In hyperparathyroidism the parathyroid hormone (PTH) level is elevated, the number of osteoblasts is markedly increased, and the bones become porous. (1)
In hyperparathyroidism BMD values can differ very much per bone, (2) and some BMD values can even be elevated (3) due to increased osteoblast activity.
So what exact influence has PTH on the bones?
PTH stimulates uptake of calcium into the bones, (4) osteoblast apoptosis (5) and deportation of calcium from the bones. This is exactly the opposite of the influence of estrogen, and since estrogen is protective, excessive PTH logically accelerates osteoporosis.
Estrogen and PTH do not just have opposite effects on bone; estrogen also prevents the PTH level from increasing too much. When estrogen level is at its lowest (around menstruation and after menopause), PTH level is at its highest. (6) That is why hyperparathyroidism is common in postmenopausal women (7) and estrogen administration is an effective therapy. (8)
If a lack of estrogen caused the hyperparathyroidism, parathyroidectomy does not result in complete bone-reparation, of course. (9)
Besides estrogen, calcitriol also inhibits PTH secretion. Though calcitriol has similar, but less strong effects on bones, supplementary calcitriol can per saldo strongly decrease uptake of calcium into the bones and deportation from the bones, (10) which is protective.
What is the biological purpose of PTH?
Primarily to co-regulate blood-calcium level, and secondarily to co-regulate the bone-calcium contents. These must be regulated because too much or too little calcium in the blood can be lethal, and too little or too much calcium in the bones is unwelcome too. Our bones are constructed according to a genetic plan. Excessive calcium has eventually to be deported since holding more calcium than is the optimum amount is not beneficial. (bone-deformations)
Thus hormones that stimulate deportation of calcium from the bones are required.
PTH collaborates with calcitriol to deport calcium from the bones. PTH stimulates secretion of calcitriol, which hormone (like PTH) both increases uptake of calcium into the bones (11) and subsequent deportation of calcium from the bones.
The difference between these two hormones is that the ffects of PTH on bone are stronger. More importantly, calcitriol (which is composed of vit. D) also increases absorption of calcium from food while PTH increases the excretion of calcium into urine.
Calcitriol inhibits secretion of PTH and PTH increases secretion of calcitriol. (see "Calcium Hormones")
But the calcitriol level is low in hyperparathyroidism.
Why is the calcitriol level low in hyperparathyroidism?
The PTH level can be elevated for various reasons besides a lack of calcitriol. (due to a thyroid malfunction, a tumor or a lack of estrogen for example). The calcitriol level has to be decreased even if PTH is not elevated due to a lack of calcitriol. Otherwise the combined influence of PTH and calcitriol would cause far too much calcium deportation from the bones.
Even if in hyperparathyroidism the calcitriol level is normal, the continued uptake of dietary calcium would add up to the accelerated fractional calcium absorption and subsequent deportation, further hastening osteoporosis.
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Abstracts of most sources can be found at The National Library of Medicine
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