Treatment of spinal osteoporosis in postmenopausal women.

Ninety-five postmenopausal women with unequivocably wedged or compressed vertebrae in whom the recognised causes of secondary osteoporosis had been excluded were studied, 41 having no treatment and the rest one or more of six different treatments. The treatment regimens comprised calcium supplements, vitamin D, calcium and vitamin D, ethinyloestradiol or--where oestrogens were contraindicated--norethisterone, 1 alpha-hydroxycholecalciferol (1 alpha-OHD3), or hormones with 1 alpha-OHD3. The seven groups were reasonably comparable in most respects except that the hormone-treated patients were younger and had a higher initial cortical area ratio than the others, and the calcium- and hormone-treated groups had the best initial radio-calcium absorption. The untreated osteoporotic patients lost cortical bone more rapidly than do normal postmenopausal women. Three treatments (calcium, hormones, and 1 alpha OHD3 plus hormones) appear to be useful in modifying the disease, and two treatments (vitamin D and 1 alpha-OHD3) useless or even harmful. Vitamin D and 1 alpha-OHD3 are more safely used in conjunction with oestrogens, which protect bone against resorption, than on their own.     

An expanded overview of postmenopausal osteoporosis

Why is the incidence of osteoporotic fracture so much higher in women than in men? The dominant medical view holds that the exaggerated skeletal fragility and fracture risk of postmenopausal women solely reflects the loss of bone following withdrawal of endogenous estrogen. Indeed, an enormous amount of research in this area has attempted to understand the rise in fractures after menopause in terms of the impact of estrogen lack on bone remodeling. Recent insights suggest that this simple view does not offer an adequate explanation for the greater susceptibility of older women to fracture compared to that of men. It seems more reasonable to view bone health as a lifelong process, reflecting the contributions and influences of myriad events occurring throughout life to skeletal acquisition and maintenance. Only recently has the medical community recognized that the amount of bone present at skeletal maturity makes a powerful contribution to lifelong skeletal status. A second area that must be incorporated into discussions of this topic relates to bone size and geometry. Women's bones are inherently smaller than those of men. A bone's strength is determined by its size as well as by its material properties. In boys, pubertal increases in the cortical thickness of long bones are achieved by (testosterone-dependent) periosteal apposition. By contrast, increased cortical thickness in girls reflects bone expansion into the medullary space, with little or no periosteal apposition, suggesting an inhibitory effect of estrogen on the latter process. Consequently, at skeletal maturity, men have wider bones of greater mechanical competence. Although estrogen is generally held to be skeletally protective, this aspect of its actions may actually render women more susceptible to some fractures. In later life, men may lose even more bone from appendicular sites than do women, but men show much greater concomitant increases in periosteal apposition than women, permitting them to maintain a relatively favorable mechanical profile. These several findings are based on cross-sectional observations of relatively few individuals and therefore require confirmation in prospective longitudinal studies. The degree to which gender-related differences in later life skeletal adaptation reflects a bone's mechanical or metabolic environment has been frequently discussed but still awaits experimental confirmation.     

Clinical problems related to postmenopausal osteoporosis]

Authors discuss current hypotheses related to the causes of osteoporosis and its possible therapy. One of the frequent menopausal disorders is osteoporosis, i.e. decrease in bone density, which may eventually lead to the pathological fractures and marked deformities of the skeleton. Etiology of the postmenopausal osteoporosis is not clearly explained. However, one may assume that hormonal disturbances, especially estrogen deficit, plays an important causative role. The treatment is difficult. It is usually aimed at preventing of bone loss.     

Progress in osteoporosis and fracture prevention: focus on postmenopausal women

In the past decade, we have witnessed a revolution in osteoporosis diagnosis and therapeutics. This includes enhanced understanding of basic bone biology, recognizing the severe consequences of fractures in terms of morbidity and short-term re-fracture and mortality risk and case finding based on clinical risks, bone mineral density, new imaging approaches, and contributors to secondary osteoporosis. Medical interventions that reduce fracture risk include sufficient calcium and vitamin D together with a wide spectrum of drug therapies (with antiresorptive, anabolic, or mixed effects). Emerging therapeutic options that target molecules of bone metabolism indicate that the next decade should offer even greater promise for further improving our diagnostic and treatment approaches.