Increased visfatin expression is associated with nuclear factor-kappa B and phosphatidylinositol 3-kinase in periodontal 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-κB1and 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.


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.


CONCLUSIONS
Understanding the role of visfatin in periodontitis will enable the development of new treatment methods for inflammation.
Department of Periodontology, Gülhane Military Medicine Academy, Dental Sciences Center, Ankara, Turkey. drdterkan@mynet.com.
Erkan
E
Özcan
Department of Periodontology, Gülhane Military Medicine Academy, Dental Sciences Center, Ankara, Turkey.
N Işıl
NI
Saygun
Department of Immunology, Gülhane Military Medicine Academy, Ankara, Turkey.
Rahşan
R
Ilıkçı
Department of Pathology, Gülhane Military Medicine Academy, Ankara, Turkey.
Yıldırım
Y
Karslıoğlu
Department of Immunology, Gülhane Military Medicine Academy, Ankara, Turkey.
Uğur
U
Muşabak
Department of Immunology, Gülhane Military Medicine Academy, Ankara, Turkey.
Sait
S
Yeşillik
D000328:Adult; D055113:Chronic Periodontitis / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D053583:Interleukin-1beta / Q000378:metabolism; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D054409:Nicotinamide Phosphoribosyltransferase / Q000378:metabolism*; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D053583:Interleukin-1beta; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human; D058539:Phosphatidylinositol 3-Kinase
Apoptosis; Nicotinamide phosphoribosyltransferase; Nuclear factor-kappa B; Periodontitis; Phosphatidylinositol 3-kinase