Related Experiment Video
Updated: May 25, 2025
Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
Bmal1 knockout aggravates Porphyromonas gingivalis-induced periodontitis by activating the NF-κB pathway
Ye Tian1, Xinran Liu2, Qiuyu Lu2
1Sichuan University, West China Hospital of Stomatology, National Clinical Research Center for Oral Diseases, State Key Laboratory of Oral Diseases, Department of Geriatric Stomatology, Chengdu, China.
Background:
Circadian rhythm disorders and NF-κB are closely linked and can exacerbate periodontitis. However, the mechanisms via which circadian rhythm-related genes influence periodontitis are not yet fully understood.
Objective:
We investigated the effect of brain and muscle Arnt-like protein-1 (BMAL1) on the NF-κB pathway and downstream inflammatory factors on periodontitis. In this study, Bmal1 homozygous knockout and periodontitis mouse models were established.
Methodology:
Bone marrow-derived macrophages (BMDMs) from Bmal1-/- mice were cultured and stimulated with lipopolysaccharides. Bone resorption was detected using micro-computed tomography and histological analyses. Gene and cytokine expression was assessed using quantitative reverse-transcription PCR and ELISA. The nuclear translocation of p65 was detected using immunofluorescence.
Results:
Our findings indicate that Bmal1 knockout exacerbates periodontitis severity in mice by activating the NF-κB signaling pathway with increased nuclear translocation of p65 (p<0.05), as well as increased expression of Il-1b, Il-6, and Tnfα (p<0.01), along with decreased Nr1d1 expression (p<0.05) in BMDMs under inflammation.
Conclusion:
The results highlight the protective role of Bmal1 in periodontitis and suggest its potential link to the circadian clock's influence on the disease.
