Introduction: Osteoporosis, especially menopause – related form, represents a condition with dramatic epidemiologic burden thus the need for clear recommendations of case finding strategies and for developing new therapies. Antisclerostin antibodies uncouple bone resorption from formation, allowing formation but not resorption. We aim to introduce a compressive approach related to antisclerostin antibodies (a PubMed- based narrative review).
General data: The inhibition of sclerostin based on human-like antibodies (like romosozumab, blosozumab) induces a consistent yet transitory bone mass elevation while the resorption is blocked. Phase two trials showed an important human skeletal effect by inducing high bone mineral density through Wnt signalling transduction. Sclerostin is presented into the body in order to control the bone formation – resorption balance.
Its blood levels are increased in patients with renal failure even if it is paradoxically more excreted. This small protein is coded by SOST gene which is found in osteocytes in response to mechanical forces on the bones thus osteocytes play an essential role as key regulators of bone remodelling. Sclerostin binds to osteoblasts to inhibit them. Its production is also found in cartilages but limited data are currently known about its specific actions but, perhaps, antibodies targeting sclerostin may be beneficial for both osteoporosis and osteoarthritis.
Conclusion: The results from ongoing trials will point out the exact role of antisclerostin antibodies as anti-osteoporotic agents, and this will probably be as second line medication on a sub-set of subjects with severe forms of osteoporosis or potentially in patients with kidney failure- related bone loss.
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