Oral hygiene and cancer risk: emerging evidence and public health perspectives

Abstract

Oral hygiene, traditionally regarded as a pillar of dental care, is increasingly recognized for its broader relevance to systemic health, including cancer prevention. Accumulating evidence suggests that poor oral hygiene may contribute to carcinogenesis through pathways involving chronic inflammation, microbial dysbiosis, and immune dysregulation. This review synthesizes epidemiological studies linking indicators of poor oral health—such as periodontal disease and tooth loss—to elevated risks of head and neck, gastrointestinal, and other cancers. It also explores biological mechanisms that plausibly connect the oral environment to systemic oncogenesis. Integrating oral health promotion into lifestyle medicine frameworks and national public health strategies presents an opportunity for low-cost, scalable interventions to mitigate cancer burden, particularly in underserved populations. Future priorities include longitudinal research to strengthen causal inference, biomarker discovery for early detection, and policy initiatives embedding oral health within comprehensive disease prevention models. Recognizing oral hygiene as an integral component of systemic health may foster more holistic and equitable approaches to cancer prevention worldwide.

Introduction

Cancer remains one of the foremost global health challenges, accounting for substantial morbidity, mortality, and disability worldwide. In 2022, an estimated 20 million new cancer cases and 9.7 million cancer-related deaths occurred globally, with one in five individuals expected to develop cancer and one in nine men or one in twelve women projected to die from it during their lifetime [1]. Cancer contributes to 16.8% of all global deaths and over 22.8% of mortality from noncommunicable diseases (NCDs), ranking among the top three causes of death in adults aged 30–69 years in 177 of 183 countries [2]. By 2050, the global cancer burden is projected to exceed 35 million cases annually, representing a 76–77% increase primarily driven by population aging, urbanization, and continued exposure to modifiable risk factors [3]. Particularly concerning is the projected near tripling of cancer incidence and mortality in low-Human Development Index (HDI) countries, where healthcare systems remain under-resourced [3, 4]. These trends underscore the need to identify additional, scalable, and low-cost preventive strategies that complement existing efforts.

Although considerable progress has been made in addressing established cancer risk factors such as tobacco use, alcohol consumption, and obesity, oral hygiene remains an underrecognized yet biologically plausible and modifiable determinant of cancer risk [5]. Traditionally confined to the domain of dental health, poor oral hygiene is now increasingly linked to systemic inflammation, microbial dysbiosis, and immune dysregulation—factors that play critical roles in carcinogenesis. Emerging epidemiologic evidence suggests that inadequate oral hygiene is associated with increased risks of cancers affecting the oral cavity, gastrointestinal tract, and pancreas [5–7]. As a widely accessible and low-cost behavior, daily toothbrushing and other oral health practices may represent pragmatic, population-level interventions—particularly in settings with limited healthcare infrastructure.

This review synthesizes the current state of evidence on the relationship between oral hygiene and cancer risk, explores plausible biological mechanisms underlying this association, and discusses public health and clinical implications. By reframing oral hygiene within the context of lifestyle-based cancer prevention, this review aims to inform interdisciplinary strategies for reducing cancer burden and improving health equity globally.

Materials and methods

This study is a SANRA-guided narrative review designed to synthesize epidemiologic evidence, biological mechanisms, and public-health implications linking oral hygiene to cancer risk [8]. We did not conduct a PRISMA flow or meta-analysis; instead, we emphasize transparent reporting of information sources, selection logic, and balanced interpretation, consistent with SANRA’s six quality domains.

Information sources and timeframe

We conducted a structured, comprehensive search of PubMed/MEDLINE, Web of Science Core Collection, Scopus, and the China National Knowledge Infrastructure (CNKI). To incorporate current practice and policy insights, we also searched websites of authoritative organizations, including the World Health Organization (WHO), U.S. Centers for Disease Control and Prevention (CDC), National Institute of Dental and Craniofacial Research (NIDCR), and the Association of State and Territorial Dental Directors (ASTDD). The predefined timeframe spanned from January 1, 2015, to May 31, 2025. While the majority of included studies were published between 2019 and 2024, milestone studies dating back to 2017 were retained to ensure mechanistic continuity, particularly those related to microbial dysbiosis and carcinogenesis. Additionally, policy documents and online reports from globally recognized institutions were included when directly relevant to the review’s objectives.

Search strategy and keywords

Title/abstract terms and controlled vocabulary were combined with Boolean operators. Core concept groups included:

• (i)exposure/phenotype: “oral hygiene,” “oral health,” “toothbrushing,” “periodontal disease/periodontitis,” “tooth loss,” “oral microbiome,” “dysbiosis”;
• (ii)outcomes: “cancer”, “neoplas*”, further refined by site (head and neck/oral cavity, esophageal, gastric, colorectal, pancreatic, lung, breast);
• (iii)mechanisms: “inflammation”, “immune”, “acetaldehyde”, “nitros*”, “Fusobacterium nucleatum”, “Porphyromonas gingivalis”, “HPV”; and,
• (iv)policy/practice: “guideline”, “health promotion”, “screening”, “integrated care”, “universal health coverage”.

Where appropriate, we added cohort or registry locators (e.g., UK Biobank, KNHANES, Golestan, China cohorts) to retrieve large population studies.

Eligibility criteria and study selection

Inclusion criteria were: (1) human observational studies (cohort, case–control, cross-sectional) assessing associations between oral hygiene/health indicators (e.g., periodontitis, tooth loss, brushing frequency, composite oral health indices) and cancer incidence or mortality; (2) high-quality evidence syntheses (systematic reviews/meta-analyses) and large secondary analyses; (3) mechanistic studies directly linking periodontal pathogens, inflammatory/immunologic pathways, or carcinogenic metabolites to oncogenesis that inform human plausibility; and (4) authoritative guidelines/policy documents relevant to clinical integration and public-health practice. We excluded non–peer-reviewed opinion pieces and conference abstracts (unless policy reports from recognized bodies), articles in languages other than English or Chinese without reliable translation, and purely preclinical studies without clear relevance to human cancer outcomes. After de-duplication, two reviewers independently screened titles/abstracts and assessed full texts against prespecified criteria; disagreements were resolved by discussion and consensus. Reference snowballing was used to identify additional key sources.

Data extraction and thematic synthesis

Key study features (design, population, exposure and outcome measures, effect estimates, confounder adjustment) were extracted and synthesized qualitatively. We organized findings under three predefined themes aligned with the aims of this review: (1) an epidemiologic perspective on site-specific cancer risks; (2) a mechanistic perspective integrating inflammation, immune dysregulation, microbiome dysbiosis, and carcinogenic metabolites; and (3) a public-health perspective covering implementation, equity, and policy translation.

Risk-of-bias and balance considerations

To mitigate bias, we prioritized large, well-adjusted cohorts and recent syntheses; explicitly considered confounding (smoking, alcohol, adiposity, socioeconomic status, comorbidities); noted differences in exposure ascertainment (self-report vs clinical periodontal indices); and highlighted geographic/population heterogeneity. Positive, null, and conflicting findings are presented to maintain balance. Remaining uncertainties and research priorities are summarized in the Discussion. By adhering to SANRA quality domains, clarity of purpose, appropriate search description, representative literature, reasoned presentation, balanced interpretation, and appropriate referencing, this narrative review aims to provide a credible and transparent synthesis.

Epidemiological evidence connecting oral health and cancer risk

A comprehensive evaluation of epidemiological evidence is critical before examining mechanistic pathways linking poor oral health to carcinogenesis. Across diverse populations, indicators of poor oral hygiene—including periodontal disease, tooth loss, and dental plaque accumulation—have been consistently associated with increased cancer incidence and mortality. While residual confounding remains a consideration, the strength and consistency of these associations support the emerging recognition of oral health as a systemic cancer risk factor. The following sections detail these associations across specific cancer sites.

Head and neck cancers

Substantial epidemiologic evidence supports a strong association between poor oral hygiene and increased risk of head and neck cancers, particularly malignancies of the oral cavity, pharynx, and larynx [9, 10]. Chronic periodontitis, a key marker of poor oral health, has been linked to approximately two-fold higher odds of developing oral squamous cell carcinoma (OSCC), as evidenced by a meta-analysis reporting a pooled odds ratio (OR) of 2.14 [10].

Indicators of poor oral hygiene, including tooth loss, heavy dental plaque accumulation, and infrequent toothbrushing, have consistently been associated with elevated risks of head and neck malignancies [9–11]. Importantly, these associations persist even after adjustment for confounding factors such as tobacco smoking and alcohol consumption, reinforcing the notion that poor oral health constitutes an independent risk factor for head and neck cancers [11, 12].

Population-based cohort studies further corroborate these findings. A Japanese cohort study demonstrated that individuals with poor oral hygiene behaviors, such as low frequency of toothbrushing and tooth loss, exhibited significantly greater risks of upper aerodigestive tract cancers [13]. Similarly, other studies have suggested that periodontal disease is associated with increased risks of head and neck cancers, independent of smoking and alcohol exposure [11].

Gastrointestinal cancers

Emerging evidence also implicates poor oral health as a potential risk factor for gastrointestinal (GI) malignancies, including cancers of the esophagus, stomach, colorectum, and pancreas.

Esophageal and gastric cancer

A large Chinese cohort study involving over 500,000 adults showed that individuals who rarely brushed their teeth had a 24% higher risk of esophageal cancer and a 27% higher risk of gastric cancer [7]. Similar associations have been reported in Korean and Japanese populations [5]. These findings are biologically plausible, given that oral bacteria involved in periodontal disease can produce nitrosamines and acetaldehyde, which may be swallowed and contribute to upper GI carcinogenesis [14].

Colorectal cancer

A meta-analysis of 11 observational studies found that individuals with periodontal disease exhibited a 20–30% higher risk of developing colorectal cancer compared to those with healthy gums [15]. Mechanistic studies have detected Fusobacterium nucleatum, a key periodontal pathogen, at significantly elevated levels within colorectal tumors. F. nucleatum promotes colon tumorigenesis by activating β-catenin signaling, impairing immune surveillance, and inducing chronic inflammation [16].

Pancreatic cancer

Periodontal disease and tooth loss have also been linked to increased pancreatic cancer risk. A large U.S. prospective study reported that individuals with higher antibody levels against Porphyromonas gingivalis had nearly a two-fold greater risk of developing pancreatic cancer [17]. Furthermore, poor oral health has been associated with systemic inflammatory responses that may facilitate pancreatic tumorigenesis.

Other cancer types

Although the strongest associations involve head and neck and gastrointestinal malignancies, emerging studies have explored links between poor oral health and other cancer types, with mixed findings.

Lung cancer

Several cohort studies have reported positive associations between periodontal disease, tooth loss, and lung cancer risk. For instance, findings from the Golestan Cohort Study indicated that poor dental health was associated with a significantly elevated risk of lung cancer, independent of smoking status [18]. However, these associations often attenuate after adjustment for smoking and other confounders, suggesting that residual confounding remains a major concern.

Breast and prostate cancer

Evidence linking periodontal disease to breast and prostate cancers is less robust. A large prospective analysis from the UK Biobank reported no significant association between self-reported poor oral health and breast cancer risk after controlling for potential confounders [19]. Similarly, studies investigating prostate cancer risk have yielded inconsistent results, with some suggesting modest associations and others reporting null findings [20].

Hematologic malignancies

Preliminary data suggest a potential link between periodontal disease and hematologic malignancies, including leukemia and lymphoma. Chronic immune activation, microbial translocation, and systemic inflammation induced by periodontal pathogens have been proposed as possible mechanisms [15]. Nonetheless, current evidence remains limited, and larger prospective studies are needed to validate these associations.

In summary, poor oral health has emerged as a significant and modifiable risk factor for the development of several major cancers, particularly those of the head and neck and gastrointestinal tract. While strong epidemiological support underpins these associations, links with other malignancies such as lung, breast, and hematologic cancers remain inconclusive and merit further investigation. To facilitate a clearer understanding of the current evidence, major epidemiological studies linking oral health indicators to cancer risk are summarized in Table 1. These findings emphasize the systemic relevance of oral hygiene beyond dental outcomes and highlight an important avenue for cancer prevention. Future research should prioritize large-scale, longitudinal studies to clarify causal relationships and to explore the mechanistic pathways linking oral health to oncogenesis. Future studies integrating oral microbiome profiling and lifestyle factors could offer new insights into the complex interplay between oral health and systemic cancer risk.

Table 1.

Summary of major epidemiological studies linking oral health indicators to cancer risk across diverse populations

Study	Country/region	Sample size	Study design	Oral health indicators	Cancer type(s)	Main findings
Enomoto et al. [21] (2024)	Japan	32,000	Cross-sectional	Brushing frequency	All-cause cancer	Lower brushing frequency associated with higher cancer prevalence
Yano et al. [18] (2024)	Iran	50,045	Prospective cohort	Dental health	Lung cancer	Poor oral health associated with higher lung cancer risk
Hu et al. [15] (2024)	Multi-country	11 studies	Meta-analysis	Periodontitis, brushing frequency	Oral, colorectal, pancreatic cancers	Consistent association with elevated cancer risk
Sheng et al [22].(2023)	China	~ 45,000	Prospective cohort	Oral hygiene combined with lifestyle factors	Various cancers	Interaction between poor oral health and lifestyle increases cancer risk
Wu et al. [19] (2023)	United Kingdom	> 469,000	Prospective cohort	Tooth loss, brushing frequency	Colorectal, liver cancers	Poor oral health linked to increased digestive system cancer risk
Kim et al. [11] (2022)	South Korea	~ 85,000	Prospective and cross-sectional	Brushing frequency, periodontitis	Gastric, pancreatic, all-cause cancer	≥ 3 times/day brushing associated with lower cancer mortality
Zhang et al. [7] (2022)	China	> 35,000	Prospective cohort	Tooth loss, periodontal status	Esophageal cancer	Poor oral health associated with elevated esophageal cancer risk
Jacob et al. [23] (2021)	Spain (National survey data)	~ 23,000	Cross-sectional	Self-reported oral health	Head and neck, gastrointestinal cancers	Poor oral health associated with increased risk of head and neck and GI cancers

Biological mechanisms linking oral hygiene and carcinogenesis

Building upon the epidemiological associations presented earlier, accumulating mechanistic evidence has elucidated several biological pathways through which poor oral hygiene may contribute to carcinogenesis. The observed biological plausibility—rooted in chronic inflammation, microbial dysbiosis, carcinogenic metabolite production, and immune dysregulation—provides critical insight into how oral health may exert systemic effects. Collectively, these mechanisms highlight the oral cavity’s integral role in systemic health and disease.

Chronic inflammation as a carcinogenic catalyst

Periodontal disease, resulting primarily from poor oral hygiene, is recognized as one of the most prevalent chronic inflammatory conditions globally [24]. The persistent accumulation of microbial plaque in periodontitis triggers a sustained immune response within periodontal tissues, characterized by elevated secretion of key pro-inflammatory cytokines, including IL-1β, IL-6, TNF-α, and prostaglandin E2 [25–27]. These inflammatory mediators can enter systemic circulation, creating a chronic inflammatory environment that fosters oxidative stress, angiogenesis, cellular proliferation, and DNA damage—hallmarks widely acknowledged in carcinogenesis [28].

Epidemiological evidence further supports the systemic implications of periodontal inflammation. Elevated systemic concentrations of inflammatory biomarkers such as C-reactive protein (CRP) and IL-6 have been consistently linked to an increased cancer risk in individuals with periodontal disease [29, 30]. Specifically, case–control studies have highlighted a significantly increased likelihood of oral squamous cell carcinoma (OSCC) among chronic periodontitis patients, even after controlling for well-established confounding factors like smoking and alcohol consumption [31–33]. This underscores the independent and critical role of chronic oral inflammation in promoting tumorigenesis.

Interventional studies offer additional support for a causal inflammatory pathway. Non-surgical periodontal therapy has been demonstrated to effectively reduce systemic inflammatory markers, suggesting the inflammatory cascade initiated by periodontal disease may be modifiable [34].

Oral microbiome dysbiosis and carcinogenesis

Oral dysbiosis, characterized by a shift from a balanced microbiota to a predominance of pathogenic species, constitutes a pivotal mechanistic link between poor oral hygiene and increased cancer risk. Periodontal disease, in particular, fosters the proliferation of anaerobic pathogens such as Fusobacterium nucleatum and Porphyromonas gingivalis, both recognized for their direct oncogenic potential [14, 15, 33].

F. nucleatum is strongly implicated in colorectal carcinogenesis, with evidence consistently demonstrating its enrichment in colorectal tumors. This bacterium promotes tumor proliferation and immune evasion by adhering to epithelial cells via its FadA adhesin, thereby activating oncogenic pathways such as β-catenin signaling [15, 22, 35]. Beyond colorectal malignancies, F. nucleatum DNA has also been detected in pancreatic tumors, highlighting its potential role in systemic tumorigenesis [14, 36]. Beyond the effects of F. nucleatum, another key periodontal pathogen, P. gingivalis, exerts profound oncogenic influences. It secretes virulence factors, including gingipains and lipopolysaccharides, which impair neutrophil and T-cell function, compromise epithelial integrity, and perpetuate chronic inflammation—ultimately facilitating immune suppression, DNA damage, and malignant progression [15, 23, 32, 37]. Notably, P. gingivalis DNA has been detected in esophageal cancer tissues, and elevated circulating antibodies against this pathogen have been associated with an increased risk of pancreatic cancer. Moreover, poor oral hygiene may promote persistent infection with high-risk human papillomavirus (HPV) strains, established drivers of oropharyngeal carcinogenesis [7, 38, 39].

Carcinogenic metabolites produced by oral bacteria

Poor oral hygiene fosters a microbial environment conducive to the endogenous production of carcinogenic metabolites. Nitrate-reducing bacteria, commonly found in dental plaque and on the tongue, can convert dietary nitrates into nitrites, which under acidic conditions may be further metabolized into N-nitroso compounds—potent human carcinogens implicated in the pathogenesis of esophageal and gastric cancers [38, 40].

In addition, alcohol-metabolizing bacteria such as Porphyromonas gingivalis can convert ethanol into acetaldehyde, a Group 1 carcinogen known to form DNA adducts, disrupt DNA repair processes, and promote mutagenesis within epithelial tissues [11, 18, 41]. This effect is particularly pronounced among individuals with poor oral hygiene who consume alcohol, as studies have reported significantly elevated salivary acetaldehyde concentrations in this population [42, 43], thereby increasing the risk for oral and pharyngeal cancers.

Furthermore, chronic oral infections and periodontitis perpetuate oxidative stress, leading to the generation of reactive oxygen and nitrogen species. These reactive intermediates cause DNA strand breaks, lipid peroxidation, and other molecular damages that represent critical precursors to malignant transformation [19, 44].

Immune modulation, viral persistence, and tumor surveillance failure

Chronic periodontal inflammation can disrupt systemic immune homeostasis, thereby weakening cancer immune surveillance mechanisms. Evidence indicates that periodontitis alters immune cell composition by increasing regulatory T cells and myeloid-derived suppressor cells, while simultaneously reducing the cytotoxic capacity of natural killer cells and T lymphocytes [45, 46]. This immunological imbalance fosters a permissive environment in which emerging tumor cells may evade detection and elimination.

At the local level, periodontal pathogens such as Porphyromonas gingivalis can modulate toll-like receptor (TLR) signaling pathways and suppress innate immune responses, further undermining mucosal defense mechanisms [47]. Severe local immune dysfunction may extend into systemic circulation, especially in individuals with advanced periodontal disease.

Beyond bacterial mechanisms, poor oral hygiene may also facilitate persistent infection with high-risk human papillomavirus (HPV) strains, well-established oncogenic drivers of oropharyngeal cancers. Case–control studies have observed higher oral HPV prevalence among individuals with poor oral hygiene, suggesting that impaired mucosal immunity may hinder viral clearance and promote viral-mediated carcinogenesis [38, 39, 48].

Clinically, poor oral health in cancer patients has been associated with impaired immune parameters and poorer clinical outcomes, particularly among those with head and neck malignancies [49, 50]. These findings highlight the systemic reach of oral immune dysfunction and its profound implications for tumor surveillance.

Collectively, these interconnected mechanisms illustrate how poor oral hygiene exerts carcinogenic influences beyond the confines of the oral cavity. Chronic inflammation, microbial dysbiosis, microbial metabolite toxicity, and immune dysregulation form a complex network of biological processes that plausibly drive cancer initiation and progression. These insights reinforce the evolving perspective that oral hygiene is not merely a dental concern, but a potentially modifiable factor in the broader landscape of systemic cancer prevention. The conceptual framework is illustrated in Fig. 1.

Fig. 1.

Conceptual Framework Linking Oral Microbiome Dysbiosis to Cancer Risk. The schematic illustrates the transition from a healthy oral microbiome (eubiosis) to microbial dysbiosis resulting from poor oral hygiene, characterized by periodontal disease and tooth loss. Dysbiosis promotes local inflammation, disrupts epithelial barrier integrity, and triggers systemic inflammatory responses, collectively contributing to carcinogenic signaling pathways. These biological alterations are associated with elevated risks of cancers involving the oral cavity, esophagus, lung, liver, pancreas, and colorectum (Created with BioRender.com)

Public health and clinical implications

The accumulating evidence linking poor oral hygiene to elevated cancer risk highlights critical opportunities for both public health and clinical interventions. Incorporating oral health into comprehensive health promotion strategies may represent a cost-effective and scalable approach to mitigating the global cancer burden, particularly among underserved populations.

Oral hygiene as a lifestyle medicine intervention

Oral hygiene practices—including daily toothbrushing, flossing, and routine dental visits—are simple, low-cost behaviors that can be widely promoted across populations. Unlike many medical interventions, maintaining good oral health requires minimal infrastructure yet confers significant systemic benefits [21, 28]. Several large-scale cohort studies have demonstrated that individuals who practice regular oral hygiene have lower risks not only of oral and oropharyngeal cancers, but also gastrointestinal malignancies such as esophageal, gastric, and pancreatic cancers [7, 32, 51].

In a 2024 cross-sectional study involving 32,000 Japanese adults, Enomoto et al. found that after multivariable adjustment individuals with consistent toothbrushing habits had significantly lower odds of cancer prevalence, supporting oral hygiene as a fundamental cancer prevention behavior [21]. Similarly, the Korean National Health and Nutrition Examination Survey (KNHANES) showed that brushing three or more times a day was associated with a reduced risk of all-cause cancer mortality [11]. These findings position oral hygiene alongside diet, physical activity, tobacco cessation, and alcohol moderation within the framework of lifestyle medicine.

In clinical settings, incorporating oral health assessment and counseling into routine preventive care could further strengthen cancer prevention efforts. Primary care providers, oncologists, and dental professionals should collaborate to educate patients on the systemic benefits of maintaining good oral hygiene [41, 49]. Thus, integrating oral health promotion into lifestyle medicine frameworks represents a pragmatic, scalable strategy to reduce cancer burden at the population level.

Health promotion strategies and integration of care

Although evidence continues to expand, recognition of the connection between oral health and systemic diseases remains insufficient among the general public. Targeted health promotion campaigns are needed to emphasize that oral health is integral to overall well-being and potentially to cancer prevention [52].

School-based oral health programs, community awareness initiatives, and workplace wellness campaigns represent effective platforms for disseminating oral hygiene education [49]. Japan's integration of dental examinations into annual health check-ups offers a successful model: national data show that routine oral screening has contributed to early detection and improved outcomes for oral and head and neck cancers [34]. At the healthcare system level, oral health services should be incorporated into universal health coverage (UHC) frameworks and chronic disease management programs [53]. Interprofessional education between medical and dental students has shown promise in improving integrated care delivery [26]. Further, oncology care pathways should include baseline and periodic oral assessments to minimize treatment-related oral complications and potentially improve survival outcomes [40, 54].

Incorporating oral hygiene promotion into national noncommunicable disease (NCD) strategies could maximize health gains. Cost-effectiveness modeling suggests that investments in oral health promotion could yield significant returns in reducing the burden of cancer, cardiovascular disease, and diabetes [41].

Addressing disparities in oral health access

Oral health disparities mirror broader inequities in healthcare access, education, and socioeconomic status. Vulnerable groups—such as rural populations, low-income individuals, and racial minorities—experience disproportionately higher rates of periodontal disease, tooth loss, and oral cancers [3, 55].

Financial barriers, lack of dental insurance, limited access to fluoridated water, and low oral health literacy contribute to persistent inequities [52]. Expanding subsidized dental services, mobile clinics, school-based sealant programs, and community oral health workers can help bridge these gaps [49]. Targeted interventions for high-risk populations are urgently needed. For example, Menya et al. demonstrated that addressing poor oral health practices in Africa's esophageal cancer corridor could significantly reduce cancer burden in these regions [56]. Additionally, culturally sensitive education campaigns can empower communities to adopt preventive oral health behaviors.

Promoting oral health equity is not merely a dental issue; it is essential for achieving broader cancer prevention and health equity goals. Closing the oral health gap could contribute meaningfully to narrowing the global cancer disparities across populations [3, 55]. Achieving oral health equity should be a global public health priority, integrated into national cancer control plans. A strategic framework for public health interventions is summarized in Fig. 2.

Fig. 2.

Strategic Framework for Public Health Interventions to Promote Oral Health and Prevent Cancer. The framework outlines a multi-level strategy for improving oral hygiene and reducing cancer risk. At the individual level, daily toothbrushing, flossing, mouthwash use, and dental visits are emphasized. Clinical-level actions include integrating oral health into primary care and oncology care. Community-level interventions focus on school-based programs and water fluoridation. At the policy level, incorporating oral health promotion into national noncommunicable disease (NCD) and cancer prevention strategies is advocated (Created with BioRender.com)

To enhance conceptual clarity and inform future research directions, this review highlights several unresolved questions. First, while associations between poor oral hygiene and cancer risk have been reported across multiple sites, causal inference remains limited by residual confounding, reverse causality, and varying definitions of exposure. Longitudinal studies with repeated oral health assessments and robust control for behavioral and socioeconomic variables are warranted to establish temporality and dose–response relationships. Second, although microbial dysbiosis, particularly involving Fusobacterium nucleatum and Porphyromonas gingivalis, has been implicated in tumorigenesis, its site-specific mechanisms across gastrointestinal, respiratory, and reproductive systems remain insufficiently mapped. Third, from a translational standpoint, integration of oral health into national cancer prevention strategies remains sporadic. Future implementation research should explore scalable screening models, interdisciplinary integration within universal health coverage, and culturally tailored risk communication strategies. Acknowledging the heterogeneity and conflicting results in the current evidence base is essential to guide balanced interpretation and hypothesis generation.

Future research directions

While substantial progress has been made in elucidating the links between oral health and cancer, several critical knowledge gaps remain. Future research should focus on strengthening causal inference, identifying reliable biomarkers, and translating findings into effective public health interventions. The following sections outline key priorities for advancing the field.

Longitudinal and interventional studies

Although numerous cross-sectional and cohort studies have demonstrated associations between poor oral health and increased cancer risk, most available evidence remains observational and cannot establish causality. To strengthen causal inference, there is an urgent need for long-term prospective cohort studies that rigorously adjust for confounders such as tobacco use, alcohol consumption, diet, socioeconomic status, and comorbidities.

Moreover, randomized controlled trials (RCTs) specifically designed to assess whether periodontal treatment or intensive oral hygiene interventions can reduce systemic inflammation, alter microbial dysbiosis, or lower cancer incidence are critically needed. Emerging pilot trials suggest that periodontal therapy can improve systemic inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) [40], but robust cancer outcome data are lacking.

Future intervention studies should aim to include diverse populations across different socioeconomic and ethnic backgrounds, with long-term follow-up for cancer incidence and mortality endpoints. Interdisciplinary collaboration among dental researchers, epidemiologists, oncologists, and public health experts will be essential to design effective trials, ensure methodological rigor, and translate findings into practice.

Biomarker discovery and microbiome-based screening

Advances in oral microbiome research and salivary diagnostics offer exciting opportunities to identify early biomarkers of cancer risk. Certain oral pathogens, such as Fusobacterium nucleatum and Porphyromonas gingivalis, have been consistently detected not only in periodontitis lesions but also in colorectal and pancreatic tumors [15, 47]. Ongoing research should explore whether oral microbial signatures, inflammatory cytokines, or microbial metabolites can serve as noninvasive biomarkers for early cancer detection. Saliva, an easily accessible biofluid, holds promise for future screening tools, especially in underserved populations. For instance, salivary detection of F. nucleatum DNA or elevated acetaldehyde levels could serve as early warning indicators for gastrointestinal cancers.

Additionally, multi-omics approaches integrating metagenomics, metabolomics, transcriptomics, and proteomics could provide comprehensive insights into the functional interactions between the oral ecosystem and systemic carcinogenesis [46]. Machine learning models trained on oral microbiome data may further enhance predictive accuracy for identifying individuals at elevated cancer risk. Future biomarker studies should prioritize large-scale, longitudinal validation in diverse cohorts and explore whether changes in the oral microbiome precede or merely reflect systemic disease. If successful, microbiome-based screening could complement traditional cancer screening strategies and offer cost-effective, noninvasive options for early detection.

Integration of oral health into public health policy

Despite mounting biological and epidemiological evidence, oral health remains underrepresented in major national and global cancer prevention frameworks. Future research should focus on policy translation, evaluating the cost-effectiveness, feasibility, and health equity impacts of incorporating oral hygiene promotion into existing noncommunicable disease (NCD) strategies.

Implementation research is needed to assess the integration of oral health education, preventive dental services, and periodontal screening into routine primary care and public health programs. For example, school-based sealant programs, community water fluoridation, and mobile dental clinics have demonstrated success in improving oral health outcomes and could serve as scalable models for broader cancer prevention efforts [41, 49]. The World Health Organization (WHO) has recently prioritized oral health in its global NCD action plan [52], and national cancer control plans should similarly recognize oral hygiene as a modifiable cancer risk factor. Future studies should investigate barriers and facilitators to the adoption of oral health interventions across different cultural, socioeconomic, and healthcare settings.

Special attention should also be given to closing oral health disparities that disproportionately affect low-income, rural, and minority populations—groups that also bear a disproportionate burden of cancer. Oral health equity must become an integral part of broader efforts to reduce global cancer disparities.

Conclusion

Oral hygiene, traditionally viewed as a cornerstone of dental care, is now increasingly recognized as a critical determinant of systemic health, particularly in cancer prevention. Accumulating mechanistic and epidemiological evidence substantiates the role of poor oral hygiene in carcinogenesis through chronic inflammation, microbial dysbiosis, production of carcinogenic metabolites, and immune dysregulation. These biologically plausible pathways are consistently reinforced by large-scale population studies linking poor oral health to elevated risks of head and neck, gastrointestinal, and other cancers.

Given the escalating global burden of cancer and the accessibility of oral hygiene interventions, integrating oral health promotion into comprehensive cancer prevention strategies offers a pragmatic, scalable, and cost-effective opportunity—especially in underserved populations facing dual burdens of poor oral health and cancer disparities. Embedding oral health within broader noncommunicable disease frameworks, primary care models, and public health policies must become a global priority.

Looking forward, longitudinal and interventional studies are urgently needed to strengthen causal inference, while innovations in salivary diagnostics and microbiome-based screening could expand avenues for early detection. Ultimately, reframing oral hygiene not merely as a dental habit but as a strategic axis of systemic disease prevention represents a transformative opportunity to advance health equity, reduce cancer burden, and foster interdisciplinary collaboration across global health domains.

Limitations

Several limitations should be acknowledged. First, most of the available evidence linking oral hygiene to cancer risk is observational in nature, limiting causal inference. These studies are prone to residual confounding,particularly from smoking, alcohol use, diet, and socioeconomic status (SES). Second, definitions of oral health and hygiene exposures varied considerably, ranging from self-reported toothbrushing frequency to clinical periodontal indices, potentially introducing misclassification bias. Third, substantial geographic heterogeneity exists in both oral health practices and cancer incidence, which may limit the generalizability of findings across populations. Finally, heterogeneity in cancer outcome definitions and adjustment strategies across studies may introduce bias. Future longitudinal studies and randomized controlled trials are needed to validate these associations and elucidate underlying mechanisms.

Author contributions

*Minhong Yin* and *Huijuan Cheng* contributed to the conception and overall design of the study, providing critical guidance on the thematic framework and structural organization. *Guodong Sun* was primarily responsible for drafting the manuscript, conducting literature review, visualizing key concepts, and integrating multidisciplinary perspectives. All authors participated in the critical revision of the manuscript for important intellectual content, contributed to the interpretation of the data and evidence, and approved the final version for submission.

Funding

This work was supported by the Gansu Province Natural Science Foundation Project (22JR5RA916), the In-House Fund of Lanzhou University First Hospital (ldyyyn2020-46), the Science and Technology Development Plan Project of Lanzhou City (2020-ZD-92), and the Scientific Research Cultivation Program for Cuiying Scholars, Second Hospital of Lanzhou University (CYXZ2023-06, CYXZ2023-08).

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

This article is a narrative review based entirely on previously published studies and publicly available data sources. No new studies involving human participants or animals were conducted by the authors. Therefore, ethical approval and informed consent were not required.

Competing interests

The authors declare no competing interests.