Conclusion
FOXM1 plays a key role in diabetes periodontitis, and this study provides theoretical support for the clinical prevention and treatment of diabetes periodontitis in humans.
Material and methods
A model of mice with diabetes periodontitis was created. The pathological damage of periodontal tissues in the mandibles of mice was assessed through hematoxylin-eosin staining. The expression of bone resorption-related, cell proliferation transcription, inflammatory, and oxidative stress-related factors in mice with diabetes periodontitis was analyzed through Western blot and quantitative reverse transcription polymerase chain reaction. Oxidative stress level was examined through enzyme-linked immunosorbent assay. Furthermore, plasmids with FOXM1 silencing were constructed using short hairpin RNA. The activity of activator protein-1 (AP-1) binding was measured via electrophoretic mobility shift assay. Reactive oxygen species (ROS) expression was detected using a dichlorodihydrofluorescein diacetate probe.
Methods
A model of mice with diabetes periodontitis was created. The pathological damage of periodontal tissues in the mandibles of mice was assessed through hematoxylin-eosin staining. The expression of bone resorption-related, cell proliferation transcription, inflammatory, and oxidative stress-related factors in mice with diabetes periodontitis was analyzed through Western blot and quantitative reverse transcription polymerase chain reaction. Oxidative stress level was examined through enzyme-linked immunosorbent assay. Furthermore, plasmids with FOXM1 silencing were constructed using short hairpin RNA. The activity of activator protein-1 (AP-1) binding was measured via electrophoretic mobility shift assay. Reactive oxygen species (ROS) expression was detected using a dichlorodihydrofluorescein diacetate probe.
Objective
Periodontitis, the sixth major complication of diabetes, has a mutually influential and mutually reinforcing relationship with diabetes. Forkhead box protein M1 (FOXM1) is essential for osteoclast differentiation, periodontitis, and diabetes. This study aims to investigate the potential action mechanisms and effects of FOXM1 on diabetes periodontitis. Material and
Results
Treatment with the ROS inhibitor N-acetylcysteine ameliorated the degree of bone destruction, attenuated the inflammatory response, and mitigated oxidative stress in mice with diabetes periodontitis. Short hairpin-FOXM1 reduced the levels of FOXM1, increased the levels of C-Jun proto-oncogene and AP-1, enhanced AP-1 binding activity, and increased ROS production in the macrophage cells. sh-FOXM1 increased the mRNA and protein levels of tartrate-resistant acid phosphatase (TRAP), osteoclast-associated receptor (OSCAR), and nuclear factor-activated T-cell c1 (NFATc1). By contrast, JUN-small interfering RNA decreased the mRNA and protein expression of TRAP, OSCAR, and NFATc1. The silencing of FOXM1-regulated ROS production mediated AP-1 activation to promote macrophage osteoclast differentiation.