• Seiji Ohtori, Kazuhisa Takahashi, and Hideshige Moriya.
• Department of Orthopaedic Surgery, School of Medicine, Chiba University, Chiba, Japan. sohtori@ucsd.edu
• Eur Spine J. 2003 Apr 1;12(2):211-5.

AbstractPatients with cervical facet lesions and facet joint injury sometimes experience diffuse neck pain, headache, and arm and shoulder pain. However, the pathophysiology of the intensity and expansion of facet joint pain has not yet been investigated. Retrograde transport of fluoro-gold (F-G) and immunohistochemistry of calcitonin gene-related peptide (CGRP) was used in 20 rats (control group, n=10; injured group, n=10). For the injured group, the whole facet capsule was incised. Of the total F-G labelled dorsal root ganglion (DRG) neurons innervating the C5/6 facet joint, the number and the cross-sectional area of cell profiles of F-G labelled CGRP-ir neurons were evaluated in the bilateral DRGs of both groups. The numbers of CGRP-ir F-G labelled DRG neurons as a percentage of all F-G labelled DRG neurons at C3, C4, C5, C6, C7, C8, T1, T2, and T3 respectively were 30, 22, 43, 47, 21, 19, 25, 36 and 30% in the control group, and 13, 15, 23, 17, 15, 8, 16, 28 and 35% in the injured group, with the injured group showing a significantly lower percentage of CGRP-ir F-G labelled neurons than the control group at C5 and C6 (P<0.05). However, the mean cross-sectional area of F-G labelled CGRP-ir cells from C3 to C8 DRGs increased from 625+/-22 micro m(2) to 878+/-33 micro m(2) in the injured group (P<0.001). Associated with the injured facet joints, the phenotypic switch to large neurons may complicate the mechanism of injured facet pain.

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