Erkan Özcan1, N Işıl Saygun2, Rahşan Ilıkçı3, Yıldırım Karslıoğlu4, Uğur Muşabak3, Sait Yeşillik3. 1. Department of Periodontology, Gülhane Military Medicine Academy, Dental Sciences Center, Ankara, Turkey. drdterkan@mynet.com. 2. Department of Periodontology, Gülhane Military Medicine Academy, Dental Sciences Center, Ankara, Turkey. 3. Department of Immunology, Gülhane Military Medicine Academy, Ankara, Turkey. 4. Department of Pathology, Gülhane Military Medicine Academy, Ankara, Turkey.
Abstract
OBJECTIVE: Visfatin is an adipocytokine that plays a role in regulating periodontal inflammation by as yet identified mechanisms. It has been suggested that visfatin mediates inflammation via activation of the nuclear factor-kappa B (NF-κB) and phosphatidylinositol 3-kinase (PI3k) signaling pathways which play a role in the inhibition of neutrophil apoptosis. The aim of this study was to investigate the expression of visfatin, NF-κB (NF-κB1 and NF-κB2), PI3k, tumor necrosis factor alpha (TNF-α), and interleukin-1 beta (IL-1β) in the tissue of healthy individuals and patients with periodontitis. MATERIALS AND METHODS: Tissue biopsy samples were obtained from 21 patients with chronic periodontitis and from the gingiva of 19 healthy individuals undergoing crown lengthening. The mRNA expression levels of visfatin, NF-κB, PI3k, TNF-α, and IL-1β were evaluated by quantitative real-time PCR (qPCR). Also, visfatin protein expression was measured by immunohistochemistry. RESULTS: Both qPCR and immunohistochemistry results revealed that the visfatin expression was higher in the tissues with periodontitis than in healthy tissues (P < 0.01). Similarly, the mRNA expression levels of NF-κB2, PI3k, and IL-1β were higher in tissues with periodontitis than in healthy gingival tissues (P < 0.01). Visfatin was positively correlated with the levels of NF-κB1 (r = 0.549, P < 0.05), NF-κB2 (r = 0.636, P < 0.05), PI3k (r = 0.682, P < 0.01), TNF-α (r = 0.558, P < 0.05), and IL-1β (r = 0.686, P < 0.01) in the tissues with periodontitis. CONCLUSIONS: Our results demonstrated that increased visfatin was associated with the expression of NF-κB and PI3k which may play a role in the pathogenesis of periodontitis. We suggest that increased visfatin may contribute to the inhibition of neutrophil apoptosis via the NF-κB and PI3k signaling pathways. CLINICAL RELEVANCE: Understanding the role of visfatin in periodontitis will enable the development of new treatment methods for inflammation.
OBJECTIVE:Visfatin is an adipocytokine that plays a role in regulating periodontal inflammation by as yet identified mechanisms. It has been suggested that visfatin mediates inflammation via activation of the nuclear factor-kappa B (NF-κB) and phosphatidylinositol 3-kinase (PI3k) signaling pathways which play a role in the inhibition of neutrophil apoptosis. The aim of this study was to investigate the expression of visfatin, NF-κB (NF-κB1 and NF-κB2), PI3k, tumor necrosis factor alpha (TNF-α), and interleukin-1 beta (IL-1β) in the tissue of healthy individuals and patients with periodontitis. MATERIALS AND METHODS: Tissue biopsy samples were obtained from 21 patients with chronic periodontitis and from the gingiva of 19 healthy individuals undergoing crown lengthening. The mRNA expression levels of visfatin, NF-κB, PI3k, TNF-α, and IL-1β were evaluated by quantitative real-time PCR (qPCR). Also, visfatin protein expression was measured by immunohistochemistry. RESULTS: Both qPCR and immunohistochemistry results revealed that the visfatin expression was higher in the tissues with periodontitis than in healthy tissues (P < 0.01). Similarly, the mRNA expression levels of NF-κB2, PI3k, and IL-1β were higher in tissues with periodontitis than in healthy gingival tissues (P < 0.01). Visfatin was positively correlated with the levels of NF-κB1 (r = 0.549, P < 0.05), NF-κB2 (r = 0.636, P < 0.05), PI3k (r = 0.682, P < 0.01), TNF-α (r = 0.558, P < 0.05), and IL-1β (r = 0.686, P < 0.01) in the tissues with periodontitis. CONCLUSIONS: Our results demonstrated that increased visfatin was associated with the expression of NF-κB and PI3k which may play a role in the pathogenesis of periodontitis. We suggest that increased visfatin may contribute to the inhibition of neutrophil apoptosis via the NF-κB and PI3k signaling pathways. CLINICAL RELEVANCE: Understanding the role of visfatin in periodontitis will enable the development of new treatment methods for inflammation.
Authors: Andressa Vilas Boas Nogueira; Marjan Nokhbehsaim; Sigrun Eick; Christoph Bourauel; Andreas Jäger; Søren Jepsen; Joni Augusto Cirelli; James Deschner Journal: Clin Oral Investig Date: 2013-02-13 Impact factor: 3.573