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Plasma TGF-β1 as a risk factor for gingival overgrowth

Lookup NU author(s): Professor Janice Ellis, Professor John Kirby, Dr John Taylor, Professor Mark Thomason

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Abstract

Background and Aims: Induction of the pro-fibrotic growth factor TGF-β1 has been suggested as a possible mechanism through which immunosuppressant drugs may induce gingival overgrowth. This study aims to investigate plasma levels of TGF-β1 and relate them to the development and severity of gingival overgrowth in immunosuppressed transplant patients. Materials and Methods: One hundred and thirty-two ciclosporin-treated and 13 tacrolimus-treated transplant patients and 24 drug-free control subjects underwent a full periodontal examination including a determination of the presence and severity of gingival overgrowth. Results: Plasma TGF-β1 concentrations were determined by ELISA, and were found to be significantly elevated in samples from the transplant patients (mean = 29.1 ng/ ml) as compared with controls (mean = 6.1 ng/ml, p < 0.0001). There was no significant difference between the levels of plasma TGF-β1 in the ciclosporin- and tacrolimus-treated patient groups. Conclusions: Furthermore, concomitant treatment with calcium channel blockers did not influence the levels of plasma TGF-β1 in the patients group. The relationship between gingival overgrowth, independent periodontal variables and TGF-β1 plasma concentrations was examined using univariate and multivariate regression analyses; low TGF-β1 plasma concentrations were found to be a risk factor for gingival overgrowth in immunosuppressed patients concomitantly receiving a calcium channel blocker. © Blackwell Munksgaard, 2004.


Publication metadata

Author(s): Ellis JS, Morgan CL, Kirby JA, Taylor JJ, Thomason JM

Publication type: Article

Publication status: Published

Journal: Journal of Clinical Periodontology

Year: 2004

Volume: 31

Issue: 10

Pages: 863-868

ISSN (print): 0303-6979

ISSN (electronic): 1600-051X

Publisher: Wiley-Blackwell

URL: http://dx.doi.org/10.1111/j.1600-051X.2004.00572.x

DOI: 10.1111/j.1600-051X.2004.00572.x

PubMed id: 15367190


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