The calcium antagonist diltiazem inhibits calcification enhanced by calcitonin in growth cartilage of rats in ethane-1-hydroxy-1,1-diphosphonate (EHDP)-induced rickets

After division of the tendo achilles in rats heterotopic bone forms in the muscle and in the tendon stumps. Tenotomy was performed in 26 male rats. Thirteen received Verapamil (36 mm/Kg) for six days per week for five months, and the remainder were not given this drug. The onset of heterotopic ossification was monitored by monthly x-rays. After five months the animals were killed and the sectioned tendons examined microscopically. The radiographs had shown that the amount of ossification was less in rats treated with Verapamil. This was confirmed at microscopy, but examination of the sections under polarised light showed that the ratio of lamellar to woven bone was the same in the two groups. Verapamil appeared to reduce the amount of heterotopic bone formation but did not influence the substitution of woven by lamellar bone.

Section: Introductionunclassified

Effet d'un inhibiteur calcique, le v�rapamil, sur le d�veloppement des ossifications h�t�rotopiques

Duriez

Flautre

Blary

et al. 1990

A comparative study of the calcification-promoting action of 1,25 (OH)2D3 and calcitonin on the growth cartilage of rats with 1-hydroxyethylidene-1, 1-biphosphonic acid (HEBP)-induced rickets

Eguchi

Shibata

Wada

et al. 1987

When HEBP (1-hydroxyethylidene-1, 1-biphosphonic acid) was administered to young rats in large doses over a short period rickets was consistently produced. When HEBP was administered concomitantly with 1,25 (OH)2D3 or calcitonin (CT), calcification appeared in the growth-plate cartilage where there had been an increase in thickness due to the inhibition of calcification. This experiment was done in an attempt to clarify differences in the calcification-promoting mechanisms of 1,25 (OH)2D3 and CT. The serum alkaline phosphatase level was reduced in rats with an accelerated calcification following the administration of 1,25 (OH)2D3, but there was no reduction in the serum alkaline phosphatase level in rats in which the calcification was accelerated by the administration of CT. The mode of appearance of calcification in the growth-plate cartilage by 1,25 (OH)2D3 or CT differed, depending on the time of administration. These results suggest that mechanisms involved in the enhancement of calcification by 1,25 (OH)2D3 and CT differ in cases where rickets are induced by HEBP.

Promotion of calcification by imidazole and its suppression by diltiazem in the growth cartilage of rats with HEBP induced rickets

Eguchi

Kawamura

Wada

et al. 1989

The object of our experiments was to determine the effect of imidazole on the growth cartilage of rats with HEBP induced rickets. When HEBP (1-hydroxyethylidene-1, 1-bisphophonic acid) was given to young rats in large doses over a short period, rickets was consistently produced. We found that imidazole had a calcification promoting action in the growth plate cartilage where there had been an increase in thickness due to the inhibition of calcification. In an attempt to clarify the mechanism of accelerated calcification due to imidazole, the effects of diltiazem, a calcium antagonist, were observed; it was found to suppress the accelerated calcification. If diltiazem inhibits the entry of calcium ions into the cells of the growth cartilage, as it does in smooth muscle and myocardial cells, then our results indicate that intracellular concentrations of calcium may play an important role in the accelerated calcification due to imidazole.