New research from South Korea suggests Streptococcus mutans—the same bacteria behind cavities—may play a surprising role in Parkinson’s disease. Discover how this finding could reshape the way we view oral-systemic health.
By Paige Anderson, CRDH
For many years, the conversation about the link between oral and systemic health has centered around periodontal disease and chronic inflammation. But new research from Sungkyunkwan University School of Medicine in South Korea suggests that caries-causing bacteria may also have systemic implications.
The study, published in Nature Communications in September of this year, has revealed a potential direct causative link between Streptococcus mutans and Parkinson’s disease (PD). While the findings are based on a mouse model and not yet definitive for humans, the results provide compelling evidence that an enzyme produced by this common cariogenic microbe could play a role in triggering Parkinson's-like changes in the brain.
Looking Beyond Periodontal Pathogens
The most well-known oral-systemic links involve periodontal bacteria such as Porphyromonas gingivalis or Fusobacterium nucleatum, which are associated with inflammatory pathways affecting the heart, brain, and joints. In contrast, S. mutans is typically viewed as a localized threat only responsible for enamel demineralization and dental caries.
The new research challenges that assumption. It suggests that even microbes we associate primarily with tooth decay may have far-reaching effects, particularly if they migrate beyond the oral cavity. This study is among the first to implicate a cariogenic rather than periodontal pathogen in a neurodegenerative process.
What We Already Knew
Over the past decade, scientists have increasingly explored connections between the gut microbiome and Parkinson’s disease. Multiple studies have found that people with PD often have altered gut microbial communities and distinct metabolic profiles.
The prevailing theory has been that oral and gut dysbiosis promotes systemic inflammation and abnormal signaling through the gut-brain axis, possibly contributing to the misfolding and aggregation of α-synuclein, the hallmark protein associated with Parkinson’s.
However, most of these studies have been correlational and have not demonstrated a causative link. That’s what makes this new finding so intriguing. It suggests a possible direct causative pathway involving a single bacterial enzyme and its metabolic product.
The New Study
Professor Ara Koh and doctoral candidate Hyunji Park collaborated with Professor Han-Joon Kim of Seoul National University College of Medicine to lead the study. Together, the group showed that S. mutans can produce an enzyme called urocanate reductase (UrdA), which converts urocanate (a compound derived from histidine) into imidazole propionate (ImP).
In turn, the study showed that ImP can enter the bloodstream, reach the brain, and contribute to the loss of dopaminergic neurons, demonstrating a direct, causative pathway from oral dysbiosis to the development of PD.
Mouse Model Findings
The researchers colonized mice with S. mutans strains that express UrdA. They also introduced engineered E. coli capable of producing the same enzyme. In both cases, mice showed elevated systemic and brain levels of ImP.
These mice developed motor impairments, loss of dopaminergic neurons, neuroinflammation, and α-synuclein aggregation, which are all hallmarks of Parkinson’s pathology. Even when ImP was administered directly (without bacteria), the same neurodegenerative effects occurred.
Further, when the scientists blocked the signaling pathway, many of these effects were reversed, suggesting a clear mechanistic link.
Limitations and Cautions
While this evidence is compelling, it’s important to recognize the limitations. Since this study used a mouse model, it obviously doesn’t completely replicate human microbiology or neurophysiology. The presence of S. mutans in the gut generally doesn’t occur in humans at levels comparable to those in the study.
Likewise, more research is needed to definitively show whether PD leads to microbial changes in humans or vice versa.
Still, these findings align with a growing body of evidence that oral bacteria and their metabolites can influence systemic inflammation, vascular function, and now, potentially, neurodegeneration.
Clinical Implications for Dental Professionals
As dental professionals, most of us are all too aware of how a Parkinson’s diagnosis can directly affect our patients’ oral health. From bruxism to difficulty maintaining adequate oral hygiene at home, PD has direct effects on oral health outcomes. Likewise, PD can affect our treatment planning, sometimes necessitating the use of sedation to calm tremors and at other times making us hesitant to recommend sedation at all.
However, this study reinforces a familiar but powerful message: oral health is whole-body health.
While the link between S. mutans and PD remains to be proven in humans, the research offers a new reason to emphasize caries prevention and bacterial load reduction, not just for dental health but also for overall wellbeing.
In practical terms, here’s how we can integrate this understanding into our daily practice:
- Reinforcing the value of home care: Encourage patients to brush twice daily with fluoride toothpaste, floss regularly, and consider antimicrobial rinses when indicated.
- Targeting caries risk factors: Control dietary sugar intake and promote remineralization strategies.
- Early detection and microbial control: Identify high caries activity early and intervene to reduce S. mutans colonization through professional cleanings, sealants, or fluoride treatments.
- Patient education: Explain that maintaining oral hygiene could play a role in protecting long-term brain health.
- Interprofessional collaboration: As systemic research evolves, collaboration between dentistry, neurology, and microbiology may yield valuable preventive insights.
Even if this microbial-Parkinson’s pathway ultimately proves to be one of several contributing mechanisms, it underscores how profoundly interconnected the mouth and body truly are.
Author: Paige Anderson is a certified registered dental hygienist with eight years of clinical experience and an English degree. She blends her two areas of expertise to create resources for dental providers so they can change lives by giving their patients the highest possible standard of care.
