Journal of Bone and Mineral Research

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Abstract
Hormonal control of skeletal growth, modeling, and remodeling is characterized by a complex interaction between the calciotropic hormones (25‐hydroxycholecalciferol, 1,25‐dihydroxycholecalciferol, parathyroid hormone, and calcitonin), growth, and thyroid hormones in addition to the estrogenic and androgenic gonadal hormones. Although both growth and thyroid hormones are essential for normal skeletal growth and modeling and also can produce detrimental skeletal effects in adults when circulating in excess concentrations, these hormones assume a minor role in the day‐to‐day bone remodeling of the mature skeleton. Following the attainment of the peak bone mass, bone mineral content begins to decline in the fourth and fifth decades of life, accelerating in females in the first 5–7 years after the menopause as a result of estrogen deficiency. Associated with this age‐dependent loss in skeletal mass are decreases in calcitonin reserve primarily in the 5–7 years following the menopause, decreases in circulating 25‐hydroxycholecalciferol, intestinal resistance to 1,25‐dihydroxycholecalciferol, and a gradual progressive rise in blood parathyroid hormone. These changes in calciotropic hormone profiles, together with poor nutritional habits, anticonvulsant, glucocorticoid, and thyroid medications, diseases such as type I diabetes, immobilization, or decreased physical activity all serve to weaken the aging skeleton. The result is a gradual and subtle change in skeletal anatomy, which progresses to alterations in vertebral structure, such as kyphosis, scoliosis, and pseudospondylolisthesis, and a variety of sciatic and nerve entrapment syndromes. Vertebral, forearm, and hip fractures and edentulism ultimately comprise the syndrome of age‐related bone loss, resulting in lifestyle disabilities, extensive morbidity, analgesic drug abuse, hospitalization, and escalating annual health care expenditures.