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1 Oral and Maxillofacial Surgery, Eastman Dental Institute, London WC1X 8LD; and 2 Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, United Kingdom
We examined the effects of
HCO3
and CO2 acidosis on
osteoclast-mediated Ca2+ release from 3-day cultures of
neonatal mouse calvaria. Ca2+ release was minimal above pH
7.2 in control cultures but was stimulated strongly by the addition of
small amounts of H+ to culture medium
(HCO3 acidosis). For example, addition of 4 meq/l
H+ reduced pH from 7.12 to 7.03 and increased
Ca2+ release 3.8-fold. The largest stimulatory effects (8- to 11-fold), observed with 15-16 meq/l added H+, were
comparable to the maximal Ca2+ release elicited by
1,25-dihydroxyvitamin D3
[1,25(OH)2D3; 10 nM], parathyroid hormone (10 nM), or prostaglandin E2 (1 µM); the action of these
osteolytic agents was attenuated strongly when ambient pH was increased
from ~7.1 to ~7.3. CO2 acidosis was a less effective
stimulator of Ca2+ release than HCO3
acidosis over a similar pH range. Ca2+ release stimulated
by HCO3 acidosis was almost completely blocked by
salmon calcitonin (20 ng/ml), implying osteoclast involvement. In whole
mount preparations of control half-calvaria, ~400 inactive
osteoclast-like multinucleate cells were present; in calvaria exposed
to HCO3 acidosis and to the other osteolytic agents
studied, extensive osteoclastic resorption, with perforation of bones,
was visible. HCO3 acidosis, however, reduced numbers
of osteoclast-like cells by ~50%, whereas
1,25(OH)2D3 treatment caused increases of
~75%. The results suggest that HCO3 acidosis
stimulates resorption by activating mature osteoclasts already present
in calvarial bones, rather than by inducing formation of new
osteoclasts, and provide further support for the critical role of
acid-base balance in controlling osteoclast function.
calcium release; carbon dioxide; bicarbonate ion; acid-base balance; osteolysis
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