Abstract
Aims: Compelling evidences suggest that increased production of osteoclastogenic cytokines by activated T cells plays a relevant role in the bone loss induced by estrogen (E) deficiency in the mouse. However, little information is available on the role of T cells in post-menopausal bone loss in humans.
Methods: To investigate this issue we have assessed the production of cytokines involved in osteoclasts (OCs) formation (RANKL, TNFα and OPG), in vitro Ocs formation in pre and postmenopausal women, the latter with or without osteoporosis. We also evaluate OC precursors in peripheral blood and the ability of peripheral blood mononuclear cells to produce TNFα in both basal and stimulated condition by flow cytometry in these subjects.
Results: Our data demonstrate that E enhances the production of the pro-osteoclastogenetic cytokines TNF alpha and RANKL and increases the number of circulating OCs precursors. Furthermore we show that T cells and monocytes from women with osteoporosis exhibit a higher production of TNF α then those from the other two groups.
Conclusions: Our findings suggest that E deficiency stimulates OCs formation both by increasing the production of TNF and RANKL and increasing the number of OCs precursors. Women with postmenopausal osteoporosis have a higher T cells activity than healthy postmenopausal subjects, T cells thus contribute to the bone loss induced by E deficiency in humans as they do in the mouse.
The abstracts were prepared by incoming Professor Elena Brach del Prever. Correspondence should be addressed to IORS – President office, Dipartimento di Traumatologia, Ortopedia e Mediciana del Lavoro, Centro Traumatologico Ortopedico - Via Zuretti, 29 I-10135 Torino, Italy.
