MATERIALS AND METHODS: The addressed focused question was "Is there a difference in the resistin levels between individuals with CP and those without CP?" four electronic databases: Medline, PubMed (National Institutes of Health, Bethesda), EMBASE, and Science direct databases from 1977 up to March 2016 for appropriate articles addressing the focused question. EMBASE and Medline were accessed using OVID interface which facilitated simultaneous search of text words, MeSH or Emtree. Unpublished studies (gray literature) were identified by searching the Open-GRAY database and references of the included studies (cross referencing) were performed to obtain new studies. In-vitro studies, animal studies, studies that reported levels of other cytokines but not resistin, letters to the editor and review papers were excluded.
RESULTS: Ten studies were included. Nine studies compared resistin levels between CP and periodontally healthy (H) individuals and reported higher mean serum and GCF levels of resistin in CP patients than the H controls. Two studies showed comparable resistin levels from GCF and serum between diabetes mellitus with CP (DMCP) and CP groups. Three studies included obese subjects and showed comparable serum and GCF resistin levels between obese subjects with CP (OBCP) and CP subjects.
CONCLUSIONS: CP patients were presented with elevated levels of GCF or serum resistin as compared with H individuals. Resistin modulates inflammation in chronic periodontal disease and may be used as surrogate measure to identify subjects at risk for periodontitis. Resistin levels in patients with CP and systemic inflammatory disorders such as diabetes, obesity, or rheumatoid arthritis was not significantly higher than the levels in patients with only CP.
METHODS: Twenty patients with periodontitis were recruited for the trial. Following random allocation of either quadrants of the selected jaw to test or control treatment, conventional non-surgical periodontal therapy (NSPT) was performed. In addition, the test side received adjunct photodynamic therapy. Probing depth (PD), clinical attachment level, bleeding on probing (BoP) and plaque scores (PS%) were recorded at phase 0 (baseline), phase 1 (immediately after NSPT), phase 2 (7 days following NSPT), phase 3 (1 month following NSPT) and phase 4 (3 months following NSPT). Subgingival plaque samples for quantification of Aa by real-time polymerase chain reaction was performed at phases 0, 1, 2 and 4.
RESULTS: There was a significant clinical improvement at phases 3 and 4 compared with baseline while BoP reduced significantly only in the test group at phase 4. However, no difference in the quantification of Aa was detected between the groups.
CONCLUSIONS: Within the limits of the study, PDT adjunct to scaling and root planing does not lead to quantitative reduction of Aa in periodontitis patients.
METHODS: This is a meta- analysis study, following the preferred reporting items for systematic reviews and meta- analyses (PRISMA). Relevant studies were searched in the health related electronic databases. Methodological quality of the included studies were assessed using the Newcastle-Ottawa Scale. For individual studies, odds ratio (OR) and its 95%confidence interval (CI) were calculated to assess the strength of association between IL10 polymorphisms (- 1082 A > G, -819C > T, - 592 A > C) and the risk of periodontitis. For pooling of the estimates across studies included, the summary OR and its 95% CIs were calculated with random-effects model. The pooled estimates were done under four genetic models such as the allelic contrast model, the recessive model, the dominant model and the additive model. Trial sequential analysis (TSA) was done for estimation of the required information size for this meta-analysis study.
RESULTS: Sixteen studies were identified for this review. The included studies were assessed to be of moderate to good methodological quality. A significant association between polymorphism of IL10-1082 A > G polymorphism and the risk of chronic periodontitis in the non-Asian populations was observed only in the recessive model (OR,1.42; 95% CI:1.11, 1.8,I2: 43%). The significant associations between - 592 A > C polymorphism and the risk of aggressive periodontitis in the non-Asian populations were observed in particular genetic models such as allele contrast (OR, 4.34; 95%CI:1.87,10.07,I2: 65%) and recessive models (OR, 2.1; 95% CI:1.16, 3.82,I2: 0%). The TSA plot revealed that the required information size for evidence of effect was sufficient to draw a conclusion.
CONCLUSIONS: This meta-analysis suggested that the IL10-1082 A > G polymorphism was associated with chronic periodontitis CP risk in non-Asians. Thus, in order to further establish the associations between IL10 (- 819 C > T, - 592 A > C) in Asian populations, future studies should include larger sample sizes with multi-ethnic groups.
METHODS: A total of 48 periodontitis subjects (obese, n = 18; normal weight, n = 30) were recruited (hereafter will be referred as participants) to participate into a prospective, before and after clinical trial. Obesity status is defined by body mass index (BMI) criteria (obese: ≥30 kg/ m2; normal weight
METHODS: Five specialist periodontal clinics in the Ministry of Health represented the public sector in providing clinical and cost data for this study. Newly-diagnosed periodontitis patients (N = 165) were recruited and followed up for one year of specialist periodontal care. Direct and indirect costs from the societal viewpoint were included in the cost analysis. They were measured in 2012 Ringgit Malaysia (MYR) and estimated from the societal perspective using activity-based and step-down costing methods, and substantiated by clinical pathways. Cost of dental equipment, consumables and labour (average treatment time) for each procedure was measured using activity-based costing method. Meanwhile, unit cost calculations for clinic administration, utilities and maintenance used step-down approach. Patient expenditures and absence from work were recorded via diary entries. The conversion from MYR to Euro was based on the 2012 rate (1€ = MYR4).
RESULTS: A total of 2900 procedures were provided, with an average cost of MYR 2820 (€705) per patient for the study year, and MYR 376 (€94) per outpatient visit. Out of this, 90% was contributed by provider cost and 10% by patient cost; 94% for direct cost and 4% for lost productivity. Treatment of aggressive periodontitis was significantly higher than for chronic periodontitis (t-test, P = 0.003). Higher costs were expended as disease severity increased (ANOVA, P = 0.022) and for patients requiring surgeries (ANOVA, P
METHODS: Databases (MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials and Cochrane Oral Health Group Trials Register databases) were searched up to and including July 2016. The primary outcome was probing depth (PD), and the secondary outcomes were changes in clinical attachment level (CAL) and bone defect (BD) fill. The mean differences (MD) of outcomes and 95% confidence intervals (CI) for each variable were calculated using random effect model.
RESULTS: Eight clinical studies were included. Seven studies used alendronate as an adjunct to SRP; of these, four studies used topical application and three used oral alendronate. Considering the effects of adjunctive bisphosphonates as compared to SRP alone, a high degree of heterogeneity for PD (Q value = 39.6, P
MATERIALS AND METHODS: Forty chronic periodontitis patients completed this study and received periodontal treatment comprising scaling and root planing plus ultrasonic debridement. Clinical data were recorded at baseline, 6 weeks (R1) after treatment completion (full-mouth or quadrant-scaling and root planing) and 25 weeks after baseline (R2). Serum samples were taken at each time point and cytokines concentrations determined by ELISA.
RESULTS: Following treatment, statistically significant reductions were noted in clinical parameters. However, IL-17A and IL-17E concentrations were significantly greater than baseline values before- and after-adjusting for smoking. The IL-17A:IL-17E ratio was lower at R1 and R2. Serum IL-6 and TNF levels were significantly lower at R1 only. Also exclusively at R1, serum IL-17A and IL-17E correlated positively with clinical parameters, while the IL-17A:IL-17E ratio correlated negatively with probing pocket depth and clinical attachment.
CONCLUSION: Increased serum IL-17E and a reduced IL-17A:IL-17E ratio may be indicative and/or a consequence of periodontal therapy. Therefore, the role of IL-17E in periodontal disease progression and the healing process is worthy of further investigation.
CLINICAL RELEVANCE: IL-17E may be a valuable biomarker to monitor the healing process following periodontal treatment as increased IL-17E levels and a reduced IL-17A:IL-17E ratio could reflect clinical improvements post-therapy. Therefore, monitoring serum IL-17E might be useful to identify individuals who require additional periodontal treatment.