Periapical Lesions Increase Macrophage Infiltration and Inflammatory Signaling in Muscle Tissue of Rats.

INTRODUCTION: Our previous studies have shown that periapical lesions (PLs) in rats cause systemic disorders such as increased tumor necrosis factor-α plasma levels, insulin resistance, and impairment in insulin signal transduction in muscle tissue. However, the mechanisms involved in these alterations are not fully understood. Under chronic inflammatory conditions such as obesity, it has been shown that the skeletal muscle is affected by inflammation, and the number of resident macrophages that are associated with impairments of insulin action and sensitivity is increased. This study aimed to investigate the presence of macrophages, activation of inflammatory pathways in muscle tissue, glycemia, and insulinemia of rats with PLs. METHODS: Sixty Wistar rats were distributed into a control group; a group with 1 PL (1PL), which was induced in the right maxillary first molar; and a group with 4 PLs (4PL), which were induced in the right upper and lower first and second molars. We quantified macrophage content by immunohistochemistry for the F4/80 protein. We evaluated Jun N-terminal kinase and IKKα/ß phosphorylation status in the muscle tissue by Western blotting. Serum levels of lipopolysaccharide (LPS) and HSP70 and plasma levels of glucose and insulin were assessed by using commercial kits. RESULTS: The 1PL and 4PL groups showed increase in macrophage content, IKKα/ß, and Jun N-terminal kinase phosphorylation status, serum LPS and HSP70 levels, and insulin resistance and no changes in glycemia and insulinemia compared with the control group. There was no difference in these parameters between the 1PL and 4PL groups. CONCLUSIONS: PLs promoted an increase in macrophage infiltration, activation of inflammatory pathways in muscle tissue, and serum concentrations of HSP70 and LPS in rats. The present study improves the knowledge on the impact of oral inflammations on the development of systemic alteration, which can induce insulin resistance.

Periapical lesions decrease insulin signal and cause insulin resistance.

INTRODUCTION: Inflammatory cytokines are associated with decreased insulin signal transduction. Moreover, local oral inflammation, such as that accompanying periodontal disease, is associated with insulin resistance and type 2 diabetes mellitus. The aim of this study was to evaluate the effect of periapical lesions (PLs) on insulin signaling and insulin sensitivity in rats. We hypothesized that PLs alter systemic insulin signaling and insulin sensitivity via elevated plasmatic tumor necrosis factor α (TNF-α). METHODS: Wistar rats were divided into control (CN) and PL groups. PLs were induced by exposing pulpal tissue to the oral environment. After 30 days, insulin sensitivity was measured using the insulin tolerance test. After euthanization, maxillae were processed for histopathology. Plasmatic concentrations of tumor necrosis factor α (TNF-α) were determined via the enzyme-linked immunosorbent assay. Insulin signal transduction was evaluated using insulin receptor substrate tyrosine phosphorylation status and serine phosphorylation status in periepididymal white adipose tissue via Western blotting. For insulin signaling and insulin tolerance tests, the analyses performed were analysis of variance followed by the Tukey post hoc test. For TNF-α analysis, the Student's t test was used. In all tests, P < .05 was considered significant. RESULTS: The rats with PLs showed higher plasmatic TNF-α, lower constant rate for glucose disappearance values, and reduced pp185 tyrosine phosphorylation status but no change in serine phosphorylation status in white adipose tissue after insulin stimulation. CONCLUSIONS: PLs can cause alterations to both insulin signaling and insulin sensitivity, probably because of elevation of plasmatic TNF-α. The results from this study emphasize the importance of the prevention of local inflammatory diseases, such as PLs, with regard to the prevention of insulin resistance.

Fluido intersticial en estadios clínicos de patología periapical crónica / Crevicular fluid in clinical stages of chronic periapical pathology

Se intentó correlacionar el momento evolutivo de la patología periapical crónica (PPC) de origen pulpar, mediante la valoración cuantitativa de fluido intersticial. En 88 pacientes se introdujo un cono de papel No.30 hasta 1 mm. del extremo apical en las piezas dentarias afectadas, inmediatamente después de la apertura del conducto radicular. Mediante un higrómetro electrónico se obtuvo la cantidad relativa de líquido embebido en el cono de papel. Los valores se dividieron en cuatro estadios. 1: estado de equilibrio, promedio 5,44; 2: estado inflamación leve, promedio 21,29; 3: estado inflamación moderada, promedio 42,73; 4: estado inflamación severa, promedio 98,71. La cantidad de fluido intersticial varía cuantitativamente de acuerdo con el momento evolutivo de la PPC, pudiendo ser proporcional a la gravedad de la lesión

Fluido intersticial en estadios clínicos de patología periapical crónica / Crevicular fluid in clinical stages of chronic periapical pathology

Se intentó correlacionar el momento evolutivo de la patología periapical crónica (PPC) de origen pulpar, mediante la valoración cuantitativa de fluido intersticial. En 88 pacientes se introdujo un cono de papel No.30 hasta 1 mm. del extremo apical en las piezas dentarias afectadas, inmediatamente después de la apertura del conducto radicular. Mediante un higrómetro electrónico se obtuvo la cantidad relativa de líquido embebido en el cono de papel. Los valores se dividieron en cuatro estadios. 1: estado de equilibrio, promedio 5,44; 2: estado inflamación leve, promedio 21,29; 3: estado inflamación moderada, promedio 42,73; 4: estado inflamación severa, promedio 98,71. La cantidad de fluido intersticial varía cuantitativamente de acuerdo con el momento evolutivo de la PPC, pudiendo ser proporcional a la gravedad de la lesión (AU)