Histological Study of Periradicular Tissue Responses to Uninfected and Infected Devitalized Pulps in Dogs
Uninfected necrotic tissue, such as that which follows amyocardial or cerebral infarct, is capable of inducing aninflammatory reaction. Eventually, the infarct is organizedby granulation tissue. Why then, does uninfected devitalizedpulp tissue, such as in traumatized teeth, not causeperiradicular inflammation and does not become organizedby granulation tissue? Four beagle dogs were usedin this experiment. A total of 48 teeth, which included 24maxillary and 24 mandibular incisors, were asepticallydevitalized, leaving residual pulp tissues in the root canals,and equally divided into two groups. Group A (24 uninfected):A sterile cotton pellet was placed deep into thecanal orifice before the pulp chamber and access openingwere closed with a layer of zinc-oxide eugenol cementfollowed by glass ionomer cement. Group B (24 infected):The teeth were left open to the oral cavity for 7 days andthen closed with a cotton pellet and zinc-oxide eugenoland glass ionomer cement. The animals were sacrificedone year after the experiment and prepared for histologicalexamination of periradicular tissue responses to uninfectedand infected devitalized pulp tissues. The resultsindicate that uninfected devitalized pulp tissues did notcontinuously release inflammatory mediators and causepersistent periradicular inflammation over a period of oneyear. However, infected devitalized pulp tissues inducedvarious degrees of periradicular inflammation. Only theapical few millimeters of uninfected devitalized pulp tissuein the root canals were organized by granulation tissuefrom vital periodontal ligament tissue.
JOE—Volume 32, Number 1, January 2006
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