A. S. Sindhura* and Abdul Khader


Hormonal changes that begin during the menopausal transition affect many biological systems. In postmenopause, long term manifestations of definite estrogen deprivation ensue, among which Osteoarthritis (OA) is one. Osteoarthritis is a chronic degenerative joint disease involving multiple physiopathological mechanisms. OA strikes women more often than men and it increases in prevalence, incidence and severity after menopause. Among the multiple physiopathological mechanisms involved in OA, those related to sex hormones have been attracting much attention, in particular those involving estrogens. The manifestation of osteoarthritis after the decline of estrogen in menopause has a different pathology compared to the osteoarthritis that occur as degenerative joint disease. The postmenopausal osteoarthritis is a subtype of osteoarthritis and it is considered as osteoporotic phenotype. This type of osteoarthritis demands anti-resorptive agents along with conventional line of management. There is increasing evidence that estrogen fulfil a relevant role in maintaining the homeostasis of articular tissues and, hence, of the joint itself. It also has anti-resorptive property. The dramatic rise in OA prevalence among post-menopausal women, presence of estrogen receptors (ERs) in chondrocytes, subchondral bone cells and sinoviocytes, suggest a link between OA and loss of ovarian function. A better understanding of the role that estrogen and its deficiency plays in the molecular mechanisms of menopause induced osteoarthritic changes that affect the different joint structures will help further development of new and precise therapeutic strategies to prevent and/or restore damaged articular tissues in OA.

Keywords: Osteoarthritis, estrogen, menopause, subchondral bone, articular cartilage, menisci.

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