Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters.

The facet joint is a common source of neck pain, particularly after excessive stretch of its capsular ligament. Peptidergic afferents have been shown to have an important role in the development and maintenance of mechanical hyperalgesia, dysregulated nociceptive signaling, and spinal hyperexcitability that develop after mechanical injury to the facet joint. However, the role of non-peptidergic isolectin-B4 (IB4) cells in mediating joint pain is unknown.

Pain from intra-articular NGF or joint injury in the rat requires contributions from peptidergic joint afferents.

Non-physiological stretch of the cervical facet joint's capsular ligament induces persistent behavioral hypersensitivity and spinal neuronal hyperexcitability via an intra-articular NGF-dependent mechanism. Although that ligament is innervated by nociceptors, it is unknown if a subpopulation is exclusively responsible for the behavioral and spinal neuronal responses to intra-articular NGF and/or facet joint injury. This study ablated joint afferents using the neurotoxin saporin targeted to neurons involved in either peptidergic ([Sar(9),Met (O2)(11)]-substance P-saporin (SSP-Sap)) or non-peptidergic (isolectin B4-saporin (IB4-Sap)) signaling to investigate the contributions of those neuronal populations to facet-mediated pain.

Thrombospondin-4 and excitatory synaptogenesis promote spinal sensitization after painful mechanical joint injury.

Facet joint injury induces persistent pain that may be maintained by structural plasticity in the spinal cord. Astrocyte-derived thrombospondins, especially thrombospondin-4 (TSP4), have been implicated in synaptogenesis and spinal sensitization in neuropathic pain, but the TSP4 response and its relationship to synaptic changes in the spinal cord have not been investigated for painful joint injury. This study investigates the role of TSP4 in the development and maintenance of persistent pain following injurious facet joint distraction in rats and tests the hypothesis that excitatory synaptogenesis contributes to such pain.

Increased interleukin-1α and prostaglandin E2 expression in the spinal cord at 1 day after painful facet joint injury: evidence of early spinal inflammation.

Study Design: This study used immunohistochemistry and an enzyme immunoassay to quantify interleukin-1α (IL-1α) and prostaglandin E2 (PGE2) levels in the spinal cord of rats at 1 day after painful cervical facet joint injury.

Objective: The objective of this study was to determine to what extent spinal inflammation is initiated early after a painful loading-induced injury of the C6-C7 facet joint in a rat model.

Summary Of Background Data: A common source of neck pain, the cervical facet joint is susceptible to loading-induced injury, which can lead to persistent pain.

Brain-derived neurotrophic factor is upregulated in the cervical dorsal root ganglia and spinal cord and contributes to the maintenance of pain from facet joint injury in the rat.

The facet joint is commonly associated with neck and low back pain and is susceptible to loading-induced injury. Although tensile loading of the cervical facet joint has been associated with inflammation and neuronal hyperexcitability, the mechanisms of joint loading-induced pain remain unknown. Altered brain-derived neurotrophic factor (BDNF) levels are associated with a host of painful conditions, but the role of BDNF in loading-induced joint pain remains undefined.

An anatomical and immunohistochemical characterization of afferents innervating the C6-C7 facet joint after painful joint loading in the rat.

Study Design: This study used retrograde neuronal tracing and immunohistochemistry to identify neurons innervating the C6-C7 facet joint and those expressing calcitonin gene-related peptide (CGRP) in the dorsal root ganglion (DRG) of rats after painful cervical facet joint injury.

Objective: The objective of this study was to characterize the innervation of the C6-C7 facet joint after painful joint injury in the rat.

Summary Of Background Data: The cervical facet joint is a source of neck pain, and its loading can initiate persistent pain.

The prostaglandin E2 receptor, EP2, is upregulated in the dorsal root ganglion after painful cervical facet joint injury in the rat.

Study Design: This study implemented immunohistochemistry to assay prostaglandin E2 (PGE2) receptor EP2 expression in the dorsal root ganglion (DRG) of rats after painful cervical facet joint injury.

Objective: To identify if inflammatory cascades are induced in association with cervical facet joint distraction-induced pain by investigating the time course of EP2 expression in the DRG.

Summary Of Background Data: The cervical facet joint is a common source of neck pain, and nonphysiological stretch of the facet capsular ligament can initiate pain from the facet joint via mechanical injury.