TY - JOUR
T1 - Alcohol-induced bone disease
T2 - Impact of ethanol on osteoblast proliferation
AU - Klein, Robert F.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1997
Y1 - 1997
N2 - The habitual consumption of even moderate quantities of alcohol (1 to 2 drinks/day) is clearly linked with reduced bone mass (osteopenia). Biochemical and histological evaluation of patients with alcoholic bone disease reveal a marked impairment in bone formation in the face of relatively normal bone resorption. Experiments using well-defined osteoblastic model systems indicate that the observed reductions in bone formation result from a direct, antiproliferative effect of ethanol on the osteoblast itself. As bone remodeling and mineralization are dependent on osteoblasts, it follows that the deleterious effect of alcohol on these cells would result in slowed bone formation, aberrant remodeling of skeletal tissue and, ultimately, osteopenia and fractures. The skeletal consequences of alcohol intake during adolescence, when the rapid skeletal growth ultimately responsible for achieving peak bone mass is occurring, may be especially harmful. The specific subcellular mechanisms whereby ethanol inhibits cell proliferation are, as yet, unknown. During the last few years, attention has shifted from nonspecific membrane perturbation effects to actions on certain signaling proteins. Specifically, there is increasing evidence that ethanol may exert significant effects on transmembrane signal transduction processes that constitute major branches of cellular control mechanisms. At present, abstinence is the only effective therapy for alcohol-induced bone disease. An improved understanding of the pathogenesis of alcohol-induced bone disease may eventually result in alternative therapeutic avenues for those who are unable to abstain.
AB - The habitual consumption of even moderate quantities of alcohol (1 to 2 drinks/day) is clearly linked with reduced bone mass (osteopenia). Biochemical and histological evaluation of patients with alcoholic bone disease reveal a marked impairment in bone formation in the face of relatively normal bone resorption. Experiments using well-defined osteoblastic model systems indicate that the observed reductions in bone formation result from a direct, antiproliferative effect of ethanol on the osteoblast itself. As bone remodeling and mineralization are dependent on osteoblasts, it follows that the deleterious effect of alcohol on these cells would result in slowed bone formation, aberrant remodeling of skeletal tissue and, ultimately, osteopenia and fractures. The skeletal consequences of alcohol intake during adolescence, when the rapid skeletal growth ultimately responsible for achieving peak bone mass is occurring, may be especially harmful. The specific subcellular mechanisms whereby ethanol inhibits cell proliferation are, as yet, unknown. During the last few years, attention has shifted from nonspecific membrane perturbation effects to actions on certain signaling proteins. Specifically, there is increasing evidence that ethanol may exert significant effects on transmembrane signal transduction processes that constitute major branches of cellular control mechanisms. At present, abstinence is the only effective therapy for alcohol-induced bone disease. An improved understanding of the pathogenesis of alcohol-induced bone disease may eventually result in alternative therapeutic avenues for those who are unable to abstain.
KW - Alcohol
KW - Ethanol
KW - Osteoblast
KW - Osteoporosis
KW - Proliferation
UR - http://www.scopus.com/inward/record.url?scp=0030916963&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030916963&partnerID=8YFLogxK
U2 - 10.1111/j.1530-0277.1997.tb03781.x
DO - 10.1111/j.1530-0277.1997.tb03781.x
M3 - Article
C2 - 9161596
AN - SCOPUS:0030916963
SN - 0145-6008
VL - 21
SP - 392
EP - 399
JO - Alcoholism: Clinical and Experimental Research
JF - Alcoholism: Clinical and Experimental Research
IS - 3
ER -