Differential effects of prostaglandin E2 and enamel matrix derivative on the proliferation of human gingival and dermal fibroblasts and gingival keratinocytes |
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| Authors: | E Weinberg M Topaz M Dard P Lyngstadaas C Nemcovsky M Weinreb |
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| Institution: | 1. Department of Oral Biology, the Maurice and Gabriela Goldschleger School of Dental Medicine, Tel‐Aviv University, Tel‐Aviv, Israel;2. Plastic Surgery Unit, Hillel Yaffe Medical Center, Hadera, Israel;3. Preclinical Research, Institut Straumann, Basel, Switzerland;4. Department of Biomaterials, Faculty of Dentistry, University of Oslo, Oslo, Norway;5. Department of Periodontology, the Maurice and Gabriela Goldschleger School of Dental Medicine, Tel‐Aviv University, Tel‐Aviv, Israel |
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| Abstract: | Weinberg E, Topaz M, Dard M, Lyngstadaas P, Nemcovsky C, Weinreb M. Differential effects of prostaglandin E 2 and enamel matrix derivative on the proliferation of human gingival and dermal fibroblasts and gingival keratinocytes. J Periodont Res 2010; 45: 731–740. © 2010 John Wiley & Sons A/S Background and Objective: Elevated levels of prostaglandins contribute to periodontal destruction but can impair gingival healing by affecting local fibroblasts. Enamel matrix derivative (EMD) has beneficial effects on supporting and gingival tissues. We showed that prostaglandin E2 (PGE2) inhibits the proliferation of human gingival fibroblasts (hGFs) and that EMD stimulates it. Prostaglandins and EMD may also affect skin healing by targeting dermal fibroblasts (DFs). Thus, we compared the effects of these two agents on the proliferation of hGFs, human gingival keratinocytes (hGKs) and hDFs. Material and Methods: Cells from healthy human gingiva or skin were treated with PGE2 and/or EMD, and proliferation was assessed by measuring cell number and DNA synthesis. Results: In hGFs, PGE2 (1 μm ) inhibited proliferation while EMD stimulated it. When present together, EMD abolished the PGE2‐induced inhibition. Serum increased (by a factor of 10) the amount of phosphorylated extracellular signal‐regulated kinase (p‐ERK), PGE2 reduced it (by 70–80%) and EMD restored it when present with PGE2. Prostaglandin E2 stimulated cAMP production in hGFs while serum or EMD did not. Enamel matrix derivative stimulated hDF proliferation, but the inhibitory effect of PGE2 was milder than with hGFs. When present together, EMD abolished the PGE2‐induced inhibition. Enamel matrix derivative inhibited the proliferation of primary hGKs, but PGE2 had no effect. Finally, we found that hDFs contained about five times less prostaglandin EP2 receptor mRNA than hGFs, while hGKs contained none. Conclusion: Prostaglandin E2 inhibits and EMD stimulates hGF proliferation via distinct pathways. The different sensitivities of hDFs and hGKs to PGE2 can be explained by the levels of EP2 expression. |
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| Keywords: | prostaglandin fibroblast prostaglandin EP2 receptor enamel matrix derivative keratinocyte |
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