Etiologic role of root canal infection in apical periodontitis and its relationship with clinical symptomatology

Abstract: Evidence shows the polymicrobial etiology of endodontic infections, in which bacteria and their products are the main agents for the development, progression, and dissemination of apical periodontitis. Microbial factors in necrotic root canals (e.g., endotoxin) may spread into apical tissue, evoking and supporting a chronic inflammatory load. Thus, apical periodontitis is the result of the complex interplay between microbial factors and host defense against invasion of periradicular tissues. This review of the literature aims to discuss the complex network between endodontic infectious content and host immune response in apical periodontitis. A better understanding of the relationship of microbial factors with clinical symptomatology is important to establish appropriate therapeutic procedures for a more predictable outcome of endodontic treatment.

Bacterial endotoxin adhesion to different types of orthodontic adhesives

Abstract Bacterial endotoxin (LPS) adhesion to orthodontic brackets is a known contributing factor to inflammation of the adjacent gingival tissues. Objective The aim of this study was to assess whether LPS adheres to orthodontic adhesive systems, comparing two commercial brands. Material and Methods Forty specimens were fabricated from Transbond XT and Light Bond composite and bonding agent components (n=10/component), then contaminated by immersion in a bacterial endotoxin solution. Contaminated and non-contaminated acrylic resin samples were used as positive and negative control groups, respectively. LPS quantification was performed by the Limulus Amebocyte Lysate QCL-1000™ test. Data obtained were scored and subjected to the Chi-square test using a significance level of 5%. Results There was endotoxin adhesion to all materials (p<0.05). No statistically significant difference was found between composites/bonding agents and acrylic resin (p>0.05). There was no significant difference (p>0.05) among commercial brands. Affinity of endotoxin was significantly greater for the bonding agents (p=0.0025). Conclusions LPS adhered to both orthodontic adhesive systems. Regardless of the brand, the endotoxin had higher affinity for the bonding agents than for the composites. There is no previous study assessing the affinity of LPS for orthodontic adhesive systems. This study revealed that LPS adheres to orthodontic adhesive systems. Therefore, additional care is recommended to orthodontic applications of these materials.

Toll-like receptor agonists Porphyromonas gingivalis LPS and CpG differentially regulate IL-10 competency and frequencies of mouse B10 cells

Abstract IL-10 expressing regulatory B cells (B10) play a key role in immune system balance by limiting excessive inflammatory responses. Effects of toll-like receptor signaling and co-stimulatory molecules on B10 activity during innate and adaptive immune responses are not fully understood. Objective This study is to determine the effects of P. gingivalis LPS and CpG on B10 cell expansion and IL-10 competency in vitro. Material and Methods Spleen B cells were isolated from C57BL/6J mice with or without formalin-fixed P. gingivalis immunization. B cells were cultured for 48 hours under the following conditions: CD40L, CD40L+LPS, CD40L+CpG, and CD40L+LPS+CpG in the presence or absence of fixed P. gingivalis. Percentages of CD1dhiCD5+ B cells were measured by flow cytometry. IL-10 mRNA expression and secreted IL-10 were measured by real-time quantitative PCR and by ELISA respectively. Results P. gingivalis LPS plus CD40L significantly increased CD1dhiCD5+ B cell percentages and secreted IL-10 levels in both immunized and non-immunized mice B cells in the presence or absence of P. gingivalis, compared with control group. Secreted IL-10 levels were significantly increased in CD40L+LPS treated group compared with CD40L treatment group in the absence of P. gingivalis. CpG plus CD40L significantly decreased CD1dhiCD5+ B cell percentages, but greatly elevated secreted IL-10 levels in immunized and non-immunized mice B cells in the absence of P. gingivalis, compared with CD40L treatment group. Conclusions P. gingivalis LPS and CpG differentially enhance IL-10 secretion and expansion of mouse B10 cells during innate and adaptive immune responses.

Host-Microbiome Interactions in Alcoholic Liver Disease

Alcoholic liver disease is a leading cause of morbidity and liver-related death worldwide. Intestinal bacterial overgrowth and dysbiosis induced by ethanol ingestion play an important role in the pathogenesis of alcoholic liver disease. After exposure to alcohol in the lumen, enteric bacteria alter their metabolism and thereby disturb intestinal homeostasis. Disruption of the mucosal barrier results in the translocation of microbial products that contribute to liver disease by inducing hepatic inflammation. In this review, we will discuss the effects of alcohol on the intestinal microbiome, and in particular, its effects on bacterial metabolism, bacterial translocation and ecological balance. A better understanding of the interactions among alcohol, the host and the microbiome will reveal new targets for therapy and lead to new treatments.

Bacterial pathogenesis and mediators in apical periodontitis: [review]

Apical periodontitis is a group of inflammatory diseases caused by microorganisms (mainly bacteria) infecting the necrotic root canal system. The pathogenesis of different types of apical periodontitis and even the same type in different individuals is unlikely to follow a stereotyped fashion with regard to the involved bacterial mediators. Disease pathogenesis is rather complex and involves a multitude of bacteria- and host-related factors. This review article discusses the bacterial pathogenesis of acute and chronic apical periodontitis, with the main focus on the bacterial mediators conceivably involved in the different stages of the infectious process, including secreted products (enzymes, exotoxins, N-formyl-methionyl-leucyl-phenylalanine peptides, heat-shock proteins and metabolic end-products) and structural components (lipopolysaccharide, peptidoglycan, lipoteichoic acid, lipoproteins, fimbriae, flagella, outer membrane proteins and vesicles, DNA, and exopolysaccharides). Knowledge of the bacterial factors involved in the pathogenesis of apical periodontitis is important to the understanding of the disease process and to help establishing proper therapeutic measures to inactivate this bacterial "artillery".

Lesões perirradiculares compreendem um grupo de doenças inflamatórias causadas por microrganismos (principalmente bactérias) infectando o sistema de canais radiculares com polpa necrosada. É improvável que a patogênese dos diferentes tipos de lesão perirradicular, e até mesmo daquelas do mesmo tipo, mas em diferentes indivíduos, obedeça um padrão estereotipado com relação aos mediadores bacterianos envolvidos. A patogênese destas doenças é complexa e envolve inúmeros fatores relacionados às bactérias e ao hospedeiro. Este artigo de revisão discute a patogênese bacteriana das lesões perirradiculares agudas e crônicas, enfatizando os fatores bacterianos que estão possivelmente envolvidos nos diferentes estágios do processo infeccioso, incluindo produtos secretados (enzimas, exotoxinas, peptídeos N-formilados, proteínas de choque térmico e produtos terminais do metabolismo) e componentes estruturais (lipopolissacarídeo, peptidoglicano, ácido lipoteicóico, lipoproteínas, fímbrias, flagelos, proteínas e vesículas de membrana externa, DNA e exopolissacarídeos). O conhecimento dos fatores bacterianos envolvidos na patogênese das lesões perirradiculares é importante para o entendimento do processo patológico bem como para ajudar no estabelecimento de medidas terapêuticas adequadas para desativação desta "artilharia" bacteriana.

Participaçäo colinérgica nos efeitos das drogas antipsicóticas na febre devida a um pirogênio bacteriano / Cholinergic participation in effects of antipsichotics drugs in the fever elicited by one bacterial pyrogen

Os resultados mostraram que a associaçäo de atropina às drogas antipsicóticas produziu reduçäo da resposta febril, quando clorpromazina e flufenazina foram os antipsicóticos utilizados. A associaçäo de atropina ao haloperidol e ao pimozide potencializou a resposta febril