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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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