Although the mechanism of bone resorption induced by estrogen deficiency is still controversial, recent studies have suggested that estrogen may modulate the secretion of bone resorption cytokines that are produced in the bone microenvironment
and
influence bone remodeling. Among them, IL-1 promotes bone resorption by stimulating the activity of mature osteoclasts and the differentiation of osteoclast precursors and the production of cytokines are mediated by estrogen. The purpose of the
this
study was to evaluate the effect of ovariectomy on bone mineral density and levels of IL-1 in the culture media of bone marrow and peripheral blood monocytes.
The experimental animals were 16 female Sprague-Dawley rats that were 8 weeks of age and weighed an average of 186.8gm at the beginning of the study. Bilateral ovariectomy was performed from a vental approach in all rats. Bone mineral
density(BMD)
of
the total body and IL-1 levels in culture media of bone marrow and peripheral blood monocytes were measured before and 8 weeks after ovariectomy with DPX-L and ELISA assay, respectively. Serum levels of LH, FSH and E were measured by RIA assay.
BMD of total body was lower after ovariectomy(0.24±0.04 g/cm2) than before ovariectomy (0.27±0.03g/cm2)(p<0.05). Serum levels of LH, FSH were higher after ovariectomy(0.87±0.36 mIU/ml, 9.47±1.26 mIU/ml) than before ovariectomy(0.10±0.06
mIU/ml,
2.09±0.41 mIU/ml)(p<0.01) and serum level of E2 was lower after ovariectomy(10.98±8.71pg/ml) than before ovariectomy(7350.77±417.29 pg/ml)(o.o1), respectively. Levels of IL-1 in culture media of bone marrow monocytes were higher after
ovariectomy(25.47±3.54 pg/ml) than before ovariectomy(9.83±1.10 pg/ml)(p<0.01), but there were no statistically significant differences in culture media of the peripheral blood monocytes(before ovariectomy: 10.59±1.03 pg/ml ; after
ovariectomy:
11.17±1.29 pg/ml)
It is possible that the increased production of IL-1 in estrogen deficiency induced by ovariectomy occurs in the bone microenvironment and this cytokine may play a critical role in inducing bone loss.
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