Salivary Antioxidant Profile in Patients with Systemic Sclerosis and Periodontitis.

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.

Association between obesity and chronic periodontitis: A nationwide population-based cohort study in Taiwan.

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 ±â€Š13.8 years and 42.0 ±â€Š14.0 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.

Evaluation of the Genetic Association and Methylation of Immune Response Pathway Genes with the Risk of Chronic Periodontitis in the Uighur Population.

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.

Pleckstrin Levels Are Increased in Patients with Chronic Periodontitis and Regulated via the MAP Kinase-p38α Signaling Pathway in Gingival Fibroblasts.

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-1ß (IL-1ß) 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-1ß and LPS significantly increased PLEK mRNA and pleckstrin protein levels. VX-745, the p38 MAP kinase inhibitor significantly decreased IL-1ß- 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.

NIK inhibitor impairs chronic periodontitis via suppressing non-canonical NF-κB and osteoclastogenesis.

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-ß 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.

Translation of mouse model to human gives insights into periodontitis etiology.

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.

Butyric Acid in Saliva of Chronic Periodontitis Patients Induces Transcription of the EBV Lytic Switch Activator BZLF1: A Pilot Study.

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.

Association between Monocyte Chemoattractant Protein-1 -2518 (A/G) Single Nucleotide Polymorphism and Chronic Periodontitis in End-stage Renal Disease Patients - A Case-control Study.

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.

Incidence of the Acute Symptom of Chronic Periodontal Disease in Patients Undergoing Supportive Periodontal Therapy: A 5-Year Study Evaluating Climate Variables.

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.

Metabolomic Status of The Oral Cavity in Chronic Periodontitis.

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 (1H-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.

Prevalence of periodontitis in a population of patients on dialysis in Colombia.

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.

El objetivo de este estudio fue establecer la prevalencia de Periodontitis Crónica (PC) en pacientes con enfermedad renal crónica (ERC) en diálisis y determinar la relación de su presencia con algunos indicadores de micro inflamación. Un total de 135 pacientes con ERC en terapia dialítica fueron incluidos en este estudio. Se evaluaron parámetros bioquímicos, nivel de inserción clínica (NIC) y profundidad de sondaje (PS), de acuerdo con la Asociación Americana de Periodoncia y el CDC de Atlanta (CDC-AAP). También fue evaluada, la gingivitis y la PC de acuerdo con la clasificación interface biopelicula-encia (BGI). La tasa de no respuesta a la encuesta fue del 10%. Un total de 2636 dientes en 135 pacientes fueron evaluados, (52.5% hombres, edad promedio 55.7 ± 1.32), 56% con antecedente de tabaquismo. 78/135 en hemodiálisis y 57/135 en diálisis peritoneal, el 55.5 % con un tiempo en diálisis mayor a tres años. La prevalencia de gingivitis por la clasificación BGI fue del 14.8% IC 95% (9.7 - 21.9) y de periodontitis 82.2% IC 95% (74.7 - 87.8). La severidad de la PC fue: sin periodontitis 14.0% 95% IC (9.1 - 21.1); leve 11.1% 95% IC (6.7 - 17.7); moderada 28.8% 95% IC (21.7 - 37.1) y severa 45.9% 95% IC (31.6-54.47) La diálisis peritoneal y el tiempo en diálisis aumentaron la chance de tener PC: OR 11.0 95% IC (2.2-53.8) y OR 7.6 95% CI (1.1-50.2) respectivamente. Por la alta prevalencia de PC en esta población, es necesario establecer programas para asegurar el cuidado de la salud periodontal en esta población en diálisis.

La plausibilidad biológica entre la periodontitis crónica y el infarto cerebral isquémico / Biological plausibility of the relationship between chronic periodontitis and ischemic stroke

Introducción: Las bolsas periodontales reales constituyen un reservorio importante de bacterias gramnegativas que pueden por diversas vías ejercer influencia en sitios distantes, lo cual provoca alteraciones sistémicas como las enfermedades derivadas de la aterosclerosis. Objetivo: Explicar los fundamentos teóricos que sustentan la propuesta de la periodontitis crónica como un factor de riesgo para el infarto cerebral isquémico. Contenido: 1) La aterosclerosis y las enfermedades cerebrovasculares, generalidades de su patogenia. 2) La microbiota periodontal, fundamentos de su asociación con la aterosclerosis y la enfermedad cerebrovascular isquémica. Exposición del tema: La inflamación es un elemento de vital importancia en todas las fases del proceso aterosclerótico, tanto en su inicio, progresión, como en sus complicaciones. La naturaleza de las enfermedades periodontales inmunoinflamatorias crónicas y la infección subgingival anaerobia asociada a ellas, representa una injuria metastásica que produce y disemina mediadores inflamatorios favorecedores de la ateroesclerosis, participando en la colonización, y ruptura de placas ateromatosas; procesos implicados en la patogenia del infarto cerebral isquémico. Consideraciones finales: El mayor conocimiento de la relación riesgosa entre periodontitis crónica e infarto cerebral isquémico, permitiría una utilización racional de estrategias de prevención y tratamiento de la enfermedad cerebrovascular, basadas en la detección de procesos inflamatorios como las periodontopatías crónicas(AU)

Introduction: True periodontal pockets are an important reservoir of gram-negative bacteria which may exert an influence on distant sites in a variety of manners, bringing about systemic alterations such as diseases derived from atherosclerosis. Objective: Explain the theoretical foundations supporting the proposal of chronic periodontitis as a risk factor for ischemic stroke. Content: 1) Atherosclerosis and cerebrovascular disease, an overview of their pathogenesis. 2) The periodontal microbiota, bases for its association with atherosclerosis and ischemic stroke Topic presentation: Inflammation is an element of vital importance in all the stages of the atherosclerotic process, be it its onset, progress or complications. By their nature, chronic immunoinflammatory periodontal diseases and the associated anaerobic subgingival infection, constitute a metastatic injury that produces and spreads inflammatory mediators leading to atherosclerosis and participating in the colonization and rupture of atheromatous plaques, which are processes involved in the pathogenesis of ischemic stroke. Final considerations: Better knowledge about the risk relationship between chronic periodontitis and ischemic stroke would allow a rational use of strategies for the prevention and treatment of cerebrovascular disease based on detection of inflammatory processes such as chronic periodontal conditions(AU)

Superoxide Dismutase, Uric Acid, Total Antioxidant Status, and Lipid Peroxidation Assay in Chronic and Aggressive Periodontitis Patients.

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.

Are Sphingolipids and Serine Dipeptide Lipids Underestimated Virulence Factors of Porphyromonas gingivalis?

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.

Relationship between human immunodeficiency virus (HIV-1) infection and chronic periodontitis.

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.

The combined and individual impact of diabetes and smoking on key subgingival periodontal pathogens in patients with chronic periodontitis.

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.

Resistin and Plasma-reactive Oxygen Metabolite Levels in Obese and Non-obese Individuals with Chronic Periodontitis in Response to Non-surgical Periodontal Therapy.

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.

Prótese total imediata em paciente com periodontite crônica associada ao tabagismo ­ relato de caso / Immediate total prosthesis in a patient with chronic periodontitis associated with smoking ­ case report

O tabagismo é uma prática que traz muitos malefícios aos usuários, tanto à saúde sistêmica quanto à oral. O efeito mais comum observado na cavidade oral é a periodontite, podendo culminar na cronificação da doença, consequentemente, levando à perda dos elementos dentários, fazendo-se necessária a intervenção protética. Este trabalho tem como objetivo relatar o tratamento reabilitador por meio de prótese total imediata em paciente portador de periodontite crônica com extensa perda óssea associada ao tabagismo. O mesmo foi diagnosticado com periodontite crônica severa associada ao tabagismo e o tratamento proposto foi a extração de todos os elementos superiores com enfoque para a reabilitação em prótese total imediata superior e confecção de prótese parcial removível inferior. Concluiu-se que o tratamento eleito proporcionou uma reabilitação satisfatória tanto no aspecto clínico quanto emocional do paciente, pois restabeleceu a capacidade mastigatória adequada, trouxe melhora na fonética, conferiu aspecto de cavidade oral saudável e, principalmente, bem-estar estético e social (AU).

Smoking is a practice that brings much harm to its users, both to systemic and oral health. The most common effect observed in the oral cavity is periodontitis, which can culminate in the chronification of the disease, consequently leading to loss of dental elements, making prosthetic intervention necessary. This work aims to report rehabilitation treatment through immediate total prosthesis in patient with chronic periodontitis with extensive bone loss associated with smoking. This patient was diagnosed with severe chronic periodontitis associated with smoking and the proposed treatment was the extraction of all the superior elements with focus on the rehabilitation in the immediate superior total prosthesis and the manufacture of lower removable partial denture. It was concluded that the elected treatment provided a satisfactory rehabilitation for both patient clinical and emotional aspects, as it reestablished adequate masticatory capacity, improved phonetics, conferred a healthy oral cavity aspect, essential aesthetic, and mainly, aesthetic and social well-being (AU).

Gingival crevicular fluid oxidative stress level in patients with periodontal disease and hyperlipidemia.

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.