Immunohistochemical demonstration of nerve fibers in the synovial fold of the human cervical facel joint

Abstract

The role of the intra-articular synovial fold as a source of facet joint pain is unclear, because the nature of nociceptive innervation in lumbar synovial folds is controversial, and there have been no such studies in cervical synovial folds. The present study aimed to demonstrate the presence of nerve fibers including nociceptive fibers in synovial folds of human cervical facet joints using immunohistochemistry. Synovial folds of cervical facet joints removed from patients undergoing cervical spine laminoplasty were analyzed immunohistochernically using antibodies to protein gene product 9.5, p 111-tubulin, substance P and calcitonin gene-related peptide. Many nerve fibers immunoreactive for protein gene product 9.5 and 111-tubulin were demonstrated both around blood vessels and as free fibers in the stroma of the synovial fold. Also, immunostaining showed the presence of free nerve fibers immunoreactive for substance P and calcitonin gene-related peptide in the stroma. The presence of putative nociceptive fibers in cervical synovial folds supports a possible role for these structures as a source of cervical facet joint pain. 0 3001 Orthopaedic Research Society. Published by

Ketorolac Reduces Spinal Astrocytic Activation and PAR1 Expression Associated with Attenuation of Pain after Facet Joint Injury

“…Color image is available online at www.liebertpub.com/neu injury. [5][6][7]43 Injured afferents release excitatory neuropeptides, such as substance P, glutamate, and calcitonin gene-related peptide, at their terminals that directly activate astrocytes and other glial cells in the spinal cord that can amplify neuronal excitability via the release of pro-inflammatory cytokines and prostaglandins. [25][26][27] Glial activation was observed here at 7 days after painful facet joint distraction (Fig.…”

“…1,2 The cervical facet joint is a common source of neck pain identified in clinical studies, 3,4 with mechanical reports also documenting nociceptor innervation of the capsule and its mechanical vulnerability for injury from non-physiologic joint and spine motions. [5][6][7] Despite reports suggesting that injury to the cervical facets is a major contributor to persistent neck pain, 8 the cellular mechanisms by which pain is initiated and maintained after joint injury have yet to be defined.…”

The influence of age, anthropometrics and range of motion on the morphometry of the synovial folds of the lateral atlanto-axial joints: a pilot study

“…At the lateral atlanto-axial joints, the synovial folds fill the ventral and dorsal articular recesses created by the incongruence of the convex hyaline articular cartilage surfaces [50]. Based on the presence of nerve fibres and the demonstration of substance-P-like and calcitonin gene-related protein-like immunoreactivity within the synovial folds, it is suggested that the synovial folds are potential sources of pain [19,21,26]. Pain originating from the synovial folds of the lateral atlanto-axial joints may manifest as neck pain, which might refer to the head, producing headache [1,6].…”

A novel rodent neck pain model of facet-mediated behavioral hypersensitivity: implications for persistent pain and whiplash injury

“…In clinical studies of patients reporting painful neck injury, the facet joint has been identified in 25-62% of cases as the site of pain (Aprill and Bogduk, 1992;Barnsley et al, 1994), with the C5-C7 spinal levels being the most commonly reported site of injury in whiplash (Barnsley et al, 1995;Bogduk and Marsland, 1998). Histologic studies of rabbit, rat, and cadaveric human tissue have identified nociceptive nerve fibers throughout the structures of the facet joint, including the joint's capsular ligament (Giles and Harvey, 1987;McLain, 1994;Cavanaugh et al, 1996;Inami et al, 2001;Ohtori et al, 2001). These studies imply that neural input from the facet joint due to loading of the entire joint or any of its tissue elements has the potential for initiating and/or modulating pain sensation.…”