Journal of clinical periodontology · 2007
Role of IL-6, TNF-A and LT-A variants in the modulation of the clinical expression of plaque-induced gingivitis.
СтатьяРандомизированное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Scapoli Chiara, Mamolini Elisabetta, Trombelli Leonardo
Аннотация
AIM: The purpose of the present study was to assess the association of interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-A) and lymphotoxin alpha (LT-A) gene polymorphisms with the clinical parameters of gingivitis in a large experimental gingivitis trial and with each of two subgroups, "high responder" (HR, n=24) and "low responder" (LR, n=24), with distinct susceptibility to gingivitis.
MATERIAL AND METHODS: Ninety-six systemically and periodontally healthy non-smokers, 46 males (mean age: 23.9+/-1.7) and 50 females (mean age: 23.3+/-1.6), were included in a randomized split-mouth localized 21-day experimental gingivitis trial. Plaque index, gingival index, gingival crevicular fluid volume and angulated bleeding score were recorded. HR and LR subgroups were characterized by substantially different severities of gingival inflammation despite a similar plaque accumulation rate. All subjects were genetically characterized for IL-6(-174), IL-6(-597), TNF-A(-308) and LT-A(+252) polymorphisms.
RESULTS: None of the variants analysed, either as single polymorphisms or as a combined genotype, was associated with the clinical parameters in the overall population. For the polymorphisms studied, genotypic distributions in HR and LR subjects were not significantly different.
CONCLUSIONS: The present results suggest an absence of association between IL-6, TNF-A and LT-A polymorphisms and subject-based clinical behaviour of the gingiva in response to de novo plaque accumulation.
MATERIAL AND METHODS: Ninety-six systemically and periodontally healthy non-smokers, 46 males (mean age: 23.9+/-1.7) and 50 females (mean age: 23.3+/-1.6), were included in a randomized split-mouth localized 21-day experimental gingivitis trial. Plaque index, gingival index, gingival crevicular fluid volume and angulated bleeding score were recorded. HR and LR subgroups were characterized by substantially different severities of gingival inflammation despite a similar plaque accumulation rate. All subjects were genetically characterized for IL-6(-174), IL-6(-597), TNF-A(-308) and LT-A(+252) polymorphisms.
RESULTS: None of the variants analysed, either as single polymorphisms or as a combined genotype, was associated with the clinical parameters in the overall population. For the polymorphisms studied, genotypic distributions in HR and LR subjects were not significantly different.
CONCLUSIONS: The present results suggest an absence of association between IL-6, TNF-A and LT-A polymorphisms and subject-based clinical behaviour of the gingiva in response to de novo plaque accumulation.