Objective To conduct a systematic review and meta‐analysis to evaluate the recent scientific literature addressing the association between periodontitis and asthma, chronic obstructive pulmonary disease (COPD), and pneumonia. Materials and Methods The search for studies was carried out using MEDLINE/PubMed, EMBASE, Lilacs, Web of Science, Scopus, and SciELO databases, including the gray literature (ProQuest). Reference lists of selected articles were also searched. Studies having varying epidemiological designs assessing the association between periodontitis and respiratory diseases in human subjects were eligible for inclusion. Three independent reviewers performed the selection of articles and data extraction. Fixed and random effects meta‐analysis were performed for the calculation of the association measurements (Odds Ratio—OR) and 95% confidence intervals (95% CI). Results A total of 3,234 records were identified in the database search, with only 13 studies meeting the eligibility criteria and 10 studies contributed data for meta‐analysis. Using a random effects models periodontitis was associated with asthma: ORadjusted: 3.54 (95% CI: 2.47–5.07), I2 = 0%; with COPD: OR adjusted: 1.78 (95% CI: 1.04–3.05), I2 = 37.9%; and with pneumonia: OR adjusted: 3.21 (95% CI: 1.997–5.17), I2 = 0%. Conclusions The main findings of this systematic review validated an association between periodontitis and asthma, COPD and pneumonia.

Our data suggest that P. gingivalis HmuY may be considered an immunogenic protein associated with host-pathogen interactions.

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.

Background Periodontitis, an inflammatory disease of multibacterial etiology that affects the protective and supporting tissues surrounding teeth, can influence the course of respiratory diseases, such as asthma, due to epithelial alterations arising from inflammatory and immunological processes, bronchial remodeling, or by the aspiration of pathogenic colonizers found in periodontal pockets. This study evaluated the levels of periodontal pathogens Prevotella intermedia, Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans in the subgingival biofilm of individuals with and without severe asthma. Methods A case‐control study enrolling 457 individuals (220 with asthma and 237 without asthma) was conducted at the Program for Control of Asthma in Bahia (ProAR) Clinic located in Salvador, Bahia, Brazil. A structured questionnaire was used to obtain data on sociodemographic, health status, and lifestyle habits. A clinical periodontal assessment was performed, including bleeding on probing, probing depth, and clinical attachment level. Subgingival biofilm was collected at the deepest site of each sextant, and bacterial DNA was extracted. Quantitative real‐time PCR analysis was performed to detect and relatively quantify periodontopathogens in the biofilm. Results Statistically significant positive associations were found between periodontitis and severe asthma, (odds ratio [OR]adjusted]: 4.00; 95% confidence interval [CI]: 2.26 to 7.10). High levels of P. intermedia were found in association with the presence of severe asthma (ORadjusted: 2.64; 95% CI: 1.62 to 4.39; P < 0.01). Conclusions The present results suggest that periodontitis and P. intermedia are associated with severe asthma. However, the functional consequences of this dysbiosis upon asthma susceptibility and its phenotypes remain unclear.

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.