4.7 Review

Periodontitis and Accelerated Biological Aging: A Geroscience Approach

期刊

JOURNAL OF DENTAL RESEARCH
卷 101, 期 2, 页码 125-132

出版社

SAGE PUBLICATIONS INC
DOI: 10.1177/00220345211037977

关键词

biomarkers; immunity; inflammation; oral-systemic diseases; periodontal diseases; periodontal medicine

向作者/读者索取更多资源

As the global population ages, periodontitis and tooth loss are of great concern for health. Recent advances in geroscience have shown that biological aging is linked to periodontitis, with individuals having accelerated aging experiencing higher risks of periodontitis and tooth loss. Furthermore, cellular and molecular mechanisms at the periodontal level play a role in the aging process, with cellular senescence, stem cell exhaustion, and immunoaging impacting periodontal homeostasis and the pathophysiology of periodontitis. Advances in senotherapy involving physical exercise, intermittent fasting, natural compounds, senolytic drugs, and cell therapy are being explored to rejuvenate oral health and potentially intercept biological aging before the onset of aging-related diseases in chronologically young individuals.
As the whole world is epidemically aging, the burden of periodontitis and tooth loss is becoming a major health concern. Growing meta-epidemiological data implicate chronic systemic inflammation/infection due to periodontitis as an independent risk factor for aging-related diseases and mortality. However, because people age differently, chronological age is not a reliable marker of an individual's functional status. Recent advances in geroscience have shown that various biomarker signatures of biological aging are longitudinally associated with declined physical function, morbidity, and mortality due to major age-related diseases, including periodontitis. Here, we emphasize novel research developments bidirectionally linking periodontitis to accelerated biological aging. Using a composite biomarker age estimator, a striking increase in periodontitis and tooth loss was observed in subjects whose biological age at baseline was higher than their chronological age. Moreover, significantly shortened telomeres were encountered in populations affected by severe periodontitis. Second, we elucidate the cellular and molecular pillars of the aging process at the periodontal level. Accumulating evidence suggests that cellular senescence, stem cell exhaustion, and immunoaging are hallmarks of biological aging implicated in the impairment of periodontal homeostasis and the pathophysiology of periodontitis. Indeed, persistent bacteria-derived lipopolysaccharide stimulation influences cellular senescence in osteocytes, driving alveolar bone resorption. Moreover, inflammaging status induced by chronic hyperglycemia elevates the burden of senescent cells in gingival tissues, impairing their barrier function. Lastly, we reviewed a recent breakthrough in senotherapy to directly target the mechanisms of aging at the periodontal level. Physical exercise and intermittent fasting, together with natural compounds, senolytic drugs, and cell therapy, are increasingly being evaluated to rejuvenate the oral cavity. Following these innovations in geroscience, further advancements could provide oral clinicians the chance to intercept biological aging when still subclinical and set interventions for halting or delaying the trajectory toward aging-related diseases while patients are still chronologically young.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据