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Osteoporosis is a systemic skeletal disorder characterized by: decreased bone mass and deterioration of bone microarchitecture. Osteopenia is a milder form of bone loss. Increased fracture risk even with minimal trauma; most common sites for bone loss and resultant fractures are thoracic and lumbar vertebrae, ribs, upper femur, lower radius. Usually causes no signs or symptoms except height loss and kyphosis until fractures occur. Pathogenesis: genetics; medications; diet; race; gender; lifestyle; physical activity. Type 1 (postmenopausal) is most common; results from sex hormone deficiency; increased recruitment/responsiveness of osteoclast precursors and increased bone resorption outpace bone formation; decreased trabecular bone leads to an increased risk of Colles and vertebral fractures; estrogen deficiency may cause bone to be more sensitive to parathyroid hormone, leading to increased calcium release from bone, decreased renal calcium excretion, and increased production of 1,25-dihydroxyvitamin D; gonadal deficiency may also increase production of cytokines that have an influence on osteoclasts. Type 2 (senile) occurs in both genders; decreased formation of bone and decreased renal production of 1,25(OH)2 D3 occurring late in life; loss of cortical and trabecular bone leads to increased fracture risk in hip, long bones, vertebrae. Type 3, secondary to medications or due to other conditions that cause increased bone loss by various mechanisms. Bone mineral density frequently used as approximate measure of bone strength. WHO defines osteoporosis as bone density 2.5 standard deviations below mean for young adult white females. Markers of bone turnover (bone specific alkaline phosphatase, osteocalcin, type I procollagen peptides, and urinary deoxypyridinoline) sometimes used to monitor response to therapy
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