Periodontal Disease May Be Linked To Leading Cause Of Stroke

​Thomas E. Bramanti, D.D.S., Ph.D.

Board-Certified Diplomate American Board of Periodontology/Implant Dentistry

Board-Certified Diplomate American Board of Oral Implantology/Implant Dentistry

​​Certified TMJ Expert, The Pankey Institute

Fellow American Academy of Implant Dentistry
Clinical Assistant Professor at UCSF in the Department of Oral and Maxillofacial Surgery

Clinical Assistant Professor UCSF-Fresno Medical Education Program, School of Medicine 

About The Author:

Thomas E. Bramanti, D.D.S., Ph.D., DABP, DABOI, FAAID is a Board-Certified Specialist in Periodontics, a Board-Certified Specialist In Oral Implantology, a Fellow of the American Academy of Implant Dentistry, and a leading authority in implant dentistry. Dr. Bramanti is a private practitioner of Periodontics, Advanced Dental Implant Dentistry, and TMJ Expert serving patients in Fresno for over 30 years, a Clinical Assistant Professor at UCSF in the Department of Oral and Maxillofacial Surgery, a Clinical Assistant Professor UCSF-Fresno Medical Education Program in the School of Medicine, and an Attending Surgeon at Community Regional Medical Center Hospital. Dr. Bramanti has a Ph.D. in microbiology and has extensively studied and published research relating to bacteria which cause gum disease and are culprits in the cause of stroke. With a passion for lifelong results, Dr. Bramanti has pioneered new standards of care for gum disease and dental implant success. He has contributed research journals and medical articles in local periodicals to raise awareness of health issues impacting the Central Valley.

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Fusobacterium nucleatum serves as a critical bridging organism in periodontal biofilm development and an emerging mechanistic link between periodontitis and ischemic stroke through systemic inflammation, bacteremia, and pro-atherogenic pathways. The specificity of the F. nucleatum–stroke association among periodontal pathogens magnifies the need for regular oral care targeting F. nucleatum which will have particular relevance for cerebrovascular disease prevention.

 In conclusion, it has been demonstrated that the qualitative positivity for F. nucleatum in the oral cavity was independently associated with high-grade brain lesions and high-grade total stroke score in patients with ischemic stroke. Thus, daily oral care and professional cleaning by your dentist targeting F. nucleatum are essential to impede stroke progression.

Periodontal disease, which is a persistent bacterial infection causing chronic inflammation in the periodontal tissues, is characterized by the loss of connective tissue and alveolar bone support, resulting in tooth loss.

Periodontitis plays a leading role in the cause of stroke, through its contribution in promoting atherosclerosis via systemic inflammation and bacteremia. This link is supported by multiple meta-analyses and has been formally recognized in a 2025 American Heart Association (AHA) Scientific Statement. Several cohort studies have demonstrated periodontal disease to be associated with an increased risk of ischemic stroke by 1.6-fold. Periodontal disease showed a dose-response relationship with stroke risk — incidence rates rose from 1.29/1000 person-years in periodontally healthy individuals to 5.03/1000 person-years in those with severe periodontal disease. Periodontal disease has been demonstrated to be significantly associated with the incidence of cardioembolic and thrombotic stroke and that regular dental care was related to a lower adjusted stroke risk. Periodontal disease is an established risk factor for ischemic stroke.

Periodontal disease is associated with increased systemic inflammatory markers through exposure to Gram-negative bacteria, which may be implicated in the cause of stroke. The oral microbiota comprises >700 bacterial species, several of which have been identified as periodontal pathogens. Fusobacterium nucleatum (F. nucleatum) appears to be associated with poor clinical outcomes following ischemic stroke. Studies have demonstrated that high relative rates of F. nucleatum in the tongue coating were significantly associated with the presence of brain lesions indicating stroke. Furthermore, positive rates for F. nucleatum were independently associated with high-grade stroke scores.

Periodontal disease has been associated with several systemic diseases, such as rheumatoid arthritis, diabetes, and atherosclerosis. One of the main mechanisms underlying these associations is low-grade inflammation, which is initiated in response to a dysbiotic microbial community in the periodontal pocket. This low-grade inflammation, with increased local and systemic pro-inflammatory cytokines levels, promotes a positive feedback loop resulting in microbial dysbiosis and continuous activation of the host immune response, producing pro-inflammatory cytokines that can reach various parts of the body, including the brain. The direct effects of certain periodontal pathogens via virulence factors have also been reported, where lipopolysaccharides (LPS) have been linked to alterations in the endothelial cells, disruption of the blood-brain barrier, and neuroinflammation. These factors presumably contribute to stroke progression.

F. nucleatum, which is a strictly anaerobic Gram-negative rod bacterium normally found in the oral cavity, is considered a periodontal pathogen as it is frequently isolated from lesions, produces several tissue irritants, and often aggregates with other periodontal pathogens as a bridge between early and late colonizers. F. nucleatum is able to pass through the blood–brain barrier, It is believed that the physiological effects of F. nucleatum are associated with stroke onset and progression. Moreover, increased serum antibody titers against F. nucleatum are associated with poor clinical outcomes following ischemic stroke.

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THOMAS E. BRAMANTI, DDS, PHD, INC 

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