Sarcopenia and osteoporosis increase the risk of bone fracture in the elderly due to the loss of muscle mass and the decrease in bone mineral density. Myostatin and Bone Morphogenetic Proteins (BMPs) are important molecules involved in muscle mass homeostasis.
In this study, we investigated the role of BMP4 and myostatin in the pathophysiogenesis of sarcopenia related to osteoporosis and osteoarthritis.
Muscle atrophy, BMP4 and myostatin expression were evaluated in 27 biopsies of osteoarthritic (OA) women and 27 biopsies from osteoporotic (OP) group by immunohistochemical reaction. Muscle stem cell niches were investigated by transmission electron microscopy analysis.
Myostatin and BMP4 expression was evaluated by counting the number of positive fibers on 25 high-power field. We found that OA muscle biopsies showed a significantly higher number of BMP4-positive fibers (37.35 ± 5.63) as compared with muscle of OP patients (9.60 ± 1.57). Unlike BMP4 expression, the number of myostatin-positive fibers in OP patients (33.95 ± 4.10) was significantly higher compared to OA group (13.86 ± 1.68). The ultrastructural analysis of BMP4-positive tissues displayed the presence of a high rate of satellite cells both single or as syncytium giving proof of muscle regeneration capability.
Our results indicated that sarcopenia and osteoporosis shared an impairment of metabolic activity. Conversely, the molecular mechanisms of OA seem to inhibit the onset of an age-related sarcopenia.
The characterization of molecular mechanisms underlying the bone-muscle crosstalk could open new therapeutic perspectives in elderly diseases.