Combined effects of caffeine and prostaglandin E-2 on the proliferation ofosteoblast-like cells (UMR106-01)

Citation
Y. Kamagata-kiyoura et al., Combined effects of caffeine and prostaglandin E-2 on the proliferation ofosteoblast-like cells (UMR106-01), J PERIODONT, 70(3), 1999, pp. 283-288
Citations number
31
Categorie Soggetti
Dentistry/Oral Surgery & Medicine","da verificare
Journal title
JOURNAL OF PERIODONTOLOGY
ISSN journal
00223492 → ACNP
Volume
70
Issue
3
Year of publication
1999
Pages
283 - 288
Database
ISI
SICI code
0022-3492(199903)70:3<283:CEOCAP>2.0.ZU;2-N
Abstract
Background: The general public widely consumes caffeine (1,3,7-trimethylxan thine), which is contained in various foods, beverages and over-the-counter medications. We have shown previously that caffeine intake could affect bo ne 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 mu g/ml of PGE(2) alone s howed any inhibitory effects on cell proliferation, the combination of caff eine and PGE2 showed significant inhibition. However, in order to have inhi bitory effects, both caffeine and PGE(2) had to be present at least 72 or 9 6 hours in the medium. Addition of the endogenous PGE(2) synthesis inhibito r, indomethacin, showed no effects on cell proliferation. Neither cAMP-indu cing agent IBMX (0.01 mM and 0.1 mM) nor forskolin (0.001 mM) inhibited cel l proliferation, but combined with PGE(2) these agents strongly inhibited p roliferation as was observed with the combination of caffeine and PGE(2), s uggesting possibly that the increase of intracellular cAMP concentration pl ays an important role in the inhibitory effects of cell proliferation. Conclusions: The present data for the first time demonstrate the possible i mplication of routine caffeine intake in the acceleration of pathological c onditions of periodontitis. Thus, we propose that chronic caffeine intake i s one of the possible risk factors in the advancement of pathology in the p eriodontitis patient. Further research in this area is warranted.