• Yoshiyuki Matsuyama, Yoshihiro Sakuma, Miyako Suzuki, Sumihisa Orita, Kazuyo Yamauchi, Gen Inoue, Yasuchika Aoki, Tetsuhiro Ishikawa, Masayuki Miyagi, Hiroto Kamoda, Gou Kubota, Yasuhiro Oikawa, Kazuhide Inage, Takeshi Sainoh, Jun Sato, Junichi Nakamura, Tomoaki Toyone, Kazuhisa Takahashi, and Seiji Ohtori.
• Department of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
• Asian Spine J. 2014 Oct 1;8(5):557-64.

Study DesignExperimental animal study.PurposeTo evaluate pain-related behavior and changes in nuclear factor-kappa B (NF-kB), receptor activator of NF-kB (RANK), and ligand (RANKL) in dorsal root ganglia (DRG) after combined sciatic nerve compression and nucleus pulposus (NP) application in rats.Overview Of LiteratureThe pathological mechanisms underlying pain from lumbar-disc herniation have not been fully elucidated. RANKL are transcriptional regulators of inflammatory cytokines. Our aim was to evaluate pain-related behavior and RANKL expression in DRG after sciatic-nerve compression and application of NP in rats.MethodsMECHANICAL HYPERALGESIA AND RANKL EXPRESSION WERE ASSESSED IN THREE GROUPS OF RATS: NP+sciatic nerve compression (2 seconds), sham-operated, and controls (n=20 each). Mechanical hyperalgesia was measured every other day for 3 weeks using von Frey filaments. RANKL expression in L5 DRGs was examined at five and ten days after surgery using immunohistochemistry.ResultsMechanical hyperalgesia was observed over the 12-day observation period in the NP+nerve compression group, but not in the control and sham-operated animal groups (p<0.05). RANKL immunoreactivity was seen in the nuclei of L5 DRG neurons, and its expression was significantly upregulated in NP+nerve compression rats compared with control and sham-operated rats (p<0.01).ConclusionsThe exposure of sciatic nerves to mechanical compression and NP produces pain-related behavior and up-regulation of RANKL in DRG neurons. RANKL may play an important role in mediating pain after sciatic nerve injury with exposure to NP.

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