Deans' stroke musings: Oral health as a modifiable risk factor for neurodegeneration: Prudent optimism and interdisciplinary action

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, June 4, 2025

Oral health as a modifiable risk factor for neurodegeneration: Prudent optimism and interdisciplinary action

Your competent? doctor has had oral health protocols for 7 years already, right? NO? So, you DON'T have a functioning stroke doctor, do you?

oral health (5 posts to March 2018)

Oral health as a modifiable risk factor for neurodegeneration: Prudent optimism and interdisciplinary action

https://doi.org/10.1016/j.jocn.2025.111354 Get rights and content

Highlights

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Periodontitis is potentially linked to neurodegeneration via different pathways.
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Tooth loss and impaired chewing may accelerate cognitive decline.
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Salivary biomarkers offer a possible tool for early neurodegeneration detection.
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Interdisciplinary collaboration between dentists and neurologists is crucial.

Abstract

Neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD), represent a growing public health burden, necessitating exploration of modifiable risk factors. Emerging evidence suggests a link between poor oral health, particularly chronic periodontitis, and neurodegeneration, mediated by systemic inflammation, direct bacterial invasion, and disruptions in the microbiota-gut-brain axis. Periodontal pathogens, such as Porphyromonas gingivalis, have been suggested to contribute to neuroinflammation, blood–brain barrier dysfunction, and amyloid-beta aggregation, all of which are implicated in AD pathology. Additionally, tooth loss and masticatory dysfunction could further exacerbate cognitive decline through reduced cerebral stimulation and impaired nutrient absorption. While the association between periodontitis and neurodegeneration is compelling, causality remains uncertain, warranting further longitudinal and interventional studies. Interdisciplinary collaboration between neurologists and dental professionals is essential to establish oral health as a potential preventive strategy for neurodegenerative diseases. Routine periodontal screenings, improved oral hygiene awareness, and early intervention could help mitigate cognitive decline. Moreover, salivary biomarkers show promise as non-invasive tools for early detection of neurodegeneration. Addressing socioeconomic and healthcare disparities in access to both dental and neurological care is crucial in minimizing disease burden. Future research should focus on mechanistic studies and randomized trials to determine whether and how periodontal interventions can influence neurodegenerative disease progression.