Biochemical and morphological changes in herniated human intervertebral disc

Ahsan, Rashedul; Tajima, Naoya; Chosa, Etsuo; Sugamata, Masao; Sumida, Michihiro; Hamada, Minoru

doi:10.1007/s007760100006

Cited by 43 publications

(47 citation statements)

References 22 publications

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“…It has been demonstrated that collagen II decreased while collagen I increased when intervertebral disc degenerates (Ahsan et al, 2001). As shown in our results, there was less collagen II expression in the calcified layer of the cartilage endplate and nucleus pulposus of aged rats compared with the young control group.…”

Section: Discussionsupporting

confidence: 83%

Features of intervertebral disc degeneration in rat’s aging process

Zhang

Sun

Liu

et al. 2009

J. Zhejiang Univ. Sci. B

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Abstract:Objective: The age-related change is important part of degenerative disc disease. However, no appropriate animal model or objective evaluation index is available. This study aimed to investigate the features of intervertebral disc degeneration in aging process of rats. Methods: 22-month-old Sprague-Dawley (SD) rats were used as spontaneously occurring intervertebral disc degeneration models and 6-month-old rats as young controls. Expression of collagen types II and X was measured by immunohistochemistry. Degenerations of intervertebral discs were scored according to Miyamoto's method. Numbers and areas of afferent vascular buds were measured. The thicknesses of non-calcified and calcified layers were measured and statistically analyzed. Results: There were less collagen type II expression and more collagen type X expression in the calcified layer of the cartilage endplates and nucleus pulposus in the rats of the aged group than in the young control. There were fewer and smaller afferent vascular buds in the rats of the aged group than in the young control group. The ratio of the non-calcified to the calcified layers in the rats of the aged group significantly decreased, compared with that of the young control group (P<0.01). Conclusion: Rats can spontaneously establish intervertebral disc age-related degeneration. The expression of collagen types II and X, numbers and areas of afferent vascular buds, the ratio of the non-calcified to the calcified layers, and water and glycosaminoglycan contents in the nucleus pulposus are sensitive indexes of intervertebral disc degeneration.

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Section: Discussionsupporting

confidence: 83%

Features of intervertebral disc degeneration in rat’s aging process

Zhang

Sun

Liu

et al. 2009

J. Zhejiang Univ. Sci. B

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“…Considering results which were obtained from disc herniation models [2,31], the initial post-traumatic and degenerative changes are likely comparatively complex. Numerous pathobiological changes and inflammatory cascades, such as the induction of programmed cell death (apoptosis), chemotactic recruitment of leukocytes and the activation of matrix-degrading metalloproteinases (MMPs) can be expected [4,27,51].…”

Section: Introductionmentioning

confidence: 99%

Vertebral endplate trauma induces disc cell apoptosis and promotes organ degeneration in vitro

et al. 2007

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There is a major controversy whether spinal trauma with vertebral endplate fractures can result in posttraumatic disc degeneration. Intervertebral discs, which are adjacent to burst endplates, are frequently removed and an intercorporal spondylodesis is performed. In any case, the biological effects within the discs following endplate factures are poorly elucidated to date. The aim of our investigations was therefore to establish a novel disc/endplate trauma culture model to reproducibly induce endplate fractures and investigate concurrent disc changes in vitro. This model is based on a full-organ disc/endplate culture system, which has been validated by the authors before. Intervertebral disc/endplate specimens were isolated from Burgundy rabbits and cultured in standard media (DMEM/ F12, 10%FCS). Burst endplate fractures were induced in half of the specimens with a custom-made fracture device and subsequently cultured for 9 days. The biological effects such as necrotic or apoptotic cell death and the expression of pro-apoptotic genes and other genes involved in organ degeneration, e.g. matrix metalloproteinases (MMPs) were analyzed. Cell damage was assessed by quantification of the lactate dehydrogenase (LDH) activity in the supernatant. The expression of genes involved in the cellular apoptotic pathway (caspase 3) and the pro-apoptotic proteins FasL and TNF-a were monitored. The results demonstrate that LDH levels increased significantly post trauma compared to the control and remained elevated for 3 days. Furthermore, a constant up-regulation of the caspase 3 gene in both disc compartments was present. The pro-apoptotic proteins FasL and TNF-a were up regulated predominantly in the nucleus whereas the MMP-1 and -13 transcripts (collagenases) were increased in both disc structures. From this study we can conclude that endplate burst fractures result in both necrotic and apoptotic cell death in nucleus and annulus tissue. Moreover, FasL and TNF-a expression by nucleus cells may lead to continued apoptosis induced by Fas-and TNF-a receptor bearing cells. In addition TNF-a over-expression has potentially deleterious effects on disc metabolism such as overexpression of matrix proteinases. Taken together, the short term biological response of the disc following endplate fracture exhibits characteristics, which may initiate the degeneration of the organ.

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“…We have been able to show similar results for osteochondrotic discs. In studies on herniated disc material, apoptosis was previously shown to play a major role [41]. In our study, the opposite side of the disc of the herniation was analysed.…”

Section: Discussionmentioning

confidence: 93%