A1 Refereed original research article in a scientific journal
The role of nickel accumulation and epithelial cell proliferation in orthodontic treatment-induced gingival overgrowth
Authors: Gursoy UK, Sokucu O, Uitto VJ, Aydin A, Demirer S, Toker H, Erdem O, Sayal A
Publisher: OXFORD UNIV PRESS
Publication year: 2007
Journal name in source: EUROPEAN JOURNAL OF ORTHODONTICS
Journal acronym: EUR J ORTHODONT
Volume: 29
Issue: 6
First page : 555
Last page: 558
Number of pages: 4
ISSN: 0141-5387
DOI: https://doi.org/10.1093/ejo/cjm074(external)
Abstract
The aim of this study was to investigate the role of nickel in orthodontic treatment-induced gingival hyperplasia. The nickel concentration in gingival tissues with and without overgrowth, histopathology of gingival overgrowths, and epithelial cell proliferation response to different nickel concentrations were analysed. Ten patients receiving orthodontic therapy (eight females and two males, mean age 15.4 years) were included in the study. Hyperplastic and healthy gingiva samples were collected from the same patients. The amount of nickel in the gingival tissue samples was analysed using the atomic absorption spectrometry technique. The tissues removed from hyperplastic areas during gingivectomy were also used for histological analysis. To analyse the effect of nickel on epithelial cell proliferation, four different nickel concentrations (0.5, 2, 5, and 10 mu g) were incubated with keratinocyte cells for 11 days. Mann-Whitney U-test, analysis of variance, and Tukey's test were used in the statistical analyses.The results did not show any difference in nickel concentration between the study and control gingiva tissue samples, but histological analysis demonstrated an increase in epithelial thickness and a significant increase (P = 0.031, 0.02, 0.02) in epithelial cell proliferation in response to low-dose nickel concentrations, with a toxic response to a higher dose. In the limitations of this study, it is plausible that the effect of a continuing low-dose nickel release to epithelium is the initiating factor of gingival overgrowth induced by orthodontic treatment.
The aim of this study was to investigate the role of nickel in orthodontic treatment-induced gingival hyperplasia. The nickel concentration in gingival tissues with and without overgrowth, histopathology of gingival overgrowths, and epithelial cell proliferation response to different nickel concentrations were analysed. Ten patients receiving orthodontic therapy (eight females and two males, mean age 15.4 years) were included in the study. Hyperplastic and healthy gingiva samples were collected from the same patients. The amount of nickel in the gingival tissue samples was analysed using the atomic absorption spectrometry technique. The tissues removed from hyperplastic areas during gingivectomy were also used for histological analysis. To analyse the effect of nickel on epithelial cell proliferation, four different nickel concentrations (0.5, 2, 5, and 10 mu g) were incubated with keratinocyte cells for 11 days. Mann-Whitney U-test, analysis of variance, and Tukey's test were used in the statistical analyses.The results did not show any difference in nickel concentration between the study and control gingiva tissue samples, but histological analysis demonstrated an increase in epithelial thickness and a significant increase (P = 0.031, 0.02, 0.02) in epithelial cell proliferation in response to low-dose nickel concentrations, with a toxic response to a higher dose. In the limitations of this study, it is plausible that the effect of a continuing low-dose nickel release to epithelium is the initiating factor of gingival overgrowth induced by orthodontic treatment.
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