Osteoporosis and Osteomalacia

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Hyperthyroidism

Thyroid hormones have a direct resorptive effect on bone. Low thyroid-stimulating hormone (TSH) and high thyroxine (T4) levels can exert a negative effect on bone resorption.1 Hyperthyroid patients have a significant negative calcium balance. Bone loss occurs more in cortical than trabecular bone. Hyperthyroid states can be compartmentalized into overt hyperthyroidism, endogenous subclinical hyperthyroidism, and exogenous subclinical hyperthyroidism due to suppressive therapy and thyroid

Hyperparathyroidism

Hyperparathyroidism is divided into primary and secondary hyperparathyroidism(Table 1). Classically, primary hyperparathyroidism is recognized as a disease of “bones, stones, and groans”; now, the condition is asymptomatic in most patients because the current biochemical profile contains serum calcium, and markedly high levels of calcium are detected sooner than in the past. Primary hyperparathyroidism is a generalized disorder of calcium, phosphate, and bone metabolism that results from an

Hypoparathyroidism

Hypothyroidism is an uncommon disease caused by insufficient PTH. The most common causes are immunologic destruction, radiation therapy, and surgical removal. Patients develop hypocalcemia and hyperphosphatemia. Idiopathic hypophosphatemia can lead to various musculoskeletal findings, including diffuse ligamentous and entheseal ossifications. A recent report describes a 50-year-old man with idiopathic hypoparathyroidism who was diagnosed with diffuse idiopathic skeletal hyperostosis when 40

Vitamin D deficiency

Vitamin D deficiency has received much attention over the past few years with the recognition of the many people deficient in Vitamin D living in northern latitudes. Vitamin D is obtained from cutaneous production when 7-dehydrocholesterol is converted to vitamin D3 (cholecalciferol) by ultraviolet B radiation or by oral intake of vitamin D2 (ergocalciferol) or vitamin D3. Fatty fish is the most important dietary source. Fortification of foods is practiced in some countries, including the

Hypophosphatemia

The 3 most common causes of hypophosphatemia are redistribution of phosphorus from extracellular fluid into cells, increased urinary excretion, and decreased intestinal absorption. The clinical manifestations depend on the severity of the condition. Early on, hypophosphatemia can cause increased bone resorption. Impaired bone mineralization causes rickets in children and osteomalacia in adults. X-linked hypophosphatemic rickets is the most common disorder of renal wasting, occurring in about 1

Hypomagnesemia

Hypomagnesemia is usually caused by loss of magnesium from the gastrointestinal tract or kidney. Hypocalcemia is a common manifestation of moderate-to-severe magnesium depletion. Both can be associated with neuromuscular hyperexcitability and tetany, as elicited by positive Chvostek and Trousseau signs. Epidemiologic studies suggest that a low magnesium diet may be a risk factor of osteoporosis. Magnesium deficiency in rats can cause a decrease in bone mass and skeletal fragility.24 Magnesium

Gonadal steroids

Estrogen and testosterone play an important role in maintaining skeletal architecture. The estrogen and testosterone decrease with aging has profound effects on the skeleton. At menopause, women undergo rapid trabecular bone loss.25 The duration of rapid bone loss can begin 1 to 2 years before menopause and continue for up to 5 years after, when there can be a loss of 20% to 30% of trabecular bone and 5% to 10% of cortical bone. About 8 to 10 years after menopause, there is a slower and

Diabetes mellitus

The incidence of diabetes continues to climb worldwide. Type I and Type II diabetes mellitus (DM) are associated with osteoporosis and fracture. The increased risk seems due to the direct effect of the metabolic syndrome associated with DM on the skeleton, the complications of DM, and an increased risk of falls. Patients with DM may have retinopathy, affecting vision and causing an increased risk of falls. Neuropathy may cause a person to be less active and to have an increased risk of falls.

Cushing syndrome

Cushing syndrome involves endogenous production of cortisol by adrenal hyperplasia or by an adrenal adenoma or malignancy. One of the myriad associated clinical features is increased bone resorption, osteoporosis, and increased risk of fracture. In patients suspected of having Cushing syndrome, 24-hour urine cortisol level is checked. If elevated, the adrenal glands are imaged. Traditionally, large, functioning adenomas are removed, thus treating the underlying condition. More recent studies

Hyperprolactinemia

Elevated prolactin levels are associated with bone loss and osteoporotic fractures.42 In has been demonstrated that treatment of hyperprolactinemia with bromocriptine restores normal values of bone-formation and bone-resorption markers.43 Many medical conditions and medications can cause hyperprolactinemia (Box 1). Much data suggest that many antipsychotics, such as risperidone, haloperidol, and chlorpromazine, are associated with lower bone density in treated patients.44 Screening patients at

CKD mineral bone disorder

CKD mineral bone disorder (MBD) has been designed to replace the term renal osteodystrophy (ROD) as knowledge about bone disease in patients with CKD has emerged, and it is now known that there are many facets to bone disease in these patients. ROD refers to skeletal pathology and CKD-MBD refers to the entire spectrum of mineral metabolism, cardiovascular, and skeletal complications of CKD.45 The earliest histologic abnormalities of bone in CKD-MBD are seen after a fairly mild reduction in the

Glucocorticoid-induced osteonecrosis

This tends to be an unpredictable and devastating consequence of glucocorticoid use. Patients experience often acute pain in a joint. MRI initially reveals bone marrow edema, most commonly in the femoral neck. The involved area of bone can go on to collapse, and the patient may require a total joint replacement. Almost any joint can be involved, but large joints are most commonly affected. It has long been thought that this process was the result of fat emboli, microvascular tamponade of blood

Summary

As the population ages, the amount of metabolic bone disease and number of fractures will increase. It is imperative that health care providers screen and treat patients at risk of metabolic bone disease. There is much research ongoing in this field and the number of treatment options will greatly expand. Focusing on ways to maximize the development of the fetal skeleton to improve peak bone mass, such as improving maternal vitamin D levels during pregnancy, may best address the treatment of

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