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Anti-RANKL antibodies decrease CGRP expression in dorsal root ganglion neurons innervating injured lumbar
Masashi Sato1, Kazuhide Inage, Yoshihiro Sakuma
1Department of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Summary
Anti-receptor activator of NF-κB ligand (RANKL) antibodies reduced inflammatory markers and sensory nerve activation in injured intervertebral discs. This suggests RANKL is a potential therapeutic target for managing disc degeneration pain.
Area of Science:
- Neuroscience
- Immunology
- Orthopedics
Background:
- Nuclear factor-κB (NF-κB), receptor activator of NF-κB (RANK), and RANK ligand (RANKL) regulate inflammatory cytokines.
- Elevated RANKL expression in dorsal root ganglion (DRG) neurons is observed in pain models and intervertebral disc herniation.
Purpose of the Study:
- To investigate the impact of anti-RANKL antibodies on sensory nerves within injured intervertebral discs.
Main Methods:
- DRG neurons innervating L5-L5 discs were labeled in rats.
- Intervertebral discs underwent puncture or sham surgery, followed by saline or anti-RANKL antibody administration.
- DRGs were analyzed for calcitonin gene-related peptide (CGRP) expression, and inflammatory markers (TNF-α, IL-6) were quantified.
Main Results:
- Injured discs showed significantly increased CGRP, TNF-α, and IL-6 levels compared to sham controls.
- Anti-RANKL antibody treatment significantly reduced CGRP, TNF-α, and IL-6 in injured discs.
Conclusions:
- Increased TNF-α, IL-6, and CGRP expression in injured discs was suppressed by anti-RANKL antibodies.
- RANKL inhibition offers a potential therapeutic strategy for pain associated with lumbar disc degeneration.
