The Journal of Bone and Joint Surgery (American). 2006;88:63-67.
doi:10.2106/JBJS.E.01411
© 2006 The Journal of Bone and Joint Surgery, Inc.
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Pain Generation in Lumbar and Cervical Facet Joints

John M. Cavanaugh, MD, Ying Lu, MS, Chaoyang Chen, MD and Srinivasu Kallakuri, MS

Corresponding author:
John M. Cavanaugh, MD
Bioengineering Center, Wayne State University, 818 West Hancock, Detroit, MI 48202.
E-mail address: cavanau{at}rrb.eng.wayne.edu

NOTE: The authors are grateful for the technical assistance of Amrita Vempati, Anita Singh, and Sowmya Surapaneni.

In support of their research for or preparation of this manuscript, one or more of the authors received grants or outside funding from the United States Centers for Disease Control and Prevention (CDC Grants # R49-CCR519751 and # R49-CE000455). None of the authors received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. A commercial entity paid or directed, or agreed to pay or direct, benefits to a research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated (a Ford Biomedical Engineering Graduate Fellowship was provided by the Ford Motor Company).

Facet joints are implicated as a major source of neck and low-back pain. Both cervical and lumbar facet syndromes have been described in the medical literature. Biomechanical studies have shown that lumbar and cervical facet-joint capsules can undergo high strains during spine-loading. Neuroanatomic studies have demonstrated free and encapsulated nerve endings in facet joints as well as nerves containing substance P and calcitonin gene-related peptide. Neurophysiologic studies have shown that facet-joint capsules contain low-threshold mechanoreceptors, mechanically sensitive nociceptors, and silent nociceptors. Inflammation leads to decreased thresholds of nerve endings in facet capsules as well as elevated baseline discharge rates. Recent biomechanical studies suggest that rear-end motor-vehicle impacts give rise to excessive deformation of the capsules of lower cervical facet joints. Still unresolved is whether this stretch is sufficient to activate nociceptors in the joint capsule.

To answer this question, recent studies indicate that low stretch levels activate proprioceptors in the facet-joint capsule. Excessive capsule stretch activates nociceptors, leads to prolonged neural afterdischarges, and can cause damage to the capsule and to axons in the capsule. In instances in which a whiplash event is severe enough to injure the joint capsule, facet capsule overstretch is a possible cause of persistent neck pain.


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