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Journal of Dental Research
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Biological

Modulation of Gingival Fibroblast Minocycline Accumulation by Biological Mediators

J.D. Walters*, R.J. Nakkula and P. Maney

Section of Periodontology, College of Dentistry, The Ohio State University Health Sciences Center, 305 West 12th Avenue, PO Box 182357, Columbus, OH 43218-2357, USA;

Correspondence: * walters.2{at}osu.edu

Gingival fibroblasts actively accumulate tetracyclines, thereby enhancing their redistribution from blood to gingiva. Since growth factors and pro-inflammatory cytokines regulate many fibroblast activities, they could potentially enhance fibroblast minocycline accumulation. To test this hypothesis, we treated gingival fibroblast monolayers for 1 or 6 hours with platelet-derived growth factor-BB (PDGF), fibroblast growth factor-2 (FGF), transforming growth factor-β1 (TGF), or tumor necrosis factor-{alpha} (TNF). Minocycline uptake was assayed at 37° by a fluorescence method. All 4 factors significantly enhanced minocycline uptake (P ≤ 0.008, ANOVA), primarily by increasing the affinity of transport. Treatment for 6 hours with 10 ng/mL FGF, PDGF, TGF, or TNF enhanced fibroblast minocycline uptake by 19% to 25%. Phorbol myristate acetate enhanced fibroblast minocycline uptake by 28%, suggesting that protein kinase C plays a role in up-regulating transport. These effects on transport provide a mechanism by which systemic tetracyclines could be preferentially distributed to gingival wound or inflammatory sites.

Key Words: tetracyclines • antimicrobial chemotherapy • aggressive periodontitis • matrix metalloproteinases

Journal of Dental Research, Vol. 84, No. 4, 320-323 (2005)
DOI: 10.1177/154405910508400405
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