Influence of cigarrete smoke inalation in apical periodontitis development: local and sistemic inflamatory anallisys in Wistar rats

• Grant number: 20/06310-5
• Support type: Regular Research Grants
• Duration: November 01, 2021 - October 31, 2023
• Field of knowledge: Health Sciences - Dentistry - Endodontics
• Principal researcher: Eloi Dezan Junior
• Grantee: Eloi Dezan Junior
• Home Institution: Faculdade de Odontologia (FOA). Universidade Estadual Paulista (UNESP). Campus de Araçatuba. Araçatuba , SP, Brazil
• Assoc. researchers: Carlos Roberto Emerenciano Bueno ; Claudia Cristina Biguetti ; Luciano Tavares Angelo Cintra ; Marco Antonio Hungaro Duarte ; Marina Tolomei Sandoval Cury ; Mariza Akemi Matsumoto

Abstract

Endodontic infection occurs mainly after contamination of the pulp tissue, leading to bacterial colonization of root canals, resulting in an inflammatory response of the periapical tissues and the formation of a periapical lesion, an Apical Periodontitis (AP). Smoking is considered a major risk factor for oral infections, studied mainly in periodontal disease, as it affects gingival tissues, periodontal ligament, vascular system, inflammatory response and bone metabolism. Observing into account these systemic changes in the technical response, the aim of this study will be to evaluate in Wistar rats the influence of smoking on the inflammatory profile of AP. Forty animals will be divided into 4 groups (n = 10): AP (rats with induced apical periodontitis); S (rats exposed to cigarette smoke); SAP (mice with induced apical periodicity and exposure to cigarette smoke); Control (rats without PA and without exposure to cigarettes). For exposure to cigarette smoke, the animals stay in a smoking chamber for 8 minutes, three times a day. The animals will be exposed to cigarette smoke 20 days before the induction of PA. For PA induction, as pulps of the upper and lower first molars, the rights will be exposed to the oral environment for 30 days, during which time the exposure of cigarette smoke will continue, totaling 50 days of exposure to smoke. Hematologic parameters will be analyzed, calcium, phosphorus and alkaline phosphatase as bone markers, nicotine and cotinine will be analyzed. After euthanasia, mandible and maxillae will be removed and mandible will be used to evaluate the volume of bone destruction in apical periodontitis by micro CT. Then, samples will be embedded in paraffin to assess the inflammatory profile via hematoxylin-eosin staining for morphological and histomorphometric analysis (characterization and quantification of inflammatory cells), macrophage detection via immunohistochemistry. Interleukin IL-6, IL-1² e TNF-± as local inflammation indicators; RANKL e OPG as bone resorption indicator, and evaluation of collagen fibers of periodontal ligament by Picrosirius red birefringence. The data obtained will be tabulated and submitted to statistical analysis with a significance level of 5%. (AU)