Sensory nerve ingrowth, cytokines, and instability of discogenic low back pain: A review

REVIEW ARTICLE

Seiji Ohtori1), Masayuki Miyagi2), Gen Inoue2)

1) Department of Orthopaedic Surgery, Graduate School of Medicine Chiba University, Chiba, Japan
2) Department of Orthopaedic Surgery, Kitasato University, School of Medicine, Kanagawa, Japan

Abstract:

Introduction: Many patients suffer from discogenic low back pain. However, the mechanisms, diagnosistic strategy, and treatment of discogenic low back pain all remain controversial. The purpose of this paper was to review the pathological mechanisms of discogenic low back pain.
Methods: Many authors have investigated the pathological mechanisms of discogenic low back pain using animal models and examining human patients. Central to most investigations is understanding the innervation and instabilities of diseased intervertebral discs and the role of inflammatory mediators. We discuss three pathological mechanisms of discogenic low back pain: innervation, inflammation, and mechanical hypermobility of the intervertebral disc.
Results: Sensory nerve fibers include C-fibers and A delta-fibers, which relay pain signals from the innervated outer layers of the intervertebral disc under normal conditions. However, ingrowth of these sensory nerve fibers into the inner layers of intervertebral disc occurs under disease conditions. Levels of neurotrophic factors and some cytokines are significantly higher in diseased discs than in normal discs. Stablization of the segmental hypermobility, which can be induced by intervertebral disc degeneration, suppresses inflammation and prevents sensitization of sensory nerve fibers innervating the disc.
Conclusions: Pathological mechanisms of discogenic low back pain include sensory nerve ingrowth into inner layers of the intervertebral disc, upregulation of neurotrophic factors and cytokines, and instability. Inhibition of these mechanisms is important in the treatment of discogenic low back pain.

Released: January 27, 2018; doi: dx.doi.org/10.22603/ssrr.2016-0018