Journal
JOURNAL OF DENTAL RESEARCH
Volume 100, Issue 12, Pages 1397-1404Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/00220345211009463
Keywords
periodontitis; aging; innate immunity; cell biology; gerontology; cytokines
Categories
Funding
- National Institutes of Health (NIA) [R01AG046282]
- National Institutes of Health (NIDCR) [K08DE029505]
- UCSF Core Center for Musculoskeletal Biology and Medicine of the NIAMS [P30AR066262]
- Russel/Engleman Arthritis Center at UCSF
- Department of Veterans Affairs Health Care System
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The prevalence of periodontal disease increases with age, likely due to systemic inflammatory dysregulation. Age-related changes to macrophages may have a detrimental effect on disease recovery in aging populations, contributing to the pathogenesis of periodontal disease.
The prevalence of periodontal disease increases with age. Systemic inflammatory dysregulation also increases with age and has been reported to contribute to the myriad of diseases and conditions that become more prevalent with advanced age. As periodontal disease involves a dysregulated host inflammatory response, the age-related inflammatory dysregulation may contribute to the pathogenesis of periodontal disease in aging populations. However, our understanding of what drives the age-related inflammatory dysregulation is limited. Here, we investigate the macrophage and its contribution to periodontal disease in old and young mice using a ligature-induced periodontal disease model. We demonstrate that control old mice present with an aged periodontal phenotype, characterized by increased alveolar bone loss and increased local inflammatory cytokine expression compared to young mice. Macrophages were demonstrated to be present in the periodontium of old and young mice in equal numbers in controls, during disease induction, and during disease recovery. However, it appears age may have a detrimental effect on macrophage activity during disease recovery. Depletion of macrophages during disease recovery in old mice resulted in decreased inflammatory cytokines within the gingiva and decreased bone loss as measured by micro-computed tomography. In young mice, macrophage depletion during disease recovery had no beneficial or detrimental effect. Macrophage depletion during disease induction resulted in decreased disease severity similarly in young and old mice. Findings from this work support the diverse roles of macrophages in disease induction as well as the active roles of disease recovery, including the resolution of inflammation. Here, we conclude that age-related changes to the macrophage appear to be detrimental to the recovery from disease and may explain, in part, the age-related increase in prevalence of periodontal disease. Future studies examining the specific intrinsic age-related changes to the macrophage will help identify therapeutic targets.
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