Animal studies, experimental models on cell lines, and epidemiological case
-control studies have all suggested the possibility that 3-hydroxy-3-methyl
glutaryl coenzyme A reductase inhibitors have a beneficial effect on bone m
etabolism. However, all epidemiological studies are not prospective in natu
re and based on either measurement of bone mineral density or fracture risk
. They also differ in recruitment criteria, definition of statin exposure,
and outcome assessment. We performed a first prospective study using specif
ic biochemical bone markers on 17 hypercholesterolaemic non-osteoporotic su
bjects treated with a therapeutic dose of simvastatin 20 mg daily for 4 wee
ks. Our results show that serum osteocalcin concentration increased signifi
cantly (p-value < 0.05) 4 weeks after therapy, whereas other bone markers i
ncluding serum bone-specific alkaline phosphatase activity, urine deoxypyri
dinoline, and urine cross-linked N-telopeptides of type I Collagen did not
show any significant changes. Our data support that simvastatin causes a be
neficial effect on bone metabolism as reflected by an increase in serum ost
eocalcin concentration. This added beneficial effect of statins on bone met
abolism could potentially allow statins to become the first effective anabo
lic agent for the treatment of osteoporosis. We urge that priority should b
e given to a randomised controlled study to re-evaluate this group of drugs
.