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.

Abstract

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.

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