Related Experiment Video
Updated: Oct 28, 2025

Author Spotlight: Insights and Innovations in Gene Expression Manipulation Techniques for Choroid Plexus Research
Published on: June 16, 2023
RANTES/CCL5 Signaling from Jawbone Cavitations to Epistemology of Multiple Sclerosis - Research and Case Studies
Johann Lechner1, Volker von Baehr2, Fabian Schick1
1Clinic for Integrative Dentistry, Munich, Germany.
Background:
The role played by signaling pathways in the cell-cell communication associated with multiple sclerosis (MS) progression has become a critical area in research. Chemokine RANTES (regulated upon activation, normal T-cell expressed and secreted), also named chemokine C-C motif ligand 5 (CCL5; R/C), is a protein that has been investigated in neuroinflammatory research due to its link to MS development.
Objective:
Research on bone marrow defects in the jawbone (BMDJ), which morphologically presents as fatty-degenerative osteonecrosis of the jawbone (FDOJ), presents overexpression of R/C signaling in affected areas. Here, we try to elucidate the potential link between jawbone-derived R/C and MS.
Methods:
Seventeen BMDJ/FDOJ samples extracted from 17 MS patients, as well as samples from 19 healthy controls, were analyzed for R/C expression using bead-based Luminex® analysis. The serum R/C levels from 10 MS patients were examined. Further, bone density, histology, and R/C expression were analyzed in two clinical case studies.
Results:
High R/C overexpression was found in all BMDJ/FDOJ samples obtained from the MS group. Serum R/C levels were also upregulated in the MS group. R/C serum levels in the MS cohort were higher than in the healthy controls. In contrast, the histology of BMDJ/FDOJ samples showed no inflammatory cells.
Discussion:
R/C-induced "silent inflammation" in MS is widely discussed in the scientific literature, along with R/C triggering of inflammation in the central nervous system, which might be key in the development of MS.
Conclusion:
The authors suspect that BMDJ/FDOJ may serve as a trigger of MS progression via R/C overexpression. As such, the dental and medical communities should be made aware of BMDJ/FDOJ in cases of MS.
Insights
Jawbone defects in multiple sclerosis (MS) patients show high levels of chemokine RANTES (CCL5). This suggests jawbone issues may trigger MS progression through RANTES signaling.
Area of Science:
- Neuroimmunology
- Oral pathology
- Biochemistry
Background:
- Cell-cell communication via signaling pathways is crucial in multiple sclerosis (MS) progression.
- Chemokine RANTES (regulated upon activation, normal T-cell expressed and secreted), also known as chemokine C-C motif ligand 5 (CCL5), is implicated in neuroinflammation and MS development.
Purpose of the Study:
- To investigate the potential link between jawbone RANTES (CCL5) overexpression and MS.
- To explore if bone marrow defects in the jawbone (BMDJ), presenting as fatty-degenerative osteonecrosis of the jawbone (FDOJ), are associated with MS.
Main Methods:
- Analysis of RANTES (CCL5) expression in 17 BMDJ/FDOJ samples from MS patients and 19 healthy controls using Luminex analysis.
- Measurement of serum RANTES (CCL5) levels in 10 MS patients.
- Histological and bone density analysis of BMDJ/FDOJ samples.
Main Results:
- Significant RANTES (CCL5) overexpression was detected in all BMDJ/FDOJ samples from the MS group.
- Elevated serum RANTES (CCL5) levels were observed in MS patients compared to healthy controls.
- BMDJ/FDOJ histology revealed no inflammatory cells, suggesting "silent inflammation".
Conclusions:
- BMDJ/FDOJ may act as a trigger for MS progression due to RANTES (CCL5) overexpression.
- The findings highlight the need for awareness of BMDJ/FDOJ in MS patients among dental and medical professionals.
- RANTES (CCL5)-mediated "silent inflammation" in the central nervous system could be a key factor in MS development.
More Related Videos
09:46Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
Published on: September 21, 2021
08:47Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Related Concept Videos
The JAK-STAT Signaling Pathway
Rous Sarcoma Virus (RSV) and Cancer
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
Cystic Fibrosis: Pathogenesis
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies