Bone Mineral Density in Polycystic Ovary Syndrome

Issue: Supplement to issue 3/2017

Author: Orbetzova, Maria М.

Clinic of Endocrinology and metabolic disorders, “Sv. Georgy” University Hospital, Medical Faculty, Medical University, Plovdiv

Abstract:

Estrogens play a key role in the development and maintenance of the appropriate bone mass in women, by acting on osteoblasts, as well as on osteoclasts. The main mechanism of androgen action on bones is believed to be linked to the aromatization of androgens to estrogens in the ovaries and extra glandular tissues. Moreover, all bone-forming cells have receptors for both andro-gens and estrogens with a predominance of andro-gen receptors on osteoblast cells.

Polycystic ovary syndrome (PCOS), charac-terized by chronic anovulation, hyperandrogene-mia, obesity, central adiposity, and insulin resist-ance, represents a unique, natural model for study of the influences of androgenic hormones on bone mass among women. In PCOS, bone mineral den-sity (BMD) appears to be maintained at levels comparable to those observed in control women, implying that the deleterious effects associated with anovulation may be attenuated by bone exposure to androgens. Various lines of evidence in both normal women and women with androgen excess tend to support an independent association of androgens with peak bone mass attainment and maintenance in premenopausal women. Gene-rally, the association of androgens and BMD мес-тата с по-голям процент трабекуларна кост (гръбначен стълб, бедрена шийка) в сравне-ние с местата с преобладаваща кортикална кост (радиус и бедро), което предполага по-тенциално по-изразени андрогенни ефекти, било то директни или индиректни, in the androgen excess populations appears to be stronger in bone sites with a greater percentage of trabecular bone (lumbar spine and femoral neck) compared to cortical bone sites (radius and hip), suggesting potentially more pronounced andro-genic effects, whether direct or indirect, in more metabolically active bone. However, no net posi-tive effect on bone was observed without the mid-cycle estradiol peak and/or luteal phase proges-terone production, suggesting again that estradiol plays a critical role. Thus the higher BMD seen in eumenorrheic, hyperandrogenic PCOS women compared to that in oligo- and amenorrheic PCOS women and normal controls may be estrogen mediated. Alternatively, androgen-dependent changes in body composition, rather than a direct effect of androgens, may be the primary influence in maintaining BMD in PCOS women. The absence of any notable differences in bone remod-eling markers between women with PCOS and healthy controls suggests that any direct effects of androgens on bone formation may be limited. Moreover, in studies of hyperandrogenic disor-ders, the bone effects attributed to androgens may be partially mediated by cytokines (interleukin-6), growth factors, or other hormones (insulin, activin, follistatin). Insulin appears to be one of the most important positive bone growth stimulators.

Finally, treatment interventions targeted at reducing androgen, estrogen, and insulin levels, without attention to their individual effects on bone mass and without subsequent restoration of normal cycling, may place a subgroup of PCOS women potentially at risk for osteoporosis later in life.

Key words: bone mineral density, androgen excess, polycystic ovary syndrome, estrogens, insulin

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