Dexamethasone enhances the effects of parathyroid hormone on human periodontal ligament cells in vitro

Abstract

Periodontal ligament cells (PDL) are thought to play a major role in promoting periodontal regeneration. Recent studies, focused on characterizing PDL cells, have been directed at establishing their osteoblast-like properties and determining biological mediators and/or factors that induce osteoblastic cell populations in the PDL. The glucocorticoid, dexamethasone (Dex), has been shown to selectively stimulate osteoprogenitor cell proliferation and to induce osteoblastic cell differentiation in many cell systems. In the present study the ability of Dex to modulate parathyroid hormone (PTH)-stimulated cAMP synthesis in cultured human PDL cells was examined. PDL cells, obtained from premolar teeth extracted for orthodontic reasons, were cultured with Dex (0–1000 nM) for 7 days prior to PTH (1–34) stimulation. The exposure of PDL cells to Dex resulted in a dose-dependent increase in cAMP production in response to PTH stimulation. This response was seen in cells obtained from three different patients. The first significant Dex effect was seen on day 7 when compared to day 1 for 100 nM Dex. PTH (1–34) stimulation caused a dose-dependent increase in cAMP synthesis after Dex (1000 nM) treatment for 7 days. Conversely, stimulation of the cells with PTH (7–34) (0–1000 nM) did not increase cAMP production in PDL cells after Dex treatment. Forskolin- (1 μM) and isoproterenol- (1 μM) stimulated cAMP synthesis was not augmented by Dex treatment. Dex treatment did not alter calcitonin-(1 μM) stimulated cAMP production in PDL cells. Glucocorticoid enhancement of PTH-stimulated cAMP synthesis in these cells supports the presence of an osteoblast-like population in the PDL, in vitro .