Musculoskeletal system and the menopause

Abstract

In 1940, an American endocrinologist, Fuller Albright, was the first to link osteoporosis to ovarian failure when he noted that 40 out of the 42 patients admitted on the orthopedic ward with osteoporotic fractures were women and all had passed the menopause. Postmenopausal osteoporosis is characterized by progressive loss of bone tissue occurring as a result of an imbalance between bone formation and bone resorption leading to the occurrence of fractures. The pathophysiology of osteoporosis is multifactorial, involving various cytokines, mediators and signaling pathways in combination with genetic, hormonal and environmental influences regulating the bone remodeling process. Bone homeostasis depends on its cellular components. The development and differentiation of osteoblasts and osteoclasts is tightly controlled by growth factors and cytokines synthesized in the bone marrow microenvironment so as to maintain a dynamic equilibrium between their formation, survival and function. The increase in osteoclastogenesis and impaired osteoblastogenesis rather than the alteration in the activity of these cells are responsible for postmenopausal osteoporosis.