Abstract

Periodontitis is a common inflammatory disease that leads to the degradation of periodontium and results in alveolar bone loss. The development of a suitable animal model of periodontitis is a prerequisite to understanding better the mechanisms that underly this disease. This study evaluated periodontal disease induction via retentive ligature, intragingival injection of lipopolysaccharide (LPS), and their combination in a rat model.Seventy-two Sprague Dawley rats were divided into four groups. The first group (control) did not receive any treatment. The second group underwent the application of 4/0 nylon ligature around the second maxillary molars. The third group was treated with an intragingival injection of Porphyromonas gingivalis LPS into the palatal mucosa of the second maxilla molars, and the fourth group was treated with a combination of ligature and LPS injection (ligature-LPS). Morphological changes in the gingival tissues were evaluated after 7, 14, and 30 days of treatment.Significant degenerative changes were observed in the periodontal tissues and alveolar bone in the third and fourth groups, which were evident as early as seven days. The lesions remained until 14 days and declined with time in the third and fourth groups. The changes induced by ligature and ligature-LPS were not different. Injection with LPS alone resulted in minimal increases in the Gingival and Plaque Indices.The ligature technique induced periodontal disease successfully, more effective than the injection of LPS. The combination of ligature with LPS injection added no significant effect compared to ligature alone.

Highlights

  • Periodontal disease is a major multifactorial oral disorder in humans, mainly caused by bacterial plaque deposition on the periodontium [1]

  • Periodontitis is a common inflammatory disease that leads to the degradation of periodontium and results in alveolar bone loss

  • This study evaluated periodontal disease induction via retentive ligature, intragingival injection of lipopolysaccharide (LPS), and their combination in a rat model

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Summary

Introduction

Periodontal disease is a major multifactorial oral disorder in humans, mainly caused by bacterial plaque deposition on the periodontium [1]. Inoculation of Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, or their pathogenic products such as lipopolysaccharide (LPS), has been described to induce periodontitis in rats. Intra-gingival injection of LPS derived from P. gingivalis could induce periodontal inflammation and bone resorption in experimental animals. A combination of ligature and inoculation of P. gingivalis has been reported to induce alveolar bone loss in the rat model [10]. The combination of ligature with a pathogenic product, such as lipopolysaccharide from P. gingivalis, which would accelerate the process, is not well described. We hypothesize that a combination of ligature and injection of LPS would induce periodontal disease in a shorter time compared to using either ligature or LPS alone. We compared the morphological changes of periodontal disease induced by ligature, injection of LPS, and a combination of ligature-LPS injection in the Sprague Dawley rat model

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