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Osteoporosis is characterized by the imbalance between the activity of the osteoblasts, the bone forming cells, and the osteoclasts, the cells that resorb the bone tissue, imbalance that favors the osteoclasts.1
Primary osteoporosis can be further subdivided into two types.
Type I, postmenopausal osteoporosis, results from decreased circulating levels of estrogen.
It is seen in postmenopausal women and affects the majority of persons older than 70 years. Bone loss is rapid. There is swift trabecular bone loss up to 8% per year. Type I osteoporosis causes primarily trabecular bone loss with only 0.5% cortical bone loss per year. Fractures occur in locations of trabecular bone loss such as the distal radius and vertebrae. The cause of primary osteoporosis is a changing hormonal milieu.
Type II, senile osteoporosis, is a consequence of aging.
It causes a more global bone loss affecting cortical and cancellous bone such as in the femoral neck. Type II osteoporosis is seen in persons older than 70 years. The female-to-male ratio is 2:1. The bone loss occurs in both the trabecular and cortical bone and averages 0.3–0.5% per year. Fractures occurring as the result of type II osteoporosis typically involve the hip, pelvis, humerus, tibia, and vertebral bodies. The causes of senile osteoporosis are those seen with aging and include calcium deficiency, decreased vitamin D, and increased parathormone activity.
Secondary Osteoporosis
Causes.
Chronic or prolonged corticosteroid use
Endocrine disorders.
Hyperthyroidism, hyperparathyroidism, diabetes, Cushing disease, and euplastic disorders.