Metabolic Bone Disorder

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Hyperparathyroidism produces bone erosion by stimulation of osteoclast activity

PTH stimulates osteoclastic resorption of bone, with the release of calcium from the bone into the plasma. Its activity is normally finely controlled by a feedback mechanism whereby PTH secretion from the parathyroid gland is suppressed by a rise in plasma calcium concentration and stimulated by a fall. Failure of the feedback mechanism leads to excessive parathormone secretion, with continuing PTH output and excessive osteoclastic destruction of bone.

There are two main patterns of hyperparathyroidism. In primary hyperparathyroidism an autonomous parathyroid tumour, usually a parathyroid adenoma, secretes excess PTH continuously outside of the control of the feedback mechanism. 

In secondary hyperparathyroidism a persistently low serum calcium level (due to excess calcium loss in the urine in chronic renal disease) leads to continuous stimulation of the parathyroids by the feedback mechanism. This results in hyperplasia of all the parathyroid glands and a constant excessive secretion of PTH.

In primary hyperparathyroidism the serum calcium level is often greatly increased (hypercalcaemia) because of the continuous release of calcium from bone in the absence of an effective feedback mechanism. In secondary hyperparathyroidism it is the presence of a pathologically low serum calcium level that stimulates PTH activity and calcium release from bone; the serum calcium level is therefore low (hypocalcaemia) or normal because any calcium mobilized from the bone is almost immediately lost through the abnormal kidneys.

Renal osteodystrophy is a metabolic bone disorder associated with chronic renal failure

The term 'renal osteodystrophy' refers to metabolic and structural abnormalities of bone caused by the presence of chronic renal failure. There are two main components to renal osteodystrophy: osteomalacia of renal origin (due to failure of conversion of 25-hydroxyvitamin D3 to the active principle 1,25-dihydroxyvitamin D3 in the kidney because of tubular damage) and secondary hyperparathyroid effects (secondary to low serum calcium because of a combination of vitamin D deficiency, excess calcium loss in urine, and phosphate retention).

The bone in renal osteodystrophy therefore shows a combination of secondary hyperparathyroidism changes, excessive bone erosion by osteoclasts, and failure of mineralization of osteoid collagen.

A further factor occurs in patients who receive long-term haemodialysis for chronic renal failure. Such patients often retain increased quantities of aluminium, which become deposited in the bone in the site in which mineralization by calcium should be taking place, blocking calcification of the osteoid, and thus playing a role in the osteomalacia.
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