Bone Abstracts

Introduction: Age-related bone diseases, such as osteoarthritis (OA) and osteoporosis (OP), are strongly associated with sarcopenia and muscle fiber atrophy. Potential mechanisms involved in the reduction of skeletal muscle mass during sarcopenia converge on the failure of satellite cells in replacing and repairing damaged muscle fibers. Myostatin and bone morphogenetic proteins (BMPs) are molecules able to regulate muscle mass homeostasis by activating satellite stem cells [4]. In this study, we investigated the role of BMP2, BMP4, and myostatin in the patho-physiogenesis of sarcopenia related to osteoporosis and osteoarthritis.

Methods: Muscle atrophy, BMP2, BMP4, and myostatin expression were evaluated in 27 biopsies of osteoarthritic (OA) women and 27 biopsies from osteoporotic (OP) by immunoistochemical reaction. Muscle stem cells niches were investigated by ultrastructural analysis.

Results: We found that OA muscle biopsies showed a significantly higher number both BMP2-positive fibers (62.79±6,205) and BMP4-positive fibers (37.35±5.63) as compared with muscle of OP patients (9.60±1.57 and 13.92±3.343). Unlike BMP2 and BMP4 expression, the number of myostatin-positive fibers in OP patients (33.95±4.10) was significantly higher compared with OA group (13.86±1.68). The ultrastructural analysis of BMPs-positive tissues displayed the presence of a high rate of satellite cells both single or as syncytium giving a proof of muscle regeneration capability.

Discussion: Our results clearly indicated that sarcopenia and osteoporosis shared an impairment of metabolic activity. Conversely, the higher expression of BMPs in OA patients seems to inhibit the onset of age-related sarcopenia. The characterization of molecular mechanisms underlying the bone–muscle crosstalk could open new therapeutics perspectives in elderly diseases.