Strontium causes osteomalacia in chronic renal failure rats

Abstract

These findings indicate that Sr accumulation in chronic renal failure rats resulted in the development of osteomalacic lesions, in contrast to the Al group where adynamic bone disease was induced in the present set-up. Further studies are required to define the mechanism by which way Sr causes osteomalacia in chronic renal failure rats.

Strontium and Bone

“…This pathology, characterized by a decreased mineralization in the absence of an increased osteoid, suggests an effect of aluminum on osteoblast activity rather than on mineralization. (27) These findings are in line with studies performed in rats with normal renal function, where aluminum administration led to a decrease in bone and matrix formation, which was not accompanied by an increase in osteoid. (61,62) It should be mentioned, however, that others in both experimental and in vitro studies have reported opposite results, i.e., found aluminum to stimulate bone formation.…”

“…(36) We were the first to demonstrate that intermediate doses of strontium (3 g/l as SrCl 2 и6H 2 O in the drinking water) can induce osteomalacia in chronic renal failure rats, as evidenced by increased osteoid in combination with reduced bone mineralization. (27) This appears to be in contrast with the positive effects of low doses of strontium administered to rats with normal renal function. In this context, the similarities of strontium with fluor in the development of a mineralization defect are worth mentioning.…”

“…Recently, by means of electron probe X-ray microanalysis (EPXMA) of bone of renal failure rats loaded with strontium, Schrooten et al found the element to be present in calcified bone in close proximity to the mineralization front. (27) Blood is the second most important bodily location of strontium. Data in the literature on normal serum strontium levels in subjects with intact renal function vary between 10 g/l and 217 g/l and greatly depend on the analytical technique used.…”

“…(59) These findings are more or less in line with another experimental study where in rats with chronic renal failure high doses of fluoride (50 mg/kg) caused osteomalacia, as evidenced by an increase in osteoid parameters and diminished bone strength. (60) Recently, Schrooten et al in a chronic renal failure rat model (27) studied the effects of both strontium and aluminum on bone. Whereas daily dietary loading of strontium (3 g/l in the drinking water) resulted in the development of osteomalacia, those receiving aluminum at a daily oral dose of Al (10 mg Al(OH) 3 /10 g of rat chow + 10 mg/l as AlCl 3 to the drinking water) developed adynamic bone disease.…”

“…(29) In an experimental study using the "remnant kidney model," oral strontium loading resulted in histologic bone lesions characterized by an increased amount of osteoid in the presence of a decreased mineralization rate, indicating the presence of osteomalacia and pointing toward a causal role of the element in the development of this particular type of renal osteodystrophy. (27) A direct effect of strontium on bone mineralization may be suggested from the element's localization in bone. Indeed, histochemically, strontium could be localized in calcified bone, mainly in new bone close to the osteoid/ calcification front, a critical site of bone mineralization.…”