ISSN:
1600-0595
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Abstract— The purpose of the present study was to evaluate the influence of bacterial infection on the pulpal and periodontal tissues in replanted teeth using germ-free and conventional rats. Forty maxillary and mandibular first molars from ten 6-week-old germ-free male Wistar rats were used. The animals and all materials were maintained in a germ-free environment inside vinyl isolators throughout the experimental periods. Twenty conventional male Wistar rats served as controls. The first molars were intentionally replanted immediately after extraction. At 3 days, and 1,2,4 and 8 weeks after replantation, animals were sacrificed and the re planted teeth were histopathologically evaluated. Diversity of pulp tissue response was notable in conventional rats, which initially showed various degrees of neutrophil infiltration and then display ed different types of response, including revascularization with reparative dentin formation and complete necrosis. Pulpal responses of germ-free rats were less variable, being characterized by an almost complete lack of neutrophil infiltration and a high frequency of bone-like tissue ingrowth. Typical inffammatory resorption was detected only in conventional rats, whereas a higher incidence of ankylosis was notable in germ-free rats. The present results may corroborate the concept that bacterial infection is a major cause of serious healing complications following tooth replantation, such as pulp necrosis and inflammatory root resorption. The difficulty in optimally controlling bacterial infection seems to be highlyrelevant to the complexity and unpredictability of the outcome of this procedure. It should also be emphasized that extensive mechanical damage to the periodontal tissues may trigger the development of unfavorable healing complications as ankylosis, even under strictly aseptic conditions.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1600-9657.1998.tb00832.x
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