Seiji Ohtori1, Gen Inoue2, Masayuki Miyagi3, Kazuhisa Takahashi2. 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.
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.
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