In hyperparathyroidism is parathyroid hormone (PTH) level elevated, is osteoblast number markedly increased, and do 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 both uptake of calcium into the bones (4) (and 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 enhances osteoporosis.


Estrogen and PTH not just have opposite effects on bone, estrogen also prevents 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?


To co-regulate blood-calcium level, and secondary, bone-calcium contents. Too much or too little calcium in the blood is lethal, and to little or too much calcium in the bones is unwelcome too. Our bones are constructed according to a genetic plan, and since holding more calcium than is the optimum amount is not beneficial, excessive calcium eventually has to be deported. And thus also hormones that stimulate deportation of calcium from the bones are required.


To deport calcium from the bones, PTH collaborates with calcitriol. PTH stimulates secretion of calcitriol, which hormone also both increases uptake of calcium into the bones (11) and subsequent deportation of calcium from the bones.


The difference between those 2 hormones is that calcitriol (which is composed of vit. D) also increases absorption of calcium from food, and that the effects of PTH on bone is stronger and that PTH also increases excretion of calcium into urine.

While PTH increases secretion of calcitriol, calcitriol inhibits secretion of PTH. (see Calcium Hormones)


But in hyperparathyroidism, calcitriol level is low.



Why is calcitriol level low in hyperparathyroidism?


Besides due to a lack of calcitriol, PTH level can be elevated for various reasons (due to a thyroid malfunction, a tumor or a lack of estrogen for example). If PTH is not elevated due to a lack of calcitriol, calcitriol level has to be decreased anyway. If not, the combined influence of PTH and calcitriol would cause far too much calcium to be deported from the bones.

And if calcitriol level is normal, also uptake of dietary calcium is not diminished, which would further enhance fractional calcium absorption and subsequent deportation, further enhancing osteoporosis.


Abstracts of most sources can be found at The National Library of Medicine


(1) Miller MA, Disparate effects of mild, moderate, and severe secondary hyperparathyroidism on cancellous and cortical bone in rats with chronic renal insufficiency. Bone1998 / 23 (3) / 257-266.

(2) Kosowicz J, et al, [Bone mineral density in primary hyperparathyroidism]. [Article in Polish] Pol. Arch. Med. Wewn. 1999 / 101 (2) / 131-138.

(3) Mazzuoli GF, et al, Primary hyperparathyroidism and osteoporosis. Aging (Milano)1998 / 10 (3) / 225-231.

(4) Kroll MH, Parathyroid hormone temporal effects on bone formation and resorption. Bull. Math. Biol. 2000 / 62 (1) / 163-188. , Chevalley T, et al, [Bone and hormones. Effects of parathyroid hormone on the bone]. [Article in French] Presse Med.1999 / 28 (10) / 547-553.

(5) Stanislaus D, In vivo regulation of apoptosis in metaphyseal trabecular bone of young rats by synthetic human parathyroid hormone (1-34) fragment. Bone 2000 / 27 (2) / 209-218.

(6) Zittermann A, et al, Physiologic fluctuations of serum estradiol levels influence biochemical markers of bone resorption in young women. J Clin Endocrinol Metab 2000 / 85 (1) / 95-101. , Riggs BL, et al, A unitary model for involutional osteoporosis: estrogen deficiency causes both type I and type II osteoporosis in postmenopausal women and contributes to bone loss in aging men. J. Bone Miner. Res. 1998 / 13 (5) / 763-773.

(7) Masiukiewicz US, et al, The role of parathyroid hormone in the pathogenesis, prevention and treatment of postmenopausal osteoporosis. Aging (Milano) 1998 / 10 (3) / 232-239.

(8) Orr-Walker BJ, et al, Effects of hormone replacement therapy on bone mineral density in postmenopausal women with primary hyperparathyroidism: four-year follow-up and comparison with healthy postmenopausal women. Arch. Intern. Med.2000 / 160 (14) / 2161-2166. , Diamond T, et al, Estrogen replacement may be an alternative to parathyroid surgery for the treatment of osteoporosis in elderly postmenopausal women presenting with primary hyperparathyroidism: a preliminary report. Osteoporos. Int.1996 / 6 (4) / 329-333.

(9) Erlichman M, et al, Bone densitometry: patients with asymptomatic primary hyperparathyroidism part I. Technical report. Health Technol. Assess. (Rockv.) 1995 / (6) / 1-30.

(10) Sairanen S, et al, Bone mass and markers of bone and calcium metabolism in postmenopausal women treated with 1,25-dihydroxyvitamin D (Calcitriol) for four years. Calcif. Tissue Int. 2000 / 67 (2) / 122-127.

(11) Erben RG, et al, Therapeutic efficacy of 1alpha,25-dihydroxyvitamin D3 and calcium in osteopenic ovariectomized rats: evidence for a direct anabolic effect of 1alpha,25-dihydroxyvitamin D3 on bone. Endocrinology1998 / 139 (10) / 4319-4328.



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