The aim of this study was the histopathological evaluation of apical and periapical tissues in dog teeth that were submitted to bacterial endotoxin, associated or not with calcium hydroxide. After removal of the pulp from 60 premolars, the teeth were divided into four groups and were filled with bacterial endotoxin (group 1), bacterial endotoxin plus calcium hydroxide (group 2), saline solution (group 3), or had induced periapical lesions with no treatment (group 4). After 30 days, animals were killed and the teeth processed histologically. The inflammatory infiltrate, the thickness of the periodontal ligament, and the presence of resorption areas were similar for groups 1 and 4. Groups 2 and 3 were similar to each other. It can be concluded that the bacterial endotoxin caused a periapical lesion and that calcium hydroxide detoxified the lipopolysaccharides in vivo.Improvement in microbiology techniques for culture and identification has shown that root canals in teeth with pulp necrosis and a chronic periapical reaction have a predominance of anaerobic microorganisms (1, 2), especially Gram-negative ones (3). This polybacterial infection is present not only in the lumen of the root canal and dentinal tubules, but also in the apical craters and the entire root canal system (2). Gram-negative microorganisms not only have different virulent factors and produce toxic products and sub-products in apical and periapical tissues, but also contain endotoxin in their cell wall. Endotoxin, which consists of lipopolysaccharides (LPS), is liberated during bacterial cell multiplication or death and is responsible for a series of important biological effects (4, 5). Its action on macrophages (6) triggers the release of a series of inflammatory, bioactive, chemical mediators, or cytokines (5), such as tumor necrosis factor (TNF) (4, 5) and interleukins-1 (5, 7), -6, and -8 (7). Endotoxin also induces fever (8), is mitogenic to B lymphocytes (5), activates the complement system (8) and the metabolism of arachidonic acid (5), and irreversibly adheres to mineralized tissues. These events lead to an inflammatory reaction and bone resorption in the periapical region. These facts emphasize the important role of LPS in the pathogenesis of periapical lesions (4, 9, 10, 11).A survey of the medical literature over the last 10 yr produced 22,450 articles dealing with endotoxin; however only four articles in dentistry (9, 10, 12, 13) evaluated the effects of LPS on apical and periapical tissues using experimental animals.Treatment of root canals in teeth with pulp necrosis and a chronic periapical reaction should not only be concerned with bacterial death, but also the inactivation of endotoxin. Safavi and Nichols (14, 15), Barthel et al. (4), and Olsen et al. (16) studied, in vitro, the effect of calcium hydroxide on bacterial LPS, because LPS may remain in the root canals between intracanal dressing sessions. However, there are no in vivo studies reporting this problem.The purpose of this study was to evaluate histopathologically the ef...