Avaliação do papel do CCR4 no reparo ósseo alveolar em camundongos

• Autor(a) principal: Bomfim, Betânia Cabral Aciole
• Data de Publicação: 2018
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da UFS
• Texto Completo: https://ri.ufs.br/jspui/handle/riufs/13885
• topic: Ossos; Doenças; Inflamação; Imunologia; Processo alveolar; Osteogênese; CCR4; Alvéolo dental; Osteogenesis; Inflammation; Immunology; CCR4; Dental alveolus

Introduction: The bone repair process depends on mechanisms which involve both osseous and immune systems. Leukocytes, cytokines and their receptors play a role in yielding immune responses during repair. The CCR4 receptor is important in recruiting T lymphocytes during immune responses. That expression of CCR4 in T cells has aroused our interest in investigating the role of that receptor in innate immunity during bone repair, since T activated lymphocytes could be the source of RANKL activation and thus interfere in osteoclastogenesis, and therefore in bone repair. Thus, the purpose of this study is to determine the role of CCR4 cells in the post-extraction alveolar bone repair process of the upper right incisor of mice. Methodology: For that, a total of 40 mice were used, divided into two groups (control group - C57 BI/6 WT) and CCR4KO (experimental group – CCR4 deficient) and had their bone repair processes analyzed during periods of 0 hour, 7, 14 and 21 days post-exodontia. Samples underwent histological processing and were analyzed by means of optical microscopy for histomorphometric characterization. Results: As an overall result of the histological analyses, it has been observed that the absence of CCR4 did not affect the end result of alveolar bone repair among CCR4KO mice, which showed a sequence of inflammatory and repair events similar to that of the control group. As for the histomorphometric analysis, results showed higher blood clot density among the CCR4KO group at 0 hour (p< 0,05); as well as a higher number of inflammatory cells over the 7-day period when compared to the control group (p< 0,05). The CCR4KO presented lower vessel density over the 7, 14 and 21- day periods, however, with a gradual increase among both groups (p< 0,05). As for the fiber density, the gap among the four groups was statistically significant when the focus was on the gradual density decrease in the CCR4KO group from the 7-day period, as well as the fibroblast density was lower in the 7, 14 and 21 days in the CCR4KO group, when compared to the control group. There was also a significant difference in bone formation, with the CCR4KO group showing higher area density of bone tissue over the 7, 14 and 21-day periods when compared to the control group (p< 0,05), with lower osteoblast activity at 7 days and higher at 14 and 21 days, and an osteoclast activity higher than that of the control group at 7, 14 and 21 days. Conclusion: The absence of the CCR4 receptor was not capable of interfering with the sequence of events which take place during alveolar bone repair of mice, but caused differences within some active components of alveolar bone repair process.