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Objective: The aim of the present study was to compare periodontal status and antioxidant profile in unstimulated saliva of systemic sclerosis (SSc) patients with periodontitis and systemically healthy periodontitis patients., Design: Twenty patients with established diagnoses of systemic sclerosis and periodontitis (SSc group) and 20 systemically healthy individuals with periodontitis (P group) were enrolled in the study. Clinical periodontal parameters (clinical attachment level (CAL), gingival recession (GR), periodontal probing depth (PPD), and gingival index (GI)) and concentration of uric acid (UA), superoxide dismutase (SOD), and glutathione peroxidase (GPX) in unstimulated saliva samples were assessed., Results: There were significantly higher mean values of CAL (4.8 ± 0.21 mm versus 3.18 ± 0.17 mm; p ≤ 0.001) and GR (1.66 ± 0.90 mm versus 0.46 ± 0.54 mm; p ≤ 0.001) in the SSc group when compared to the P group. Significantly higher level of GPX ( p ≤ 0.001) and SOD ( p ≤ 0.001) in unstimulated saliva was detected in the SSc group in comparison with the P group. The specific activity of UA did not significantly differ between the two groups ( p = 0.083)., Conclusion: The results may indicate higher periodontal destruction and antioxidant perturbations in unstimulated saliva of SSc patients with periodontitis compared to systemically healthy periodontitis patients., Competing Interests: The authors declare no conflict of interest., (Copyright © 2023 Stefan I. Sredojevic et al.)

Chronic periodontitis (CP) is a bacteria-driven inflammatory disease characterized by the breakdown of gingival tissue, the periodontal ligament, and alveolar bone, leading ultimately to tooth loss. We previously reported the pleckstrin gene ( PLEK ) to be highly upregulated in gingival tissue of patients with CP and the only gene concurrently upregulated in other inflammatory diseases including rheumatoid arthritis and cardiovascular diseases. Using saliva from 169 individuals diagnosed with CP and healthy controls, we investigated whether pleckstrin could serve as a novel biomarker of periodontitis. Additionally, we explored signal pathways involved in the regulation of PLEK using human gingival fibroblasts (HGFs). Pleckstrin levels were significantly higher (p < 0.001) in the saliva samples of patients with CP compared to controls and closely associated with CP severity. Immunohistochemical analysis revealed the expression of pleckstrin in inflammatory cells and gingival fibroblasts of CP patients. To explore the signal pathways involved in pleckstrin regulation, we stimulated HGFs with either interleukin-1β (IL-1β) or lipopolysaccharides (LPS) alone, or in combination with inhibitors targeting c-Jun N-terminal kinase, tyrosine kinase, protein kinase C, or p38 MAP kinase. Results showed that IL-1β and LPS significantly increased PLEK mRNA and pleckstrin protein levels. VX-745, the p38 MAP kinase inhibitor significantly decreased IL-1β- and LPS-induced pleckstrin levels at both the mRNA and the protein level. Together, these findings show that pleckstrin could serve as a salivary biomarker for the chronic inflammatory disease periodontitis and a regulator of inflammation via the p38 MAP kinase pathway., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Alim, Njenda, Lundmark, Kaminska, Jansson, Eriksson, Kats, Johannsen, Arvidsson, Mydel and Yucel-Lindberg.)

Abstract: Previous studies have suggested that obesity might be associated with chronic periodontitis (CP); however, no clear conclusions have been reached so far. In this retrospective cohort study, we aimed to investigate the association between obesity and CP by using a large population-based dataset in Taiwan.A population-based retrospective cohort study was conducted using the Longitudinal Health Insurance Database 2010 (LHID2010) derived from the National Health Insurance Research database in Taiwan, from 2000 to 2013. Obesity and non-obesity groups were matched with sex, age, urbanization level, socioeconomic status, and the related comorbidities by using the propensity score method at a 1:2 ratio.An obese cohort (n = 4140) and a non-obese cohort (n = 8280) were included in this study, with an average age of 41.7 ± 13.8 years and 42.0 ± 14.0 years, respectively. The risk of CP for the patients with obesity was 1.12-fold compared with those without obesity (hazard ratio, 1.12; 95% confidence interval, 1.01-1.25). In the subgroup analysis according to age and sex, the hazard ratio of CP were 1.98 (95% confidence interval, 1.22-3.22) in the subgroup of age equal to or older than 65 years. The risk of CP showed no difference between obesity and non-obesity groups in both sex.This population-based cohort study demonstrated that obesity was associated with the development of CP in Taiwan., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.)

Aim: The aim of this study was to explore the possible associations between single nucleotide polymorphisms (SNPs) and DNA methylation levels of seven genes in the inflammatory response pathway with susceptibility to chronic periodontitis (CP) among the Uighur population of the Xinjiang Autonomous Region of China. Methods: A total of 444 eligible subjects (279 CP patients and 165 healthy controls) were enrolled in the study. Genomic DNA was obtained from gingival tissue for genotyping eight SNPs and performing methylation measurements of seven genes. Results: SNP rs2070745 in the formyl peptide receptor 1 ( FPR1 ) gene achieved statistical significance in a standard allelic association analysis for CP ( p  = 0.02). The frequency of the rs2070745 minor allele G was higher in the cases than in controls (0.367 vs. 0.291). Additionally, rs2070745 was significantly associated with CP under the dominant genetic model ( p  = 0.03). Using logistic regression analysis, rs2070745 was found to be consistently associated with CP under the additive dominant model, and this association remained significant after covariates were taken into account [odds ratio (OR) = 1.49 (1.09-2.05), p  = 0.014; OR = 1.58 (1.04-2.40), p  = 0.031, respectively]. No significant gene-gene interactions were identified. Although we did not find a polymorphism in interleukin 6 ( IL6 ) associated with CP in our study, the methylation level of a CpG island region located within the promoter region of IL6 was significantly less in CP patients compared with controls ( p  < 0.05). Conclusions: The genetic polymorphism rs2070745 in FPR1 and the methylation level of the promoter region of IL6 might be associated with CP in the Uighur population of China.

Monocyte chemoattractant protein 1 (MCP-1) plays an important role in the development of periodontitis. The purpose of this investigation was to evaluate association of the  MCP-1 gene polymorphism with chronic periodontitis in patients with end-stage renal disease (ESRD). One hundred fifty ESRD patients with chronic periodontitis (CP), 100 without CP and 190 healthy controls were included in this study. Genomic DNA from all participants was genotyped for the -2518 (A/G) polymorphism by a polymerase chain reaction - restriction fragment length polymorphism (PCR--RFLP) assay. Significant differences were observed in the genotype and allele frequencies between patients with ESRD and CP and controls.  The G allele frequency was significantly higher in patients than in control subjects, with odds ratio 1.77 (95 % CI 1.2-2.5), p = 0.0014. For the GG genotype the OR was 3.63 (95 % CI 1.5-8.76), p = 0.041.  No significant differences in the polymorphism distribution were observed between ESRD patients  without CP and control subjects. Comparison of the MCP-1 gene polymorphism distribution in ESRD patients with various primary diseases leading to ESRD did not show any significant differences. The mean MCP-1 serum levels were compared between subgroups. They were significantly higher in ESRD patients with CP (582 ± 112 pg/ml) than in patients without CP (309 ± 103 pg/ml) and controls (265 ± 85 pg/ml). Our results suggest that the  MCP-1 -2518 A/G  polymorphism might be a novel risk factor for developing chronic periodontitis in patients with ESRD.

Periodontitis is an inflammatory disease that causes damages to periodontium and alveolar bone. Overactivation and formation of osteoclasts can cause bone destruction, which contributes to periodontitis development. Receptor activator of nuclear factor κB ligand (RANKL)-mediated NF-κB signaling plays an essential role in osteoclasts differentiation. We aimed to study the effects of NIK-SMI1, an NF-κB-inducing kinase (NIK) inhibitor, on the osteoclastogenesis in vitro and periodontitis progression in vivo. A ligature-induced mice model of periodontitis was incorporated to test the potential therapeutic effect of NIK-SMI1 on periodontitis. The target protein and mRNA expression levels were determined by Western blot assay and real-time PCR assay, respectively. We found that the administration of NIK-SMI1 strongly inhibited the RANKL-stimulated non-canonical NF-κB signaling as demonstrated by decreased nuclear p52 expression and activity. Blocking NIK activity also resulted in reduced osteoclasts specific genes expression and enhanced IFN-β expression. NIK-SMI1 treatment resulted in attenuated periodontitis progression and pro-inflammatory cytokines expression in vivo. Our study suggested that NIK-SMI1 exerts beneficial effects on the mitigation of osteoclastogenesis in vitro and periodontitis progression in vivo. Application of NIK-SMI1 may serve as a potential therapeutic approach for periodontitis., (© The Author(s) 2020. Published by Oxford University Press on behalf of FEMS.)

To suggest candidate genes involved in periodontitis, we combined gene expression data of periodontal biopsies from Collaborative Cross (CC) mouse lines, with previous reported quantitative trait loci (QTL) in mouse and with human genome-wide association studies (GWAS) associated with periodontitis. Periodontal samples from two susceptible, two resistant and two lines that showed bone formation after periodontal infection were collected during infection and naïve status. Differential expressed genes (DEGs) were analyzed in a case-control and case-only design. After infection, eleven protein-coding genes were significantly stronger expressed in resistant CC lines compared to susceptible ones. Of these, the most upregulated genes were MMP20 (P = 0.001), RSPO4 (P = 0.032), CALB1 (P = 1.06×10 -4 ), and AMTN (P = 0.05). In addition, human orthologous of candidate genes were tested for their association in a case-controls samples of aggressive (AgP) and chronic (CP) periodontitis (5,095 cases, 9,908 controls). In this analysis, variants at two loci, TTLL11/PTGS1 (rs9695213, P = 5.77×10 -5 ) and RNASE2 (rs2771342, P = 2.84×10 -5 ) suggested association with both AgP and CP. In the association analysis with AgP only, the most significant associations were located at the HLA loci HLA-DQH1 (rs9271850, P = 2.52×10 -14 ) and HLA-DPA1 (rs17214512, P = 5.14×10 -5 ). This study demonstrates the utility of the CC RIL populations as a suitable model to investigate the mechanism of periodontal disease.

Background/aim: Epstein-Barr virus (EBV) associates with human chronic periodontitis (CP) progression. We previously demonstrated that butyric acid (BA), produced by periodontopathic bacteria, induced EBV lytic switch activator BZLF1 expression. We investigated whether short chain fatty acids (SCFAs) in CP patients' saliva enabled EBV reactivation., Materials and Methods: Saliva was collected from seven CP patients and five periodontally healthy individuals. SCFAs were quantified using HPLC. BZLF1 mRNA and its pertinent protein ZEBRA were determined with Real-time PCR and western blotting. Histone H3 acetylation (AcH3) was further examined., Results: BZLF1 mRNA expression and transcriptional activity in EBV-infected Daudi cells were induced only when treated with the CP saliva. Among SCFAs, BA alone correlated significantly with the BZLF1 transcription (r=0.88; p<0.02). As expected, CP patients' saliva induced AcH3., Conclusion: BA in saliva may play a role in EBV reactivation and hence contribute to EBV-related disease progression in CP patients., (Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Although patients under supportive periodontal therapy (SPT) have a stable periodontal condition, the acute symptom of chronic periodontal disease occasionally occurs without a clear reason. Therefore, in the present study, to obtain a better understanding of this relationship in patients undergoing SPT, we hypothesized that the acute symptom of chronic periodontal disease might be affected by climate factors. We conducted a questionnaire study and carried out oral examinations on patients undergoing SPT who had been diagnosed as having the acute symptom of chronic periodontal disease. We collected climate data from the local climate office in Okayama city, Japan. We predicted parameters that affect the acute symptom of chronic periodontal disease with unidentified cause and divided patients into high and low groups in terms of climate predictors. Then we defined the cut-off values of parameters showing significant differences in the incidence of the acute symptom of chronic periodontal disease. The incidence of the acute symptom of chronic periodontal disease with unidentified cause was significantly different when the cases were classified according to the maximum hourly decrease in barometric pressure (1.5 and 1.9 hPa) ( p = 0.04 and p = 0.03, respectively). This suggests that climate variables could be predictors of the acute symptom of chronic periodontal disease. Therefore, gaining a better understanding of these factors could help periodontal patients undergoing SPT prepare to avoid the acute symptom of chronic periodontal disease.

Chronic periodontitis is an inflammatory disease of tooth-supporting tissues associated with Porphyromonas gingivalis. Expansion and invasion of this bacterium into the periodontium is associated with changes in the metabolome of the oral cavity., Materials and Methods: Metabolomics analysis of mouth washout and tongue swab samples based on proton nuclear magnetic resonance ( 1 H-NMR) method was employed to determine metabolic status of the oral cavity in chronic periodontal disease., Results: Mouth washout extracts contained a total of 23 metabolites and tongue swab extracts contained 17. Identified metabolites partially overlap with the content of saliva and gingival crevicular fluid. The colonization of the oral cavity of patients with periodontitis by bacteria was manifested in the change in levels of eight metabolites., Conclusion: NMR-based metabolomics analysis is a potentially useful methodological approach for monitoring the pathological processes observed in the oral cavity in the course of periodontitis., (Copyright© 2019, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

The aim of this study is to establish the prevalence of Chronic Periodontitis (CP) in patients with Chronic Kidney Disease (CKD) and to ascertain its relationship with several factors or indicators of micro inflammation. One hundred and thirty-jive CKD patients on dialysis treatment were included. Biochemical parameters, clinical attachment level and pocket depth were recorded according of the American Academy of Periodontology and the CDC (CDC-AAP). Gingivitis and CP were recorded based on the biofilm-gingival interface (BGI) periodontal diseases classification. The rate of non-response to the survey was 10 percent. A total 2,636 teeth in 135 patients were examined, of whom 52.5% were males. Average age was 55.7 years (SD ± 1.32); 41.4% had a smoking history; 78/135 patients were on hemodialysis and 57/135 on peritoneal dialysis; 55.5% had been on dialysis for more than three years. Prevalence of gingivitis and periodontitis was 14.8%, 95% CI (9.7-21.9) and 82.2%, 95% CI (74.7 - 87.8), respectively; according to the BGI Index. Severity of CP was: No periodontitis, 14.0% 95% CI (9.1 - 21.1); mild, 11.1% 95% CI (6.7 -17.7); moderate, 28.8% 95% CI (21.7- 37.1); and severe, 45.9% 95% CI (31.6-54.47). Peritoneal dialysis and time on dialysis > 3 years increase the chance of having periodontitis, OR 11.0 95% CI (2.2-53.8) and OR 7.6 95% CI (1.1-50.2), respectively. In view of the high prevalence of CP in this population, programs designed to ensure better periodontal and gingival care in the population on dialysis need to be established., (Sociedad Argentina de Investigación Odontológica.)

Aim: To assess and compare the impact of non-surgical periodontal therapy on plasma reactive oxygen metabolites and resistin values in chronic periodontitis obese and non-obese patients., Materials and Methods: Total 200 subjects were included in the present study and were broadly divided into two study groups with 100 patients in each group as follows: group A: Obese patients with chronic periodontitis, group B: Non-obese, normal weight patients with chronic periodontitis. Various following periodontal parameter were calculated at the baseline time and two months after the non-surgical periodontal therapy. Plasma reactive oxygen metabolite (RM) and serum and GCF resistin levelswere evaluated. Assessment of all the results was done by Statistical Package for Social Sciences (SPSS) software., Results: Significant results were obtained while doing an inter-group comparison of clinical attachment levels between two study groups. Significant results were obtained while comparing the clinical attachment levels in both the study groups at different time intervals. Significant 9 reduction in the RM was seen in Group B subjects in comparison to Group A subjects 2 months after non-surgical periodontal therapy., Conclusion: In patients with chronic periodontitis, obesity can be considered as an important factor in the alteration of resistin levels., Clinical Significance: Obese patients should be motivated for reducing weight so that periodontal therapy and other treatment modalities could be carried out more effectively.

Aim: It has been suggested that periodontitis may be associated with increased oxidative stress. The objective of this study is to evaluate the possible differences in antioxidant status between chronic periodontitis (CP) and aggressive periodontitis (AP), by assessing the concentrations of antioxidants with total antioxi-dant status (TAS) and lipid peroxidation status in serum and gingival crevicular fluid (GCF) of these patients., Materials and Methods: Forty-six patients with CP, 32 patients with AP, and 50 healthy controls were included in this study. The level of enzymatic antioxidant, superoxide dismutase (SOD), nonenzymatic antioxidant uric acid, and TAS with lipid peroxidation measured in serum and GCF of patients suffering from CP and AP were compared with the healthy controls., Results: The TAS is decreased and malondialdehyde (MDA) level is increased in both serum and GCF in CP and AP compared with healthy controls (p < 0.001). Superoxide dismutase activities in GCF and serum are found to be low in both the groups of periodontitis (p < 0.001). The uric acid levels are found to be inconsistent in GCF and serum in both the groups of periodontitis., Conclusion: Lipid peroxidation and TAS were affected at systemic level in serum and in GCF of the periodontal pockets, in CP and AP. Similar comments may be made for the decrease in SOD activities and inconsistent uric acid levels., Clinical Significance: Increased oxidative stress may have a role in the pathogenesis of periodontal disease activity.

The keystone periodontal pathogen Porphyromonas gingivalis produces phosphorylated dihydroceramide lipids (sphingolipids) such as phosphoethanolamine dihydroceramide (PE DHC) and phosphoglycerol dihydroceramide (PG DHC) lipids. Phosphorylated DHCs (PDHCs) from P. gingivalis can affect a number of mammalian cellular functions, such as potentiation of prostaglandin secretion from gingival fibroblasts, promotion of RANKL-induced osteoclastogenesis, promotion of apoptosis, and enhancement of autoimmunity. In P. gingivalis , these lipids affect anchoring of surface polysaccharides, resistance to oxidative stress, and presentation of surface polysaccharides (anionic polysaccharides and K-antigen capsule). In addition to phosphorylated dihydroceramide lipids, serine dipeptide lipids of P. gingivalis are implicated in alveolar bone loss in chronic periodontitis through interference with osteoblast differentiation and function and promotion of osteoclast activity. As a prerequisite for designation as bacterial virulence factors, bacterial sphingolipids and serine dipeptide lipids are recovered in gingival/periodontal tissues, tooth calculus, human blood, vascular tissues, and brain. In addition to P. gingivalis , other bacteria of the genera Bacteroides , Parabacteroides , Porphyromonas , Tannerella , and Prevotella produce sphingolipids and serine dipeptide lipids. The contribution of PDHCs and serine dipeptide lipids to the pathogenesis of periodontal and extraoral diseases may be an underappreciated area in microbe-host interaction and should be more intensively investigated., (Copyright © 2018 American Society for Microbiology.)

Background and Objective: Comprehension of the similarities and differences in the composition of the subgingival microbiota of patients with diabetes mellitus (DM), smokers or smokers with DM is an important step in developing therapies specific for these groups at risk for periodontitis. Therefore, the aim of this study was to compare the combined and individual effects of DM and smoking on the levels and prevalence of key subgingival periodontal pathogens in patients with chronic periodontitis., Material and Methods: One hundred patients with generalized chronic periodontitis were allocated into one of the following groups: DM (n = 25, non-smokers with type 2 DM); S (n = 25, non-diabetic smokers); SDM (n = 25, smokers with type 2 DM); and control (n = 25, non-diabetic non-smokers). Two subgingival biofilm samples from healthy sites (probing depth and clinical attachment level ≤3 mm and no bleeding) and 2 from diseased sites (probing depth and clinical attachment level ≥5 mm and bleeding on probing) were analyzed by quantitative polymerase chain reaction for Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Eubacterium nodatum, Parvimonas micra, Fusobacterium nucleatum ssp. and Prevotella intermedia., Results: There were no differences among groups in the mean counts of the bacterial species studied, considering all sampled sites (healthy plus diseased sites). There were also no differences among groups regarding the prevalence of any bacteria species in healthy and diseased sites (P > .05). The mean P. micra count was significantly higher in the healthy sites of both smoking groups, than in those of the control group (P < .05)., Conclusion: The subgingival levels and prevalence of the bacterial species studied are not significantly different in subjects with chronic periodontitis presenting DM, smokers or smokers with DM. In addition, DM and smoking, jointly and individually, do not considerably affect the subgingival levels of target periodontal pathogens in patients with chronic periodontitis., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Introduction: Current studies show that, even in the era of antiretroviral therapies, HIV-1 infection is associated with more severe and frequent refractory chronic periodontitis. Areas covered: This review, based on a systematic analysis of the literature, intends to provide an update on factors that may be involved in the pathogenesis of periodontal disease in HIV-1-infected patients, including local immunosuppression, oral microbial factors, systemic inflammation, salivary markers, and the role of gingival tissue as a possible reservoir of HIV-1. Expert commentary: The therapeutic revolution of ART made HIV-1 infection a chronic controllable disease, reduced HIV-1 mortality rate, restored at least partially the immune response and dramatically increased life expectancy of HIV-1-infected patients. Despite all these positive aspects, chronic periodontitis assumes an important role in the HIV-1 infection status for activating systemic inflammation favoring viral replication and influencing HIV-1 status, and also acting as a possible reservoir of HIV-1. All these issues still need to be clarified and validated, but have important clinical implications that certainly will benefit the diagnosis and management of chronic periodontitis in HIV-1-infected patients, and also contributes to HIV-1 eradication.

This study aimed to assess the impact of hyperlipidemia on healthy and diseased periodontal tissue by evaluating oxidative stress biomarkers in gingival crevicular fluid (GCF). Clinical periodontal parameters and blood serum lipid, GCF malondialdehyde (MDA), protein carbonyl (PC), and total antioxidant capacity (TAOC) levels were evaluated in six age and sex-matched groups (n = 15 each) of normolipidemic and hyperlipidemic individuals as follows: normolipidemic + periodontally healthy (H), normolipidemic + gingivitis (G), normolipidemic + chronic periodontitis (CP), hyperlipidemic + periodontally healthy (HH), hyperlipidemic + gingivitis (HG), and hyperlipidemic + CP (HCP). GCF MDA, and PC levels varied among groups, with patients with periodontitis having the highest MDA and PC levels [CP > G > H (p < 0.01) and HCP > HG > HH (p < 0.01)] and the lowest TAOC levels [CP < G < H (p < 0.01) and HCP < HG < HH (p < 0.01)]. Furthermore, paired comparisons showed MDA and PC levels to be higher and TAOC levels to be lower in HCP compared with NCP (p < 0.01). In patients with hyperlipidemia, GCF, MDA, and PC levels positively correlated with clinical assessments and serum triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL) levels and negatively correlated with serum high-density lipoprotein cholesterol (HDL) levels, whereas GCF TAOC levels negatively correlated with clinical assessments and serum TG, TC, and LDL levels, but positively correlated with serum HDL levels (p < 0.01). In normolipidemic patients, GCF, MDA, and PC levels positively correlated with clinical assessments and serum TG levels and negatively correlated with serum HDL levels, whereas GCF TAOC levels negatively correlated with clinical assessments and serum TG levels and positively correlated with serum HDL levels (p < 0.01). In conclusion, abnormal serum lipid subfractions could be considered a risk factor for enhancing oxidative stress in GCF in the presence of periodontal disease.

Background and Objective: The relationship between atherothrombotic cardiovascular disease (ATCD) and localised infections in teeth, including caries and chronic apical periodontitis (CAP) has not been studied much and is not well defined., Method: A systematic search was performed using the scientific databases PubMed and Medline from 1989 to 2016., Results: A significant relationship was observed with ATCD in 10 out of 10 studies addressing the degree of oral hygiene, in 14 of 17 that included loss of teeth, in 6 of 12 that analysed caries and in 11 of 15 that included CAP. However, there was a huge methodological heterogeneity., Conclusions: It can be concluded that there is an association between CAP and ATCD. Patients with ATCD present a worse oral hygiene status and fewer teeth., (Copyright © 2017 Elsevier España, S.L.U. All rights reserved.)

Objective: To determine risk factors for chronic periodontitis in 30-60 year olds in Sri Lanka. Cases and controls for this population based unmatched case-control study were identified from a broader cross-sectional study which was conducted to determine the prevalence of chronic periodontitis in 30-60 year old adults in Colombo district Sri Lanka. The study included 694 cases and 706 controls. Data were collected by means of a pre-tested interviewer administered questionnaire to obtain information about socio-demographic and behavioural factors, a physical examination to record anthropometric measurements and an oral examination., Results: Being a male, a Muslim, belonging to the 45-60 year old age group, having less than 12 years of education, using the finger to clean teeth, current smoking, current betel quid chewing, self-reported diabetes and hypertension emerged as risk factors for chronic periodontitis., Conclusions: Several socio-demographic and behavioural factors as well as co-morbid conditions emerged as independent risk factors for chronic periodontits in this population. The findings could be used for planning programmes to reduce the burden of chronic periodontits in Colombo district Sri Lanka.

Objective: Alendronate (ALN) inhibits osteoclastic bone resorption and triggers osteostimulative properties both in vivo and in vitro, as shown by increase in matrix formation. This study aimed to explore the efficacy of 1% ALN gel as local drug delivery (LDD) in adjunct to scaling and root planing (SRP) for the treatment of chronic periodontitis among smokers., Material and Methods: 75 intrabony defects were treated in 46 male smokers either with 1% ALN gel or placebo gel. ALN gel was prepared by adding ALN into carbopol-distilled water mixture. Clinical parameters [modified sulcus bleeding index, plaque index, probing depth (PD), and periodontal attachment level (PAL)] were recorded at baseline, at 2 months, and at 6 months, while radiographic parameters were recorded at baseline and at 6 months. Defect fill at baseline and at 6 months was calculated on standardized radiographs by using the image analysis software., Results: Mean PD reduction and mean PAL gain were found to be greater in the ALN group than in the placebo group, both at 2 and 6 months. Furthermore, a significantly greater mean percentage of bone fill was found in the ALN group (41.05±11.40%) compared to the placebo group (2.5±0.93%)., Conclusions: The results of this study showed 1% ALN stimulated a significant increase in PD reduction, PAL gain, and an improved bone fill compared to placebo gel in chronic periodontitis among smokers. Thus, 1% ALN, along with SRP, is effective in the treatment of chronic periodontitis in smokers.

Background: Periodontitis is an inflammatory disease caused by bacterial triggering of the host immune-inflammatory response, which in turn is regulated by microRNAs (miRNA). Polymorphisms in the miRNA pathways affect the expression of several target genes such as tumor necrosis factor-α and interleukins, which are associated with progression of disease., Objective: The objective of this study was to identify the association between the MiR-146a single nucleotide polymorphisms (SNPs) (rs2910164, rs57095329, and rs73318382), the MiR-196a2 (rs11614913) SNP and chronic periodontitis., Methods: Genotyping was performed for the MiR-146a (rs2910164, rs57095329, and rs73318382) and the MiR-196a2 (rs11614913) polymorphisms in 180 healthy controls and 190 cases of chronic periodontitis by the direct Sanger sequencing technique. The strength of the association between the polymorphisms and chronic periodontitis was evaluated using logistic regression analysis. Haplotype and linkage analyses among the polymorphisms was performed. Multifactorial dimensionality reduction was performed to determine epistatic interaction among the polymorphisms., Results: The MiR-196a2 polymorphism revealed a significant inverse association with chronic periodontitis. Haplotype analysis of MiR-146a and MiR-196a2 polymorphisms revealed 13 different combinations, of which 5 were found to have an inverse association with chronic periodontitis., Conclusion: The present study has demonstrated a significant inverse association of MiR-196a2 polymorphism with chronic periodontitis.

Periodontitis is one of the most common oral inflammatory diseases, and results in connective tissue degradation and gradual tooth loss. It manifests with formation of periodontal pockets, in which anaerobic and Gram‑negative bacteria proliferate rapidly. Consequently, alteration of the subgingival microbiota is considered the primary etiologic agent of periodontitis. Previous studies have reported that smokers are at increased risk of periodontal disease, in both prevalence and severity, indicating that smoking is a risk factor for the onset and progression of the pathology. In the present study, 16S rRNA sequencing was employed to assess the subgingival microbiota in 6 smoker patients with chronic periodontitis, 6 non‑smoker patients with chronic periodontitis and 8 healthy controls. The results demonstrated significant alterations in the microbial structure of periodontitis patients. High relative abundance of Parvimonans, Desulfubulbus, Paludibacter, Haemophilus, and Sphaerochaeta genera characterized subgingival microbiota of periodontitis patients, both smokers and non‑smokers. Due to the high precision and sensitivity of the 16S rRNA sequencing method, analysis for low‑abundant genera (including Pedobacter, Granulicatella, Paracoccus, Atopobium, Bifidobacterium, Coprococcus, Oridobacteriu, Peptococcus, Oscillospira and Akkermansia) was feasible, and revealed novel phylotypes associated with periodontitis. Of note, a major microbial community alteration was evident in smoker patients, suggesting an association between smoking and severity of subgingival dysbiosis. The present study confirmed that chronic periodontitis is a polymicrobial disease where changes in the equilibrium of subgingival microbiota contribute to severity of pathology.

The aim of this longitudinal prospective study was to evaluate the effects of periodontal treatment on the clinical, microbiological and immunological periodontal parameters, and on the systemic activity (ESSDAI) and subjective (ESSPRI) indexes in patients with primary Sjögren's Syndrome (pSS). Twenty-eight female patients were divided into four groups: pSS patients with or without chronic periodontitis (SCP, SC, respectively), and systemically healthy patients with or without chronic periodontitis (CP, C, respectively). Periodontal clinical examination and immunological and microbiological sample collection were performed at baseline, 30 and 90 days after nonsurgical periodontal treatment (NSPT). Levels of interleukin IL-1β, IL-8 and IL-10 in saliva and gingival crevicular fluid (GCF) were evaluated by ELISA, as well as the expression of Porphyromonas gingivalis (Pg), Aggregatibacter actinomycetemcomitans, (Aa) Tannerella forsythia (Tf), and Treponema denticola (Td), by qPCR. Systemic activity and pSS symptoms were evaluated by ESSDAI and ESSPRI. NSPT resulted in improved periodontal clinical parameters in both SCP and CP groups (p>0.05). Pg, Aa, and Tf levels decreased after NSPT only in CP patients (p<0.05). Significantly greater levels of IL-10 in GCF were verified in both SCP and CP groups (p<0.05). SCP patients showed increased salivary flow rates and decreased ESSPRI scores after NSPT. In conclusion, NSPT in pSS patients resulted in improved clinical and immunological parameters, with no significant effects on microbiological status. pSS patients also showed increased salivary flow and lower ESSPRI scores after therapy. Therefore, it can be suggested that NSPT may improve the quality of life of pSS patients.

In old aged patients with chronic generalized periodontitis and cardiovascular diseases the level lipoperoxidation increased and antioхidation protection decreased in saliva and blood. After the course of treatment myocardial ischemia and diseases chronic periodontal inflammation the level of lipoperoхidation was changed insignificant accompanied with decreased of TBK-active substance in saliva and blood. Change of nitric oхide after by treatment was depended it initial level before treatment and often had an opposite orientation.

Purpose: To evaluate the awareness of cigarette smoking as a risk factor for chronic periodontitis in patients either undergoing active periodontal treatment (APT) or enrolled in supportive periodontal therapy (SPT)., Materials and Methods: Comprehensive tobacco use history was collected with a questionnaire in 50 patients before and after APT (test) and in 50 patients (control) enrolled in SPT at the School of Dental Medicine, University of Bern. Carbon monoxide (CO) exhalation levels were measured in both APT and SPT patients., Results: In the test group, 94% (n = 47) completed the study. Before APT, 48% of these (n = 24) knew about the association between smoking and periodontal disease, while 42% (n = 21) assumed a possible association and 10% (n = 5) did not. Following APT, 53% (n = 25) knew about the association, while 34% (n = 17) still assumed a possible association and 10% (n = 5) did not. In the control group, 60% (n = 30) of SPT patients knew about the association of smoking with periodontal disease, while 30% (n = 15) assumed an association and 10% (n = 5) were not aware of any association. In both APT and SPT patients, neither between-group nor baseline to follow-up differences were detected (p > 0.05)., Conclusions: Brief interventions for tobacco cessation during APT or SPT failed to increase periodontal patients' awareness of smoking as a risk factor for chronic periodontitis. In order to both increase awareness and motivation to quit tobacco use, more counseling than conventional brief interventions may be needed. Key words: chronic periodontitis, exhaled carbon monoxide, patient education, risk factor, smoking, smoking cessation.

The purpose of this 24-month study was to identify predictors of smoking cessation in a cohort of smokers with chronic periodontitis, attending a multidisciplinary smoking cessation program. Of the 286 subjects screened, 116 were included and received non-surgical periodontal treatment and smoking cessation therapy, which consisted of lectures, cognitive behavioral therapy, and pharmacotherapy, according to their individual needs. During initial periodontal treatment, dentists actively motivated the study subjects to stop smoking, using motivational interviewing techniques. Further smoking cessation counseling and support were also provided by the dentists, during periodontal maintenance sessions at 3, 6, 12 and 24 months of follow-up. Smoking status was assessed by means of a structured questionnaire, and was validated by exhaled carbon monoxide (CO) measurements. The Fagerström Test for Cigarette Dependence was used to assess smoking dependence. Of the 61 individuals that remained up to the 24-month examination, 31, 21 and 18 declared that they were not smoking at 3, 12 and 24 months, respectively. Smoking cessation after 24 months was associated with the male gender (OR = 3.77, 95%CI = 1.16-12.30), baseline CO levels less than 10ppm (OR = 5.81, 95%CI 1.76-19.23), not living or working with another smoker (OR = 7.38, 95%CI 1.76-30.98) and a lower mean Fagerström test score (OR = 5.63, 95%CI 1.55-20.43). We concluded that smoking cessation was associated with demographic, smoking history and cigarette dependence variables.

Background/aims: This study examined prevalence and risk factors of periodontitis in representative samples of Korean adults, with and without diabetes mellitus (DM)., Methods: Data from the 2012 Korean National Health and Nutritional Examination Survey were analyzed. A total of 4,477 adults (≥ 30 years old) were selected from 8,057 individuals who completed a nutrition survey, a self-reported general health behavior questionnaire, an oral examination, an oral hygiene behaviors survey, and laboratory tests. DM was defined as a fasting plasma glucose ≥ 126 mg/dL, or self-reported diagnosed diabetes, or current use of oral hypoglycemic agents and/or insulin. The community periodontal index was used to assess periodontitis status and comparisons between the periodontitis and the non-periodontitis group, were performed, according to the presence of DM. Risk factors for periodontitis in adults with DM and without DM were evaluated by multiple logistic regression analysis., Results: The prevalence of periodontitis was significantly higher in adults with DM (43.7%) than in those without DM (25%, p < 0.001). In adults without DM, risk factors for periodontitis were older age, male, urban habitation, waist circumference, smoking, oral pain, and less frequent tooth brushing. Significant risk factors for periodontitis in adults with DM were the smoking, oral pain, and not-using an oral hygiene product., Conclusions: Adults with DM have an increased risk of periodontitis than those without DM. Current smoking and oral pain increase this risk. Using an oral hygiene product can reduce risk of periodontal disease in adults with DM., Competing Interests: No potential conflict of interest relevant to this article was reported.

Objectives: To determine the prevalence and dose-response relationship of chronic periodontitis among smokers in Pakistan., Methods:   This is a cross-sectional study among participants seeking dental care in Karachi Medical and Dental College, Karachi, Pakistan. A total of 443 participants with a mean age of 44.3 (±6.5) participated in the study from April 2011 to December 2011. Males comprised 64.7%, and females comprised 35.2%. Participants were interviewed on social demographics and oral habits. Participants with shallow pockets (3.5-5.5 mm) and deep pockets (greater than 5.5 mm) were considered suffering from chronic periodontitis. The characteristics of participants were assessed using frequency distribution for categorical variables and mean (standard deviation) for continuous variables. , Results: Among 443 participants, smokers were distributed as 55.1% and non-smokers as 44.9%. Smoking was found to be significantly related to young adults (p less than 0.007), male gender (p less than 0.001), and lower education level (p less than 0.01). Overall prevalence of chronic periodontitis among smokers was estimated at 81.6%. Heavy smoking was found to have significantly high prevalence (p less than 0.001) and severity (p less than 0.001) of periodontitis as compared with moderate and light smokers. The multivariate unadjusted model depicted 3.5 times higher risk of chronic periodontitis among smokers (p less than 0.001)., Conclusion: Chronic periodontitis had a high prevalence among smokers. Heavy smoking was found to have a higher risk for having periodontitis.

Objective: To investigate the effect of smoking on the expression levels of matrix metalloproteinase (MMP)-1, MMP-9, tissue inhibitor of metalloproteinase-1 (TIMP-1), and the concentrations of TNF-α and IL-10 in patients with chronic periodontitis (ChP)., Methods: This is an ex-vivo study. Our study consisted of 78 cases, all of which were diagnosed with ChP and were selected according to the inclusion and exclusion criteria. Among these 78 cases, 38 patients were classified into the smoking group (S-ChP group), and 40 patients in the non-smoking group (NS-ChP group). The clinical periodontal parameters of all patients were recorded, including the plaque index (PLI), probing depth (PD), loss of attachment (LA) and sulcus bleeding index (SBI). Serum was collected from forearm blood to establish a Porphyromonas gingivalis (Pg) internalizing KB cell model. Enzyme-linked immunosorbent assay (ELISA) was used to determine the concentrations of MMP-1, MMP-9 and TIMP-1 in the KB cell lysis solution as well as IL-10 and TNF-α in the gingival crevicular fluid (GCF)., Results: Fewer Pg internalizing KB cell colonies were observed in the NS-ChP group than in the S-ChP group (P<0.01). When 400μL serum was added, there were remarkable differences in the concentrations of MMP-1 and TIMP-1 secreted from the KB cells between the S-ChP and NS-ChP groups (MMP-1: t=-21.71, P<0.01; TIMP-1: t=64.35, P<0.001). Additionally, when 800μL serum was added, there were significant differences in the concentrations of MMP-1, MMP-9 and TIMP-1 in the KB cells between the S-ChP and NS-ChP groups (MMP-1: t=-81.89, P<0.001; MMP-9: t=-15.67, P<0.001; TIMP-1: t=109.4, P<0.001). The TNF-α levels were higher, but the IL-10 levels were lower in the GCF from the ChP patients in the S-ChP group than those in the NS-ChP group (both P<0.001)., Conclusion: The serum of S-ChP patients can enhance the concentrations of MMP-1 and MMP-9, but reduce TIMP-1 secreted from Pg internalizing KB cells. However, the concentration of TNF-α was increased and IL-10 was decreased. Abnormal concentrations of ChP-associated biomarkers may be conducive to the development and progression of ChP., (Copyright © 2016 Elsevier Inc. All rights reserved.)

The periodontopathogen Aggregatibacter actinomycetemcomitans synthesizes several virulence factors, including cytolethal distending toxin (CDT). The active CDT holoenzyme is an AB-type tripartite genotoxin that affects eukaryotic cells. Subunits CdtA and CdtC (B-components) allow binding and intracellular translocation of the active CdtB (A-component), which elicits nuclear DNA damage. Different strains of A. actinomycetemcomitans have diverse virulence genotypes, which results in varied pathogenic potential and disease progression. Here, we identified an A. actinomycetemcomitans strain isolated from two patients with advance chronic periodontitis that has a regular cdtABC operon, which, however, codes for a unique, shorter, variant of the CdtB subunit. We describe the characteristics of this CdtBΔ116-188, which lacks the intact nuclear localisation signal and the catalytic histidine 160. We show that the A. actinomycetemcomitans DO15 isolate secretes CdtBΔ116-188, and that this subunit cannot form a holotoxin and is also not genotoxic if expressed ectopically in HeLa cells. Furthermore, the A. actinomycetemcomitans DO15 isolate is not toxic, nor does it induce cellular distention upon infection of co-cultivated HeLa cells. Biological significance of this deletion in the cdtB remains to be explained.

Chronic periodontitis is a progressive, infectious inflammation disease, caused by the dysbiosis of oral resident flora, leading to the destruction of periodontium. The onset of pathogenic microorganisms is the etiological factor of periodontitis, while the immuno-inflammatory response affects the progression of the disease. Under chronic periodontitis, oxidative stress occurs when excessive reactive oxygen species are produced and exceed the compensative capacity of the organism. Oxidative stress leads to the destruction of periodontium, in a direct way(damaging the biomolecule) or an indirect way(enhancing the produce of inflammatory cytokine and destructive enzymes). Therefore, as the antagonist of the reactive oxygen species, antioxidants may be helpful to treat the chronic periodontitis. This paper reviewed relevant literatures about the destructive role of excessive reactive oxygen species and protective role of antioxidants in chronic periodontitis.

It has earlier been reported that individuals with poorly controlled diabetes have severe periodontal disease (PD) compared to well-controlled diabetes. This longitudinal interventional study compared periodontal treatment outcomes with HbA1c level changes in four groups of diabetic and non-diabetic patients with or without PD, respectively. HbA1c, bleeding on probing (BOP), plaque index and periodontal pocket depth (PPD) 4 < 6 mm and ≥6 mm were recorded at baseline to 3 months after non-surgical treatment and 3-6 months for surgical treatment in subjects with or without T2D, and with or without PD. A total of 129 patients were followed from baseline to 6 months. Diabetics with PD and without PD showed reductions in HbA1c levels with a mean value of 0·3% after 3 months and mean values of 1% and 0·8%, respectively, after 6 months. Diabetics with PD showed higher levels of BOP versus non-diabetics without PD (P < 0·01) and versus diabetics without PD (P < 0·05) at baseline. After 6 months, diabetics with PD showed higher number of PPD 4 < 6 mm versus diabetics without PD (P < 0·01) and non-diabetics with PD (P < 0·01). Diabetics without PD showed higher levels of PPD 4 < 6 mm versus non-diabetics without PD (P < 0·01). Surgical and non-surgical periodontal treatment in all groups improved periodontal inflammatory conditions with a decrease in HbA1c levels in a period of three and 6 months. No change was seen in the number of pockets PPD 4 < 6 mm in diabetic subjects with PD after non-surgical and surgical treatment., (© 2015 John Wiley & Sons Ltd.)

To investigate the cytokine profile as biomarkers in the gingival crevicular fluid (GCF) of chronic periodontitis (CP) patients with and without obesity, MEDLINE/PubMed, EMBASE, ScienceDirect, and SCOPUS databases were combined with handsearching of articles published from 1977 up to May 2016 using relevant MeSH terms. Meta-analyses were conducted separately for each of the cytokines: resistin, adiponectin, TNF- α , leptin, IL-6, IL-8, and IL-1 β . Forest plots were produced reporting standardized mean difference of outcomes and 95% confidence intervals. Eleven studies were included. Three studies showed comparable levels of leptin among obese and nonobese patients with CP. Four studies reported comparable levels of interleukin- (IL-) 6 and resistin whereas five studies reported comparable levels of adiponectin. Two studies reported similar levels of CRP in patients with periodontitis with and without obesity. One study showed higher levels of tumor necrosis factor-alpha in obese patients with CP. One study showed higher levels of IL-1 β and IL-8 in obese patients with CP. The level of localized periodontal inflammation may have a greater influence on the GCF proinflammatory biomarker levels as compared to systemic obesity. Whether patients having chronic periodontitis with obesity have elevated proinflammatory GCF biomarkers levels compared to nonobese individuals remains debatable.

Here, we report the diagnosis and treatment of an extraoral cutaneous sinus tract originating in a mandibular second molar with a C-shaped root canal system. The patient was referred to our department by a dermatologist after a series of unsuccessful treatments, including antibiotics. Diffuse radiolucency on a preoperative radiograph revealed that earlier root canal treatment had been only partially successful. Consequently, we performed retreatment of the root canal comprising removal of the former restoration and gutta-percha, cleaning and shaping, and passive irrigation with sodium hypochlorite. The patient responded well, and the cutaneous lesion completely resolved uneventfully within 1 month postoperatively. Preoperative recognition and thorough knowledge of the root canal anatomy and conventional methods of obturation are necessary in performing successful endodontic treatment.

Porphyromonas gingivalis is a periodontal pathogen strongly associated with loss of attachment and supporting bone for teeth. We have previously shown that the total lipid extract of P. gingivalis inhibits osteoblast differentiation through engagement of Toll-like receptor 2 (TLR2) and that serine dipeptide lipids of P. gingivalis engage both mouse and human TLR2. The purpose of the present investigation was to determine whether these serine lipids inhibit osteoblast differentiation in vitro and in vivo and whether TLR2 engagement is involved. Osteoblasts were obtained from calvaria of wild type or TLR2 knockout mouse pups that also express the Col2.3GFP transgene. Two classes of serine dipeptide lipids, termed Lipid 654 and Lipid 430, were tested. Osteoblast differentiation was monitored by cell GFP fluorescence and osteoblast gene expression and osteoblast function was monitored as von Kossa stained mineral deposits. Osteoblast differentiation and function were evaluated in calvarial cell cultures maintained for 21 days. Lipid 654 significantly inhibited GFP expression, osteoblast gene expression and mineral nodule formation and this inhibition was dependent on TLR2 engagement. Lipid 430 also significantly inhibited GFP expression, osteoblast gene expression and mineral nodule formation but these effects were only partially attributed to engagement of TLR2. More importantly, Lipid 430 stimulated TNF-α and RANKL gene expression in wild type cells but not in TLR2 knockout cells. Finally, osteoblast cultures were observed to hydrolyze Lipid 654 to Lipid 430 and this likely occurs through elevated PLA2 activity in the cultured cells. In conclusion, our results show that serine dipeptide lipids of P. gingivalis inhibit osteoblast differentiation and function at least in part through engagement of TLR2. The Lipid 430 serine class also increased the expression of genes that could increase osteoclast activity. We conclude that Lipid 654 and Lipid 430 have the potential to promote TLR2-dependent bone loss as is reported in experimental periodontitis following oral infection with P. gingivalis. These results also support the conclusion that serine dipeptide lipids are involved in alveolar bone loss in chronic periodontitis., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Pro-inflammatory cytokine release (IL-8, IL-6, TNF-α, IL-1β) by peripheral blood neutrophils, isolated from periodontitis patients (before/after therapy) and matched controls, was determined after 18 h culture in the presence/absence of Escherichia coli LPS, opsonised Staphylococcus aureus, heat-killed Fusobacterium nucleatum and Porphyromonas gingivalis. All cultures demonstrated differences in the amounts of each cytokine detected (P < 0.0001), with a clear release pattern (IL-8 > IL-6 > TNF-α = IL-1β). Median cytokine release from unstimulated patient neutrophils was consistently, but non-significantly, higher than from control cells. Stimulated cytokine release from untreated patient neutrophils was also consistently higher than from control cells. This hyper-reactivity was significant for all tested cytokines when data for all stimuli were combined (P < 0.016). In terms of individual stimuli, significant hyper-reactivity was detected with LPS (IL-8), F. nucleatum (IL-8, TNF-α), opsonised S. aureus (IL-8, TNF-α, IL-1β) and P. gingivalis (IL-8, IL-1β). Cytokine production by patient neutrophils did not reduce following successful non-surgical periodontal therapy and, except for responses to F. nucleatum, the cytokine hyper-reactivity detected pre-therapy was retained. These data demonstrate that chronic periodontitis is characterised by neutrophils that constitutively exhibit cytokine hyper-reactivity, the effects of which could modulate local and systemic inflammatory-immune responses and influence the risk and severity of periodontitis-associated systemic inflammatory diseases., (© The Author(s) 2015.)

We evaluated the effects of nonsurgical periodontal therapy in 100 patients with type 2 diabetes and chronic periodontitis. The participants were classified as having good (n = 48) or poor (n = 52) glycemic control and were further randomly allocated to receive either scaling and root planning treatment group or no treatment (n = 50 each). The effect of nonsurgical periodontal therapy was compared among diabetic patients with good glycemic control, those with poor glycemic control, and 25 nondiabetic individuals. Periodontal and metabolic status was recorded at baseline, 3 months, and 6 months. In patients receiving treatment, periodontal parameters significantly improved and HbA1c decreased by 10.8%. Improvements in gingival index and bleeding on probing were greater in the nondiabetic participants and the treated patients with good glycemic control than in the treated patients with poor glycemic control (P < 0.05). Regression analysis showed that improvement in periodontal status was independently associated with glycemic improvement. Nonsurgical periodontal therapy improved glycemic control and periodontal health in patients with type 2 diabetes. However, patients with poor baseline glycemic control had less clinical improvement than did those without diabetes and those with good glycemic control.

The acute phase of chronic periodontitis may occur even in patients during supportive periodontal therapy. However, the details are not fully understood. Since the natural environment, including meteorology affects human health, we hypothesized that weather conditions may affect occurrence of acute phase of chronic periodontitis. The aim of this study was to investigate the relationship between weather conditions and acute phase of chronic periodontitis in patients under supportive periodontal therapy. Patients who were diagnosed with acute phase of chronic periodontitis under supportive periodontal therapy during 2011-2013 were selected for this study. We performed oral examinations and collected questionnaires and meteorological data. Of 369 patients who experienced acute phase of chronic periodontitis, 153 had acute phase of chronic periodontitis without direct-triggered episodes. When using the autoregressive integrated moving average model of time-series analysis, the independent covariant of maximum hourly range of barometric pressure, maximum hourly range of temperature, and maximum daily wind speed were significantly associated with occurrence of acute phase of chronic periodontitis (p < 0.05), and 3.1% of the variations in these occurrence over the study period were explained by these factors. Meteorological variables may predict occurrence of acute phase of chronic periodontitis.

Alzheimer's disease, an affliction of old age, is one of the leading causes for dementia worldwide. Various risk factors including family history, genetics and infections have been implicated in its pathogenesis. The cognitive decline in this condition is mainly a result of the formation of amyloid deposits that provoke neuroinflammation, ultimately resulting in cell death. Recently, an association between peripheral inflammation and Alzheimer's disease was hypothesized. It was suggested that chronic systemic inflammation worsened the inflammatory processes in the brain. This was mainly attributed to increased levels of pro-inflammatory mediators, such as interleukin-1, interleukin -6 and tumor necrosis factor-α in the plasma. As chronic periodontitis is a widespread peripheral immunoinflammatory condition, it has been proposed to play a significant role in the aggravation of Alzheimer's disease. With this background, the current review focuses on the relationship between Alzheimer's disease and chronic periodontitis, and its therapeutic implications., (© 2014 Japan Geriatrics Society.)

Cysteine proteases (gingipains) from Porphyromonas gingivalis are key virulence factors in chronic periodontitis. Innate immune receptors CD14, Toll-like receptor (TLR) 2 and TLR4 are important in P. gingivalis recognition. We examined the ability of gingipains to cleave CD14, TLR2 and TLR4, and the consequences for the cellular response to bacterial challenge. Macrophages were exposed to Arg (RgpA and RgpB)- and Lys (Kgp)-gingipains, and residual expression of TLR2, TLR4 and CD14 was determined by flow cytometry. The cellular response to live bacteria following exposure to purified gingipains was evaluated by TNFα production and bacterial phagocytosis. RgpA and Kgp decreased CD14 detection in a concentration (p = 0.0000002)- and time (p = 0.03)-dependent manner, whereas RgpB had no significant effect. TLR2 and TLR4 expression were unaffected. Reduction in CD14 expression was more efficient with Lys-gingipain than with Arg-gingipain. A reduced CD14 surface level correlated with decreased TNFα secretion and bacterial phagocytosis following challenge with live P. gingivalis, but the response to heat-killed bacteria was unaffected. Therefore, gingipains reduce CD14 expression without affecting expression of the bacterial-sensing TLRs. Reduced CD14 expression depends on the gingipain hemagglutinin/adhesion site and results in macrophage hyporesponsiveness to bacterial challenge. Further studies are needed to determine if reduced CD14 expression is linked to periodontitis induced by P. gingivalis., (© 2014 S. Karger AG, Basel.)

Aim: Evaluate the effects of smoking on dendritic cells (DCs), cytokines, clinical periodontal parameters, and number of teeth in samples of human chronic periodontitis (CP)., Material and Methods: Gingival samples were obtained from 24 smokers and 21 non-smokers with CP. Periodontal examination was carried out. Immunohistochemical staining was performed to identify Factor XIIIa+ immature, CD1a+ immature, and CD83+ mature DCs. The inflammatory infiltrate was counted, and IL-2, IL-10, IL-4, IL-6, IFN-γ, TNF-α, and IL-17A were measured using the cytometric bead array (CBA). Inflammatory infiltrate, DCs, cytokines, classification of CP, clinical periodontal parameters, number of teeth, smoking habit in years (SH/years), and number of cigarettes smoked per day (C/day) were correlated and compared., Results: CD83+ mature DCs decreased in the smokers group. Negative correlations could be observed between the number of C/day with levels of IL-17A and number of teeth. Correlations between smoking, periodontal disease status, and other cytokines were not observed., Conclusions: Smoking decreases mature DCs in chronic periodontitis. Moreover, a dose-dependent relation can be observed between C/day and number of teeth and levels of IL17A observed. Smokers show a different modulation of the CP immune response., (Copyright © 2014 Elsevier GmbH. All rights reserved.)

Unlabelled: Diabetes has been associated with periodontitis, but the mechanisms through which periodontal diseases affect the metabolic control remain unclear., Objective: This study aimed to evaluate serum leveis of inflammatory markers, IL-8, IL-6 and monocyte chemoattractant protein 1 (MCP-1), in type 2 diabetic patients in the presence of chronic periodontitis., Material and Methods: Forty two individuals were enrolled in this study and assigned to one of five groups: diabetes mellitus with inadequate glycemic control and periodontitis (DMI+P, n = 10), diabetes mellitus with adequate glycemic control and periodontitis (DMA+P, n = 10), diabetes mellitus without periodontitis (DM, n = 10), periodontitis without diabetes (P, n=6), and neither diabetes nor periodontitis (H, n = 6). Periodontal clinical examination included visible plaque index (PL), gingival bleeding index (GB), probing depth (PD), attachment level (AL) and bleeding on probing (BP). Glycemic control was evaluated by serum concentration of glycated hemoglobin (HbAlc). Inflammatory serum markers IL-8, IL-6 and (MCP-1) were measured by ELISA., Results: DMI+P and DMA+P groups presented higher PD (p=0.025) and AL (p=0.003) values when compared to the P group. There were no significant differences among groups for IL-6, IL-8 and MCP-1 serum levels., Conclusions: Although periodontitis was more severe in diabetic patients, the serum levels of the investigated inflammatory markers did not differ among the groups.

Periodontal disease is a chronic inflammatory disease that results in the breakdown of the tooth-supporting tissues, and can ultimately lead to resorption of the alveolar bone. Recently, several studies have shown a close relationship between increased interleukin-18 (IL-18) levels and the pathogenesis of chronic periodontitis, a major cause of tooth loss. However, it has yet to be shown whether chronic periodontitis results from or causes an increase in IL-18 after bacterial infection. In the present study, we investigated how IL-18 overexpression relates to periodontal disease using IL-18 transgenic (Tg) mice. IL-18Tg and wild-type mice were inoculated intraorally with Porphyromonas (P.) gingivalis, which has been implicated in the etiology of chronic periodontitis. Seventy days after P. gingivalis infection, alveolar bone loss and gingival cytokine levels were assessed using histo-morphological analysis and enzyme-linked immuno-absorbent assay, respectively. Periodontal bone loss was evoked in IL-18Tg mice, but not in wild-type mice. Interestingly, levels of bone-resorptive cytokines, including IL-1α, IL-1β, tumor necrosis factor-α, and IL-6, were unchanged in the gingival tissues of IL-18Tg mice infected with P. gingivalis, although levels of interferon γ (a proinflammatory T-helper 1 cytokine) decreased. RT-PCR analysis showed elevated expression of mRNAs for receptor activator of nuclear factor kappa-B ligand (a key stimulator of osteoclast development and activation) and CD40 ligand (a marker of T cell activation) in the gingiva of IL-18Tg mice infected with P. gingivalis. We conclude that increased IL-18 in the gingival tissues evokes chronic periodontitis after bacterial infection, presumably via a T cell-mediated pathway.

As many diseases have been shown to have several or indirect causes (i.e. are multifactorial) the question is what is the relative importance of each factor in a given disease? Also, what happens when some diseases, although apparently disparate, share causative factors and/or tissue pathologies? Host inflammation response mechanisms are largely shared by the body's different tissues and systems and only recently has special attention been paid to the possible linkages among chronic periodontitis and other chronic systemic diseases. The aim of this review was to consider and discuss the mounting evidence that the basis for the inter-relationships between chronic periodontitis and atheromatous disease and diabetes lie at a fundamental intracellular level, namely oxidative stress and mitochondrial dysfunction, as a meeting background among such chronic diseases and periodontitis., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

All cells and organisms across the evolutionary spectrum, from the most primitive to the most complex, are mechanosensitive. As the cytoskeleton is a key in controlling the normal basal prestress of cells and therefore is involved in virtually all physiological cellular processes, abnormalities in this essential cellular characteristic may result in diseases. Indeed, many diseases have now been associated with abnormalities in cytoskeletal and nucleoskeletal proteins. We propose that adult periodontitis is, at least in part, such a cytoskeletal disease. It is well established that adult periodontitis starts by bacterial invasion at the interface between the tooth surface and marginal gingiva that induces a local inflammatory response. The inflammatory cells release metalloproteinases which degrade gingival collagenous fibrous tissue and loss of local tissue integrity that reduces the normal prestressed cell-extracellular matrix network. This is a major signaling trigger that induces a local and rapid release of ATP, which then activates P2X receptors and stimulates a calcium influx, further activating osteoclastic resorption of the alveolar bone. As periodontitis is a chronic disease, it seems reasonable to suggest that agents that maintain cytoskeletal tensegrity, for example, inhibitors of ATP receptors, may diminish the bone loss and may have a role in future periodontal therapy., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: The aim of the present study is to investigate the clinical correlates of a novel lateral-flow immunoassay with bleeding on probing (BOP), oral hygiene, and periodontal probing depth. This report offers a simple, rapid, and highly sensitive tool that addresses two issues important to periodontists: 1) detecting active periodontitis, and 2) predicting chronic periodontitis., Methods: Seventy-six of 86 males requiring seminal fluid analysis as part of a separate study were serially recruited into the study. After basic dental and periodontal examination under natural light and with the use of the community periodontal index of treatment needs (CPITN) probe, debris and calculus indices were recorded per participant. Participants were subsequently grouped into "good," "fair," and "poor" oral hygiene categories based on a simplified oral hygiene index. BOP was assessed with the ball-ended tip of the probe, and periodontitis was assessed with pocket probing as well as a lateral flow of neutrophil collagenase-2 immunoassay, which measures levels of matrix metalloproteinase-8., Results: Neutrophil collagenase-2 immunoassay was 96% sensitive for poor oral hygiene, 95% sensitive for chronic periodontitis (defined as at least two sites with periodontal pockets), and 82.6% sensitive for at least two sites with BOP., Conclusion: Neutrophil collagenase-2 immunoassay had a high sensitivity for at least two sites with BOP and two sites with periodontal pockets but a lower relationship for single-site pockets and BOP.

Background: The immunosuppresion in HIV patients makes them highly susceptible to microbial infections. The aim of the study was to establish whether HIV stage (as depicted by CD4+ T lymphocyte counts) could independently be associated with periodontal status (as revealed by the measurement of clinical indices)., Methods: One hundred and twenty HIV-infected patients attending an infectious diseases clinic in the Western Cape, South Africa were included in the study. The periodontal clinical indices such as plaque index, gingival index, pocket probing depth and clinical attachment levels were measured on the mesial aspect of the six Ramfjord teeth. The CD4 + T cell counts were taken from the patients' medical records and patients' HIV stage determined and grouped according to their CD4+ T cell counts into A (<200 cells /mm3), B (200-500 cells /mm3) and C (>500 cells /mm3)., Results: The mean age of 120 HIV-positive patients was 33.25 years and the mean CD4 + T cell count was 293.43 cells/mm3. The probing depth and clinical attachment loss were found to be significantly associated with the total CD4 + T cell counts but not with HIV stage. Significant correlations were found between age and all clinical indices except for clinical attachment loss. No correlation was found between age and HIV stage of the patients. The use of antiretroviral therapy was significantly associated with probing depth and clinical attachment loss, but not with plaque nor gingival index. Significant associations were observed between smoking and all of the clinical indices except for the gingival index. A significant association was observed between the use of interdental aids and all the clinical indices except for probing depth, while brushing was significantly associated with plaque index only. CD4 + T cell counts were significantly associated with brushing frequency (p = 0.0190) and the use of interdental aids (p = 0.0170)., Conclusion: The findings of this study conclude that HIV stage, ART and age are not independent risk factors for changes in the periodontal status of HIV-positive subjects but rather that smoking and oral hygiene habits determine their susceptibility to disease.