Introductory remarks.

The cause of osteoporosis, a condition in which bone mass is decreased to a point where structural failure may occur, is unknown; many factors that contribute to the development of osteoporosis are known.Bone mass increases until the late twenties, the time when people attain peak bone mass. For a time after peak bone mass is reached, bone loss and formation are approximately equal. Soon after that, probably in the early thirties, an uncoupling of bone synthesis and bone resorption occurs, and a net loss of bone mass begins, a process that can ultimately result in osteoporosis.Bone loss occurs most rapidly in white females immediately after menopause. The bone most affected is the spongy, trabecular bone of the vertebrae and pelvis and the ends of long bones.Osteoporosis is classified into two syndromes, which are not distinct but have overlapping features and may have the same pathogenetic mechanism. Type I, or postmenopausal osteoporosis, is associated with estrogen deficiency and is characterized by loss of trabecular bone in the vertebrae and the distal radius (the wrist). Vertebral fractures and wrist fractures (also called Colles' fractures) result. Type II, or senile osteoporosis, is age-related, occurs in men as well as women, and is characterized by fractures of the hip and humerus. There is a loss of cortical as well as trabecular bone.Estrogen deficiency, increasing age, smoking, high alcohol intake, large amounts of caffeine and protein, and lean body mass favor decreased bone density, whereas estrogen replacement after menopause, adequate dietary calcium, and moderate amounts of weight-bearing exercise tend to favor increased bone density.Standard X-rays, computed tomography, single and dual photon absorptiometry, and neutron activation analysis are noninvasive techniques used in evaluating osteoporosis.Calcium, estrogen, and calcitonin are approved drug therapies for osteoporosis.