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  • Osteoporosis is defined as bone fragility due to reduced bone mineral density (BMD) or loss of bone trabecular microarchitecture.

  • Fragility fractures occur most frequently in the wrists, forearms, spine, and hips.

  • The incidence of osteoporosis increases with age, independent of sex, but the disease is most prevalent in postmenopausal women.

  • The risk of spinal fracture increases with chronic glucocorticoid doses as low as 2.5 mg of prednisone daily.

  • Prednisone doses higher than 7.5 mg daily increase the risk of spine fractures fivefold and double the risk of hip fracture.

  • Risk of osteoporosis is associated not only with glucocorticoids but with other medications as well, including chronic use of PPIs, anticonvulsants, SSRIs, and warfarin.

  • Preventive measures and treatment options are effective at reducing fractures.

General Considerations

Bone remodeling occurs throughout life, such that the average skeleton is turned over every 10 years. Bone remodeling units include three main cell types: osteoclasts (OCs) that resorb bone; osteoblasts (OBs) that form new bone; and osteocytes (OCYs), embedded within the bone, that regulate the activity of OCs and OBs by producing paracrine factors locally. OCYs are the main producers of sclerostin, which regulates OB against producing more bone. OCYs also produce receptor activator of nuclear factor κB ligand (RANKL), which recruits OC precursors and stimulates bone resorption. Bone catabolism and anabolism normally remain coupled to maintain bone integrity. However, in many disease states such as hyperparathyroidism, hormonal changes such as those occurring in menopause, and the use of medications such as glucocorticoids, bone formation becomes uncoupled from bone resorption. This process ultimately leads to osteoporosis. The degree to which bone cells are regulated by the immune system has been recognized and defined only within the last two decades, and it is now clear that many endocrine and autoimmune disease states are associated with osteoporosis because the cross-talk between the immune system and bone cells has become dysregulated.

Men and women have significant differences in peak bone mass and the rates of bone loss over their life spans (Figure 51–1). Men achieve higher peak bone mass than do women and have only slow bone loss in middle to late age. They therefore maintain a higher bone mineral density (BMD) until late in life. Women undergo an early rapid phase of postmenopausal bone loss followed by a slow but persistent rate of bone loss until death. The lower peak bone mass attained by women coupled with the early rapid phase of menopause-related bone loss means that women typically have lower BMDs than men of the same age. Thus, women have an earlier onset of the typical osteoporotic fractures (hip, vertebral, and distal forearm [Colles]) compared with men (Figure 51–2). Osteoporotic fractures occur in men on average 10 years later than women do. The impact of older age at hip fractures is that men have substantially higher morbidity and mortality ...

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