Inflammatory Cells in Experimental Intervertebral Disc Injury

Kanerva, Anna; Kommonen, Bertel; Grönblad, Mats; Tolonen, Jukka; Habtemariam, Aklilu; Virri, Johanna; Karaharju, Erkki

doi:10.1097/00007632-199712010-00002

Cited by 57 publications

(43 citation statements)

References 14 publications

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“…Different animal models of the annular defect have shown that the healing is defective and probably initiates degeneration of the disc. [29][30][31][32] The tears demonstrated at the periphery of the annulus fibrosus may play a critical role in discogenic low back pain and the initiation of degenerative changes. The formation of vascularised granulation tissue may be a physiological response to repair the injury to the annulus.…”

Section: Discussionmentioning

confidence: 99%

The pathogenesis of discogenic low back pain

Peng

Wu²,

Hou³

et al. 2005

The Journal of Bone and Joint Surgery. British volume

309

202

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Discogenic low back pain is a common cause of disability, but its pathogenesis is poorly understood. We collected 19 specimens of lumbar intervertebral discs from 17 patients with discogenic low back pain during posterior lumbar interbody fusion, 12 from physiologically ageing discs and ten from normal control discs. We investigated the histological features and assessed the immunoreactive activity of neurofilament (NF200) and neuropeptides such as substance P (SP) and vasoactive-intestinal peptide (VIP) in the nerve fibres.The distinct histological characteristic of the painful disc was the formation of a zone of vascularised granulation tissue from the nucleus pulposus to the outer part of the annulus fibrosus along the edges of the fissures. SP-, NF-and VIP-immunoreactive nerve fibres in the painful discs were more extensive than in the control discs. Growth of nerves deep into the annulus fibrosus and nucleus pulposus was observed mainly along the zone of granulation tissue in the painful discs. This suggests that the zone of granulation tissue with extensive innervation along the tears in the posterior part of the painful disc may be responsible for causing the pain of discography and of discogenic low back pain.

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Section: Discussionmentioning

confidence: 99%

The pathogenesis of discogenic low back pain

Peng

Wu²,

Hou³

et al. 2005

The Journal of Bone and Joint Surgery. British volume

309

202

View full text Add to dashboard Cite

show abstract

“…Disc tissue, especially NP, has been reported to possess inflammatory properties [7,4], and can secrete cytokines [14] that are closely related to the metabolism of osteoblast [17]. Furthermore, exposure of NP, which is normally excluded from circulation, to the fusion environment may also cause some immune reactions [4,7,13]. Our previous in vitro study showed that disc tissue could influence the metabolism of osteoblastlike cells [9].…”

Section: Haisheng LI Xuenong Zou Malene Laursen Niels Egund Martin Limentioning

confidence: 99%

The influence of intervertebral disc tissue on anterior spinal interbody fusion: an experimental study on pigs

Zou

Laursen

et al. 2002

European Spine Journal

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Intervertebral disc has been shown to be related to low back pain and nerve root injury in pathologic conditions. However, little is known about its influence on spinal fusion. With the development of minimal invasive operations, such as laparoscopic anterior spinal fusion with cages, insufficient discectomy may occur. With its inflammatory properties, the residue nucleus pulposus may have an effect on spinal fusion. In this study, a two-level lumbar spine interbody fusion (L3/4, L5/6) with a Brantigan cage was performed on ten Danish Landrace pigs. Each level was randomly assigned to one of the following methods: (1) implantation of Brantigan cage filled with autogenous iliac crest bone graft, or (2) implantation of Brantigan cage filled with a mixture of autograft and the nucleus pulposus tissue harvested from the disc level in which it was to be inserted. Each level was stabilized with two staples. The pigs were followed for 12 weeks in the same standardized condition. After sacrifice, the lumbar spines were taken out, and plain X-ray, computed tomographic (CT) scanning and histomorphometry were performed to study the fusion mass inside the cages. From plain radiographs, new bone formation could be seen inside and around the cage. CT evaluation showed that the nucleus pulposus level had a 20% (2/10) fusion rate, while the pure autograft level had a 70% (7/10) fusion rate ( P=0.07). The histological fusion rate was even lower in the nucleus pulposus level (10%), and was significantly different from the autograft level (70%, P=0.02). Histomorphometric parameters of new bone formation, bone marrow space and fibrous tissue differed significantly between the two levels ( P=0.04; P=0.02; P=0.04 respectively). We conclude that when nucleus pulposus is mixed with the autogenous bone graft, it can delay or decrease the bone formation inside the cage, thus influencing the final fusion.

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“…Although mechanical nerve root compression may contribute to the symptoms of radiculopathy, it is currently believed that an inflammatory or immune component is the key mediator of radicular pain (1,2). The nucleus pulposus (NP) tissue may be autoantigenic; this theory is supported by the accumulation of lymphocytes in regional lymph nodes following exposure to autologous NP (3) and injury to the annulus fibrosus (4). A number of animal studies applied healthy autologous NP to spinal nerve roots, as a model of non-compressive disc herniation, which induced an inflammatory and immune response resulting in neuronoglial apoptosis, a decrease in nerve conduction velocity, the onset of gait abnormality, mechanical allodynia and thermal hyperalgesia (5)(6)(7)(8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Role of interleukin-17 in chondrocytes of herniated intervertebral lumbar discs

Tian¹,

Li²,

Fu³

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Lumbar disc herniation (LDH) is a common cause of lumbosacral radiculopathy. An autoimmune response to a herniated nucleus pulposus (NP) has been suggested to play an important role in the initiation of radiculopathy. Interleukin-17 (IL-17) is a cytokine associated with inflammation and autoimmunity. The presence of IL-17 has been studied in patients with LDH; however, extensive investigation into the expression of IL-17 in different disc pathologies of LDH has not yet been conducted. The aim of the present study was to investigate the role of neovascularization and hypertrophic chondrocytes in herniated intervertebral lumbar discs. Fifty-two intervertebral lumbar disc specimens were extracted from 46 patients with LDH and were subsequently classified as either contained or non-contained disc herniation (CDH and NCDH, respectively). The specimens were stained with hematoxylin and eosin or toluidine blue, or were immunostained with polyclonal antibodies to IL-17 using the streptavidin-peroxidase method. The neovascular tissue and staining results were graded to establish the histological differences between the two herniation types. The intervertebral discs (IVDs) obtained from patients with NCDH showed significantly more neovascularization and granulation tissue than the discs obtained from patients with CDH (P<0.05). Furthermore, hypertrophic chondrocytes were more abundant in the NCDH specimens than in the CDH specimens (P<0.05). Similarly, the number of IL-17-immunoreactive cells was significantly higher in the NCDH specimens than that in the CDH specimens (P<0.01).In conclusion, local inflammation and autoreactive immune activation may play an important role in the pathogenesis of LDH. These results also suggest a role of chondrocytes in the repair of herniated IVDs.

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Inflammatory Cells in Experimental Intervertebral Disc Injury

Cited by 57 publications

References 14 publications

The pathogenesis of discogenic low back pain

The pathogenesis of discogenic low back pain

The influence of intervertebral disc tissue on anterior spinal interbody fusion: an experimental study on pigs

Role of interleukin-17 in chondrocytes of herniated intervertebral lumbar discs

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