Aging and Oral Health: Biological and Sociobehavioral Perspectives

Oral Health and Well-being in an Aging World: A Call for Integrated Solutions

Poor oral health can undermine nutrition, communication, self-esteem, and quality of life, especially in aging populations (World Health Organization 2022). Slack-Smith et al. (2023) propose ecosocial and intersectional theories and argue that these theories offer a way forward for improving oral health equity in older populations. Their synergistic critical perspectives reveal the need for broad upstream solutions targeting structural drivers of health inequities. Three longitudinal studies provide evidence that tooth loss and diabetes—alone or together—accelerate cognitive decline in older age. Jones et al. (2023) found that older birth cohorts experienced steeper declines in cognitive function and that edentulism predicted worsening over 10 y, adjusting for other risk factors. Kiuchi et al. (2023) estimated the impact of hypothetically preventing tooth loss at various levels, finding that retaining at least 10 to 19 teeth could slow decline relative to edentulism. Effects were additive, supporting tooth retention for healthy cognition. Wu et al. (2023) showed co-occurring diabetes and edentulism associated with worse cognitive function and faster decline for those in the 65- to 74-y-old group relative to neither condition. Diabetes alone mattered for this group, while edentulism predicted decline for younger and older adults. Though diabetes effects diminished with age, tooth loss remained influential across different age groups (65 to 74 y and 75 to 84 y). Findings suggest that these chronic diseases may interact to influence cognitive trajectories, underscoring the importance of coordinating medical and dental care in older populations with complex needs. Maintaining oral health is not only vital to healthy cognitive aging but also stands to benefit social connectivity and relationships as people get older. Cooray et al. (2023) argue that tooth retention enables social connections vital for well-being and healthy aging. This study examined how the number of teeth affects social participation over 6 y, controlling for time-varying factors, and found that each tooth loss scenario progressively reduced social engagement. Promoting good oral care and education is key to keeping older adults socially connected, with benefits for health, independence, and reduced risks of isolation. Mao et al. (2023) provide novel evidence on the social determinants of dental care access for older Chinese immigrants in the United States. Their findings point to the need for comprehensive solutions beyond the medical realm to reduce risks of isolation and promote well-being in marginalized aging populations. Nelson et al. (2023) propose recommendations for integrating oral health into primary care for older adults. The authors recommend electronic health record–embedded workflows prompting oral health screening, counseling, and referrals. Multilevel theory-based interventions are needed to change behaviors and address oral health disparities. The authors issue a call to action for progress on oral health in older populations through care model and electronic health record innovations, education, policy changes, and outcome-driven research. In this context, Schoebrechts et al. (2023) performed an international consensus study to validate previously optimized guidelines in oral health care as a section of the interRAI assessment system. By applying a Delphi approach with experts from 34 countries, a consensus was reached on all criteria used to provide caregivers with assistance regarding daily oral care and/or the need of referral to a dentist of care-dependent older individuals. In summary, these articles present compelling arguments and evidence for why oral health should be a priority in caring for aging populations. Teeth and gums are vital not just for eating but for cognition, social interaction, and well-being—all of which decline with age but can accelerate when oral diseases are left unaddressed. Tackling persistent challenges around access, education, and coordination of dental services will require political will and a commitment to equity. But the potential benefits to individual and public health make this an urgent issue that deserves integrated solutions and a seat at the table alongside other priorities in aging research, policy, and practice.

Unravelling the Aging-Associated Molecular Mechanisms in Oral Tissues and Cells

The other articles presented in this special issue focus on potential mechanisms of cellular aging in oral tissues. Cellular senescence is a central hallmark of the biological process of aging. In his critical review, Aquino-Martinez (2023) discusses how the integrated interaction between a persistent dysbiotic biofilm and several risk factors leads to premature senescent cells that ALTER—accumulate, limit regenerative potential, transmit senescence to heathy cells, exacerbate chronic inflammation, and dysregulate tissue remodeling—the periodontal microenvironment, amplifying inflammation and tissue destruction. The author also refers to current therapeutic strategies targeting senescent cells as potential approaches to delay age-related inflammatory pathologies, including periodontitis. In this context of cellular aging, inflammation, and periodontal tissue destruction, Wang et al. (2023) reported a potential regulatory mechanism of the osteoblastic transcription factor FoxO1 in age-related alveolar bone loss by activation of the NLRP3 inflammasome innate immune sensor under high levels of oxidative stress. An article on cellular senescence investigated the changes in self-renewal and osteogenic differentiation of murine and human dental pulp stromal cells (DPSCs) as a result of chronological and replicative senescence (Yao et al. 2023). DPSCs exhibit similar properties to bone marrow mesenchymal stem cells and have a high regenerative potential for application on tissue engineering (Mattei et al. 2021). The authors showed a decrease in the number and self-renewal capacity of DPSCs in both types of cellular aging, whereas impaired osteogenic differentiation was observed only in replicative senescence. Thus, recognition of distinct age-related patterns of DPSCs will help to determine specific guidelines for a successful stem cell therapeutic application in regenerative medicine. Compromised autophagy was recently listed as a new integrative hallmark of aging (Schmauck-Medina et al. 2022). Increasing evidence indicates that impaired autophagy leads to the accumulation of damaged cells and aging by various mechanisms, including an increase of cellular senescence and associated secretory phenotype, activation of NLRP3 inflammasome, promotion of neurodegeneration, tumorigenesis, and dysregulated immune responses. Considering the plausible interplay among aging, cognitive decline, and dysfunctional autophagy, Goto’s group (Sonoda et al. 2023) explored the impact of age-related autophagy and degeneration of the trigeminal nervous system on the formation of amyloid-β oligomers, commonly observed in progressive dementia such as Alzheimer disease. In a series of experiments using mouse models of Alzheimer disease, the authors observed that increased extracellular diffusion of amyloid-β oligomers in the trigeminal mesencephalic nucleus (Vmes) of older animals was associated with the decline in neuronal autophagy (indicated by elevated expression of Rubicon) or neuronal degeneration induced by tooth extraction. The data suggest that autophagy represents an additional mechanism of homeostasis in Vmes neurons, which progressively decreases with aging. Age and sex/gender are major risk determinants in the susceptibility to periodontal diseases. Despite that, the role of these biological variables in the disease pathogenesis is understudied (Ioannidou 2017). Here, Ebersole et al. (2023) analyzed the transcriptomic profiles of health gingival tissues with regard to sex and age in nonhuman primates. Differences in gene expression in healthy gingiva between sexes increased with age. Of interest, older female animals showed an elevated expression of genes related to innate and adaptive immune responses, which could partially support the higher severity and extent of periodontitis in males. Finally, distinct patterns of correlations between gingival gene expression and periodontal bleeding and probing were generally sex specific. These findings offer important insights regarding the effects of sex/gender biology on aging as relevant determinants to be addressed in investigations of risk assessment and pathogenesis of periodontal diseases. The impact of periodontitis on biological aging and mortality was further analyzed in a large prospective cohort study from the Third National Health and Nutrition Examination Survey (Liu et al. 2023). Accelerated phenotypic aging was determined by biochemical biomarkers and chronological age. Significant relationships between phenotypic age and all-cause/cause-specific mortality risks were observed. Further analyses indicated that moderate/severe periodontitis increased the effect of phenotypic age on all-cause mortality. Accumulation of advanced glycation end products (AGEs) on proteins is a major component of the aging process. AGE formation on collagen leads to significant structural and functional modifications on tissue properties, including oral tissues such as dentin and periodontal ligament. In their article, Leiva-Sabadini et al. (2023) demonstrated that AGE-modified collagen promoted an increased adhesion of Streptococcus mutans but not Streptococcus sanguinis on this substrate as compared with native collagen. Additionally, in silico computational docking simulation suggested that this altered substrate resulted in a larger contact area of interactions with the collagen-binding protein SpaP of S. mutans. Therefore, exposure of AGE-altered dentinal collagen with aging may favor early adhesion of cariogenic bacteria. The data presented in this issue emphasize the multifaceted and multifactorial aspect of the aging process and provide a better understanding of an array of potential biological and molecular mechanisms that affect oral tissue/cell homeostasis and immune responses during our life span. Overall, these mechanisms will offer valuable therapeutic targets for delaying and alleviating age-related oral and systemic disorders to promote oral health aging and quality of life.

We are very thankful to all of those outstanding scientists, clinicians, academic professionals, and colleagues for their dedication and contribution to this special issue. We wish you all an enjoyable reading!

Author Contributions

A.P. Colombo, B. Wu, contributed to data conception and design, drafted and critically revised the manuscript. All authors gave final approval and agree to be accountable for all aspects of the work.