Objective: Mitochondria are strained by microbial stimuli in the periodontal niche. Damaged mitochondria are cleared by mitophagy. The purpose of the study was to explore whether mitophagy participated in the progress of periodontitis and whether activation of mitophagy can inhibit inflammatory responses to bacterial infection in macrophages.
Methods: Mitophagy-related genes were measured in the healthy and inflamed human gingiva. Bone marrow-derived macrophages (BMDMs) were infected with Porphyromonas gingivalis. Dexmedetomidine, urolithin A, and resveratrol were used to activate mitophagy, while small interference RNA was utilized to knock down PTEN-induced putative protein kinase 1 (PINK1). Activation of mitophagy-related genes and colocalization of them were detected by Western blot and confocal imaging. Damages of mitochondria, accumulation of mitochondrial reactive oxygen species (mtROS), and production of IL-1β, IL-6, and TNF-α were measured.
Results: Levels of mitophagy-related genes were decreased in inflamed periodontal tissues and P. gingivalis-infected BMDMs. Dexmedetomidine, urolithin A, and resveratrol activated mitophagy, leading to reduced mitochondria damages, decreased mtROS generation, and inhibited IL-1β, IL-6, and TNF-α production. PINK1 knockdown reduced dexmedetomidine, urolithin A, and resveratrol-induced anti-inflammatory effect.
Conclusion: Inhibited mitophagy participated in the progress of periodontitis. Activation of mitophagy may become a therapeutic target during the progress of periodontitis by reducing mtROS.
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http://dx.doi.org/10.1111/odi.14286 | DOI Listing |
Dent J (Basel)
December 2024
Oral Biology & Diagnostic Sciences, Dental College of Georgia, Augusta University, Augusta, GA 30912, USA.
The incidence of obesity has dramatically increased worldwide. Obesity has been shown to exacerbate the progression of periodontal disease. Studies suggest a sex difference in periodontitis, whereby males are more sensitive to periodontal inflammation compared to females.
View Article and Find Full Text PDFCase Rep Dent
January 2025
Department of Cranio-Maxillofacial Surgery, Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham, Kochi, India.
For managing peri-implantitis, a variety of treatment modalities involving both surgical and nonsurgical methods including implantoplasty have been proposed. Implants that are placed in a free fibula flap are more prone to peri-implantitis due to the absence of firm, keratinized mucosa. Prosthetic design that offers adequate hygiene access should be designed whenever possible; otherwise, it may lead to the accumulation of plaque or biofilm that may lead to peri-implant diseases.
View Article and Find Full Text PDFKorean J Orthod
January 2025
Private Practice, Ankara, Türkiye.
Objective: The effect of different attachment positions on torque control during the labialization of maxillary lateral incisors with clear aligners was evaluated using finite element analysis.
Methods: Anatomical data acquired through cone-beam computed tomography, combined with the design of 0.625-mm-thick aligners and horizontal attachments, were integrated into the software.
Oral Dis
January 2025
Bahrain Defence Force Royal Medical Services, Riffa, Bahrain.
Objective: Tumour-associated macrophages (TAMs) are crucial in the progression and treatment response of oral squamous cell carcinoma (OSCC). TAMs infiltrate OSCC, adopting an M2-like phenotype that promotes tumour growth, metastasis and immune suppression. The current narrative review explored the roles of TAMs in OSCC, focusing on their impact on the tumour microenvironment, invasion, metastasis, angiogenesis, immunosuppression and potential therapeutic targeting.
View Article and Find Full Text PDFOral Dis
January 2025
Central Laboratory, Peking University School and Hospital of Stomatology, Beijing, China.
Objective: To review current knowledge of the various processes of programmed cell death and their roles in immunoregulation in periodontitis.
Methods: Relevant literature in the PubMed, Medline, and Scopus databases was searched, and a narrative review was performed. Programmed cell death and the regulation of its various pathways implicated in periodontal infection were reviewed.
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