Influência da obesidade na progressão da doença periodontal experimental induzida em ratos: análise histológica, microtomográfica e proteômica
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Data
2021-06-23
Autores
Lopes, Maria Eduarda Scordamaia
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Universidade Estadual Paulista (Unesp)
Resumo
Estudos têm sido conduzidos para se entender melhor os mecanismos moleculares de progressão da doença periodontal nos diferentes tecidos periodontais. Porém, a literatura ainda é escassa sobre a influência da obesidade nesses mecanismos. O objetivo do presente estudo foi avaliar in vivo o efeito da obesidade na progressão da doença periodontal. Um total de 16 ratos foram distribuídos em 2 grupos experimentais: grupo indução de doença periodontal experimental (P) e indução de obesidade seguido de indução de doença periodontal experimental (OP). A indução de obesidade foi realizada com dieta rica em gordura por 90 dias. A massa corporal dos animais foi registrada semanalmente. Após 21 dias do início da indução da doença periodontal os animais foram sacrificados e os tecidos adiposos foram removidos e pesados em balança de precisão. Análise sorológica foi realizada para observar o perfil lipídico e os níveis de glicemia. Análise microtomográfica foi realizada nas hemimaxilas para medir o percentual de volume ósseo alveolar (BVF), densidade óssea alveolar (BMD) e análise linear de perda óssea. A perda óssea alveolar foi mensurada histologicamente por histometria. A proporção dos componentes teciduais foi determinada histologicamente por estereometria. A composição proteica do ligamento periodontal foi avaliada através de análise proteômica. A partir desta análise, foram selecionadas 3 proteínas com diferenças significantes entre os grupos, e que apresentam função relevante para o processo inflamatório, para validação de sua presença no ligamento periodontal por meio de imuno-histoquímica. Foi utilizado teste estatístico t-student e adotado um nível de significância de 5%. Houve aumento significativo da massa corporal e peso dos tecidos adiposos nos animais do grupo OP. Os grupos não apresentaram diferença estatística nas análises de perda óssea. Na análise proteômica, um total de 819 proteínas foram identificadas. Na condição clínica de doença periodontal associada a obesidade, as proteínas Spondina 1, Vinculina e TRAP apresentaram-se em maior abundância e foram selecionadas por sua relevância clínica. Concluímos que embora a obesidade não tenha favorecido a progressão da doença periodontal no parâmetro de perda óssea, a caracterização proteica do ligamento periodontal em condições de doença periodontal, associado ou não à obesidade, pode ser um método auxiliar de estudo para a identificação de novos biomarcadores associados a doenças, demonstrando alterações moleculares e favorecendo estudos para alvos terapêuticos para a doença periodontal.
Many studies have been conducted to understand better the molecular mechanism of periodontal disease progression in different periodontal tissues. However, the literature is limited on the influence of obesity on these mechanisms. This study aimed to evaluate in vivo the effect of obesity on periodontal disease progression. Sixteen Holtzman rats were distributed into 2 groups: ligature-induced periodontal disease (P), and obesity induction followed by ligature-induced periodontal disease (OP). Obesity was induced by a high-fat diet for 90 days. The body mass of the animals was recorded weekly. After 21 days of the induction of periodontal disease, the animals were sacrificed and the adipose tissues were removed and weighed on precision scales. Serological analysis was performed to observe the lipid profile and blood glucose levels. Microtomographic analysis was performed on the hemimaxillae to measure the percentage of alveolar bone volume (BVF), alveolar bone density (BMD), and linear analysis of bone loss. Alveolar bone loss was measured histologically by histometry. The proportion of tissue components was determined histologically by stereometry. The protein composition of the periodontal ligament was evaluated by proteomic analysis. From this analysis, three proteins with significant differences between groups and that have a relevant function in the inflammatory process were selected to validate their presence in the periodontal ligament by immunohistochemistry. The statistical t-student test was used and a 5% significance level was adopted. There was a significant increase in body mass and adipose tissue weight in the animals of the OP group. The groups showed no statistical difference in the analyses of bone loss. In the proteomic analysis, a total of 819 proteins were identified. In the clinical condition of periodontal disease associated with obesity, the proteins Spondin 1, Vinculin and TRAP were more abundant and were selected for their clinical relevance. We conclude that although obesity has not favoured the progression of periodontal disease in the alveolar bone loss parameter, the protein characterization of the periodontal ligament in periodontal disease conditions, associated or not with obesity, may be an auxiliary method of study for the identification of new disease-associated biomarkers, demonstrating molecular changes and favouring studies for therapeutic targets for periodontal disease.
Many studies have been conducted to understand better the molecular mechanism of periodontal disease progression in different periodontal tissues. However, the literature is limited on the influence of obesity on these mechanisms. This study aimed to evaluate in vivo the effect of obesity on periodontal disease progression. Sixteen Holtzman rats were distributed into 2 groups: ligature-induced periodontal disease (P), and obesity induction followed by ligature-induced periodontal disease (OP). Obesity was induced by a high-fat diet for 90 days. The body mass of the animals was recorded weekly. After 21 days of the induction of periodontal disease, the animals were sacrificed and the adipose tissues were removed and weighed on precision scales. Serological analysis was performed to observe the lipid profile and blood glucose levels. Microtomographic analysis was performed on the hemimaxillae to measure the percentage of alveolar bone volume (BVF), alveolar bone density (BMD), and linear analysis of bone loss. Alveolar bone loss was measured histologically by histometry. The proportion of tissue components was determined histologically by stereometry. The protein composition of the periodontal ligament was evaluated by proteomic analysis. From this analysis, three proteins with significant differences between groups and that have a relevant function in the inflammatory process were selected to validate their presence in the periodontal ligament by immunohistochemistry. The statistical t-student test was used and a 5% significance level was adopted. There was a significant increase in body mass and adipose tissue weight in the animals of the OP group. The groups showed no statistical difference in the analyses of bone loss. In the proteomic analysis, a total of 819 proteins were identified. In the clinical condition of periodontal disease associated with obesity, the proteins Spondin 1, Vinculin and TRAP were more abundant and were selected for their clinical relevance. We conclude that although obesity has not favoured the progression of periodontal disease in the alveolar bone loss parameter, the protein characterization of the periodontal ligament in periodontal disease conditions, associated or not with obesity, may be an auxiliary method of study for the identification of new disease-associated biomarkers, demonstrating molecular changes and favouring studies for therapeutic targets for periodontal disease.
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Palavras-chave
Obesidade, Doenças periodontais, Perda do osso alveolar, Proteínas, Ligamento periodontal, Obesity, Periodontal diseases, Alveolar bone loss, Proteins, Periodontal ligament