牙周炎中衰老的分子特征:临床见解。

Journal of dental research Pub Date : 2024-07-01 Epub Date: 2024-06-14 DOI:10.1177/00220345241255325
K Rattanaprukskul, X-J Xia, M Jiang, E Albuquerque-Souza, D Bandyopadhyay, S E Sahingur
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引用次数: 0

摘要

大多数老年人都患有牙周病,给全世界的健康造成了负担。细胞衰老是衰老的标志之一,与多种慢性并发症有关。衰老细胞会产生多种有害分泌物,统称为衰老相关分泌表型(SASP)。这会破坏邻近细胞,导致衰老进一步扩散,并引发慢性炎症,即所谓的 "炎症"。组织微环境中的有害反响可在较年轻时触发衰老,加速生物衰老,并推动疾病的发生或发展。在这里,我们通过评估关键衰老标志物(p16、脂质褐素和β-半乳糖苷酶)和炎症介质(白细胞介素[IL]-1β、IL-6、IL-8、基质金属蛋白酶[MMP]-1、MMP-3 和肿瘤坏死因子-α)的水平,研究了健康和患病牙龈组织中衰老的生物学特征。我们的研究结果表明,与所有年龄组的健康部位相比,牙周炎患者上皮组织和结缔组织的衰老特征(包括 p16、脂褐素和 β-半乳糖苷酶)均明显增加,这表明炎症微环境也会引发年轻病变牙龈组织的衰老样改变。随后使用特异性细胞标记物进行双重染色分析发现,β-半乳糖苷酶在成纤维细胞和巨噬细胞中富集。同时,从牙周炎病变中获取的牙龈活检组织中与 SASP 一致的炎症介质也有所增加。总之,我们的研究结果提供了第一份临床报告,揭示了牙龈组织易受衰老和炎症环境升高的影响,这与衰老分泌组一致,因此衰老是口腔黏膜病理事件的驱动因素之一,也是有针对性干预的新策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular Signatures of Senescence in Periodontitis: Clinical Insights.

Most of the elderly population is afflicted by periodontal diseases, creating a health burden worldwide. Cellular senescence is one of the hallmarks of aging and associated with several chronic comorbidities. Senescent cells produce a variety of deleterious secretions, collectively termed the senescence-associated secretory phenotype (SASP). This disrupts neighboring cells, leading to further senescence propagation and inciting chronic inflammation, known as "inflammaging." Detrimental repercussions within the tissue microenvironment can trigger senescence at a younger age, accelerate biological aging, and drive the initiation or progression of diseases. Here, we investigated the biological signatures of senescence in healthy and diseased gingival tissues by assessing the levels of key senescence markers (p16, lipofuscin, and β-galactosidase) and inflammatory mediators (interleukin [IL]-1β, IL-6, IL-8, matrix metalloproteinase [MMP]-1, MMP-3, and tumor necrosis factor-α). Our results showed significantly increased senescence features including p16, lipofuscin, and β-galactosidase in both epithelial and connective tissues of periodontitis patients compared with healthy sites in all age groups, indicating that an inflammatory microenvironment can trigger senescence-like alterations in younger diseased gingival tissues as well. Subsequent analyses using double staining with specific cell markers noted the enrichment of β-galactosidase in fibroblasts and macrophages. Concurrently, inflammatory mediators consistent with SASP were increased in the gingival biopsies obtained from periodontitis lesions. Together, our findings provide the first clinical report revealing susceptibility to elevated senescence and inflammatory milieu consistent with senescence secretome in gingival tissues, thus introducing senescence as one of the drivers of pathological events in the oral mucosa and a novel strategy for targeted interventions.

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