RESUMO
OBJECTIVE: To investigate neuroinflammation under different periodontal status. MATERIALS AND METHODS: Experimental periodontitis was induced by molar ligation (Lig group) or periodontal injection of lipopolysaccharide (LPS, Lps group). Periodontal status was assessed by alveolar bone resorption and periodontal inflammation. Micro-computed tomography and haematoxylin-eosin staining were performed to assess alveolar bone resorption and periodontal inflammation, respectively. Neuroinflammation was assessed by glial cell proliferation and proinflammatory factor expression. Microgliosis was determined by immunofluorescence. Astrogliosis was determined by immunohistochemistry. Expressions of tumour necrosis factor-alpha (TNF-α) and interleukin (IL)-1ß were assessed by enzyme-linked immunosorbent assay. RESULTS: Microgliosis and astrogliosis in the Lig group were notable with molar ligation for 2 weeks and 4 weeks (p < .05), but were only slightly different similar from the control group by week 12. Microgliosis and astrogliosis in the Lps group were significant with LPS injection for 4 and 8 weeks (p < .05). The groups displayed a positive correlation between the degree of periodontal inflammation and the number of glial cells (p < .05). Expressions of IL-1ß and TNF-α in the Lps group were significantly increased with LPS injection for 8 weeks (p < .05). In the Lig group, only TNF-α was highly expressed with molar ligation for 12 weeks (p < .05). CONCLUSION: Both models demonstrated that the inflammatory response in the hippocampus of mice can change during periodontitis depending on the periodontal inflammation status.