E2 ModeratePreliminaryPEM unclearObservationalPeer-reviewedMachine draft
Undetected Jawbone Marrow Defects as Inflammatory and Degenerative Signaling Pathways: Chemokine RANTES/CCL5 as a Possible Link Between the Jawbone and Systemic Interactions?
Lechner, Johann, Schmidt, Marlene, von Baehr, Volker et al. · Journal of inflammation research · 2021 · DOI
Quick Summary
This study examined jawbone abnormalities in 301 patients with various chronic illnesses, including ME/CFS. Researchers found that patients with bone loss in the jawbone had elevated levels of a chemical messenger called RANTES/CCL5, which promotes inflammation. These findings were consistent across all disease groups studied, suggesting that jawbone problems may contribute to systemic inflammation in multiple conditions.
Why It Matters
For ME/CFS patients, this study suggests that undetected jawbone pathology could be a previously overlooked source of systemic inflammation via chemokine signaling. If validated, identifying and treating BMDJ might represent a novel therapeutic approach to reducing the chronic inflammation associated with ME/CFS and other immune-mediated conditions.
Observed Findings
- All 301 patients with BMDJ showed significantly decreased bone density (negative Hounsfield unit values indicating osteolysis)
- All BMDJ cases demonstrated consistently elevated RANTES/CCL5 expression regardless of disease classification
- BMDJ and R/C overexpression were detected across all seven disease groups without disease-specific patterns
- Bone density measurements and R/C expression were correlated in all surgical cases examined
Inferred Conclusions
- Bone marrow defects of the jawbone may represent a shared inflammatory mechanism across diverse systemic immune diseases
- RANTES/CCL5 chemokine signaling arising from jawbone pathology could contribute to systemic inflammation in multiple conditions including ME/CFS
- BMDJ may be an underrecognized but potentially modifiable source of chronic inflammatory signaling
Remaining Questions
- Is BMDJ actually more prevalent in patients with these diseases compared to healthy controls, and what is the baseline prevalence in the general population?
- Does surgical treatment of BMDJ actually improve patient outcomes and disease symptoms, particularly in ME/CFS?
- What is the mechanistic relationship between BMDJ and systemic R/C elevation—is it causative or correlative?
What This Study Does Not Prove
This study does not establish causation—it cannot prove that BMDJ causes systemic disease or that treating BMDJ will improve ME/CFS symptoms. It lacks a control group of healthy patients without BMDJ, so it cannot determine whether BMDJ and elevated RANTES/CCL5 are truly abnormal or how prevalent they are in the general population. The cross-sectional design and small sample sizes within disease subgroups limit generalizability.
Tags
Symptom:PainFatigue
Biomarker:Cytokines
Method Flag:Weak Case DefinitionNo ControlsExploratory OnlyMixed Cohort
Metadata
- DOI
- 10.2147/JIR.S307635
- PMID
- 33911892
- Review status
- Machine draft
- Evidence level
- Single-study or moderate support from human research
- Last updated
- 8 April 2026
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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