Pray for P.
Google
To regulators, research institutions, and professional bodies overseeing dental and neurological health,
Rates of neurodegenerative disease have risen during the same period in which invasive dental interventions have become routine and lifelong. Temporal overlap does not establish causation. It does establish an obligation to investigate correlation with rigor proportionate to potential harm.
Modern dentistry assumes that devitalizing or sealing teeth reliably eliminates pathogenic risk. This assumption conflicts with established microbiological principles: bacteria persist in sequestered anatomy, biofilms resist eradication, and immune activation can continue in the absence of pain. These facts are well documented across medicine. Their implications for dentistry—particularly endodontic procedures—remain insufficiently examined.
Root canal therapy warrants specific scrutiny. It intentionally devitalizes tissue and depends on achieving asepsis, not sterility, within anatomically complex spaces that cannot be directly verified in vivo. These spaces are largely inaccessible to immune surveillance. Absence of pain is treated as evidence of success despite limited means of confirming durable microbial resolution, particularly given the diagnostic limitations of standard two-dimensional imaging in detecting chronic periapical pathology.
Separately, oral pathogens, inflammatory markers, and microbial byproducts have been identified in extra-oral tissues, including the central nervous system. Research linking Porphyromonas gingivalis and its gingipain enzymes to Alzheimer’s pathology underscores the plausibility of oral–neurological pathways. While periodontal disease has received primary attention, the contribution of endodontically treated teeth as long-term microbial reservoirs remains comparatively under-studied.
Tooth extraction must therefore be included as a biological comparator. Unlike tooth-preserving procedures, extraction removes the entire diseased structure and eliminates the local microbial reservoir by definition. While extraction carries functional and economic tradeoffs, it does not depend on unverifiable assumptions of internal microbial control.
In parallel, routine preventive dental care requires critical re-evaluation. Professional cleanings indisputably involve repeated mechanical abrasion using sharp, rigid instruments of largely unchanged design. By their nature, these tools cause cumulative enamel and dentin damage. The long-term consequences of this repeated micro-trauma—particularly its role in increasing susceptibility to decay, infection, and subsequent invasive intervention—remain insufficiently quantified.
The development and adoption of demonstrably lower-damage cleaning technologies would permit more frequent preventive care without cumulative structural harm.
This letter makes no accusation. It calls for resolution.
Josef Bartol
