Abstract
Recent data demonstrate the anabolic effect of oxytocin on bone. Bone cells express oxytocin receptors. Oxytocin promotes osteoblasts differentiation and function, leading to an increased bone formation with no effect on bone resorption and an improvement of bone microarchitecture. Oxytocin is synthetized by osteoblasts, and this synthesis is stimulated by estrogen. Animal studies demonstrate a direct action of oxytocin on bone, as the systemic administration of oxytocin prevents and reverses the bone loss induced by estrogen deficiency. Although oxytocin is involved in bone formation in both sexes during development, oxytocin treatment has no effect on male osteoporosis, underlining the importance of estrogen that amplifies its local autocrine and paracrine secretion. There are few human data showing a decrease in the oxytocin serum level in anorexia nervosa independently of estrogen and in amenorrheic women associated with impaired bone microarchitecture; in post-menopausal women a higher oxytocin serum level is associated with higher bone density, but not in osteoporotic men. Oxytocin displays many effects that may be beneficial in the management of osteoporosis, cardiovascular diseases, cognitive disorders, breast cancer, diabetes and body fat gain, all age-related diseases affecting elderly women, opening exciting therapeutic perspectives, although the issue is to find a single route, dosage and schedule able to reach all these targets.
Highlights
Bone mass is maintained by the balance between bone formation assumed by osteoblasts, which share a common mesenchymal precursor with adipocytes, and bone resorption assumed by osteoclasts [7]
This paradoxical effect is explained by a down regulaall these data show that OT has a direct action on the skeleton that appears to be related tion of OT receptors on bone cells summary, action action of OT on bone metabopredominantly to a peripheral action of OTInmore than anthe indirect through the central lism is mainly an anabolic action mediated by osteoblast
It is well established that OT exerts an anabolic action on bone metabolism, in females, as its action is amplified by estrogen, and that OT can prevent or reverse ovariectomy-induced osteoporosis in animals
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Osteoporosis is the most common metabolic skeletal disorder, characterized by a decrease in bone mass and alterations of the microarchitecture, leading to skeletal fragility and an increased risk of fractures [6]. Bone mass is maintained by the balance between bone formation assumed by osteoblasts, which share a common mesenchymal precursor with adipocytes, and bone resorption assumed by osteoclasts [7]. The composition of bone marrow shifts to an increase in adipocyte formation, decrease in osteoblast functions and a major increase in osteoclast activity, resulting in osteoporosis [7]. Osteoporosis is a multifactorial disease with risk factors including aging, gonadal insufficiency, glucocorticoids and diabetes [7]. We will present current data on the role of OT in bone metabolism and osteoporosis and the potential future applications of OT as a therapeutic target in the treatment of osteoporosis, post-menopausal or secondary causes of osteoporosis and, more generally, in menopause-related diseases
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