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间质干细胞与衰老过程中牙种植体的骨整合:从机制到治疗。

Mesenchymal stem cells and dental implant osseointegration during aging: from mechanisms to therapy.

机构信息

Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Hangzhou, China.

Nanjing Jinling Hospital: East Region Military Command General Hospital, Nanjing, China.

出版信息

Stem Cell Res Ther. 2023 Dec 20;14(1):382. doi: 10.1186/s13287-023-03611-1.

Abstract

Dental implants are widely used to replace missing teeth, providing patients with unparalleled levels of effectiveness, convenience, and affordability. The biological basis for the clinical success of dental implants is osseointegration. Bone aging is a high-risk factor for the reduced osseointegration and survival rates of dental implants. In aged individuals, mesenchymal stem cells (MSCs) in the bone marrow show imbalanced differentiation with a reduction in osteogenesis and an increase in adipogenesis. This leads to impaired osseointegration and implant failure. This review focuses on the molecular mechanisms underlying the dysfunctional differentiation of aged MSCs, which primarily include autophagy, transcription factors, extracellular vesicle secretion, signaling pathways, epigenetic modifications, microRNAs, and oxidative stress. Furthermore, this review addresses the pathological changes in MSCs that affect osseointegration and discusses potential therapeutic interventions to enhance osseointegration by manipulating the mechanisms underlying MSC aging.

摘要

种植牙被广泛用于替代缺失的牙齿,为患者提供无与伦比的有效性、便利性和可负担性。种植牙临床成功的生物学基础是骨整合。骨老化是种植牙骨整合和存活率降低的高风险因素。在老年个体中,骨髓中的间充质干细胞 (MSCs) 表现出分化失衡,成骨减少,脂肪生成增加。这导致骨整合受损和种植体失败。本综述重点介绍了导致衰老 MSCs 功能失调分化的分子机制,主要包括自噬、转录因子、细胞外囊泡分泌、信号通路、表观遗传修饰、microRNAs 和氧化应激。此外,本综述还讨论了影响骨整合的 MSCs 的病理变化,并探讨了通过操纵 MSC 衰老的机制来增强骨整合的潜在治疗干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb95/10734190/634183d58c16/13287_2023_3611_Fig1_HTML.jpg

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