The Role of Muscle Loading on Bone (Re)modeling at the Developing Enthesis

摘要: Muscle forces are necessary for the development and maintenance of a mineralized skeleton. Removal loads leads to malformed bones impaired musculoskeletal function due changes in bone (re)modeling. In current study, junction at interface between muscle was examined under normal loading conditions. Unilateral mouse rotator cuff muscles were paralyzed using botulinum toxin A birth. Control groups consisted contralateral shoulders injected with saline separate group mice. It hypothesized that unloading would suppress formation enhance resorption enthesis, unloading-induced bony defects could be rescued by suppressing osteoclast activity. order modulate activity, mice bisphosphonate alendronate. Bone measured tendon enthesis alizarin calcein fluorescent labeling surfaces followed quantitative histomorphometry histologic sections. volume architecture micro computed tomography. Osteoclast surface determined via tartrate resistant acid phosphatase stained resulted delayed initiation endochondral ossification but did not impair rate. Unloading led severe trabecular architecture. These partially suppression activity through alendronate treatment, effect dose dependent. Similarly, rate increased increasing across groups. The caused therefore likely maintained high which normally decreases from neonatal mature timepoints. results have important implications treatment conditions such as brachial plexus palsy, shoulder paralysis birth subsequent humeral head.