Immunohistochemical and Stereologic Analysis of NF-κB Activation in Chronic Periodontitis (original) (raw)

Role of Nuclear Factor‐Kappa B (NF‐κB) in Inflammation, Periodontitis, and Atherogenesis

Annals of Periodontology, 2001

Atherosclerosis, the major cause of death and disability in the United States, is a chronic disease with inflammatory components. The first objective of this review is to explain how activation of NF‐κB contributes to atherosclerosis. The second objective is to describe a potential link between inflammation, activation of NF‐κB, and periodontitis. The nuclear transcription factor NF‐κB controls the expression of many genes linked to atherogenesis including those involved with inflammation. We hypothesize that one unifying mechanism in this complex disease is the activation of NF‐κB. The mechanism(s) that activates NF‐κB in atherogenesis is unknown and the effect of inhibiting NF‐κB activation on atherogenesis is untested. Periodontal disease has now been established as a risk factor for atherosclerosis and its thrombotic complications. It is unknown if periodontal disease contributes to the initiation or progression of atherosclerosis. We hypothesize that the chronic and intense inf...

Levels of Cytokine Receptor Activator of Nuclear Factor κB Ligand in Gingival Crevicular Fluid in Untreated Chronic Periodontitis Patients

Journal of Periodontology, 2004

Background: Receptor activator of nuclear factor κB ligand (RANK-L) is a cytokine involved in the regulation of osteoclastogenesis in bone remodeling and inflammatory osteolysis. One of the major causes of tooth loss in humans is bone destruction. The aim of our study was to determine the presence of RANK-L in gingival crevicular fluid (GCF) samples from adult patients with untreated chronic periodontitis and in healthy controls. We also identified the RANK-L present in lesions undergoing episodic attachment loss from GCF. Methods: GCF samples were collected from two periodontally affected sites (probing depth ≥5 mm, attachment loss ≥3 mm) in 20 patients (N = 40). After monitoring for 4 months, seven patients showed active periodontal disease, and GCF samples were collected from one active and one inactive site (N = 14 samples). The comparison with healthy controls was carried out by collecting GCF samples from 12 healthy volunteers (N = 24 samples). GCF was collected using a paper strip, and enzymelinked immunosorbent assay (ELISA) was performed to determine the total amount of RANK-L. Results: RANK-L was found in a higher proportion (85%) of samples from patients than from controls (46%). The total amount of RANK-L was significantly higher in patients (115.53 ± 78.18 picograms [pg]) than in healthy subjects (63.08 ± 55.08 pg) (P = 0.003). Active sites, presumably associated with tissue destruction, had significantly higher levels of RANK-L than their inactive counterparts (125.95 pg versus 91.80 pg, P = 0.007). Conclusion: GCF total amount of RANK-L is significantly increased in periodontal disease, supporting its role in the alveolar bone loss developed in this disease.

Receptor activator NF κB ligand (RANKL) and osteoprotegerin (OPG) protein expression in periodontitis

Journal of Periodontal Research, 2003

Little is known about the process of alveolar bone loss that occurs in periodontitis. The inflammation and tissue destruction seen in periodontitis is associated with granulomatous tissue containing inflammatory cells, such as T and B lymphocytes, plasma cells and many cells of the monocytes/macrophage lineage. These cells are thought to produce a variety of inflammatory mediators. High levels of several inflammatory cytokines, such as inter-leukin-1a (IL-1a), IL-b, IL-6, prostaglandin E 2 (PGE 2) and tumour necrosis factor a (TNFa), have been found in the tissue and gingival crevicular fluid of patients suffering advanced periodontitis (1-4). Similar

Differential activation of NF-κB and gene expression in oral epithelial cells by periodontal pathogens

Clinical and Experimental Immunology, 2007

Summary To investigate the molecular effects of the periodontopathogens Fusobacterium nucleatum (FN) and Porphyromonas gingivalis (PG) on the oral epithelium, the H400 oral epithelial cell line was cultured in the presence of non-viable bacteria. Following confirmation of the presence of transcripts for the bacterial pattern recognition receptors in H400 cells, Toll-like receptors -2, -4 and -9, and components of the NF-κB signalling pathway, immunocytochemical analyses were performed showing that NF-κB was activated within 1 h of exposure to both periodontopathogens. A significantly greater number of NF-κB nuclear translocations were apparent following H400 cell exposure to FN as compared with PG. Gene expression analyses indicated that transcripts known to be regulated by the NF-κB pathway, including cytokines/chemokines TNF-α, IL-1β, IL-8, MCP-1/CCL2 and GM-CSF, were up-regulated following 4 and 24 h of exposure to both periodontopathogens. In addition, H400 periodontopathogen ex...

Levels of Cytokine Receptor Activator of Nuclear Factor B Ligand in Gingival Crevicular Fluid in Untreated Chronic Periodontitis Patients

Journal of Periodontology, 2004

Background: Receptor activator of nuclear factor κB ligand (RANK-L) is a cytokine involved in the regulation of osteoclastogenesis in bone remodeling and inflammatory osteolysis. One of the major causes of tooth loss in humans is bone destruction. The aim of our study was to determine the presence of RANK-L in gingival crevicular fluid (GCF) samples from adult patients with untreated chronic periodontitis and in healthy controls. We also identified the RANK-L present in lesions undergoing episodic attachment loss from GCF. Methods: GCF samples were collected from two periodontally affected sites (probing depth ≥5 mm, attachment loss ≥3 mm) in 20 patients (N = 40). After monitoring for 4 months, seven patients showed active periodontal disease, and GCF samples were collected from one active and one inactive site (N = 14 samples). The comparison with healthy controls was carried out by collecting GCF samples from 12 healthy volunteers (N = 24 samples). GCF was collected using a paper strip, and enzymelinked immunosorbent assay (ELISA) was performed to determine the total amount of RANK-L. Results: RANK-L was found in a higher proportion (85%) of samples from patients than from controls (46%). The total amount of RANK-L was significantly higher in patients (115.53 ± 78.18 picograms [pg]) than in healthy subjects (63.08 ± 55.08 pg) (P = 0.003). Active sites, presumably associated with tissue destruction, had significantly higher levels of RANK-L than their inactive counterparts (125.95 pg versus 91.80 pg, P = 0.007). Conclusion: GCF total amount of RANK-L is significantly increased in periodontal disease, supporting its role in the alveolar bone loss developed in this disease.

Cytokines’ Involvement in Periodontal Changes

Cytokines, 2020

The bacterial challenge on the periodontal tissues triggers an inflammatory reaction, driven by pro-inflammatory cytokines, that eventually leads to the periodontal structures' damage. The pathogenic mechanisms of this inflammatory reaction are complex and are influenced by the type of host-immune response and certain local and systemic factors. These factors can influence periodontal inflammation, through the action of the various pro-inflammatory cytokines. Periodontal disease and certain systemic conditions can have a mutual association, as the pathogenic mechanisms of these diseases can involve similar molecular and cellular elements. The concept of 'periodontal medicine' comprises these pathogenic connections, focusing on the key role that periodontal health has on the general homeostasis and well-being.

The Association between Changes in Serum Biomarkers of Inflammatory Mediators and Periodontal Disease

Journal of Babol University of Medical Sciences, 2023

Background and Objective: Periodontal diseases are chronic inflammatory diseases leading to damage to soft and hard tissue. Due to the importance of periodontal health in people, this study was designed to investigate the association between changes in the inflammatory mediators with the development of periodontal disease. Methods: The case-control study was conducted on 120 individuals who referred to University of Baghdad, Dentistry School, Department of Periodontics in three groups: healthy group, periodontitis group, and gingivitis group, every group containing 40 individuals (20 men and 20 women). The demographic data of all individuals were recorded in the information form. Periodontal parameters, including bleeding on probing (BOP), plaque index (PI), clinical attachment loss (CAL), probing pocket depth (pd) and the serum levels of Interleukin-6 (Il-6), Immunoglobulin G (IgG) by ELISA technique, C-reactive protein (CRP) were evaluated using colorimetric technique. Findings: The mean range of IL-6 was 17.3940±1.509, 17.1432±2.214, 11.3846±1.119, for periodontitis, gingivitis, and healthy groups, the mean range of CRP was 5.4477±3.771, 3.5853±3.483, 2.3813±1.134 for periodontitis, gingivitis, healthy groups, and the mean range of IgG was 12.3875±2.073, 15.0109±2.380, 9.4851±1.081 for periodontitis, gingivitis, healthy groups, respectively. Biochemical and periodontal parameters showed highly significant increase in periodontitis and gingivitis groups compared to healthy group (p<0.05). Conclusion: According to the results of this study, the high levels of inflammatory mediators are associated with periodontal disease, and increase with the progression of periodontal disease, and the transition from gingivitis to periodontitis, and the study's cutoff values can be applied to estimate healthy cases or patients with periodontal disease.