Medicina endodôntica: associação entre desordens sistêmicas ou hábitos deletérios e a periodontite apical

• Ano de defesa: 2022
• Autor(a) principal: Pinto, Karem Paula
• Outros Autores: [e-mail]
• Orientador(a): Sassone, Luciana Moura , Silva, Emmanuel João Nogueira Leal da
• Banca de defesa: Fidalgo, Tatiana Kelly da Silva , Fischer, Ricardo Guimarães , Ferreira, Cláudio Malizia Alves , Lima, Carolina Oliveira de , Oliveira, Henrique Eduardo
• Tipo de documento: Tese
• Tipo de acesso: Acesso embargado
• Idioma: por
• Instituição de defesa: Universidade do Estado do Rio de Janeiro
• Programa de Pós-Graduação: Programa de Pós-Graduação em Odontologia
• Departamento: Centro Biomédico::Faculdade de Odontologia
• País: Brasil
• Palavras-chave em Português: Alcoolismo; Medicina endodôntica; Microtomografia de raios-X; Periodontite apical; Tabagismo
• Palavras-chave em Inglês: Alcoholism; Endodontic medicine; X-Ray microtomography; Apical periodontitis; Smoking
• Área do conhecimento CNPq: CIENCIAS DA SAUDE::ODONTOLOGIA::ENDODONTIA
• Link de acesso: http://www.bdtd.uerj.br/handle/1/21631

The endodontic medicine assesses the bidirectional relationship between systemic disorders and apical periodontitis. There is evidence that both apical periodontitis can influence systemic changes, as the opposite. However, there is a need to clarify the mechanisms involved in this relationship. This thesis was divided into two studies seeking to evaluate the metabolic alterations that may be involved in the association between systemic disorders or deleterious habits and apical periodontitis and to carefully review the existing literature. The study 1 evaluated the periapical bone pattern and the serum levels of pro-inflammatory cytokines, biochemical markers and metabolites in rats submitted to chronic consumption of alcohol and/or nicotine and induction of apical periodontitis. Twenty-eight male Wistar rats were assigned to Control, Alcohol, Nicotine and Alcohol+Nicotine groups. The groups submitted to alcohol were exposed to self-administration of 25% alcohol solution and the groups submitted to nicotine received daily intraperitoneal injections of a solution with 0.19 μl of nicotine/mL. The pulps of the lower left first molars were exposed for 28 days to induce periapical lesions. After euthanasia, the mandibles were removed and the periapical bone was evaluated by microcomputed tomography images. Blood samples were collected and the serum samples were submitted to Luminex assay for measurement of pro-inflammatory cytokines, biochemical and metabolomic analyses. The groups submitted to alcohol or nicotine consumption showed altered bone patterns indicating lower bone density and higher levels of IL-1β, IL-6 and TNF-α, in relation to the Control group. Significant differences were also observed in the levels of several biochemical markers and metabolites. Most of these parameters were even more altered in the simultaneous consumption of both substances, compared to the single consumption. The study 2 evaluated the systematic reviews that assessed the association between apical periodontitis and chronic systemic diseases through an umbrella review. A systematic search was performed in PubMed, Virtual Health Library, Scopus, Cochrane Library, Embase, Web of Science and Open Gray databases. Nine studies that met the eligibility criteria were included. The AMSTAR-2 tool was used to assess the quality of each included systematic review, which showed “low” to “high” quality of evidence. There was a positive association between diabetes and apical periodontitis with limited evidence, no association between HIV and apical periodontitis, and a positive association between apical periodontitis and cardiovascular disease, blood disorders, chronic liver disease, osteoporosis and autoimmune diseases with moderate evidence. Based on the studies, it was concluded that systemic disorders can exacerbate inflammation in apical periodontitis, as periapical lesions can interfere with systemic diseases. The chronic consumption of alcohol or nicotine has harmful effects on apical periodontitis through the alteration of metabolic pathways that lead to an increase in the production of pro-inflammatory mediators, which was even more intense in the simultaneous consumption of both substances.