Serum from Postmenopausal Women Causes Adipocyte Differentiation of Osteoprogenitor Cells

It has been suggested that osteoporosis may be a risk factor for periodontal disease, but a conclusive relationship between these two disorders remains to be resolved. Following menopause the porosity of mandibular cortical bone, and alveolar bone in particular, increases markedly. Oestrogen deficiency causes accelerated bone loss through enhanced bone remodelling whereby bone resorption exceeds new bone formation during each bone remodelling cycle. However, the molecular and cellular mechanism(s) underlying post-menopausal bone loss remain to be elucidated. Understanding those mechanism(s) may help clarify the role of osteoporosis in the etiology of periodontal disease. OBJECTIVES: Since serum factors are known to influence the differentiation of marrow cells we wished to determine whether pre- and post-menopausal serum had differing effects on osteoprogenitor cell differentiation. METHODS: The human adipocytic/osteoblastic clonal cell line, hOP-7, was incubated with 10% foetal bovine serum (FBS), 10% rabbit serum (RS - known inducer of marrow cell adipocytogenesis), or 10% pre- or post-menopausal human serum. After 4-7 days, cells were fixed and stained for lipids with Oil Red O. mRNA analyses were also performed to determine the expression of adipocyte markers lipoprotein lipase (LPL) and glycerol phosphate 3-hydrogenase (GPD). RESULTS: As expected, RS induced adipocytogenesis of hOP-7 cells as determined by increased Oil Red O cell staining, and LPL and GDP expression. Little or no adipocytogenesis occurred in hOP-7 cells incubated with FBS, or pre-menopausal serum. However, in contrast, a highly significant (p<0.01) increase in adipocytogenesis was seen in hOP-7 cells incubated with post-menopausal serum. CONCLUSIONS: Factors in post-menopausal serum are capable of inducing adipocytic differentiation of hOP-7 cells. Changes to the regulation of marrow osteoprogenitor cell differentiation should therefore be considered as a pathologic mechanism for limiting new bone formation during post-menopausal bone remodelling, and in influencing the rate of alveolar bone loss that leads to periodontal disease.