as non-union and revision surgery. Sclerostin is produced by osteocytes and binds to the LRP5/6 receptor. This inhibits the Wnt signalling pathway and thereby reduces bone formation.
Areas covered: Targeted deletion of the sclerostin gene has been found to enhance bone formation and fracture healing in rodent models. A number of in vivo studies have investigated the effect of sclerostin antibody on bone density with promising results. It also has an ability to promote fracture healing, screw fixation and metaphyseal bone healing in vivo. Early clinical studies have also demonstrated that it can increase bone mineral density, whilst being safe and well tolerated by patients.
Expert opinion: The data support the further investigation of this agent for the promotion of fracture healing. We aim to review the current literature and present an update on the use of this agent to promote bone formation and healing.
Notes
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