You must be signed in to read the rest of this article.
Registration on CDEWorld is free. You may also login to CDEWorld with your DentalAegis.com account.
Periodontitis is an inflammatory disease driven by a dysbiotic microbial community that results in the destruction of the periodontal ligament, cementum, and alveolar bone.1 Because periodontitis is one of the most widespread diseases globally, it presents a significant public health challenge. According to the results of the most recent Global Burden of Disease study, more than 1 billion people experienced severe periodontitis in 2021, with a global age-standardized prevalence of 12.50%.2 Projections indicate a sharp increase in the impact of periodontitis, with the number of individuals suffering from severe disease expected to rise by 44.32% by 2050 and surpass 1.5 billion cases.2
Through both inflammatory and bacterial mechanisms, ongoing research has established a connection between periodontitis and a range of systemic diseases and conditions, including multiple forms of cancer.3 Emerging evidence suggests that both chronic infection and inflammation play significant roles in cancer development.4,5 This concept was first proposed in 1863 by Rudolf Virchow, who hypothesized that chronic inflammation could trigger cancer formation. Recent studies involving in vitro models, animal research, and human epidemiological data have further reinforced this link.4,5 Specific examples of the association between chronic inflammation and cancer include the association between inflammatory bowel disease and colon cancer, hepatitis B and C infections and liver carcinoma, and chronic Helicobacter pylori infection and gastric cancer.6 Similarly, the incidence, exposure, and severity of periodontitis have been associated with the onset and progression of several chronic systemic diseases, including cancer.7,8 This article summarizes the current evidence linking periodontal disease to cancer.
Periodontitis: Epidemiology and Pathogenesis
Periodontitis is a chronic inflammatory disease characterized by the loss of hard and soft tissues that support the teeth. The disease arises as a result of complex interactions between microbial agents and an individual’s immune response. Periodontitis is initiated by dysbiosis, which is defined as a microbial imbalance that leads to pathogenic shifts in the microbial community. These shifts activate host immune and inflammatory pathways and ultimately lead to destruction of the periodontal attachment apparatus.9
This complex interaction between the microbial invasion and the host’s immune defense demonstrates the multifaceted nature of the development and progression of periodontitis. Understanding the biologic mechanisms that govern disease progression is essential to developing targeted therapies and effective prevention strategies as well as recognizing secondary risk factors associated with disease progression and the interaction between periodontitis and systemic health. By focusing on both microbial control and modulation of the host immune response, modern periodontal treatments aim to restore oral health and prevent further tissue destruction.10-12
Cancer: Epidemiology and Pathogenesis
According to the World Health Organization, cancer is a broad term encompassing a diverse group of diseases that can develop in any part of the body. A key characteristic of cancer is the rapid formation and replication of abnormal cells. These cells may invade nearby tissues and spread to other organs in a process known as metastasis. The spread of cancer through widespread metastasis is the leading cause of cancer-related death.13
Cancer ranks as the second leading cause of death globally, and it is responsible for approximately 10 million deaths annually. Each year, about 19 million new cases of cancer are diagnosed, with breast, lung, colorectal, pancreatic, and gastric cancers being the most prevalent. Despite advances in research, effective prevention and treatment remain challenging. Further progress in addressing cancer requires a deeper understanding of its molecular mechanisms and the identification of modifiable risk factors that can be targeted for intervention.14
Although some cancers have been associated with genetic influence, a substantial proportion of cases (ie, approximately 30% to 70%) can be linked to modifiable risk factors, such as tobacco use, alcohol consumption, high body mass index (BMI), and chronic infections.15,16 In recent years, growing attention has been paid to the host microbiome as a key player in cancer initiation and progression. Concurrently, chronic local inflammation and its systemic effects have been recognized as a critical foundation that promotes several hallmark features of malignancies.16
The Cancer Connection
Research has linked periodontitis with the development of several different types of cancer, including head and neck cancers, lung cancer, breast cancer, esophageal and gastric cancers, pancreatic cancer, and colorectal cancer (Table 1).
Head and Neck Cancers
Head and neck cancers rank as the sixth most common malignancies globally, with a significantly higher prevalence in South-Central Asia, where they are the third most common. Among head and neck cancers, oral squamous cell carcinoma is the most prevalent. Oral squamous cell carcinoma is especially prevalent in developing countries; however, changes in lifestyles and risk factors have led to a rise in cases in developed nations as well. Populations from low socioeconomic backgrounds, particularly in developing countries, face a higher risk of developing oral squamous cell carcinoma. This increased risk is often attributed to limited awareness and greater exposure to preventable risk factors such as tobacco use and alcohol consumption.17
In 2018, approximately 354,864 new cases of lip and oral cavity cancer and 92,887 new cases of oropharyngeal cancer were reported worldwide.13 This represented approximately 2% and 0.5%, respectively, of all new cancer diagnoses. Each year, about 4 in 100,000 individuals are diagnosed with lip and oral cavity cancer and 1.1 in 100,000 individuals are diagnosed with oropharyngeal cancer.13 In 2018, 177,384 people died from oral cancer, which represented a mortality rate of 2 deaths per 100,000 individuals.13 For oropharyngeal cancer, the mortality rate was 0.57 deaths per 100,000 individuals.13 Head and neck cancers demonstrate a predilection for men over women. When compared with men, who develop oral cancer at a rate of approximately 5.8 per 100,000 people, women develop oral cancer at a rate of only 2.3 per 100,000 people.13
Emerging evidence suggests a biologic link between periodontitis and head and neck cancers through microbial dysbiosis, genetic susceptibility, and immuno-epigenetic alterations. Porphyromonas gingivalis, a key periodontal pathogen, promotes inflammation and carcinogenic changes, while genetic polymorphisms in IL-1 and TNF-α suggest shared susceptibility. Chronic inflammation and epigenetic modifications, such as DNA methylation, may further contribute to tumor progression. Although observational studies indicate an association, further research is needed to confirm causality. Given the global burden of both diseases, integrating oral health strategies into oral cancer prevention strategies could be a valuable public health approach.18 Modifiable risk factors of oral cancer include tobacco use and heavy alcohol consumption, either on their own or together. When combined, tobacco and alcohol are responsible for more than 80% of oral cancer cases, and people who both smoke and drink heavily are at up to 38 times greater risk of developing oral cancer than those who do neither.19 Because electronic nicotine delivery systems are still relatively new, their harmful effects on oral health may not yet be fully known. Therefore, healthcare professionals should be cautious about treating or promoting electronic nicotine delivery systems as safe tools for tobacco use risk reduction and smoking cessation until more research is conducted to confirm their long-term safety and health impact.20
Lung Cancer
Studies on the periodontitis-lung cancer link have been inconclusive. Although one cohort found no association in nonsmokers,21 others have reported a higher risk with severe periodontitis.22 A recent systematic review supported this association with a relative risk of 1.39.22 The oral microbiome may also play a role, with bacteria such as Prevotella spp., Veillonella spp., and P. gingivalis entering the lungs via microaspiration. Research has shown that P. gingivalis is found more frequently in lung cancer tissues than in controls, and it has been linked to poorer survival when found in the lung tissues of cancer patients. In lung cancer cases, oral bacteria may be secondary colonizers due to enhanced permeation and retention in cancer tissues.23
Breast Cancer
Epidemiologic and cohort studies have demonstrated a statistically significant association between periodontitis and breast cancer development. A study by Nwizu and colleagues found that postmenopausal women with a self-reported history of periodontal disease had a 13% higher risk of developing breast cancer (HR: 1.13; 95% CI: 1.03–1.23).24 Oral bacteria, particularly Fusobacterium nucleatum, have also been detected in cancerous human breast tissues. The potential role of periodontal pathobiont-induced bacteremia in breast tumorigenesis has been investigated in a murine model.25 Systemically introduced F. nucleatum resulted in a 100-fold increase in bacterial abundance in tumor tissues when compared with controls.25
Esophageal and Gastric Cancers
Given the shared microbiome between the oral cavity and other areas of the gastrointestinal tract, research has been conducted to investigate the potential relationship between periodontitis and esophageal and gastric cancers. Self-reported periodontitis has been linked to esophageal cancer in postmenopausal women, and a smaller but significant association was found in a mixed-gender study, which also found a link between periodontitis and gastric cancer.24,26 Other studies have linked periodontitis with particular forms of malignancy. For example, periodontal disease was found to increase the risk of esophageal adenocarcinoma by 43% (HR: 1.43; 95% CI: 1.10–1.86) and gastric adenocarcinoma by 52% (HR: 1.52; 95% CI: 1.20–1.94).26 Periodontal disease resulting in tooth loss was found to further elevate these risks, providing more evidence of a potential link between oral health and upper gastrointestinal cancers.26
Although the mechanisms remain unclear, P. gingivalis and F. nucleatum are linked to esophageal and gastric cancers, possibly via chronic inflammation and immune modulation.27,28 Periodontal pockets may also harbor H. pylori, a known carcinogen.29 Conversely, commensal bacteria such as Neisseria spp. and Streptococcus pneumoniae may reduce esophageal adenocarcinoma risk. These findings may suggest that oral bacteria play a role in the development of gastrointestinal cancer.30,31 These bacteria may directly damage and/or impact precancerous cells or potentiate the impact of mild carcinogens through transformation by bacterial enzymes into more potent carcinogenic compounds.30,31
Pancreatic Cancer
An association between pancreatic cancer and periodontitis has been shown in both case-control and cohort studies.32,33 Although the etiology of pancreatic cancer is unclear, microbial dysbiosis has been suggested as a risk factor along with smoking, pancreatitis, and obesity.34 Pancreatic tumors harbor distinct microbiomes, and F. nucleatum and Granulicatella adiacens have been shown to be more abundant in high-grade tumors and linked to worse outcomes.35,36 Oral pathogens contribute to pancreatic cancer via virulence factors such as Treponema denticola’s dentilisin, which is detected in 65% of pancreatic tumors.37 The presence of P. gingivalis and Aggregatibacter actinomycetemcomitans has also been linked to increased pancreatic cancer risk.38 These bacteria evade immunity, impair natural killer cells, and activate inflammatory pathways (TLR4/NF-κB), potentially contributing to cancer development.39,40
Colorectal Cancer
Evidence of a link between periodontitis and colorectal cancer is heterogeneous. Some studies, especially in nonsmokers, show no association, whereas others report a moderate link.24 Interestingly, one cohort study suggests that periodontitis may increase the risk of benign colorectal tumors but not malignant ones.41
Colorectal cancer tissues have been found to contain F. nucleatum, which potentially reaches tumors via enteral or hematogenous routes.42 In addition to direct bacterial effects, systemic inflammatory burden, including that from periodontitis, may contribute to the development of colorectal cancer. Furthermore, inflammatory cells, such as Th17 lymphocytes, may promote gut dysbiosis and inflammation. These mechanisms highlight the need for further research into periodontitis and colorectal cancer.23
Mechanisms Underlying the Periodontitis-Cancer Link
The connection between periodontitis and cancer is thought to involve several mechanisms, including the following (Figure 1)23:
• Chronic inflammation and free radical production associated with periodontitis may cause DNA damage and malignant transformation.
• Toxins and metabolites from oral bacteria may induce epithelial barrier damage.
• Altered gene expression may be triggered by oral pathogens through epigenetic DNA methylation or carboxylation.
• Immune modulation by oral bacteria may disrupt critical cellular checkpoints and impair programmed cell death processes.
It has been proposed that oral pathogens and dysbiotic biofilm may influence cancer pathogenesis and disease progression through mechanisms that alter gene expression and produce toxins and metabolites, which then cause cellular damage.45 An altered microbiome can contribute to carcinogenesis through its toxins and metabolites, which induce genetic damage in epithelial cells. Individual periodontal pathogens have been associated with such damage. For example, A. actinomycetemcomitans produces carcinogens such as cytolethal distending toxin, reactive oxygen and nitrogen species, sulfides, nitrosamines, and acetaldehyde. These compounds may cause DNA alkylation and mutations as well as impair DNA repair mechanisms.46
Ethanol metabolism by oral bacteria such as Streptococcus salivarius and Corynebacterium generates acetaldehyde, a recognized carcinogen that damages DNA and promotes malignant cell proliferation.45,46 Individuals with periodontal disease exhibit higher salivary acetaldehyde levels after ethanol exposure, which indicates microbial enhancement of alcohol’s carcinogenic potential.45,46 Similarly, nicotine metabolism by oral bacteria leads to the formation of nitrosamines, which are potent carcinogens associated with oral, esophageal, and lung cancers. The presence of periodontal dysbiosis can amplify these harmful metabolic processes.47,48 Direct impacts of oral bacteria on host cell DNA structure and gene expression have also been demonstrated,49-52 and a dysbiotic oral environment may also potentiate the presence and virulence of bacteria and viruses impacting cancer transformation.53,54
The link between periodontitis and cancer is shaped by multiple risk factors, both direct and indirect. Chronic inflammation in periodontitis leads to persistent oxidative stress and immune dysregulation, which promotes DNA damage and carcinogenesis. In addition, systemic comorbidities, such as diabetes, obesity, and cardiovascular diseases, share inflammatory pathways with periodontitis, so they may potentially mediate its link to cancer.23 Biologic aging and immunosenescence further contribute to multimorbidity, reinforcing periodontitis as a marker of broader systemic dysfunction. Poor oral hygiene and lifestyle factors, including smoking, alcohol consumption, and an unhealthy diet, can amplify this risk, and socioeconomic disparities often correlate with limited access to healthcare, increasing susceptibility. Targeting these interconnected factors through preventive strategies, periodontal treatment, and lifestyle modifications may mitigate cancer risk while improving overall health outcomes.55
Public Health and Clinical Implications
The early detection and management of periodontitis can offer significant public health benefits for oral and overall health, including in reducing the risk of certain cancers.56 Regular dental checkups can help prevent disease progression and reduce systemic inflammation linked to cancer. In addition, public health initiatives promoting oral hygiene, smoking cessation, and healthy diets can help to further lower the prevalence of periodontitis and its associated health risks, including cancer (Figure 2).57
Recent advancements have also highlighted the potential of noninvasive methods, such as the use of diagnostic oral rinses and/or other methods of oral biomarker sampling, in the early detection of gastric cancer. Studies have demonstrated that analyzing the oral microbiome through a simple “swish-and-spit” test can identify bacterial signatures associated with gastric cancer risk. This approach not only facilitates early diagnosis but also underscores the interconnectedness of oral health and systemic diseases, reinforcing the importance of maintaining periodontal health as a component of overall cancer prevention strategies.58
Prioritizing the early detection and treatment of periodontitis, along with managing its risk factors, presents a valuable opportunity to enhance public health outcomes and reduce the burden of cancer.
Conclusion
Periodontitis has been linked to cancer through chronic inflammation, microbiome dysbiosis, and systemic effects. Elevated risks for oral, esophageal, pancreatic, and gastric cancers have been associated with periodontal conditions. Although the specific mechanisms remain under study, periodontal pathogens and inflammation resulting from periodontitis may contribute to cancer development and progression. Prioritizing early detection, oral hygiene, and lifestyle changes, such as smoking cessation, can reduce systemic risks. Further research is needed to confirm causality and develop targeted interventions.
Queries regarding this course may be submitted to authorqueries@conexiant.com
About the Authors
Layal Bou Semaan, DDS, MSc
Periodontology Resident
Department of Periodontology
University of Alabama at Birmingham
School of Dentistry
Birmingham, Alabama
Matthew Litz, DMD, MS
Adjunct Assistant Professor
Department of Periodontology
University of Alabama at Birmingham
School of Dentistry
Birmingham, Alabama
Spectra Dental Specialists
Hoover, Alabama
Maria L. Geisinger, DDS, MS
Diplomate
American Board of Periodontology
Professor and Acting Chair
Department of Periodontology
University of Alabama at Birmingham
School of Dentistry
Birmingham, Alabama
References
1. Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: consensus report of workgroup 2 of the 2017 world workshop on the classification of periodontal and peri-implant diseases and conditions. J Periodontol. 2018;89(Suppl 1):S173-S182.
2. Nascimento GG, Alves-Costa S, Romandini M. Burden of severe periodontitis and edentulism in 2021, with projections up to 2050: The Global Burden of Disease 2021 study. J Periodontal Res. 2024;59(5):823-867.
3. Jepsen S, Caton JG, Albandar JM, et al. Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S237-S248.
4. de Martel C, Georges D, Bray F, et al. Global burden of cancer attributable to infections in 2018: a worldwide incidence analysis. Lancet Glob Health. 2020;8(2):e180-190.
5. Golemis EA, Scheet P, Beck TN, et al. Molecular mechanisms of the preventable causes of cancer in the United States. Genes Dev. 2018;32(13-14):868-902.
6. De Flora S, Bonanni P. The prevention of infection-associated cancers. Carcinogenesis. 2011;32(6):787-795.
7. Li TJ, Hao YH, Tang YL, Liang XH. Periodontal pathogens: a crucial link between periodontal diseases and oral cancer. Front Microbiol. 2022;13:919633.
8. Linden GJ, Lyons A, Scannapieco FA. Periodontal systemic associations: review of the evidence. J Periodontol. 2013;84(Suppl 14): S8-S19.
9. Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis: framework and proposal of a new classification and case definition. J Periodontol. 2018;89(Suppl 1):S159-S172.
10. Könönen E, Gursoy M, Gursoy UK. Periodontitis: a multifaceted disease of tooth-supporting tissues. J Clin Med. 2019;8(8):1135.
11. Abdulkareem AA, Al-Taweel FB, Al-Sharqi AJ, et al. Current concepts in the pathogenesis of periodontitis: from symbiosis to dysbiosis. J Oral Microbiol. 2023;15(1):2197779.
12. Haque MM, Yerex K, Kelekis-Cholakis A, Duan K. Advances in novel therapeutic approaches for periodontal diseases. BMC Oral Health. 2022;22(1):492.
13. World Health Organization International Agency for Research on Cancer. Data visualization tools for exploring the global cancer burden in 2022. WHO website. https://gco.iarc.fr/today/fact-sheets-populations. Accessed August 4, 2025.
14. Sung H, Ferlay J, Siegel RL, et al. Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2021;71(3):209-249.
15. Plummer M, de Martel C, Vignat J, et al. Global burden of cancers attributable to infections in 2012: a synthetic analysis. Lancet Glob Health. 2016;4(9):e609-e616.
16. Hanahan D. Hallmarks of cancer: new dimensions. Cancer Discovery. 2022;12(1):31-46.
17. Sarode G, Maniyar N, Sarode SC, et al. Epidemiologic aspects of oral cancer. Dis Mon. 2020;66(12):100988.
18. Gasparoni LM, Alves FA, Holzhausen M, et al. Periodontitis as a risk factor for head and neck cancer. Med Oral Patol Oral Cir Bucal. 2020;26(4):e430-e436.
19. Warnakulasuriya S. Living with oral cancer: epidemiology with particular reference to prevalence and life-style changes that influence survival. Oral Oncol. 2010;46(6):407-410.
20. Sultan AS, Jessri M, Farah CS. Electronic nicotine delivery systems: oral health implications and oral cancer risk. J Oral Pathol Med. 2021;50(3):316-322.
21. Michaud DS, Lu J, Peacock-Villada AY, et al. Periodontal disease assessed using clinical dental measurements and cancer risk in the ARIC study. J Natl Cancer Inst. 2018;110(8):843-854.
22. Wang J, Yang X, Zou X, et al. Relationship between periodontal disease and lung cancer: a systematic review and meta-analysis. J Periodont Res. 2020;55(5):581-593.
23. Baima G, Minoli M, Michaud DS, et al. Periodontitis and risk of cancer: mechanistic evidence. Periodontol 2000. 2024;96(1):83-94.
24. Nwizu N, Wactawski-Wende J, Genco RJ. Periodontal disease and cancer: epidemiologic studies and possible mechanisms. Periodontol 2000. 2020;83(1):213-233.
25. Parhi L, Alon-Maimon T, Sol A, et al. Breast cancer colonization by Fusobacterium nucleatum accelerates tumor growth and metastatic progression. Nat Commun. 2020;11(1):3259.
26. Lo CH, Kwon S, Wang L, et al. Periodontal disease, tooth loss, and risk of oesophageal and gastric adenocarcinoma: a prospective study. Gut. 2021;70(3):620-621.
27. Gao S, Li S, Ma Z, et al. Presence of Porphyromonas gingivalis in esophagus and its association with the clinicopathological characteristics and survival in patients with esophageal cancer. Infect Agents Cancer. 2016;11:3.
28. Boehm ET, Thon C, Kupcinskas J, et al. Fusobacterium nucleatum is associated with worse prognosis in Lauren’s diffuse type gastric cancer patients. Sc Rep. 2020;10(1):16240.
29. Zarić S, Bojić B, Janković LJ, et al. Periodontal therapy improves gastric Helicobacter pylori eradication. J Dent Res. 2009;88(10):946-950.
30. Peters BA, Wu J, Pei Z, et al. Oral microbiome composition reflects prospective risk for esophageal cancers. Cancer Res. 2017;77(23):6777-6787.
31. Li X, Zhu S, Zhang T, Chen X. Association between oral microflora and gastrointestinal tumors. Oncol Rep. 2021;46(2):160.
32. Michaud DS, Joshipura K, Giovannucci E, Fuchs CS. A prospective study of periodontal disease and pancreatic cancer in US male health professionals. J Natl Cancer Inst. 2007;99(2):171-175.
33. Maisonneuve P, Amar S, Lowenfels AB. Periodontal disease, edentulism, and pancreatic cancer: a meta-analysis. Ann Oncol. 2017;28(5):985-995.
34. Klein AP. Pancreatic cancer epidemiology: understanding the role of lifestyle and inherited risk factors. Nat Rev Gastroenterol Hepatol. 2021;18(7):493-502.
35. Archibugi L, Signoretti M, Capurso G. The microbiome and pancreatic cancer: an evidence-based association? J Clin Gastroenterol. 2018;52:S82-S85.
36. Gaiser RA, Halimi A, Alkharaan H, et al. Enrichment of oral microbiota in early cystic precursors to invasive pancreatic cancer. Gut. 2019;68(12):2186-2194.
37. Nieminen MT, Listyarifah D, Hagström J, et al. Treponema denticola chymotrypsin-like proteinase may contribute to orodigestive carcinogenesis through immunomodulation. Br J Cancer. 2018;118(3):428-434.
38. Fan X, Alekseyenko AV, Wu J, et al. Human oral microbiome and prospective risk for pancreatic cancer: a population-based nested case-control study. Gut. 2018;67(1):120-127.
39. Tan Q, Ma X, Yang B, et al. Periodontitis pathogen Porphyromonas gingivalis promotes pancreatic tumorigenesis via neutrophil elastase from tumor-associated neutrophils. Gut Microbes. 2022;14(1):2073785.
40. Gnanasekaran J, Binder Gallimidi A, Saba E, et al. Intracellular Porphyromonas gingivalis promotes the tumorigenic behavior of pancreatic carcinoma cells. Cancers (Basel). 2020;12(8):2331.
41. Fu MM, Chien WC, Chung CH, et al. Is periodontitis a risk factor of benign or malignant colorectal tumor? A population-based cohort study. J Periodont Res. 2022;57(2):284-293.
42. Gopinath D, Kunnath Menon R, Veettil SK, et al. Periodontal diseases as putative risk factors for head and neck cancer: systematic review and meta-analysis. Cancers (Basel). 2020;12(7):1893.
43. Corbella S, Veronesi P, Galimberti V, et al. Is periodontitis a risk indicator for cancer? A meta-analysis. PloS One. 2018;13(4):e0195683.
44. Maisonneuve P, Amar S, Lowenfels AB. Periodontal disease, edentulism, and pancreatic cancer: a meta-analysis. Ann Oncol. 2017;28(5):985-995.
45. Karpiński TM. Role of oral microbiota in cancer development. Microorganisms. 2019;7(1):20.
46. Lin KY, Chung CH, Ciou JS, et al. Molecular damage and responses of oral keratinocyte to hydrogen peroxide. BMC Oral Health. 2019;19(1):10.
47. Salaspuro MP. Acetaldehyde, microbes, and cancer of the digestive tract. Crit Rev Clin Lab Sci. 2003;40(2):183-208.
48. Fitzpatrick SG, Katz J. The association between periodontal disease and cancer: a review of the literature. J Dent. 2010;38(2):83-95.
49. Gabusi A, Gissi DB, Grillini S, et al. Shared epigenetic alterations between oral cancer and periodontitis: A preliminary study. Oral Dis. 2023;29(5):2052-2060.
50. Geng F, Zhang Y, Lu Z, et al. Fusobacterium nucleatum caused DNA damage and promoted cell proliferation by the Ku70/p53 pathway in oral cancer cells. DNA Cell Biol. 2020;39(1):144-151.
51. Yost S, Stashenko P, Choi Y, et al Increased virulence of the oral microbiome in oral squamous cell carcinoma revealed by metatranscriptome analyses. Int J Oral Sci. 2018;10(4):32.
52. Groeger S, Herrmann JM, Chakraborty T, et al. Porphyromonas gingivalis W83 membrane components induce distinct profiles of metabolic genes in oral squamous carcinoma cells. Int J Molec Sci. 2022;23(7):3442.
53. Hormia M, Willberg J, Ruokonen H, Syrjänen S. Marginal periodontium as a potential reservoir of human papillomavirus in oral mucosa. J Periodontol. 2005;76(3):358-363.
54. Tezal M, Scannapieco FA, Wactawski-Wende J, et al. Local inflammation and human papillomavirus status of head and neck cancers. Arch Otolaryngol Head Neck Surg. 2012;138(7):669-675.
55. D’Aiuto F, Parkar M, Andreou G, et al. Periodontitis and systemic inflammation: control of the local infection is associated with a reduction in serum inflammatory markers. J Dent Res. 2004;83(2):156-160.
56. Nwizu N, Wactawski-Wende J, Genco RJ. Periodontal disease and cancer: epidemiologic studies and possible mechanisms. Periodontol 2000. 2020;83(1):213-233.
57. Janakiram C, Dye BA. A public health approach for prevention of periodontal disease. Periodontol 2000. 2020;84(1):202-214.
58. ASCO Post Staff. Oral rinse could provide early screening for gastric cancer. The ASCO Post website. https://ascopost.com/news/may-2024/oral-rinse-could-provide-early-screening-for-gastric-cancer/. Published May 13, 2024. Accessed August 4, 2025.
