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.

Mesenteric lymph reperfusion after superior mesenteric artery occlusion shock exacerbates endotoxin translocation in brain

PURPOSE: To determine the role of mesenteric lymph reperfusion (MLR) on endotoxin translocation in brain to discuss the mechanism of brain injury subjected to superior mesenteric artery occlusion (SMAO) shock. METHODS: Twenty-four rats were randomly assigned to MLR, SMAO, MLR+SMAO and sham groups. MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h and then allowing reperfusion for 2 h in the MLR group; SMAO involved clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h in the SMAO group; occlusion of both the SMA and MLD for 1 h was followed by reperfusion for 2 h in the MLR+SMAO group rats. RESULTS: SMAO shock induced severe increased levels of the endotoxin, lipopolysaccharide receptor, lipopolysaccharide-binding protein, intercellular adhesion molecule-1 and tumor necrosis factor-α. Concurrently, MLR after SMAO shock further aggravates these deleterious effects. CONCLUSION: Mesenteric lymph reperfusion exacerbated the endotoxin translocation in brain; thereby increased inflammatory response occurred, suggesting that the intestinal lymph pathway plays an important role in the brain injury after superior mesenteric artery occlusion shock. .

Ativação imune-inflamatória na insuficiência cardíaca / Immune-inflammatory activation in heart failure

Apesar de relativamente recente, nota-se um acúmulo crescente e robusto de evidências experimentais e clínicas que apontam um estado gradativo de ativação imune-inflamatória em pacientes com insuficiência cardíaca (IC). Níveis elevados de diversas citocinas são encontrados na circulação e no músculo cardíaco de indivíduos com IC, correlacionando-se, invariavelmente, com o grau de gravidade da doença e agindo na disfunção endotelial, no estresse oxidativo, na indução de anemia, na apoptose miocitária e na perda gradativa de massa muscular esquelética - no que se convencionou denominar o paradigma inflamatório da IC. Não só o miocárdio, mas diversos tecidos parecem sintetizar tais citocinas e perpetuar esse contínuo estado de inflamação em baixo grau, inclusive leucócitos, monócitos, células musculares esqueléticas e endoteliais - em resposta a estímulos hemodinâmicos, infecciosos, à hipóxia, ao estresse oxidativo e à ativação neuro-humoral, entre outros. Desse modo, forma-se uma rede de moléculas que interagem entre si, estabelecendo, ainda, conexões com outros eixos que efetivamente contribuem para a deterioração clínica dos pacientes - o que se encaixa no modelo fisiopatológico de acometimento multissistêmico que tem sido cada vez mais atribuído à IC. Ainda que a dosagem periférica desses biomarcadores reúna evidências bastante sólidas de poder prognóstico, os resultados dos ensaios terapêuticos que modularam em fase clínica a alça imune-inflamatória foram, até então, pouco encorajadores. Desse modo, acreditamos que é fundamental compreender melhor a ativação inflamatória e sua multifacetada relação com os eixos de descompensação da doença, para que possamos estabelecer novas perspectivas terapêuticas com impacto de relevância em um futuro próximo.

Despite being relatively recent, a growing and significant accumulation of experimental and clinical evidence has been observed that points to a gradual state of immune-inflammatory activation in patients with heart failure (HF). High levels of several cytokines are found in the circulation and cardiac muscle of individuals with HF, and invariably correlate with the severity of the disease. These cytokines act on endothelial dysfunction, oxidative stress, induction of anemia, myocyte apoptosis, and on the progressive loss of skeletal muscle mass - which is conventionally called the inflammatory paradigm of HF. Not only the myocardium, but also several tissues seem to synthesize these cytokines and perpetuate this continuous inflammatory state at a low degree, including leukocytes, monocytes, skeletal muscle cells and endothelial cells - in response to hemodynamic and infectious stimuli, to hypoxia, to oxidative stress, to neurohumoral activation, and others. Thus, a network of molecules that interact with each other is formed, and connections with other axes that effectively contribute to the clinical deterioration of the patients are also established - which fits into the pathophysiological model of multisystemic involvement that has been increasingly attributed to HF. Although the determination of these biomarkers in peripheral blood provides solid evidence of prognostic power, the results of therapeutic trials that modulated the immune-inflammatory loop in the clinical phase have been, so far, hardly encouraging. Therefore, we believe that a better understanding of the inflammatory activation and its multifaceted relation with the axes of decompensation of the disease is key for new therapeutic perspectives with a relevant impact to be established in the near future.

Factor de necrosis tumoral Alfa (TNF-alfa) / Alpha tumor necrosis factor (TNF-alpha)

Esta revisión presenta el conocimiento reciente sobre el factor de necrosis tumoral alfa (TNF-alfa), en especial los mecanismos de liberación desde macrófagos y su relación con enfermedades inflamatorias y estrés oxidativo. En odontología, TNF-alfa se relaciona con rápida pérdida de hueso alveolar en enfermedad periodontal. La inducción de apoptosis es otro de sus interesantes efectos

Participation of the central serotonergic pathway in the endotoxin-stimulated hypothalamo-pituitary-adrenal axis function

The aim of the present study was to determine whether the central serotoninergic pathway (5HT) plays any stimulatory/inhibitory role in endotoxin-stimulated hypothalamo-pituitary-adrenal (HPA) axis function in the male rat. For this purpose, animals inhibited or not of central 5HT synthesis were injected with vehicle alone or containing endotoxin (LPS) and killed 2 h later. The results indicate that the inhibition of the 5HT pathway did not modify the LPS-induced hypoglycemia but that significantly reduced ACTH release in plasma. Although the inhibition of 5HT did not modify the CRH-ergic system, it diminished hypothalamic vasopressin (AVP) content in basal condition. After LPS injection, rats inhibited of 5HT synthesis showed a significant activation of the hypothalamic AVP-ergic system whereas control rats did not. These data clearly indicate that decreased HPA axis function after 5HT inhibition could be partially compensated by the facilitation of the AVP neuronal activity.

Sepsis: avances en fisiopatología y tratamiento 1993-1994

Sepsis is a term used to define a group of clinical manifestations caused by the response to the presence of microorganisms, of different types, in the blood stream. This paper reviews is a minute fashion recent knowledge regarding the role of endotoxin in the pathogenesis of the disease as well as that of cytokines as mediators of the process, and finally some of the new therapeutic approaches

Chemical and biological properties of endotoxin from leptospira interrogans serovars canicola and icterohaemorrhagiae

Endotoxin-like activity was extracted with phenol-chloroform-petroleum ether (PCP) from Leptospira interrogans serovars icterohaemorrhagiae and canicola. Chemical analysis of leptospiral cells obtained from the PCP extract i9ndicated the following distribution of lipopolysaccharide (LPS), protein and polysaccharide in mg/ml:3.0, 4.5 anmd 1.0 for icterohaemorrhagiae and 3.,3, 5.6 and for canicola. The preparations presented several biological activities: positive Limulus test (1.0 pg/ml) for icterohaemorraahagiae and canicola PCP extract and 0.5 pg/ml for E. coli 0111:B4 LPS, lethality for chicken embryos (LD 50 45, 25 and 1.0) for ecterohaemorrhagiae, canicola and E. coli 0111:B4 LPS, pyrogenicity in rabbits with an average increase in rectal temperature of 0.6 grade C, 0.9 grade C and 2.2 grade C for canicola, icterohaemorrhagiae and E. coli 0111: B4 LPS, reacted with complement inhibiting the lysis of sheep red blood cells 62%, 75% and 90% for 2.0 ug/ml of icterohaemorrhagiae, canicola PCP extract and E. coli 0111:B4 LPS. The PCP extract showed no cytotoxicity on chicken embryo fibroblasts and epithelial cells