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Combined Effects of Caffeine and Prostaglandin E 2 on the Proliferation of Osteoblast‐Like Cells (UMR106‐01)
Author(s) -
KamagataKiyoura Yusuke,
Ohta Mitsuhiro,
Cheuk Gina,
Yazdani Malektaj,
Saltzman Marty J.,
Nakamoto Tetsuo
Publication year - 1999
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1999.70.3.283
Subject(s) - caffeine , forskolin , prostaglandin e , prostaglandin e2 , cell growth , chemistry , ibmx , osteoblast , prostaglandin , in vitro , endocrinology , in vivo , endogeny , pharmacology , inhibitory postsynaptic potential , intracellular , medicine , biochemistry , biology , microbiology and biotechnology
Background: The general public widely consumes caffeine (1,3,7‐trimethylxanthine), which is contained in various foods, beverages and over‐the‐counter medications. We have shown previously that caffeine intake could affect bone metabolism in vivo. Methods: Because prostaglandin E 2 (PGE 2 ) is shown to be elevated in the periodontally diseased site, the possible interaction between caffeine and PGE 2 was investigated in the present study using UMR106‐01 rat osteoblast‐like cells in vitro. Results: Although neither 0.1 mM caffeine nor 0.1 µg/ml of PGE 2 alone showed any inhibitory effects on cell proliferation, the combination of caffeine and PGE 2 showed significant inhibition. However, in order to have inhibitory effects, both caffeine and PGE 2 had to be present at least 72 or 96 hours in the medium. Addition of the endogenous PGE 2 synthesis inhibitor, indomethacin, showed no effects on cell proliferation. Neither cAMP‐inducing agent IBMX (0.01 mM and 0.1 mM) nor forskolin (0.001 mM) inhibited cell proliferation, but combined with PGE 2 these agents strongly inhibited proliferation as was observed with the combination of caffeine and PGE 2 suggesting possibly that the increase of intracellular cAMP concentration plays an important role in the inhibitory effects of cell proliferation. Conclusions: The present data for the first time demonstrate possible implication of routine caffeine intake in the acceleration of pathological conditions of periodontitis. Thus, we propose that chronic caffeine intake is one of the possible risk factors in the advancement of pathology in the periodontitis patient. Further research in this area is warranted. J Periodontol 1999;70:283‐288.