Gingival Crevicular Fluid TNF-α Research Articles

The effect of interleukin-20 on periodontal tissue destruction in individuals with periodontitis.

Periodontitis is an inflammatory disease that destroys periodontal tissues. Interleukin-20 (IL-20), on the other hand, is known as a potent angiogenic, chemotactic, and pro-inflammatory cytokine associated with various chronic inflammatory disorders. IL-20 has a significant role in the regulation of osteoclastogenesis and osteoblastogenesis. This study aimed to evaluate the effect of IL-20 on periodontal destruction. In this study, a total of 60 participants were included, 30 of whom were systemically and periodontally healthy (control group), and 30 were systemically healthy but had periodontitis (periodontitis group). Gingival crevicular fluid (GCF) and serum samples were collected from the participants for biochemical analysis. Enzyme-linked immunosorbent assay was used to determine the levels of IL-20, tumor necrosis factor (TNF)-α, IL1β/IL-10, RANKL/osteoprotegerin (OPG), and matrix metalloproteinase-8 (MMP8). For statistical analysis, the independent t-test, Pearson correlation coefficients, and the Chi-square test were used. GCF IL-20, RANKL, RANKL/OPG, serum IL-20, RANKL, RANKL/OPG, MMP-8, TNF-α, IL-1B, and IL-1β/IL-10 values were found to be statistically significantly higher in the periodontitis group than in the control group. GCF OPG and serum IL-10 values were found to be statistically significantly higher in the control group than in the periodontitis group. No statistically significant difference was observed between the groups in serum OPG values. A statistically significantly positive correlation was observed between serum IL-20 value and serum RANKL, RANKL/OPG, MMP-8, TNF-α, IL-1β values, and periodontal clinical parameters. The ROC curves showed: AUC = 0.788 for GCF IL-20, and AUC = 1.000 for serum IL-20. According to the results of the study, IL-20 was found to be associated with periodontitis. The role of IL-20 in periodontal pathogenesis is related to osteoclastogenesis and collagen degradation. It is conceivable that IL-20 may increase bone destruction by both affecting the RANKL/OPG ratio and proinflammatory cytokines.

Periostin in the relation between periodontal disease and atherosclerotic coronary artery disease: A pilot randomized clinical study.

The aim of this study was to analyze the effects of periodontal treatment on markers of atherosclerotic coronary artery disease and circulating levels of periostin. Periostin is necessary for periodontal stability, but it is highly present in atherosclerotic plaques. Treatment of periodontal disease, with low levels of local periostin, is thought to reduce systemic levels of periostin. Thus, this may contribute to cardiovascular health. A pilot randomized controlled clinical trial was designed to include patients with severe periodontal disease and history of atherosclerotic coronary artery disease. Samples of gingival crevicular fluid (GCF) and serum were collected before and after periodontal treatment by periodontal surgery or non-surgical therapy. The levels of several markers of inflammation and cardiovascular damage were evaluated including CRP, IFN-γ, IL-1ß, IL-10, MIP-1α, periostin, and TNF-α in GCF and CRP, Fibrinogen, IFN-γ, IL-1ß, IL-6, IL-10, L-Selectin, MIP-1α, Periostin, TNF-α, and vWF in serum. A total of 22 patients with an average of 56 years old were recruited for participating in this study. Twenty of them were male. Most of them (82%) had suffered an acute myocardial event and underwent surgery for placing 1, 2, or 3 stents in the coronary arteries more than 6 months ago but less than 1 year. The treatment of periodontal disease resulted in an overall improvement of all periodontal parameters. Regarding the evaluation of GCF and serum, a significant increase of periostin in the GCF was observed after periodontal surgery. In contrast, although other markers in GCF and serum improved, no significant correlations were found. Treatment of periodontal disease through periodontal surgery induces a local and transient increase in the levels of periostin in the gingival crevicular fluid. The effects on systemic markers of inflammation and cardiovascular function have not been confirmed.

Obesity Is Associated with a Weakened Gingival Inflammatory Cytokine Response.

Background and Objectives: An obesity-related elevated body mass index (BMI) across life is associated with chronic low-grade inflammation and increased levels of C-reactive protein (CRP) in blood. CRP is a marker and promoter of inflammation. The objectives of this study were to examine the effect of obesity on the relationship between peripheral and gingival CRP levels and to examine the effects of gingival CRP levels on gingival fluid inflammatory cytokines in periodontitis-resistant obese individuals. Materials and Methods: Thirty-nine participants in good periodontal health were recruited. Twenty patients were classified as lean and nineteen as obese based on their BMI levels. A thorough periodontal assessment was carried out. Gingival crevicular fluid (GCF) and blood samples were collected. Both GCF and blood samples were analyzed for interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), interleukin-17A (IL-17A), and CRP. Results: GCF CRP levels were significantly higher in the obese than in the lean individuals. No statistically significant differences were noted between the two groups in either GCF or blood in terms of any of the inflammatory cytokine levels. IL-17A was not detected in the GCF of most subjects in both groups. GCF CRP levels were positively associated with blood CRP levels, and the association tended to be stronger in the obese individuals. GCF CRP showed no associations with GCF IL-10 in both groups. Although GCF CRP levels were positively associated with multiple GCF inflammatory cytokines (e.g., IL-1β, IL-6, IL-8, and TNF-α) in all subjects, the associations tended to be weaker in the obese individuals (e.g., IL-1β, IL-6, and TNF-α). Furthermore, the levels of the GCF inflammatory cytokines IL-6 and TNF-α were decreased in the obese individuals. Conclusions: Obesity unfavorably influences the relationship between blood and GCF CRP levels and promotes increased CRP levels in GCF. Collectively, the findings suggest a weakened inflammatory cytokine response in the gingival tissues of obese individuals.

Periodontal Disease in Young Adults as a Risk Factor for Subclinical Atherosclerosis: A Clinical, Biochemical and Immunological Study.

Although a strong relationship between periodontal disease (PD) and atherosclerosis was shown in adults, little data are published in younger PD patients. Therefore, this study aimed to investigate and correlate clinical parameters of PD, pro- and immunoregulatory cytokines in gingival crevicular fluid (GCF) and serum, biochemical and hematological parameters associated with atherosclerosis risk, and carotid intima-media thickness (IMT) in our younger study participants (n = 78) (mean age 35.92 ± 3.36 years) who were divided into two equal groups: subjects with and without PD. PD patients had higher values of IMT, hs-CRP, triglycerides, total cholesterol, and LDL; most proinflammatory and Th1/Th17-associated cytokines in GCF; and IL-8, IL-12, IL-18, and IL-17A in serum compared to subjects without PD. These cytokines in GCF positively correlated with most clinical periodontal parameters. Clinical periodontal parameters, TNF-α and IL-8 in GCF and IL-17A, hs-CRP, and LDL in serum, had more significant predictive roles in developing subclinical atherosclerosis (IMT ≥ 0.75 mm) in comparison with other cytokines, fibrinogen, and other lipid status parameters. Hs-CRP correlated better with the proinflammatory cytokines than the parameters of lipid status. Except for serum IL-17A, there was no significant association of clinical and immunological PD parameters with lipid status. Overall, these results suggest that dyslipidemia and PD status seem to be independent risk factors for subclinical atherosclerosis in our younger PD population.

Effects of autologous leukocyte-platelet rich fibrin (L-PRF) on the rate of maxillary canine retraction and various biomarkers in gingival crevicular fluid (GCF): A split mouth randomized controlled trial

Primary objective: To evaluate the effect of L-PRF on the rate of maxillary canine retraction. To validate the rate of maxillary canine retraction by identifying the levels of Interleukin-1β (IL-1β) and Tumour Necrosis Factor-α (TNF-α) in the Gingival Crevicular Fluid (GCF). Fifteen females (age range, 18-25 years) with Class I bimaxillary dentoalveolar protrusion malocclusions were included. After levelling and alignment of maxillary arches, 1st premolars were extracted from both sides. Canines were retracted immediately after the extraction of 1st premolars in control sides and placement of L-PRF plugs in the experimental sides. The amount of canine retraction was evaluated from study models recorded before the extraction of 1st premolars (T0) and at 1-week (T1), 2-weeks (T2), 4-weeks (T3), and 8-weeks (T4) after the beginning of canine retraction by using digital model superimpositions. The concentrations of IL-1β and TNF-α were evaluated from the GCF collected at T0, T1, T2, T3, and T4 by using commercially available human IL-1β and TNF-α ELISA kits. The amount of canine retraction in the experimental sides was statistically greater during T0-T1 (P=0.038),T1-T2 (P=0.002), and T2-T3 (P=0.011) periods. Total canine retraction during T0-T4 was statistically greater in experimental sides (2.43±0.46mm) than control sides (2.08±0.28mm) (P=0.001). The concentration of IL-1β increased significantly in the experimental sides at T1 (P=0.000),T2 (P=0.000), and T3 (P=0.032). The concentration of TNF-α increased both in the control and experimental sides, but it was statistically greater in the experimental sides compared to control sides at T1 (P=0.000) and T2 (P=0.006). A positive but not statistically significant correlation was noted between the rate of canine retraction and the concentrations of cytokines such as IL-1β and TNF-α in GCF. Over an 8-week period, autologous L-PRF statistically accelerated the rate of maxillary canine retraction, but only by 0.35mm. This small acceleration occurred mainly in the first 4 weeks. During the following 4 weeks, the amount of canine retraction was comparable on the experimental and control sides.

Gingival crevicular fluid lipocalin-2 and semaphorin3A in stage III periodontitis: Non-surgical periodontal treatment effects.

Identification of biomarkers to assess individual risk and monitor periodontal health status is important. Research on lipocalin-2 (LCN2) and semaphorin3A (Sema3A) is lacking. This study aimed to evaluate gingival crevicular fluid (GCF) LCN2, Sema3A, and tumor necrosis factor-α (TNF-α) levels in periodontally healthy (H), gingivitis (G), and periodontitis (P) patients, and their changes following non-surgical periodontal therapy. Sixty systemically healthy and non-smoker participants, diagnosed as periodontally healthy, gingivitis, and stage III grade C periodontitis, were recruited (n=20/group). Clinical periodontal parameters were recorded and GCF samples were obtained at baseline from all groups; for group P, these were repeated one and three months following non-surgical periodontal treatment. GCF LCN2, Sema3A, and TNF-α levels were evaluated with enzyme-linked immunosorbent assay. GCF LCN2, Sema3A, and TNF-α total amounts were significantly higher in disease groups than group H (p<.001). Between P and G groups, only TNF-α levels were significantly different (p<.001). Non-surgical periodontal therapy resulted in significant improvement of all clinical parameters and significant decreases of GCF LCN2 and TNF-α levels, at both time points, compared with baseline (p<.001). Sema3A levels remained unchanged following treatment (p>.05). LCN2 and TNF-α levels were significantly positively correlated with clinical parameters. LCN2 (AUC [area under the curve]=0.94) and TNF-α (AUC=0.98) levels were similarly accurate in differentiating between periodontal disease (whether G or P) and healthy controls. LCN2 and TNF-α levels in GCF are correlated with clinical parameters and could prove useful as non-invasive screening tools for periodontitis.

The neutrophil elastase-upregulated placenta growth factor promotes the pathogenesis and progression of periodontal disease.

Periodontal disease is a chronic inflammatory disease. Given its high prevalence, especially in aging population, the detailed mechanisms about pathogenesis of periodontal disease are important issues for study. Neutrophil firstly infiltrates to periodontal disease-associated pathogen loci and amplifies the inflammatory response for host defense. However, excessive neutrophil-secreted neutrophil elastase (NE) damages the affected gingival. In lung and esophageal epithelium, NE had been proved to upregulate several growth factors including placenta growth factor (PGF). PGF is an angiogenic factor with proinflammatory properties, which mediates the progression of inflammatory disease. Therefore, we hypothesize excessive NE upregulates PGF and participates in the pathogenesis and progression of periodontal disease. In gingival epithelial cells (GEC), growth factors array demonstrated NE-increased growth factors and further be corroborated by Western blot assay and ELISA. The GEC inflammation was evaluated by ELISA. In mice, the immunohistochemistry results demonstrated ligature implantation-induced neutrophil infiltration and growth factor upregulation. By multiplex assay, the ligature-induced proinflammatory cytokines level in gingival crevicular fluid (GCF) were evaluated. Finally, alveolar bone absorption was analyzed by micro-CT images and H &amp; E staining. NE upregulated PGF expression and secretion in GEC. PGF promoted GEC to secret IL-1β, IL-6, and TNF-α in GCF In periodontal disease animal model, ligature implantation triggered NE infiltration and PGF expression. Blockade of PGF attenuated the ligature implantation-induced IL-1β, IL-6, TNF-α and MIP-2 secretion and ameliorated the alveolar bone loss in mice. In conclusion, the NE-induced PGF triggers gingival epithelium inflammation and promotes the pathogenesis and progression of periodontal disease.

Pro-inflammatory profiles in cardiovascular disease patients with peri-implantitis.

To investigate the pro-inflammatory cytokine profiles in patients with or without cardiovascular disease (CVD) and with or without peri-implantitis. Serum, peri-implant crevicular fluid (PICF), and gingival crevicular fluid (GCF) were collected from patients with (n=82) or without CVD (n=46) at the most severe peri-implantitis site including sites with periodontitis. A panel of proinflammatory molecules including high-sensitivity C-reactive protein (hsCRP), fibrinogen, interleukin-1 beta (IL-1β), IL-6, plasma tumor necrosis factor-alpha (TNF-α), matrix metallo-proteinase-8 (MMP-8), osteoprotegerin (OPG), vascular endothelial growth factor (VEGF), IL-17, IL-8, tissue inhibitor of metalloproteinase-2 (TIMP-2), myeloperoxidase (MPO), and prostaglandin E2 (PGE2 ) were analyzed using human custom Quantibody arrays. Krunskal-Wallis test was used to compare groups. The diagnostic ability of each biomarker was assessed using chi-square test and ROC analysis. Serum IL-1β, TNF-α and fibrinogen were significantly higher in CVD patients than those without. Serum fibrinogen displayed a trend of higher concentration in patients with radiographic bone loss (RBL) ≥2mm (P=0.08). PICF TNF-α exhibited a significantly higher detection level in the CVD patients that is coincided with the local peri-implant inflammation. In addition, PICF MMP-8 was significantly higher in the RBL ≥2mm sites than the healthy implants; whereas IL-1β, IL-8, MMP-8, and TIMP-2 proved to be the significant predictors for peri-implant disease. GCF TNF-α collected from patients with periodontitis was significantly associated with CVD cases. The augmented expression of local and systemic pro-inflammatory cytokines found in the current study supports the weak association between the chronic peri-implantitis with increasing severity and CVD.

Evaluation of Level of TNF-α among Obese Patients with and without Chronic Periodontitis.

Aim:The purpose of this case-control study was to evaluate the role of TNF-α in gingival crevicular fluid among obese women with chronic periodontitis.Materials and Methods:A total of 60 subjects were randomly selected for the study. The study population was further divided into three groups (Group 1, Obese women without periodontitis; Group 2, Non-obese women without periodontitis; Group 3, Obese with chronic periodontitis). Gingival crevicular fluid samples were taken for assessment based on clinical parameters like probing depth, bleeding on probing, and BMI.Results:There was significant increase in the level of TNF-α in gingival crevicular fluid from obese patients with chronic periodontitis and a positive correlation was found between TNF-α levels and values of the plaque index, OHI –I and BMI.Conclusion:Based on these results, it can be concluded that GCF level of TNF-α was significantly higher in obese patients with and without chronic periodontitis, and highest in obese patients with chronic periodontitis group.

Effect of probiotic Lactobacillus paracasei on tumor necrosis factor-alpha level in gingival crevicular fluid of patients undergoing impacted third molar removal.

This study was conducted to evaluate the effects of the probiotic Lactobacillus paracasei in patients undergoing removal of impacted mandibular third molars, focusing on tumor necrosis factor alpha (TNF-α) levels in gingival crevicular fluid, pain, swelling, trismus, and interincisal distance. Thirty patients were divided into two groups: (1) wound irrigation with the probiotic, and (2) irrigation with 0.9% normal saline. The data were collected at the baseline, and at 24 h and 7 days after the operation. The TNF-α level in gingival crevicular fluid was determined using the ELISA technique. In the experimental group, the probiotic L. paracasei MSMC39 reduced the TNF-α level in gingival crevicular fluid to a significantly greater degree than in the control group (P < 0.05). Pain, swelling and trismus evaluated in terms of a visual analog scale (VAS) score were lower in the experimental group than in the control group, but not to a statistically significant degree (P > 0.05). The mean interincisal distance in the experimental group was higher than that in the control group (P = 0.014). The probiotic L. paracasei is able to reduce the level of TNF-α in gingival crevicular fluid and can ameliorate postoperative complications after mandibular molar removal.

Increased risk of periodontitis occurrence in patients with rheumatoid arthritis and its association with the levels of IL-1β and TNF-α in gingival crevicular fluid.

Periodontitis (PD) is a chronic inflammatory disease caused by infection of the periodontal supporting tissues. Clinical studies have reported that rheumatoid arthritis (RA) patients have a higher prevalence of PD. This study aimed to explore the correlation between RA and PD. A total of 307 RA patients (RA group) and 324 healthy individuals (control group) who received physical examinations during the same period were recruited to this study. The incidence of PD in the two groups was analyzed, and the periodontal disease index (PDI) and bleeding on probing (BOP) were recorded. Then, 42 RA patients with PD and 56 control group patients with PD were selected for further analysis. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the gingival crevicular fluid (GCF) of the two groups. For patients with both RA and PD, the level of serum C-reactive protein (CRP) and the duration of morning stiffness were also recorded. The prevalence of PD in the RA group (51.5%) was significantly higher than that in the control group (31.2%), and the prevalence of PD also increased notably with the increase of age and the duration of the disease in RA patients. The levels of TNF-α and IL-1β in the PDI and the GCF in the concurrent RA and PD group were significantly higher than those in the PD group (P<0.05). Partial correlation analysis showed that TNF-α in the GCF positively correlated with the BOP of patients with RA and PD. Multiple linear regression analysis showed that the level of TNF-α in the GCF and serum CRP were independent influencing factors of the level of IL-1β in the GCF (the r values were 1.074 and 3.851, respectively; P<0.01). The presence of RA can increase risk of PD occurrence and is positively correlated with the levels of IL-1β and TNF-α in the GCF.

Evaluation of galectin-3, peptidylarginine deiminase-4, and tumor necrosis factor-α levels in gingival crevicular fluid for periodontal health, gingivitis, and Stage III Grade C periodontitis: A pilot study.

Comparing the gingival crevicular fluid (GCF) levels of galectin-3, peptidylarginine deiminase 4 (PAD4) and tumor necrosis factor-alpha (TNF-α) in individuals with stage III grade C periodontitis and gingivitis and with healthy periodontium was the purpose of this clinical research. Sixty systemically healthy and non-smoker individuals consisting of stage III grade C periodontitis (group S3P/n=20), gingivitis (group G/n=20), and periodontally healthy (group HP/n=20) were recruited for this research. Clinical parameters such as probing depth, clinical attachment level, gingival index, plaque index, and bleeding on probing were recorded in periodontal charts. Enzyme-linked immunosorbent assay method was used in evaluating the GCF levels of galectin-3, PAD4, and TNF-α for study groups. The GCF galectin-3 total amount was highest in group S3P compared with group G and group HP (P<0.05). Its total amount was also higher in group G compared with group HP (P<0.05). The GCF PAD4 total amount was higher in group S3P compared with group HP (P<0.05) but was similar with group G (P >0.05). Its total amounts were also similar in group G and group HP (P >0.05). The GCF TNF-α total amounts were similar in group S3P and group G (P >0.05) but significantly greater than the group HP (P ˂0.05). The GCF galectin-3, PAD4, and TNF-α concentrations were lower in the group S3P and group G compared with the group HP (P<0.05). There were significant positive correlations between GCF galectin-3 total amount and all clinical parameters (P ˂0.01) and also between GCF galectin-3 and TNF-α total amounts (P ˂0.01). There was no correlation between PAD4 and clinical parameters, or between PAD4 and TNF-α (P >0.05). Galectin-3 and PAD4 may be involved in the periodontal disease pathogenesis considering the elevated levels of these molecules in periodontal disease. These biomarkers may be used in the diagnosis of periodontal diseases.

Influence of Ceramic Lumineers on Inflammatory Periodontal Parameters and Gingival Crevicular Fluid IL-6 and TNF-α Levels—A Clinical Trial

The aim was to evaluate the effect of ceramic lumineers on inflammatory periodontal parameters, gingival crevicular fluid (GCF) flow rate and cytokine profile. Patients were provided with lumineers using standardized technique including minimal to no preparation. Ceramic lumineers were etched with hydrofluoric acid and teeth with phosphoric acid followed by adhesive cementation. Periodontal parameters (Plaque index (PI), bleeding on probing (BOP), periodontal pocket depth (PPD), and clinical attachment loss (CAL)) were recorded at baseline and after 4, 12, and 24 weeks of lumineer cementation. Assessment of GCF flow rate and levels of IL-6 and TNF-α was made using enzyme linked immunosorbent assay (ELISA). The statistical significance was determined by the t-test, analysis of variance and post hoc Tukey’s test. It was found that PI, BOP, PPD, and CAL at baseline and 24 weeks were comparable (p &gt; 0.05). The GCF volume at baseline was comparable to the GCF at week 24 (p &gt; 0.05). The IL-6 levels at baseline (5.4 ± 3.6) were similar to those at 24 week (7.4 ± 5.2) (p &gt; 0.05). The TNF-α at week 4 (65.3 ± 16.2), 12 (25 ± 10.2), and 24 (21.3 ± 7.6) was higher than the baseline (13.7 ± 5.8) (p &lt; 0.05). Clinical periodontal parameters and GCF volume among patients treated with ceramic lumineers at baseline and twenty-four week follow-up were comparable. The GCF TNF-α levels significantly increased after ceramic lumineer cementation at 24-week follow-up.

Efficacy of a novel post-foaming dental gel on gingival inflammation: A randomized controlled clinical trial.

A pilot randomized controlled clinical trial was performed to evaluate the efficacy of a post-foaming dental gel containing cetylpridinium chloride (CPC), hydrogen peroxide (H2 O2 ), sodium bicarbonate, and antioxidants on periodontal/oral health. Individuals with gingivitis or mild-moderate periodontitis (n=36) were included and randomly assigned to Group 1 and 2 with foaming gel loaded on a mouthpiece with a light source and controlled warming heat built-in unit or on a toothbrush, respectively, in addition to regular twice-daily brushing. Group 3 served as control with twice daily brushing and further assigned split-mouth to Group 3a-un-flossed and Group 3b-flossed. Gingival index (GI) and bleeding on probing (BOP) were evaluated in addition to plaque index (PI), pocket depth, and clinical attachment level at days 14, 28, 42 (treatment), and 60 (maintenance). Subgingival plaque microbial profiles and gingival crevicular fluid (GCF) cytokine levels were determined by DNA-DNA hybridization and multiplexing assays, respectively. Exploratory analyses included esthetic outcomes: changes in tooth color and levels of volatile sulfur compounds in breath. Statistical analyses were conducted using ANOVA with a post hoc analysis of Fisher's LSD. Use of post-foaming gel in both test groups resulted in significant changes in GI and BOP at Day 42 compared to control and un-flossed control (P<0.05). Device-enhanced foaming gel significantly reduced the PI in Group 1 at Day 42 compared to control and un-flossed control (P=0.02; P=0.007, respectively). GCF IL-6 and TNF-α levels were significantly reduced in Group 2 compared to control (PIL-6 =0.01, PTNF-α =0.02). Post-foaming gel resulted in greater reductions in periodontopathogens, whereas health-associated species remained stable. Despite cessation of adjunct treatments, Group 1 and 2 continued having reduced levels of GI, BOP, and PI at Day 60 (P<0.05). The novel post-foaming dental gel improves oral health by reducing gingival inflammation at the local site in addition to better esthetic outcomes.

Effect of non-surgical periodontal treatment on gingival crevicular fluid hypoxia inducible factor-1 alpha, vascular endothelial growth factor and tumor necrosis factor-alpha levels in generalized aggressive periodontitis patients.

Hypoxia-inducible angiogenic pathway involving hypoxia inducible factor-1 alpha (HIF-1α), vascular endothelial growth factor (VEGF) and tumor necrosis factor-alpha (TNF-α) may regulate several biological processes related to inflammation. The present study aimed to assess the effect of non-surgical periodontal treatment on gingival crevicular fluid (GCF) HIF-1α, VEGF, and TNF-α levels in generalized aggressive periodontitis (G-AgP). Twenty G-AgP patients and 20 periodontally healthy individuals were included. G-AgP patients received scaling and root planning (SRP), per quadrant at a 1-week-interval, performed with ultrasonic and periodontal hand instruments. GCF samples were collected and clinical periodontal parameters including probing depth, clinical attachment level, gingival index and plaque index were recorded at baseline, 1 and 3 months after treatment. Biomarker levels in GCF were analyzed by ELISA. At baseline all clinical parameters and GCF HIF-1α, VEGF, and TNF-α levels were significantly higher in G-AgP patients compared to healthy control (P<0.05). All clinical parameters improved over the 3-month-period in G-AgP patients (P<0.05). GCF HIF-1α levels in G-AgP reduced at 1 and 3 months post-treatment, however, this did not reach to statistical significance (P>0.05). GCF VEGF and TNF-α levels remained unchanged throughout the study period (P>0.05). Within the limitations of the present study, although HIF-1α seems to possess a potential diagnostic value for G-AgP, it might not be a proper predictor of clinically favorable treatment outcome. SRP plus different adjunctive therapies could provide better information about the prognostic role of hypoxia-inducible angiogenic pathway in G-AgP.

Inflammatory mediators in saliva and gingival fluid of children with congenital heart defect.

(a) To compare levels of pro- and anti-inflammatory mediators in saliva and gingival crevicular fluid (GCF) in children with and without congenital heart defects (CHDcases and controls) and to test whether a systemic component exists in CHD cases by controlling for gingivitis and plaque scores. (b) To correlate the levels of pro- and anti-inflammatory mediators in GCF and saliva with plaque bacterial composition among CHD cases and controls. Whole un-stimulated saliva and GCF samples were collected (60 CHD cases, 60 controls [Sudan]) and were analysed for levels of prostaglandin E2 (PGE2), interleukin-1β (IL-1β), tumour necrosis factor-α (TNF-α), interleukin-1ra (IL-1ra) and interleukin-10 (IL-10) levels. These levels were correlated with the previously reported levels of four red complex bacteria. Significantly elevated levels of PGE2 and IL-1β in GCF and IL-1β and TNF-α in saliva were detected among CHD cases compared with controls. General linear model (GLM) analyses revealed that PGE2 and IL-1β levels remained significantly higher in GCF and saliva samples, respectively, among CHD cases after controlling for gingivitis and plaque score, whereas TNF-α and IL-10 levels were significantly lower in their GCF samples. Additionally, IL-1β level was significantly positively correlated to the counts of the four red complex species in their GCF. In addition to higher levels of some pro-inflammatory mediators in saliva and GCF corresponding to more gingivitis in CHD cases, also a systemic inflammatory component exists and is reflected in these two oral fluids.

Assessment of saliva and gingival crevicular fluid soluble urokinase plasminogen activator receptor (suPAR), galectin‐1, and TNF‐α levels in periodontal health and disease

The aim of the study is to evaluate saliva and gingival crevicular fluid (GCF) levels of suPAR and galectin-1 in different periodontal health status and relationship between these molecules and TNF-α to understand the roles of these molecules in periodontal inflammation process. Soluble urokinase plasminogen activator receptor (suPAR) has been described as a biological marker of inflammation and immunological activation. Galectin-1, a member of the galectin family, is an anti-inflammatory cytokine. However, to date, levels of these two molecules in periodontal health and disease have not been well documented. A total of 60 individuals, 20 with chronic periodontitis (group P), 20 with gingivitis (group G), and 20 with healthy periodontium (group H) were recruited for this study. Full-mouth clinical periodontal measurements were recorded in periodontal charts. GCF and whole saliva samples were collected to determine the levels of suPAR, galectin-1, and TNF-α in study groups using enzymelinked immunosorbent assay (ELISA) method. The GCF total amount of suPAR, galectin-1, and TNF-α in GCF was similar in group P and G (P>.05). The GCF total amounts of these molecules in GCF were higher in the group G and P compared to the group H (P<.05), whereas the GCF concentrations of suPAR and galectin-1 were lower in the group G and P compared to the group H (P<.05).The saliva concentration of suPAR was significantly higher in group P compared to the group G and H (P<.05). It was also higher in the group G compared to the group H but there is no significant difference between the groups (P>.05). Salivary galectin-1 levels were similar in the study groups (P>.05). Increased levels of GCF suPAR, galectin-1, and saliva suPAR in periodontal disease suggest that these molecules may play a role in the periodontal inflammation. suPAR and galectin-1 may be considered as potential biomarkers in periodontal disease.

Effects of exercise on periodontal parameters in obese women.

Several studies have demonstrated an association between obesity, periodontitis, and exercise. This study aimed to investigate the effects of regular exercise on obese women with periodontal disease, using serum, saliva, and gingival crevicular fluid (GCF) samples. A before-after study design was adopted to evaluate the effects of 12 weeks of regular exercise on obese women grouped according to periodontal status, without a control group (no exercise). The study sample comprised of 15 patients without periodontitis (NP group) and 10 patients with chronic periodontitis (CP group), from whom periodontal parameters were measured and serum, saliva, and GCF samples were collected. Body mass index (BMI), anthropometric measurements, somatotype-motoric tests, and maximal oxygen consumption (VO2max) were recorded at baseline and after exercise. Med Calc was used for statistical analysis. After exercise, a significant decrease in BMI and a significant increase in VO2max were observed in both groups. A significant decrease in probing depth and clinical attachment loss, serum leptin, GCF tumor necrosis factor-α(TNF-α) and leptin, and a significant increase in GCF resistin were observed in the CP group. A significant decrease in serum TNF-α and leptin levels and a significant increase in serum resistin and GCF TNF-α, leptin, resistin, and adiponectin levels were observed in the NP group. Significant correlations between bleeding on probing and levels of interleukin-1β and leptin in GCF were observed in the CP group. This study showed that regular exercise exerts different impacts with respect to clinical and biochemical aspects of periodontal and systemic conditions in obese women.

Quantification of TNF-α in Patients with Periodontitis and Type 2 Diabetes.

Objective The present study aimed to compare variations in quantified tumor necrosis factor-alpha (TNF-α) levels in patients with periodontitis stage 2 grade B (POD2B) and/or type 2 diabetes (T2D) and to identify any relationships between this cytokine and these diseases. Methods Levels of the cytokine TNF-α in gingival crevicular fluid in patients with POD2B and/or T2D were evaluated. A total of 160 subjects were distributed into four groups: those with POD2B (n=44); those with T2D (n=37); those with POD2B/T2D (n=40); and healthy subjects (n=39). Glycosylated hemoglobin (HbA1c) and blood glucose (BG) levels were quantified in each subject. Data were collected on body mass index (BMI), loss of insertion (LI), and probe depth (PD). Gingival crevicular fluid samples were collected from the most acutely affected periodontal pocket and gingival sulcus in each subject, and TNF-α was quantified by multiplex analysis. Results Kruskal Wallis tests was used to identify differences in TNF-α levels, LI, PD, BMI, BG, and HbA1c by group. Differences (p<0.001) were found for LI, PD, BG, and HbA1c. A Spearman test was used to calculate possible correlations between TNF-α levels and LI or PD identified a weak but significant negative correlation of TNF-α with LI (Rho=-0199; p=0.012), and a moderately positive correlation of LI with PD (Rho=0.509; p < 0.001). Conclusions No variation was found between TNF-α levels and the presence of POD2B, POD2B/T2D, or T2D, suggesting the absence of any direct relationship between progression of these diseases and TNF-α levels. However, a correlation was present between low TNF-α concentrations and greater LI.

Relationship between TNF-α, MMP-8, and MMP-9 levels in gingival crevicular fluid and the subgingival microbiota in periodontal disease.

Periodontitis is modulated by a complex dysbiotic microbiota, these species stimulate upward the production of pro-inflammatory cytokines such as TNF-α, which, in turn, upregulates the production of bone resorption molecules. Enzymes such as MMP-8 and 9 have been associated with the destructive disease. This study evaluated the composition of periodontal microbiota with the checkerboard hybridization technique and its correlation with TNF-α, MMP-8, and MMP-9 evaluated with ELISA, of 80 patients (45 healthy, and 35 with chronic periodontitis). The frequency of the 18 species evaluated was higher in patients with bone loss compared with control group. TNF-α in gingival crevicular fluid was significantly higher in bone loss group (p < 0.01); MMP-8 (p = 0.34) by MMP-9 (p < 0.05) in bone loss group obtained lower values than in control group. Positive correlation of TNF-α was obtained with Aggregatibacter actinomycetemcomitans (rho = 0.38; p < 0.01), Fusobacterium nucleatum (rho = 0.25; p < 0.05) and Porphyromonas gingivalis (rho = 0.26; p < 0.05); negative correlation of MMP-8 with A. actinomycetemcomitans (rho = 0.26; p < 0.01), Capnocytophaga sputigena (rho = 0.33; p < 0.01), and F. nucleatum (rho = 0.21; p < 0.05); also negative correlation of MMP-9 with F. nucleatum (rho = 0.23; p < 0.05), P. gingivalis (rho = 0.23; p < 0.05), and Tannerella forsythia (rho = 0.26; p < 0.01). TNF-α increased due to the increase in each count of A. actinomycetemcomitans (β = 0.57; p = 0.00). The presence of A. actinomycetemcomitans (β = 1.88; p = 0.00), Campylobacter rectus (β = 0.78; p = 0.01), F. nucleatum (β = 0.65; p = 0.04), and P. gingivalis (β = 0.65; p = 0.04) significantly increases TNF-α levels. TNF-α in gingival crevicular fluid, despite the minimal amounts collected, is a good biomarker of periodontal disease; since levels of TNF-α increases with the increase of the most harmful species to the periodontium.