Can One Develop a Means to Treat Sarcopenia Derived from Present Osteoporosis Medications?
Osteoporosis is the loss of bone strength and density, while sarcopenia is the loss of muscle mass and strength. Both of these are near universal in the aging population, the only question being when they rise to the level of frailty. Researchers have noted mechanistic connections between these two conditions, and some data suggests that osteoporosis treatments can improve sarcopenia. Is there a path leading from current osteoporosis medications to therapies that can slow the progression of sarcopenia? That would likely require more dedicated research and development programs than are currently taking place, and it is unclear as to whether the outcome would be better than a continuation of present independent efforts to find therapies to treat sarcopenia.
Sarcopenia is a progressive and systemic skeletal muscle disorder associated with aging that usually occurs with age in the elderly. Sarcopenia currently lacks effective pharmacological treatment modalities. Multiple pharmacological intervention modalities are available for osteoporosis, a comprehensive disease characterized by decreased systemic bone mass, degradation of bone microarchitecture, and increased bone fragility. Several recent studies have shown an extremely strong correlation between sarcopenia and osteoporosis, leading to the concept of "osteosarcopenia". Therefore, it is possible to alleviate sarcopenia simultaneously by improving osteoporosis.
There are still no drugs for sarcopenia that can be effectively treated, and as the aging society progresses, it is crucial to find a treatment for sarcopenia. Current studies have shown conflicting results between anti-osteoporosis treatment and improvement of sarcopenia, with some drugs relying on a common pathway between the bone and muscle to improve sarcopenia alongside anti-osteoporosis treatment, such as denosumab and tibolone. Multiple mechanisms could explain the improvement in sarcopenia after anti-osteoporosis treatment.
Current evidence suggests that denosumab binds to RANKL and antagonizes the negative regulatory effect of RANKL on myocytes, while tibolone binds to oestrogen receptors in muscle and directly increases muscle anabolism. Furthermore, in addition to the common pathway, it does not mean that bone is negligible, through the effect of the paracrine bone factors on skeletal muscle. In conclusion, the current study suggests that anti-osteoporotic therapy offers a lasting and easy to use program for patients with sarcopenia in general.