Lechner, J, Huesker, K, Von Baehr, V · Journal of biological regulators and homeostatic agents · 2017
This study investigated whether inflammation in the jawbone might contribute to ME/CFS. Researchers compared jawbone tissue from 21 ME/CFS patients with tissue from 19 healthy people and found that ME/CFS patients had significantly higher levels of inflammatory proteins (RANTES and FGF-2) in areas of jawbone that had undergone incomplete healing. The authors suggest that this hidden jawbone inflammation might be a previously unknown trigger for ME/CFS.
If confirmed, this research could identify a treatable source of inflammation in ME/CFS patients, potentially opening new diagnostic and therapeutic avenues. The hypothesis that localized jawbone pathology contributes to systemic ME/CFS symptoms expands understanding of potential disease mechanisms and may explain why some patients report symptom improvement after dental interventions.
This study does not prove that FDOJ causes ME/CFS—it only shows correlation in a small sample. The cross-sectional design cannot establish temporal relationships or rule out reverse causation. Additionally, elevated inflammatory markers in jawbone tissue do not necessarily establish that this tissue is the primary driver of systemic ME/CFS symptoms rather than a secondary manifestation.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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