THERE IS NO DIFFERENCE IN SPONTANEOUS AND 17-BETA-ESTRADIOL-INDUCED INTERLEUKIN-1-BETA RELEASE BY PERIPHERAL-BLOOD MONONUCLEAR-CELLS FROM NONOSTEOPOROTIC WOMEN WITH DIFFERENT RATES OF EARLY POSTMENOPAUSAL BONELOSS
Akm. Hogasen et al., THERE IS NO DIFFERENCE IN SPONTANEOUS AND 17-BETA-ESTRADIOL-INDUCED INTERLEUKIN-1-BETA RELEASE BY PERIPHERAL-BLOOD MONONUCLEAR-CELLS FROM NONOSTEOPOROTIC WOMEN WITH DIFFERENT RATES OF EARLY POSTMENOPAUSAL BONELOSS, The Journal of clinical endocrinology and metabolism, 80(8), 1995, pp. 2480-2484
Interleukin-1 (IL-1, is a potent stimulator of bone resorption, and a
causal role for IL-1 has been suggested in postmenopausal bone loss. W
e have examined IL-1 beta release in vitro by peripheral blood mononuc
lear cells (PBMC) isolated from nonosteoporotic women 9-15 yr after me
nopause. These women had presented 6 yr previously with significant di
fferences in the rate of early postmenopausal bone loss. Ten women wit
h low rates of bone loss (median 2.0% per year) and 10 women with high
rates of bone loss (median 4.9% per year) were included in the study.
The women with a high rate of bone loss had a significantly lower bon
e mass of the lumbar vertebrae compared with that of the other group,
but there were no differences in biochemical markers of bone metabolis
m between the groups (pyridinoline/creatinine ratio in urine and colla
gen 1 c-terminal telopeptide and bone gla protein in serum). Moreover,
there was no difference in spontaneous IL-1 beta release by PBMCs bet
ween the two groups and no correlation between IL-1 beta release and p
resent bone turnover, as judged by biochemical markers. Treatment of P
BMCs with 10 nmol/L 17 beta-estradiol in vitro significantly stimulate
d IL-1 beta production in both groups. We conclude that IL-1 beta prod
uction by PBMCs in vitro does not correlate with the rate of early pos
tmenopausal bone loss.