Carlos Marcelo da Silva Figueredo

Periodontal Therapy Reduces Plasma Levels of Interleukin-6, C-Reactive Protein, and Fibrinogen in Patients With Severe Periodontitis and Refractory Arterial Hypertension

BACKGROUND Recent epidemiologic studies suggest that inflammation is the link between periodontal diseases and cardiovascular complications. This study aimed to evaluate the effects of non-surgical periodontal treatment on plasma levels of inflammatory markers (interleukin [IL]-6, C-reactive protein [CRP], and fibrinogen) in patients with severe periodontitis and refractory arterial hypertension. METHODS Twenty-two patients were examined and randomly divided into two groups. The test group was composed of 11 patients (mean age, 48.9 +/- 3.9 years) who received periodontal treatment, whereas the control group had 11 patients (mean age, 49.7 +/- 6.0 years) whose treatment was delayed for 3 months. Demographic and clinical periodontal data were collected, and blood tests were performed to measure the levels of IL-6, CRP, and fibrinogen at baseline and 3 months later. RESULTS The clinical results showed that the mean percentages of sites with bleeding on probing, probing depth (PD) 4 to 5 mm, PD > or =6 mm, clinical attachment loss (CAL) 4 to 5 mm, and CAL > or =6 mm were significantly reduced in the test group 3 months after periodontal treatment. There were no significant differences between the data at baseline and 3 months in the control group. Periodontal treatment significantly reduced the blood levels of fibrinogen, CRP, and IL-6 in the test group. CONCLUSION Non-surgical periodontal therapy was effective in improving periodontal clinical data and in reducing the plasma levels of IL-6, CRP, and fibrinogen in hypertensive patients with severe periodontitis.

Decreased Interleukin-1β and Elastase in the Gingival Crevicular Fluid of Individuals Undergoing Anti-Inflammatory Treatment for Rheumatoid Arthritis

BACKGROUND The primary aim of this study was to compare the inflammatory activity in the gingival crevicular fluid (GCF) in a group of patients with rheumatoid arthritis (RA) and a group of matched controls. Secondarily, we aimed to evaluate the effect of rheumatologic treatment on periodontal inflammation. METHODS Seventeen individuals with RA with a mean duration of disease of 12.1 (± 9.9) years and the same number of systemically healthy individuals matched for age, gender, periodontal status, and tobacco use were selected. Medication data were registered, and GCF was collected by means of an intracrevicular washing method. Besides clinical registrations, periodontal inflammation was assessed by analysis of the cytokines interleukin (IL)-1β and -18 and of elastase activity. RESULTS Amounts of IL-1β and total elastase were significantly lower in the patient group. IL-1β and total elastase had a significant and strong correlation in the RA group (rs = 0.883). This correlation was not observed in the control group. CONCLUSION The anti-inflammatory treatment taken by RA patients might influence the periodontal inflammation status represented by IL-1β and elastase in the GCF.

Extent and severity of chronic periodontitis in chronic kidney disease patients

UNLABELLED BACKGROUND AND OBJECTVE: Chronic inflammatory diseases have been investigated as a possible source of inflammation in chronic kidney disease patients; however, there is a shortage of information about the prevalence of periodontitis in such individuals. Therefore, the aim of this cross-sectional study was to determine the extent and severity of periodontitis in chronic kidney disease patients undergoing the following three different treatment modalities: predialysis; continuous ambulatory peritoneal dialysis (CAPD); and hemodialysis (HD); and to compare the findings with those from systemically healthy individuals. MATERIAL AND METHODS Forty CAPD patients (mean age 52±12 years), 40 HD patients (mean age 50±10 years), 51 predialysis patients (mean age 54±11 years) and 67 healthy individuals (mean age 50±7 years) were examined. The periodontal examination included probing pocket depth, clinical attachment loss, bleeding on probing and presence of plaque. Patients with at least four sites with clinical attachment loss ≥6 mm were considered to have severe chronic periodontitis, and those with at least 30% of sites with clinical attachment loss ≥4 mm were considered to have generalized chronic periodontitis. RESULTS Predialysis and HD patients had significantly more sites with clinical attachment loss ≥6 mm than healthy individuals. The CAPD patients had similar periodontal condition to healthy subjects. There were significantly more cases of severe chronic periodontitis in predialysis and HD patients. CONCLUSION Predialysis and HD are associated with a higher prevalence of severe periodontitis compared with healthy individuals and CAPD patients.

Matrix metalloproteinases and chemokines in the gingival crevicular fluid during orthodontic tooth movement.

Matrix metalloproteinases (MMPs) and monocyte chemoattractants are key modulators of the biological mechanisms triggered in the periodontium by mechanical forces. The gingival crevicular fluid (GCF) provides a non-invasive method to assess longitudinally the release of inflammatory mediators during orthodontic tooth movement. The goal of this study was to examine the GCF levels of MMP-3, MMP-9, and MMP-13 and of the chemokines macrophage inflammatory protein (MIP)-1β, monocyte chemoattractant protein (MCP)-1, and regulated on activation normal T cells expressed and secreted (RANTES) at different time points during orthodontic tooth movement. Fourteen subjects (three males and 11 females, 18.8 ± 4.8 years of age; range from 12 to 28 years) had their maxillary canines retracted. Thirty-second GCF samples were collected from the tension and pressure sides 7 days prior to the activation of the orthodontic appliance, on the day of activation, and after 1 and 24 hours, and 14, 21, and 80 days of constant force application. The volume of GCF was measured and samples analysed using a multiplexed bead immunoassay for the content of the six target molecules. Differences in the mean GFC volumes and mean level for each analyte over time were assessed using the Friedman test, and differences between the tension and pressure sides at each time point with the Mann-Whitney test. The mean levels of the three MMPs changed significantly over time but only at the compression side (P < 0.05, Friedman test). The GCF levels of the three chemokines were not affected by the application of mechanical stress. The levels of MMPs in GCF at the pressure side are modulated by the application of orthodontic force.

Subgingival microflora in inflammatory bowel disease patients with untreated periodontitis.

Objective To analyze the subgingival microflora composition of inflammatory bowel disease (IBD) patients with untreated chronic periodontitis and compare them with systemically healthy controls also having untreated chronic periodontitis. Method Thirty IBD patients [15 with Crohn’s disease (CD) and 15 with ulcerative colitis (UC)] and 15 control individuals participated in the study. All patients had been diagnosed with untreated chronic periodontitis. From every patient, subgingival plaque was collected from four gingivitis and four periodontitis sites with paper points. Samples from the same category (gingivitis or periodontitis) in each patient were pooled together and stored at −70°C until analysis using a checkerboard DNA–DNA hybridization technique for 74 bacterial species. Results Multiple-comparison analysis showed that the groups differed in bacterial counts for Bacteroides ureolyticus, Campylobacter gracilis, Parvimonas micra, Prevotella melaninogenica, Peptostreptococcus anaerobius, Staphylococcus aureus, Streptococcus anginosus, Streptococcus intermedius, Streptococcus mitis, Streptococcus mutans, and Treponema denticola (P<0.001). CD patients had significantly higher levels of these bacteria than UC patients either in gingivitis or in periodontitis sites (P<0.05). CD patients harbored higher levels of P. melaninogenica, S. aureus, S. anginosus, and S. mutans compared with controls both at gingivitis and at periodontitis sites (P<0.05). UC patients harbored higher levels of S. aureus (P=0.01) and P. anaerobius (P=0.05) than controls only in gingivitis sites. Conclusion Our study showed that even with similar clinical periodontal parameters, IBD patients harbor higher levels of bacteria that are related to opportunistic infections in inflamed subgingival sites that might be harmful for the crucial microbe–host interaction.

Cytokines expression in saliva and peri-implant crevicular fluid of patients with peri-implant disease.

OBJECTIVE This study aimed to measure the levels of GM-CSF, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IFN-γ and TNF-α in peri-implant crevicular fluid (PICF) and saliva from patients with peri-implant disease. METHODS Twenty two total edentulous patients were divided into two groups: Mucositis (MU) patients with bone loss around the implants until the first thread and pocket depth ≤3 mm, and Peri-implantitis (PI) patients with at least one implant with bone loss around two or more threads and pocket depth ≥4 mm. The clinical parameters evaluated were probing pocket depth, bleeding on probing, and percentage of plaque. PICF samples were collected from MU sites, and from shallow (SPI) and deep (DPI) sites in PI. Unstimulated whole and parotid duct saliva was collected from all patients. The cytokines were measured by a multiplexed immunoassay. RESULTS PI patients had a higher percentage of plaque compared with MU (P = 0.02). MU sites had lower pocket depth compared to SPI (P = 0.001) and to DPI (P ≤ 0.001). In PICF, the levels of IL-1β were significantly higher in SPI sites compared to MU (P = 0.03). In the saliva from parotid, IL-8 and IL-12 were significantly higher in patients with PI (P = 0.04). CONCLUSION Elevated levels of IL-1β in PICF seem to be a characteristic trait of patients with peri-implantitis. The parotid duct saliva showed a significant increase in expression of IL-8, which might be related to a systemic response.

Nitric Oxide and Oral Diseases: Can We Talk About It?

Nitric oxide (NO) is a short-lived intercellular messenger with multiple biological implications, such as regulation of blood pressure, inhibition of platelet adhesion and aggregation, bacterial-challenge and cytokine stimulation, and regulation of mineralized tissue function. NO synthase (NOS) catalyses the conversion of cationic amino acid L-arginine to L-citrulline and NO. Recently there is an increasing interest in the role of NO in the physiopathology of periodontal disease (PD). PD is a chronic inflammatory disease of the attachment structures of the teeth, which is found in 40-50% of most adult populations worldwide and may result in tooth loss. The potential sources of NO in periodontum are inflammatory cells, keratinocytes, fibroblasts, osteoclastics and blood vessels. Etiological periodontitis factors, such as inflammatory cytokines and periodontopathogens are evolved in enhanced NO levels, which may be part of a nonspecific natural defense mechanism or may lead to periodontal damage. This review gives detail of recent research data focusing on NO bioavailability and its involvement in periodontitis pathogenesis and the modulation of NO for better control of this disease.

Periodontal and inflammatory bowel diseases: Is there evidence of complex pathogenic interactions?

Periodontal disease and inflammatory bowel disease (IBD) are both chronic inflammatory diseases. Their pathogenesis is mediated by a complex interplay between a dysbiotic microbiota and the host immune-inflammatory response, and both are influenced by genetic and environmental factors. This review aimed to provide an overview of the evidence dealing with a possible pathogenic interaction between periodontal disease and IBD. There seems to be an increased prevalence of periodontal disease in patients with IBD when compared to healthy controls, probably due to changes in the oral microbiota and a higher inflammatory response. Moreover, the induction of periodontitis seems to result in gut dysbiosis and altered gut epithelial cell barrier function, which might contribute to the pathogenesis of IBD. Considering the complexity of both periodontal disease and IBD, it is very challenging to understand the possible pathways involved in their coexistence. In conclusion, this review points to a complex pathogenic interaction between periodontal disease and IBD, in which one disease might alter the composition of the microbiota and increase the inflammatory response related to the other. However, we still need more data derived from human studies to confirm results from murine models. Thus, mechanistic studies are definitely warranted to clarify this possible bidirectional association.

Cytokine expression in gingival and intestinal tissues of patients with periodontitis and inflammatory bowel disease: An exploratory study

OBJECTIVE To evaluate the expression of the cytokines IFN-γ, IL-1β, IL-4, IL-6, IL-10, IL-21, IL-22, IL-23, IL-25, IL-31, IL-33, IL-17A, IL-17F, sCD40L, and TNF-α in gingival tissue and intestinal mucosa of patients having both periodontitis and inflammatory bowel disease (IBD) and assess how they cluster in both tissues. METHODS This cross-sectional study selected 28 patients with periodontitis (18 with Crohns disease and 10 with ulcerative colitis) from the IBD gastroenterology outpatient clinic at the Pedro Ernesto University Hospital. Patients were assessed using questionnaire, medical chart check and periodontal examination. Gingival and intestinal biopsies were collected and homogenized using a cell disruptor. Cytokines expression was evaluated through multiplex technology. Cluster analysis was performed based on cytokinés correlation strength and presented in dendrograms. RESULTS Crohns disease and ulcerative colitis patients exhibited no significant difference between them in cytokine levels (p>0.05), so they were analysed together. Significantly higher levels of IL-17A, IL-17F, IL-22, IL-25, IL-33, IL-10, and INF-γ were found in gingival tissues in comparison with intestinal mucosa (p<0.05). In gingival tissue, cytokines formed the following clusters: IL-25/IL-10/IL-33 (r=0.775), IL-22/IL-23/IL-6 (r=0.681) and IL-6/IL-25/IL-33/IL-10 (r=0.660). In intestinal mucosa, the following clusters were formed: IL-6/IL-21/IL-10 (r=0.880), IL-17A/IL-6/IL-21/IL-10 (r=0.826), IL-I7F/IL-33/IL-25 (r=0.813) and IL-23/IL-2/IL-17A/IL-6/IL-21/IL-10 (r=0.785). CONCLUSION Expression of IL-17A, IL-17F, IL-22, IL-25, IL-33, IL-10, and INF-γ was significantly increased in gingival tissue in comparison with intestinal mucosa of patients with periodontitis and IBD. The cytokine clustering pattern was different in gingival and intestinal tissues.

Severe Chronic Periodontitis Is Associated With Endothelial and Microvascular Dysfunctions: A Pilot Study

BACKGROUND Periodontitis is an inflammatory chronic disease that has been implicated as a risk factor for cardiovascular disease (CVD). Endothelium has a central role in CVD pathogenesis, and chronic inflammation can make it dysfunctional, contributing to CVD emergence. Thus, the aim of this study is to investigate the existence of an association between severe chronic periodontitis (CP) and nailfold microvascular, gingival microvascular, and endothelial functions. METHODS Twenty-three patients were included, 13 with severe periodontitis (median age, 46 years; interquartile range, 9.5 years) and 10 healthy control patients (median age, 35.5 years; interquartile range, 12.5 years). Clinical and laboratorial variables were gathered, and patients were examined by the following: 1) nailfold videocapillaroscopy to assess functional capillary density (FCD), capillary diameters, red blood cell velocity at rest (RBCV) and after 1-minute arterial occlusion (RBCVmax), and time taken to reach RBCVmax (TRBCVmax); 2) side-stream dark-field imaging to determine gingival capillary density (GCD); and 3) venous occlusion plethysmography to assess endothelium-dependent (% Hyper) and endothelium-independent vasodilatation (% Nitro). RESULTS Patients with CP have smaller values for FCD, RBCV, RBCVmax, and % Hyper and higher values for TRBCVmax and GCD compared with controls (P <0.05). There were significant correlations between periodontal parameters with FCD, RBCV, RBCVmax, TRBCVmax, GCD, and % Hyper. There was also a negative correlation between FCD and GCD (r = -0.7; P <0.01). Associations between periodontitis and FCD, RBCVmax, TRBCVmax, GCD, and % Hyper remained significant after adjustments for age and systolic blood pressure. CONCLUSION Severe CP was directly associated with endothelial and microvascular dysfunctions.