Molecular Signatures of Senescence in Periodontitis: Clinical Insights.

Autor:	Rattanaprukskul K; Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA.; Department of Periodontology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand., Xia XJ; Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA., Jiang M; Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA., Albuquerque-Souza E; Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA.; Lipid Mediator Unit, William Harvey Research Institute, Queen Mary University of London, London, UK., Bandyopadhyay D; Department of Biostatistics, School of Population Health, Virginia Commonwealth, Richmond, VA, USA., Sahingur SE; Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Jazyk:	angličtina
Zdroj:	Journal of dental research [J Dent Res] 2024 Jul; Vol. 103 (8), pp. 800-808. Date of Electronic Publication: 2024 Jun 14.
DOI:	10.1177/00220345241255325
Abstrakt:	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. Competing Interests: Declaration of Conflicting InterestsThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Databáze:	MEDLINE
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