Soraya Castro Trindade

Does Periodontal Infection Have an Effect on Severe Asthma in Adults

BACKGROUND The effect of periodontal infection on systemic diseases and conditions has been the subject of numerous studies worldwide. It is considered that periodontitis may influence the hyperinflammatory response in patients with severe asthma as a result of immuno-inflammatory changes. This study aims to evaluate the influence of periodontitis on severe asthma in adults. METHODS A case-control study was carried out, comprising 220 adult individuals: 113 diagnosed with asthma (case group) and 107 without asthma diagnosis (control group). The diagnosis of periodontitis was established after a full clinical examination using probing depth, clinical attachment level, and bleeding on probing. The diagnosis of severe asthma was based on the criteria recommended by the Global Initiative of Asthma (2012). Descriptive analyses of the variables were performed, followed by bivariate analyses, using the χ(2) test. Association measurements (odds ratio [OR]), with and without adjustment for potential confounders, were obtained. A significance level of 5% was used. RESULTS The ORunadjusted for the main association was 4.38 (95% confidence interval [CI] = 2.47 to 7.75). In the logistic regression model, after adjusting for age, education level, osteoporosis, smoking habit, and body mass index, the ORadjusted was 4.82 (95% CI = 2.66 to 8.76), which was statistically significant. Individuals with periodontal infection showed, approximately, five times more likelihood to have bronchial inflammation than those without such periodontal tissue infection. CONCLUSION The findings demonstrate the influence of periodontitis on severe asthma, given that the frequency of periodontitis is higher in individuals with severe asthma than in those without a diagnosis of bronchial inflammation.

Influence of Periodontitis in the Development of Nosocomial Pneumonia: A Case Control Study

BACKGROUND Although a number of studies on the role of periodontitis in the development of nosocomial pneumonia (NP) have been published, the debate surrounding the existence and nature of this association continues. The present study investigates the influence of periodontitis in NP. METHODS This case-control study involved 315 individuals: 85 cases (with NP) and 230 controls (without NP), at a general hospital in Feira de Santana, Bahia, Brazil. Sociodemographic characteristics, health conditions, and lifestyle habits were recorded. A full-mouth periodontal examination was performed and periodontal condition assessed. The diagnosis of NP was made in accordance with established medical criteria, after physical, microbiologic, and/or radiographic examination. Logistic regression was used to calculate the strength of the association between periodontitis and NP. RESULTS Individuals with periodontitis were three times as likely to present with NP (unadjusted odds ratio [OR unadjusted] = 3.06, 95% confidence interval [95% CI]: 1.82 to 5.15) as those without periodontal disease. After adjusting for age, time between hospitalization and data collection, last visit to dentist, smoking habit, and present occupation, the association measurement had a slight decrease (OR adjusted = 2.88, 95% CI: 1.59 to 5.19), but the results continued to be statistically significant. CONCLUSION These findings suggest that periodontal infection may influence the development of NP, highlighting that periodontitis is a factor positively associated with this respiratory tract infection.

Porphyromonas gingivalis HmuY-induced production of interleukin-6 and IL-6 polymorphism in chronic periodontitis.

BACKGROUND In chronic periodontitis (CP), the gene polymorphism of interleukin-6 (IL-6) to 174C/G has been associated with the altered production of this cytokine. The aim of this pilot study is to compare the allelic and genotypic frequencies in patients with CP with control individuals without periodontitis (NP) and to measure the production of IL-6 by whole blood cells stimulated with Porphyromonas gingivalis HmuY protein. METHODS DNA was isolated from peripheral blood cells of 49 patients with CP and 60 control individuals classified as NP, and genotyping was performed by polymerase chain reaction using sequence-specific primers. Whole blood cells from 29 patients with CP and 30 control individuals were stimulated for 48 hours with HmuY, and IL-6 levels were measured using enzyme-linked immunosorbent assay. RESULTS The proportion of individuals carrying the G allele at position -174 of the IL-6 gene was higher in the group with CP (85.7%) than in the normal control group (73.3%; P <0.03). P. gingivalis HmuY-induced production of IL-6 was higher in the group with CP (P <0.05). CONCLUSIONS Our findings suggest that P. gingivalis HmuY may be associated with increased IL-6 production during CP. Furthermore, patients with periodontitis and individuals with higher HmuY-induced production of IL-6 show a high frequency of the G allele at position -174.

Induction of interleukin (IL)-1β, IL-10, IL-8 and immunoglobulin G by Porphyromonas gingivalis HmuY in humans.

BACKGROUND AND OBJECTIVE Porphyromonas gingivalis, an anaerobic gram-negative bacterium, is associated with chronic periodontitis. This study was undertaken to evaluate the production of interleukin (IL)-1β, IL-8 and IL-10 by human peripheral blood mononuclear cells (PBMC) stimulated with P. gingivalis antigens and to assess the levels of serum immunoglobulin (Ig)G, IgA and IgG subclasses raised against P. gingivalis HmuY protein. MATERIAL AND METHODS PBMC from patients with chronic periodontitis (CP) and from nonperiodontitis (NP) control subjects were stimulated with P. gingivalis antigens, and the cytokine levels in the culture supernatants were determined by ELISA. The specificity of serum antibodies raised against HmuY was analyzed by Western blotting and by ELISA. RESULTS Compared with the NP controls, the CP patients produced higher levels of total serum IgG and IgG1 specific for P. gingivalis HmuY. No differences were found between CP and NP groups in the production of IL-1β and IL-8 by PBMC stimulated with total P. gingivalis antigens. Only P. gingivalis lipopolysaccharide (LPS) induced higher levels of IL-10 in the CP group. Higher levels of IL-1β and IL-10 were induced by HmuY than by other antigens derived from the wild-type P. gingivalis strains. In contrast, total antigens derived from the hmuY-deletion mutant strain induced the production of significantly higher levels of IL-8 and significantly lower levels of IL-1β. CONCLUSION Our data suggest that P. gingivalis HmuY may be considered an immunogenic protein associated with host-pathogen interactions.

Effect of osteoporosis on periodontal therapy among post-menopausal women

OBJECTIVE This intervention study aimed to investigate the effect of osteoporosis on periodontal condition among 48 post-menopausal women undergoing periodontal therapy. MATERIAL AND METHODS The experimental group, which underwent non-surgical periodontal therapy, was composed of 16 women with periodontitis to be treated, and the control group was formed by 32 women without periodontitis. Oral condition was assessed on three occasions: at the start of the treatment (first examination), 1 month (first re-examination) and 4 months after the end of the therapy (second re-examination). In the second re-examination, recurrence of periodontal disease was evaluated by comparing the clinical measurements obtained pre- and post-treatment. The diagnosis of osteoporosis was made by investigating densitometry reports obtained previously. Descriptive analysis, analysis of variance and the Bonferroni post hoc test were applied to the data gathered, with statistical significance level of 5%. RESULTS The frequency of periodontitis was 50% in the treated group and 25% in the group without periodontitis. In both groups, this recurrence was greater in subjects with osteoporosis (37.5 and 18.75%, respectively) than in the individuals without osteoporosis (12.5 and 6.25%, respectively). CONCLUSIONS The preliminary results indicate that osteoporosis possibly has an influence on periodontal condition among individuals undergoing non-surgical periodontal treatment.

Porphyromonas gingivalis HmuY stimulates expression of Bcl-2 and Fas by human CD3 + T cells

BackgroundApoptosis is a highly controlled process of cell death that can be induced by periodontopathogens. The present study aimed to investigate the expression of Fas and Bcl-2 proteins by CD3+ T cells in vitro under stimulation by total Porphyromonas gingivalis antigens and purified recombinant P. gingivalis HmuY protein.ResultsCD3+ T cells derived from CP patients and stimulated with HmuY expressed higher levels of Bcl-2 compared to identical cells stimulated with P. gingivalis crude extract or cells derived from NP control subjects (p = 0.043).ConclusionThe authors hypothesize that P. gingivalis HmuY plays a role in the pathogenesis of chronic periodontitis, possibly by reducing or delaying apoptosis in T cells through a pathway involving the Bcl-2 protein.

Porphyromonas gingivalis antigens differently participate in the proliferation and cell death of human PBMC

OBJECTIVE Modulation of cell-mediated immunity by microorganisms in periodontal diseases has been widely studied; however, the proliferative activity and/or programmed death of mononuclear cells under periodontopathogenic stimuli are not yet well understood. The aim of this study was to investigate in vitro proliferation and death of peripheral blood mononuclear cells (PBMC) upon stimulation with Porphyromonas gingivalis (Pg) antigens. DESIGN In 19 patients with chronic periodontitis (CP) and 16 controls without periodontitis (NP) the following clinical parameters were evaluated: bleeding on probing, probing depth, and clinical attachment level. PBMC were cultured under Pg stimuli and apoptosis/necrosis and proliferation assays were carried out for 18 and 48 h, respectively. Fluorescence of labelled cells was determined using flow cytometry. RESULTS PBMC of CP and NP subjects exhibited a lower proliferative response to Pg LPS (p<0.05) and HmuY protein (p<0.001) compared with non-stimulated cells. Early apoptosis was induced by Pg LPS (p<0.01) and Pg extract (p<0.05), whilst all antigens induced late apoptosis (Pg LPS: p<0.001; Pg extract: p<0.001; HmuY: p<0.01) and necrosis (Pg LPS: p<0.01; Pg extract: p<0.001; HmuY: p<0.001). Pg LPS induced higher late apoptosis than HmuY (p<0.05). Only Pg LPS-induced necrosis tended to be higher in CP compared with NP. CONCLUSIONS The inhibitory effect of cell proliferation caused by Pg LPS and HmuY protein is not observed when these antigens comprise Pg extract. Despite induced apoptosis, some still unknown mechanism determines the inflammatory outcome in cell death stimulated by HmuY.

Association between osteoporosis treatment and severe periodontitis in postmenopausal women.

Objective: To estimate the association between osteoporosis treatment and severe periodontitis in postmenopausal women. Methods: This cross-sectional study comprised of 492 postmenopausal women, 113 women in osteoporosis treatment, and 379 not treated. Osteoporosis treatment consisted of systemic estrogen alone, or estrogen plus progestin, and calcium and vitamin D supplements, for at least 6 months. Severe periodontitis was defined as at least two interproximal tooth sites with clinical attachment loss of at least 6 mm, and at least one interproximal site with probing depth of at least 5 mm; and dental caries experience was measured using the decayed, missing, and filled teeth (DMFT) index. Analysis included descriptive statistics and Poisson multivariate analysis with robust variance. Results: Women receiving osteoporosis treatment had less periodontal probing depth, less clinical attachment loss, and less gingival bleeding than women not receiving treatment for osteoporosis (P ⩽ 0.05). In the osteoporosis treatment group, the estimated mean DMFT index score was approximately 20, the most frequent component being the number of missing teeth, and in the nontreated group, the DMFT index was approximately 19. The prevalence of severe periodontitis was 44% lower in the osteoporosis treatment group than in the nontreatment group. The prevalence ratioadjusted was 0.56, 95% confidence interval was 0.31 to 0.99 (P = 0.05), after adjustments for smoking, age, family income, and visit to the dentist. Conclusions: The results suggest that women treated with estrogen for postmenopausal osteoporosis have a lower prevalence of severe periodontitis than women not receiving treatment.

Immune response of macrophages induced by Porphyromonas gingivalis requires HmuY protein.

The main etiologic agent and a key pathogen responsible for initiation and progression of chronic periodontitis is Porphyromonas gingivalis. We examined the role of P. gingivalis, with particular interest to HmuY protein, in expression of genes involved in Toll-like receptor (TLR)-induced signaling pathways using cell-based infection model. U937 and THP-1 cells differentiated toward macrophages by PMA treatment responded to P. gingivalis-caused infection in slightly different gene expression pattern, mainly by higher expression of genes encoding NF-κB, TLR7, TLR2, TLR8, pro-inflammatory cytokines (IL-1β, IL-6, TNFα), anti-inflammatory cytokine (IL-10), and chemokines (CCL3L1, CCL4, CXCL10, CXCL11, PTX3). P. gingivalis lacking functional hmuY gene stimulates immune response of macrophages, albeit in a different manner as compared with the wild-type strain, mainly by lower expression of genes encoding NF-κB, IL-1β, IL-10, CD80, PTX3, and CCL31L. The purified HmuY protein alone induced expression of genes encoding IL-6, IL-10, TNFα, CCL3L1, and CCL4. We conclude that macrophages respond to P. gingivalis infection mostly by TLR7-induced pathway(s). Moreover, P. gingivalis HmuY is one of important virulence factors, which allows P. gingivalis for in vivo growth in the heme-limited host environment, resulting in efficient immune response of macrophages.

MAPK involvement in cytokine production in response to Corynebacterium pseudotuberculosis infection

BackgroundCaseous lymphadenitis (CL) is a contagious infectious disease of small ruminants caused by Corynebacterium pseudotuberculosis. Is characterized by the formation of abscesses in the lymph nodes and intestines of infected animals, induced by inflammatory cytokines. The production of cytokines, such as IL-10, TNF-α, IL-4 and IFN-γ, is regulated by mitogen-activated protein kinase (MAPK) pathway activation. The present study investigated the involvement of MAPK pathways (MAPK p38, ERK 1 and ERK 2) with respect to the production of cytokines induced by antigens secreted by C. pseudotuberculosis over a 60-day course of infection. CBA mice (n = 25) were divided into three groups and infected with 102 colony forming units (CFU) of attenuated strain T1, 102 CFU of virulent strain VD57 or sterile saline solution and euthanized after 30 or 60 days. Murine splenocytes were treated with specific inhibitors (MAPK p38 inhibitor, ERK 1/2 inhibitor or ERK 2 inhibitor) and cultured with secreted antigens obtained from pathogenic bacteria (SeT1 or SeVD57).ResultsThe MAPK pathways evaluated were observed to be involved in the production of IL-10, under stimulation by secreted antigens, while the MAPK p38 and ERK 1 pathways were shown to be primarily involved in TNF-α production. By contrast, no involvement of the MAPK p38 and ERK 1 and 2 pathways was observed in IFN-γ production, while the ERK 2 pathway demonstrated involvement in IL-4 production only in the mouse splenocytes infected with VD57 under stimulation by SeT1.ConclusionThe authors hypothesize that MAPK p38 and ERK 1 pathways with respect to TNF-α production, as well as the MAPK p38 and ERK 1 and 2 pathways in relation to IL-10 production under infection by C. pseudotuberculosis are important regulators of cellular response. Additionally, the lack of the MAPK p38 and ERK 1/2 pathways in IFN-γ production in infected CBA murine cells stimulated with the two secreted/excreted antigens, in IL-4 production showing involvement only via the ERK 2 pathway under stimulation by SeT1 antigen during 60-day infection period with the virulent strain, suggests that these pathways regulated the production of pro-inflammatory and regulatory cytokines in the splenic cells of CBA mice.