Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?
The recent identification of senescent cells in periodontal tissues has the potential to provide new insights into the underlying mechanisms of periodontal disease etiology. DNA damage-driven senescence is perhaps one of the most underappreciated delayed consequences of persistent Gram-negative bact...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2020-10-01
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| Series: | International Journal of Molecular Sciences |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1422-0067/21/20/7441 |
| _version_ | 1797551465108078592 |
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| author | Ruben Aquino-Martinez Sundeep Khosla Joshua N. Farr David G. Monroe |
| author_facet | Ruben Aquino-Martinez Sundeep Khosla Joshua N. Farr David G. Monroe |
| author_sort | Ruben Aquino-Martinez |
| collection | DOAJ |
| description | The recent identification of senescent cells in periodontal tissues has the potential to provide new insights into the underlying mechanisms of periodontal disease etiology. DNA damage-driven senescence is perhaps one of the most underappreciated delayed consequences of persistent Gram-negative bacterial infection and inflammation. Although the host immune response rapidly protects against bacterial invasion, oxidative stress generated during inflammation can indirectly deteriorate periodontal tissues through the damage to vital cell macromolecules, including DNA. What happens to those healthy cells that reside in this harmful environment? Emerging evidence indicates that cells that survive irreparable genomic damage undergo cellular senescence, a crucial intermediate mechanism connecting DNA damage and the immune response. In this review, we hypothesize that sustained Gram-negative bacterial challenge, chronic inflammation itself, and the constant renewal of damaged tissues create a permissive environment for the abnormal accumulation of senescent cells. Based on emerging data we propose a model in which the dysfunctional presence of senescent cells may aggravate the initial immune reaction against pathogens. Further understanding of the role of senescent cells in periodontal disease pathogenesis may have clinical implications by providing more sophisticated therapeutic strategies to combat tissue destruction. |
| first_indexed | 2024-03-10T15:46:26Z |
| format | Article |
| id | doaj.art-1aa63188a12b4e2d8173450ae8a1b300 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T15:46:26Z |
| publishDate | 2020-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-1aa63188a12b4e2d8173450ae8a1b3002023-11-20T16:25:34ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-10-012120744110.3390/ijms21207441Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?Ruben Aquino-Martinez0Sundeep Khosla1Joshua N. Farr2David G. Monroe3Department of Medicine, Division of Endocrinology, Mayo Clinic College of Medicine, Rochester, MN 55905, USADepartment of Medicine, Division of Endocrinology, Mayo Clinic College of Medicine, Rochester, MN 55905, USADepartment of Medicine, Division of Endocrinology, Mayo Clinic College of Medicine, Rochester, MN 55905, USADepartment of Medicine, Division of Endocrinology, Mayo Clinic College of Medicine, Rochester, MN 55905, USAThe recent identification of senescent cells in periodontal tissues has the potential to provide new insights into the underlying mechanisms of periodontal disease etiology. DNA damage-driven senescence is perhaps one of the most underappreciated delayed consequences of persistent Gram-negative bacterial infection and inflammation. Although the host immune response rapidly protects against bacterial invasion, oxidative stress generated during inflammation can indirectly deteriorate periodontal tissues through the damage to vital cell macromolecules, including DNA. What happens to those healthy cells that reside in this harmful environment? Emerging evidence indicates that cells that survive irreparable genomic damage undergo cellular senescence, a crucial intermediate mechanism connecting DNA damage and the immune response. In this review, we hypothesize that sustained Gram-negative bacterial challenge, chronic inflammation itself, and the constant renewal of damaged tissues create a permissive environment for the abnormal accumulation of senescent cells. Based on emerging data we propose a model in which the dysfunctional presence of senescent cells may aggravate the initial immune reaction against pathogens. Further understanding of the role of senescent cells in periodontal disease pathogenesis may have clinical implications by providing more sophisticated therapeutic strategies to combat tissue destruction.https://www.mdpi.com/1422-0067/21/20/7441periodontitisperiodontal diseasepathogenesisinflammationbacterial infectionimmune response |
| spellingShingle | Ruben Aquino-Martinez Sundeep Khosla Joshua N. Farr David G. Monroe Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? International Journal of Molecular Sciences periodontitis periodontal disease pathogenesis inflammation bacterial infection immune response |
| title | Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? |
| title_full | Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? |
| title_fullStr | Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? |
| title_full_unstemmed | Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? |
| title_short | Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? |
| title_sort | periodontal disease and senescent cells new players for an old oral health problem |
| topic | periodontitis periodontal disease pathogenesis inflammation bacterial infection immune response |
| url | https://www.mdpi.com/1422-0067/21/20/7441 |
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