The purpose of this study was to compare the effectiveness of antibacterial agents and mineral trioxide aggregate in the healing of bacterial contaminated primate pulps. The experiment required four adult male primates (Cebus opella) with 48 teeth prepared with buccal penetrations into the pulpal tissues. The preparations were performed under general anesthesia and the exposed pulps were exposed to cotton pellets soaked in a bacterial mixture consisting of microorganisms normally found in human pulpal abscesses obtained from the Endodontic Clinic of UNESP. Following bacterial inoculation (30 minute exposure), the pulpal tissue was immediately treated with either sterile saline, Cipro HC Otic solution (12), diluted Buckley' formecresol solution (12) or Otosporin otic solution (12) for 5 minutes. After removal of the pellet, hemostasis was obtained and a ZOE base applied to the DFC treated pulps and the non-treated controls (12). After hemostasis, the other exposed pulps were covered with mineral trioxide aggregate (ProRoot). The pulpal bases were all covered with a RMGI (Fuji II LC). The tissue samples were collected at one day, two days, one week and over four weeks (34 days). Following perfusion fixation, the samples were demineralized, sectioned, stained and histologically graded. After histologic analysis, presence of neutrophilic infiltrate and areas of hemorrhage with hyperemia were observed. The depth of the neutrophilic infiltrate depended on the agent or material used. The pulpal tissue treated with Otic suspensions demonstrated significantly less inflammation (Kruskal Wallis non parametric analysis, H = 9.595 with 1 degree of freedom; P = 0.0223) than the formocresol and control groups. The hard tissue bridges formed over the exposure sites were more organized in the MTA treatment groups than in the control and ZOE groups (Kruskal Wallis non parametric analysis, H = 18.291 with 1 degree of freedom; P = 0.0004). Otic suspensions and MTA are effective in treating bacterial infected pulps and stimulate the production of a hard tissue bridge over the site of the exposure.
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