The fundamental foundations of periodontal aging. Part 3

Moiseev D.A.; Zueva A.A.; Kopetsky I.S.; Daurova F.Yu.; Tomaeva D.I.

doi:https://doi.org/10.17116/operhirurg2025904168

Moiseev D.A.

Pirogov Russian National Research Medical University

ORCID: 0000-0001-7811-7741

Zueva A.A.

Pirogov Russian National Research Medical University

ORCID: 0009-0006-3605-6163

Kopetsky I.S.

Pirogov Russian National Research Medical University

ORCID: 0000-0002-4723-6067

Daurova F.Yu.

Vladimirsky Moscow Regional Research Clinical Institute

ORCID: 0000-0003-0085-1051

Tomaeva D.I.

Vladimirsky Moscow Regional Research Clinical Institute

ORCID: 0000-0001-8771-2438

The fundamental foundations of periodontal aging. Part 3

Authors:

Moiseev D.A., Zueva A.A., Kopetsky I.S., Daurova F.Yu., Tomaeva D.I.

More about the authors

Journal: Russian Journal of Operative Surgery and Clinical Anatomy. 2025;9(4): 68‑74

DOI: 10.17116/operhirurg2025904168

Read: 525 times

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To cite this article:

Moiseev DA, Zueva AA, Kopetsky IS, Daurova FYu, Tomaeva DI. The fundamental foundations of periodontal aging. Part 3. Russian Journal of Operative Surgery and Clinical Anatomy. 2025;9(4):68‑74. (In Russ.)
https://doi.org/10.17116/operhirurg2025904168

Подписка 2026 Оперативная хирургия и клиническая анатомия (Пироговский научный журнал) (Russian Journal of Operative Surgery and Clinical Anatomy)

Использование инфографики авторами научных работ

BACKGROUND

Destructive processes in periodontitis leading to tooth loss are multifactorial and are not limited to inflammatory diseases. Along with the generally recognized role of the pathogenic microbiota, increasing attention is being paid to the mechanisms of biological aging and oxidative stress as key drivers of tissue destruction. Part 3 of our systematic review summarizes current data on the molecular and cellular mechanisms underlying periodontal aging and destruction.

OBJECTIVE

To summarize and analyze the available scientific data on the aging of periodontal tissues.

MATERIAL AND METHODS

A systematic review of the literature data was conducted, and 5897 publications were found in international electronic databases: PubMed, Cochrane, Google Search, Ebsco, Embase, Web of Science, ScienceDirect, SciELO, and eLibrary from 2000 to 2025. The inclusion criteria were met by original studies and reviews on the role of reactive oxygen species (ROS), autophagy, inflammasomes, changes in cytokine profile, and age-related changes in periodontal cells. The methodology of this study meets the requirements for PRISMA systematic reviews and meta-analyses. Based on the selection criteria, 29 publications were included in the systematic review.

RESULTS

It has been established that the main integrating mechanism of periodontal destruction is chronic oxidative stress. The key role of NLRP3 inflammasome activation and imbalance in the autophagy system is shown. The aging of fibroblasts, periodontal ligament cells, and osteoblasts is accompanied by a decrease in their regenerative potential and a change in the synthesis of extracellular matrix components.

CONCLUSION

Periodontal destruction is a complex process in which infectious, inflammatory and fundamental mechanisms of aging are intertwined. The central role of oxidative stress unites these pathways, creating a vicious cycle of inflammation and tissue damage. Promising areas of therapy include not only antimicrobial strategies, but also targeted effects on RedOx balance and age-related changes in periodontal cells.

Keywords:

periodontitis

periodontal aging

oxidative stress

reactive oxygen species (ROS)

fibroblasts

cytokines

Authors:

Moiseev D.A.

Pirogov Russian National Research Medical University

ORCID: 0000-0001-7811-7741

Zueva A.A.

Pirogov Russian National Research Medical University

ORCID: 0009-0006-3605-6163

Kopetsky I.S.

Pirogov Russian National Research Medical University

ORCID: 0000-0002-4723-6067

Daurova F.Yu.

Vladimirsky Moscow Regional Research Clinical Institute

ORCID: 0000-0003-0085-1051

Tomaeva D.I.

Vladimirsky Moscow Regional Research Clinical Institute

ORCID: 0000-0001-8771-2438

Received:

09.09.2025

Accepted:

10.09.2025

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References:

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