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Although epigallocatechin-3-gallate (EGCG) from green tea has been successfully used in the prevention and treatment of several infectious and immunoinflammatory diseases because of its proven anti-inflammatory, antioxidant, antimicrobial, and antiresorptive role, its use as an intracanal dressing has not been proposed. The aim of this study was to develop a formulation based on EGCG for endodontic use by assessing its physicochemical and biological properties. Initially, physicochemical characterization of EGCG was performed by ultraviolet-visible and fluorescence spectroscopy to evaluate if the properties were maintained in acidic pH and time (1–6, 24, and 27 hours). After that, biological studies evaluated the developed formulation of EGCG at different concentrations (1.25, 5, 10, and 20 mg/mL). The tissue compatibility with subcutaneous tissue of mice was evaluated by plasma leakage after 24 hours and the examination of macroscopic and microscopic features at 7, 21, and 63 days after the insertion of polyethylene tubes containing the formulations. The repair of experimentally induced periapical lesions in dog's teeth by radiographic and histopathologic analysis was also evaluated. The scores were statistically analyzed by the chi-square and Fisher exact test. Analysis of variance followed by the Tukey posttest were used for the quantitative analysis. The significance level was 5%. The physicochemical characterization performed under ultraviolet-visible spectrophotometry showed that the EGCG properties remained unaltered in acid pH and function of time, keeping its wavelength to 274 nm. Macroscopic parameters evaluated at 7, 21, and 63 days showed that all concentrations presented no epithelial ulceration or presence of mild superficial tissue necrosis, edema, or vascularization with no significant difference in the control group. During all periods of microscopic examination, all groups presented the absence of abscess foci and edema and the presence of fibrous capsule and neovascularization. The presence of reparative tissue with a gentle presence of neutrophilic inflammatory cells was also observed for all groups, except for the calcium hydroxide paste group, which presented a more pronounced inflammation and tissue necrosis at days 7 and 21 (P <.001). At day 63, all groups presented an absence of inflammatory infiltrate and necrosis. The evaluation of dog teeth showed that treatment with the EGCG formulation provided a reduction of the periapical radiolucent area and allowed the repair of apical and periapical tissues (P >.05). The developed formulation based on EGCG from green tea presented physicochemical stability and tissue compatibility and provided the repair of periapical lesions when used as an intracanal dressing. [ABSTRACT FROM AUTHOR]

Introduction Although studies have recently shown that osteocytes embedded in mineralized bone matrix play an important role in bone diseases, the participation of cementocytes in apical periodontitis has not been evaluated. The aim of the present study was to evaluate the possible involvement of cementocytes in the development of apical periodontitis. Methods Apical periodontitis was experimentally induced in the lower first molars of wild-type mice by pulp exposure to the oral environment. At 0, 7, 21, and 42 days after pulp infection, the animals were euthanized, and the jaws were prepared for analysis under conventional and fluorescence microscopy (morphologic and morphometric analysis), immunohistochemistry and immunofluorescence (receptor activator of nuclear factor kappa-B [RANK], receptor activator of the nuclear factor kappa-B ligand [RANKL], and osteoprotegerin [OPG]), enzyme histochemistry (osteoclasts and cementoclasts), and real-time polymerase chain reaction (RANK, RANKL, OPG, and cathepsin K). Results At 7, 21, and 42 days after pulp exposure, there was a progressive increase in periodontal ligament, cementum and bone resorption areas, osteoclasts, and cementoclast counts as well as higher messenger RNA levels of RANK, RANKL, OPG, and cathepsin K. In intact teeth, cementocytes and osteocytes did not express RANKL. After infection, RANKL was strongly expressed in cementocytes, but not in osteocytes, and its expression increased with lesion progression. Conclusions Our findings show that cementocytes express RANKL in response to endodontic infection and may be involved in the pathogenesis of apical periodontitis. [ABSTRACT FROM AUTHOR]

Abstract: Because chlorhexidine (CHX) has been recommended as either an endodontic irrigant or root canal dressing, this study aimed to characterize, in vivo, the lesion induced by injections of CHX in the paw of mice at selected time intervals (24 and 48 hours and 7 and 14 days) and, in vitro, the mode of cell death, necrosis and/or apoptosis, and the cellular stress caused by exposition of cultured L929 fibroblasts to ascending concentrations of CHX for 24 hours. CHX injected in the subplantar space of the hind paw of mice induced severe toxic effects, as evidenced by necrotic changes in the epidermis, dermis, and subcutaneous tissue in association with reactive inflammatory response, particularly at higher concentrations. In addition, in cultured fibroblasts, CHX induced apoptosis at lower concentrations and necrosis at higher concentrations and increased expression of heat-shock protein 70, an indicator of cellular stress. Taken together, these findings suggest that CHX may have an unfavorable effect on the resolution of apical periodontitis. [Copyright &y& Elsevier]