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• W4315702959 abstract "The ligature-induced periodontitis model is an effective approach to induce inflammation and bone loss similar to that of human periodontitis. Previous clinical and in vitro studies have shown the involvement of lymphocytes in periodontitis, while, the local and systemic profile of immune cells associated with periodontitis in the ligature-induced periodontitis model in mice remains unclear. Experimental periodontitis was constructed in mice by ligating around the maxillary second molars for 14 and 28 days, respectively. Alveolar bone loss was assessed by micro-computed tomography (micro-CT). Hematoxylin and eosin (H&E) and tartrate-resistant acid phosphatase (TRAP) staining were used to evaluate the histological changes in the periodontal tissues. B and T cells in the cervical lymph nodes, spleen, and peripheral blood were analyzed by flow cytometry. The 14-day ligation effectively induced significant periodontal inflammation and alveolar bone loss in C57BL/6J mice, which were progressive and maintained for a relatively long-term period until day 28. In addition, CD3+ T cells and CD19+ B cells were the dominant population in both health and disease, and the B cell population within the cervical lymph nodes (LN) increased significantly under periodontitis condition, while, no significant differences of the T and B cell population among the spleen and peripheral blood were observed. The ligature-induced periodontitis mice model was established to perform a longitudinal assessment of changes in periodontal tissues morphologically and histologically, meanwhile, explore the local and systemic changes of the predominant immune-associated cells." @default.
• W4315702959 created "2023-01-12" @default.
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• W4315702959 date "2023-10-01" @default.
• W4315702959 modified "2023-10-16" @default.
• W4315702959 title "Evaluation of morphological, histological, and immune-related cellular changes in ligature-induced experimental periodontitis in mice" @default.
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• W4315702959 doi "https://doi.org/10.1016/j.jds.2023.01.002" @default.
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