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Role of nuclear factor kappa‐ B in phenytoin‐induced gingival overgrowth
Author(s) -
Arabaci T,
Köse O,
Kizildağ A,
Albayrak M,
Çiçek Y,
Kara A
Publication year - 2014
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.12111
Subject(s) - gingivitis , phenytoin , pathogenesis , medicine , connective tissue , transforming growth factor , immunohistochemistry , dentistry , pathology , psychiatry , epilepsy
Objective This study investigates the expression of transcription factor nuclear factor‐kappa B ( NF ‐κ B ) and its relation to various cellular mediators that act in the pathogenesis of phenytoin‐induced gingival overgrowth. Materials and methods Eighteen epileptic patients had phenytoin‐induced gingival overgrowth ( PHT ‐ GO ), 20 patients with plaque‐induced gingivitis (Gingivitis), and 20 periodontally and systemically healthy individuals (Control) were included in this study. The expression of activated NF ‐κ B subunits (p50 and p65), IL ‐1β, TNF ‐α and TGF β‐1 levels were examined in the gingival sections obtained from each participant. Results The results demonstrated a significantly higher expression of p65 in fibroblasts in PHT ‐ GO group with respect to Gingivitis ( P < 0.05) and control groups ( P < 0.01). However, we found no statistically significant differences between PHT ‐ GO and Gingivitis groups according to the immunohistochemical staining in macrophages ( P > 0.05). Immune‐reactive TGF β‐1 levels in the gingival connective tissue cells were statistically higher in PHT ‐ GO group with respect to Gingivitis group( P < 0.05). Statistically significant correlations were found between the HI and activated TGF β‐1 and p65 levels in PHT ‐ GO group. Conclusion The results of this study showed that NF ‐κ B is activated in PHT ‐related gingival overgrowth. This study may provide a basis for future research into specific NF ‐κ B inhibition for preventing of the side effects of this drug.