Short-term course of 1,25(OH)2D3 stimulates osteoblasts but not osteoclasts in osteoporosis and osteoarthritis

Abstract

We investigated the effect of short-term, 1,25-dihydroxyvitamin D3 therapy (4 micrograms/day for 4 days) on calcium metabolism in 27 postmenopausal women (11 cases with osteoporosis and 16 cases with osteoarthritis). Bone mass at the axial and appendicular skeleton was higher in osteoarthritis than in osteoporosis. Initial values of calcium metabolism were similar. Osteoporotic and osteoarthritic patients responded with a similar significant increase in serum osteocalcin (+61% and +54%, respectively), fasting urinary calcium excretion (+178% and +124%, respectively) and 24 hour calcium excretion (+148% and +142%, respectively). Parathyroid hormone (PTH) levels decreased significantly in both groups (-30% and -18%, respectively). Osteoclastic bone resorption, evaluated by urinary hydroxyproline excretion, was not stimulated in either group. We conclude that in osteoporosis and also in osteoarthritis (1) 1,25-dihydroxy-vitamin D3 (1,25(OH)2D3) stimulation of osteoblast function is similar in production of osteocalcin; (2) the vitamin D target tissues react adequately to 1,25(OH)2D3 stimulation; (3) short-term high dose of 1,25(OH)2D3 does not stimulate bone resorption; and (4) the differences in bone mass between osteoarthritis and osteoporosis are not related to an alteration of the responsiveness to stimulation by 1,25 (OH)2D3.

Bone mineral density loss during adjuvant chemotherapy in pre-menopausal women with early breast cancer: is it dependent on oestrogen deficiency?

“…Long-term use of oral glucocorticoids is known to induce loss of BMD, and there is evidence that short-term use suppresses bone formation at least in men, as shown in a study of prednisolone 20mg daily for 7 days [24], where osteocalcin and PICP were reduced by 35% and 26% respectively compared with a placebo group though, interestingly, this study found no change in Bone-ALP. Also there was no change in bone resorption (as measured by CTX) in the prednisolone-treated group, in agreement with other studies which showed no change in osteoclasts activity on exposure to corticosteroids [25,26].…”

The Role of Calcitriol in the Treatment of Osteoporosis

“…Moreover, a complex array of interactions between the "calciotropic" hormones family, which characterize senescence, is further exemplified by the fact that age-related increases in PTH production are less likely to be suppressed by low circulatory 1,25(OH) 2 D 3 and that defective 1,25(OH) 2 D 3 synthesis by the aging kidney increases the skeletal response to both gonadal hormone deficiency and PTH excess [10,11]. Finally, increments in serum osteocalcin levels observed in humans treated with 1,25(OH) 2 D 3 , and animal studies demonstrating an increased number of bone marrow osteoblast precursors during 1,25(OH) 2 D 3 administration are consistent with the hypothesis that abnormalities in the production and skeletal distribution of 1,25(OH) 2 D 3 must also contribute to the defects in osteoblast function and bone formation observed histologically in both humans and experimental animal models with osteoporotic syndromes [12][13][14][15][16]. …”

Generalized osteoarthritis associated with increased insulin‐like growth factor types i and ii and transforming growth factor β in cortical bone from the iliac crest. possible mechanism of increased bone density and protection against osteoporosis

“…Since neither of these two growth factors is under the direct influence of growth hormone, it does not seem likely that the elevated growth hormone level can be the entire explanation for the greater bone density in this disease compared with osteoporosis. Dynamic tests to elucidate hormone reserves did not disclose any differences in responsiveness to pharmacologic doses of 1,25-dihydroxyvitamin D3 (12), calcitonin (43), or insulin (11).…”