Identification of Senescent Cells in Peri-Implantitis and Prevention of Mini-Implant Loss Using Senolytics

• Published in: International journal of molecular sciences Vol. 24; no. 3; p. 2507
• Main Authors: Yang, Niuxin, Nakagawa, Masato, Nishiura, Aki, Yamada, Masahiro, Morikuni, Hidetoshi, Honda, Yoshitomo, Matsumoto, Naoyuki
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 28-01-2023; MDPI
• Subjects: Alzheimer's disease; Animals; Bacterial infections; Bone Resorption; Cell cycle; Cellular Senescence; Chronic illnesses; Cytokines; Dasatinib; Dental Implants; Infections; Inflammation; Inflammatory diseases; mini-implant; Orthodontic Anchorage Procedures; Orthodontics; peri-implantitis; Peri-Implantitis - drug therapy; Peri-Implantitis - prevention & control; Phosphatase; Quercetin; Rats; Senescence; senolytics; Signs and symptoms; Transplants & implants; mini-implant; senescence; Dasatinib; orthodontics; Quersetin; senolytics; peri-implantitis
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms24032507

Peri-implantitis is a disease that causes the detachment of orthodontic mini-implants. Recently, stress-induced senescent cells have been reported to be involved in various inflammatory diseases. Senescent cell-eliminating drugs, termed "senolytics", can improve the symptoms of such diseases. However, the relationship between peri-implantitis and senescent cells remains unclear. In this study, we evaluated the presence of senescent cells in a rat peri-implantitis model developed with a gum ring. The effect on bone resorption and implant loss was also investigated with and without senolytics (Dasatinib and Quercetin). The number of senescence markers (p19, p21, and p16) was found to increase, and implant detachment occurred in 24 days. After the administration of senolytics, the number of senescence markers decreased and implant detachment was inhibited. This study suggests that senescent cells aggravate peri-implantitis and senolytic administration latently reduces implant loss by inhibiting senescence-related mechanisms.