• Masayuki Miyagi, Seiji Ohtori, Tetsuhiro Ishikawa, Yasuchika Aoki, Tomoyuki Ozawa, Hideo Doya, Tomoko Saito, Hideshige Moriya, and Kazuhisa Takahashi.
• Department of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, 260-8670 Chiba, Japan.
• Eur Spine J. 2006 Jun 1; 15 (6): 953-8.

AbstractThe rat L5/6 facet joint, from which low back pain can originate, is multisegmentally innervated from the L1 to L5 dorsal root ganglia (DRG). Sensory fibers from the L1 and L2 DRG are reported to non-segmentally innervate the paravertebral sympathetic trunks, while those from the L3 to L5 DRGs segmentally innervate the L5/6 facet joint. Tumor necrosis factor alpha (TNFalpha) is a mediator of peripheral and central nervous system inflammatory response and plays a crucial role in injury and its pathophysiology. In the current study, change in TNFalpha in sensory DRG neurons innervating the L5/6 facet joint following facet joint injury was investigated in rats using a retrograde neurotransport method and immunohistochemistry. Neurons innervating the L5/6 facet joints, retrogradely labeled with fluoro-gold (FG), were distributed throughout DRGs from L1 to L5. Most DRG FG-labeled neurons innervating L5/6 facet joints were immunoreactive (IR) for TNFalpha before and after injury. In the DRG, glial fibrillary acidic protein (GFAP)-IR satellite cells emerged and surrounded neurons innervating L5/6 facet joints after injury. These satellite cells were also immunoreactive for TNFalpha. The numbers of activated satellite cells and TNFalpha-IR satellite cells were significantly higher in L1 and L2 DRG than in L3, L4, and L5 DRG. These data suggest that up-regulation of glial TNFalpha may be involved in the pathogenesis of facet joint pain.

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