Extract

Estrogen is critical for maintaining normal bone remodeling in women and also in men (1). Postmenopausal osteoporosis is characterized by an imbalance between increased osteoclast activity and decreased osteoblast function, resulting in increased bone remodeling, bone microarchitectural deterioration, and skeletal fragility. Estrogen deficiency may be responsible for both the accelerated phase of bone loss at the menopause and the slower phase of age-related bone loss later in life. Recently, this dogma has been challenged by the assertion that the concomitant increase in serum FSH levels at the time of the menopause may be the principal cause of the increase in bone resorption and accelerated bone loss occurring during the menopause transition.

The identification of women with rapid perimenopausal bone loss is important to target aggressive early intervention. The diagnosis of osteoporosis based on T-scores alone or through stratification for a high fracture risk by the WHO Fracture Risk Assessment Tool (FRAX) or other fracture risk calculator tools will exclude these women who are rapidly losing bone. Because all antiosteoporosis therapies, in particular the bisphosphonates, reduce bone loss, some experts propose aggressive, short-term therapy with a goal to reduce bone loss, stabilize bone density, and prevent microarchitectural deterioration for these women with rapid perimenopausal bone loss (2).

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