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Spine J. 2015 Jun 1;15(6):1347-55. doi: 10.1016/j.spinee.2013.07.490. Epub 2014 Mar 20.

Pathomechanisms of discogenic low back pain in humans and animal models.

Author information

1
Department of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan. Electronic address: sohtori@faculty.chiba-u.jp.
2
Department of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
3
Department of Orthopaedic Surgery, Kitasato University, School of Medicine, 1-15-1 Kitasato, Minami, Sagamihara, Kanagawa, 252-0374, Japan.

Abstract

BACKGROUND CONTEXT:

Although explored in humans and animal models, the pathomechanisms of discogenic low back pain (LBP) remain unknown.

PURPOSE:

The aim of this study was to review the literature about the pathomechanisms of discogenic LBP.

METHODS:

Animal models of discogenic pain and specimens from degenerated human intervertebral discs (IVDs) have provided clues about the pathomechanisms of discogenic LBP. Painful discs are characterized by a confluence of innervation, inflammation, and mechanical hypermobility. These three possible mechanisms are discussed in this review.

RESULTS:

Animal models and specimens from humans have revealed sensory innervation of lumbar IVDs and sensory nerve ingrowth into the inner layer of IVDs. Cytokines such as tumor necrosis factor-α and interleukins induce this ingrowth. Nerve growth factor has also been recently identified as an inducer of ingrowth. Finally, disc degeneration induces several collagenases; their action results in hypermobility and pain.

CONCLUSIONS:

To treat discogenic LBP, it is important to prevent sensitization of sensory nerve fibers innervating the IVD, to suppress pathogenic increases of cytokines, and to decrease disc hypermobility.

KEYWORDS:

Hypermobility; Inflammation; Intervertebral disc; Pain; Psychosocial factors; Sensory nerve

PMID:
24657737
DOI:
10.1016/j.spinee.2013.07.490
[Indexed for MEDLINE]
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