Effect of calcium hydroxide on proinflammatory cytokines and neuropeptides

Calcium hydroxide, a widely used intracanal medicament, is known to exert an antimicrobial effect and to degrade bacterial-derived lipopolysaccharides. However, little is known about the effect of Ca(OH)(2) on endogenous inflammatory mediators such as interleukin-1 alpha (IL-1 alpha), tumor necrosis factor-alpha (TNF-alpha), and calcitonin gene-related peptide (CGRP). This is an important gap in knowledge because these inflammatory mediators play an important role in mediating the pathogenesis of periradicular periodontitis. We tested the hypothesis that Ca(OH)(2) denatures IL-1 alpha, TNF-alpha, and CGRP. Human IL-1 alpha (0.125 ng/mL), TNF-alpha (0.2 ng/mL), and CGRP (0.25 ng/mL) were incubated with Ca(OH)(2) (0.035 mg/mL) for 1-7 days. At the end of the incubation period, the pH of the samples was neutralized, and the concentrations of the mediators were measured by immunoassays. Data were analyzed with one-way analysis of variance and Bonferroni multiple comparison tests. The results indicate that Ca(OH)(2) denatures IL-1 alpha, TNF-alpha, and CGRP by 50%-100% during the testing periods (P < .001). We concluded that denaturation of these proinflammatory mediators is a potential mechanism by which Ca(OH)(2) contributes to the resolution of periradicular periodontitis.