Aluminum alters calcium influx and efflux from bone in vitro

Aluminum alters calcium influx and efflux from bone in vitro. Aluminum retention can cause osteomalacia and adynamic lesions of bone in patients undergoing long-term dialysis. It is not known, however, whether aluminum inhibits the mineralization of bone directly or whether alterations in osteoblastic function mediate this response. To examine this issue, the uptake of 45Ca by 14-day embryonic chick calvaria was measured in vitro. Comparative studies were done in living and devitalized tissues to evaluate the role of bone cells in aluminum-related changes in 45Ca uptake. Aluminum was added to serum-free media as the citrate complex, and paired hemicalvaria maintained in equimolar sodium citrate served as controls. Aluminum citrate decreased the uptake of 45Ca into bone during 24 hour incubations to 76 ± 3% and 38 ± 2% (x ± SD) of control values at 10 µM and 100 µM aluminum, respectively. No change in 45Ca uptake was observed at the end of four hour incubations with 100 µM aluminum citrate, whereas 45Ca uptake decreased from 356 ± 48 to 266 ± 36 cpm/µg bone, P < 0.05, at eight hours and from 327 ± 22 to 269 ± 41 cpm/µg bone, P < 0.05, at 24 hours. The inhibitory effects of 10 µM and 100 µM aluminum on 45Ca uptake were eliminated, however, in devitalized tissues, and reductions in 45Ca uptake during incubations with aluminum were markedly attenuated by lowering the media phosphorus level from 4.0mM to 2.0mM. In separate studies, both 10 µM and 100 µM aluminum increased 45Ca release from live calvaria by 62 ± 6% and 73 ± 4%, respectively, during 24 hour incubations; this response was only partially blunted in devitalized bones. The results suggest that bone cells participate in aluminum-induced reductions in tissue calcification in vitro. Aluminum may also enhance calcium mobilization from bone by a cell-independent mechanism