On the Mechanical Behaviour of Intervertebral Discs

Kb, Broberg

doi:10.1097/00007632-198303000-00006

Cited by 121 publications

(67 citation statements)

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“…The annulus fibrosus of lumbar IVDs were dissected free from their upper and lower vertebrae after the NP and inner AF as well as the surrounding ligaments were discarded. AF tissues were minced into small pieces (\1 mm 3 ) and then digested with 0.2% pronase (Roche) for 90 min followed by overnight digestion with 0.025% collagenase Type II (Sigma), 0.01% hyaluronidase Type V (Sigma) in a gyratory shaker (110 rev/min) at 37°C. Then tissue debris was passed through a 70 lm mesh to obtain a single-cell suspension.…”

Section: Methodsmentioning

confidence: 99%

Cyclic stretch-induced apoptosis in rat annulus fibrosus cells is mediated in part by endoplasmic reticulum stress through nitric oxide production

et al. 2011

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Various mechanical stresses in vivo induce disc cell apoptosis and intervertebral disc (IVD) degeneration, but the underlying molecular mechanism is not fully known. The aim of this study was to investigate the role of endoplasmic reticulum stress in cyclic stretch-induced apoptosis of rat annulus fibrosus (AF) cells. Flexercell Tension Plus system was used to apply cyclic stretch to rat annulus fibrosus cells at a frequency of 0.5 Hz with 20% elongation for 12, 24, 36, or 48 h. Apoptosis was detected by flow cytometry, and nuclei morphologic changes were visualized by Hoechst 33258 staining and caspase-8, 9 activity assays. The expression of the markers of endoplasmic reticulum stress including CHOP, GRP78, and caspase-12 were determined by RT-PCR and Western blot. Mitochondrial membrane potential change was observed by JC-1 staining in situ. In addition, the levels of the nitric oxide (NO) were determined with the Griess reaction and fluorescence staining. The results indicated that cyclic stretch at a frequency of 0.5 Hz with 20% elongationinduced apoptosis in rat AF cells. Prolonged exposure of the unphysiologically cyclic stretch to AF cells caused NO overproduction, up-regulation of endoplasmic reticulum stress markers including CHOP, GRP78, and caspase-12, depolarization of mitochondria and activation of caspase-9. However, cyclic stretch at this level had no effect on caspase-8 activity. In addition, specific inhibitor of caspase-12 (Z-ATAD-FMK) and caspase-9 (Z-LEHD-FMK) partly suppressed cyclic stretch-induced AF cell apoptosis and the anti-apoptotic effects of the caspase inhibitors were additive. Our data suggest that endoplasmic reticulum stress, likely mediated by NO, contributes to the AF cell apoptosis induced by cyclic stretch in addition to the mitochondrial pathway. These findings could be helpful to understand the mechanism of disc cell apoptosis, the root cause of IVD degeneration.

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Section: Methodsmentioning

confidence: 99%

Cyclic stretch-induced apoptosis in rat annulus fibrosus cells is mediated in part by endoplasmic reticulum stress through nitric oxide production

et al. 2011

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“…Both endplates have load-bearing functions and prevent the IVD from entering the vertebrae [7], and in humans, is involved in vertebral growth [32]. The VEP, with its relatively thick epiphyseal ring at the outer margin in the adult spine, where there is no CEP, is thinner and more porous in the centre [39], [40]; similarly the depth of the CEP becomes narrower towards its centre [27], [19].…”

Section: Introductionmentioning

confidence: 99%

Staying connected: structural integration at the intervertebral disc–vertebra interface of human lumbar spines

et al. 2016

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Purpose:To investigate the microscopic fibrous integration between the intervertebral disc, cartilage endplates and vertebral endplates in human lumbar spines of varying degrees of degeneration using differential interference contrast (DIC) optics. Weakness at these junctions is considered to be an important factor in the aetiology of disc herniations. Methods:Magnetic resonance images (MRIs) of cadaveric lumbar spines were graded for degeneration and motion segments from a range of degenerative grades isolated and bisected sagittally. Following fixation and decalcification, these were cut into segments containing anterior or posterior annulus fibrosus or nucleus pulposus. The segments were cryo-sectioned and sections visualised using both standard light and DIC microscopy. Results:Detachment at the interface between the disc and vertebrae increased with greater degenerative grade (from 1.9% in Grade I to 28% in Grade V), especially at the boundary between the cartilage and vertebral endplates. DIC microscopy revealed the fibrous organisation at the IVD-cartilage endplate interface with structural features, such as annular lamellae branching and nodal insertions in the nucleus pulposus region; these have been previously observed in ovine spines, but were less uniform in humans.Structural integrity of the IVD and cartilage endplate was also lost with increasing degeneration. Conclusions:This preliminary study shows that microscopic structural features may act to maintain attachment between the IVD and CEP in the human spine. Loss of structural integrity in this region may destabilise the spine, possibly altering the mechanical environment of the cells in the disc and so potentially contribute to the aetiopathogenesis of IVD degeneration.

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“…At the cranial and caudal ends of each disc are the endplates that separate the vertebral bone from the disc itself and prevent the highly hydrated nucleus from bulging into the adjacent vertebrae. The endplates also absorb the considerable hydrostatic pressure that results from mechanical loading of the spine [10]. The endplates are typically less than 1 mm thick, and while this varies considerably across the width of any single disc, they tend to be thinnest in the central region adjacent to the nucleus [16,44].…”

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confidence: 99%

The vertebral endplate: disc degeneration, disc regeneration

2006

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The vertebral endplates are critical for maintaining disc function yet like other components of the disc are vulnerable to degeneration. This paper provides an overview of the development and normal function of the endplates as well as an impression of what happens when they undergo progressive degeneration. Recent research suggests that the degenerative process can be retarded or reversed.Keywords Disc AE Endplate AE Degeneration AE Regeneration ManuscriptDespite all that is known from decades of research the intervertebral disc remains an enigma. It is a unique and remarkable entity and perhaps the one aspect that is responsible for much of its mystery is that such a large structure is able to survive and function under the most difficult physiological conditions. The discs of the human spine are the largest non-vascularised structures in the body, and in the largest of them (in the lumbar spine) some cells can be 20 mm from the nearest direct blood supply. Despite their apparent resilience however, the resident cells are not immortal. It is not unusual for discs to show signs of deterioration by the age of 25 years and it is in this regard that the vertebral endplate plays an important role.Discs are roughly cylindrical structures that vary in size and shape progressively from the cervical to the lumbar region. They all comprise a well-hydrated central nucleus pulposus that is surrounded by the firm but flexible collagenous lamellae of the annulus fibrosus [40]. At the cranial and caudal ends of each disc are the endplates that separate the vertebral bone from the disc itself and prevent the highly hydrated nucleus from bulging into the adjacent vertebrae. The endplates also absorb the considerable hydrostatic pressure that results from mechanical loading of the spine [10]. The endplates are typically less than 1 mm thick, and while this varies considerably across the width of any single disc, they tend to be thinnest in the central region adjacent to the nucleus [16,44].The endplates are identifiable from an early embryological stage and have an osseous as well as a hyaline cartilage component [50]. The cartilaginous component appears to generate great interest since it persists throughout normal maturation while the adjacent vertebrae undergo ossification. It comprises a gel of hydrated proteoglycan molecules reinforced by a network of collagen fibrils. Unlike the articular cartilage of the synovial joints the collagen fibrils do not connect the endplate directly to the vertebral bone [22], although the endplate does have intimate contact with the disc through the lamellae of the inner annulus [21]. A network of microscopic blood vessels penetrates the endplates during development of the growing spine, principally to provide nutrition for the disc, before disappearing around the time of skeletal maturity [50]. Apart from a sparse vascular supply in the outer

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On the Mechanical Behaviour of Intervertebral Discs

Cited by 121 publications

References 0 publications

Cyclic stretch-induced apoptosis in rat annulus fibrosus cells is mediated in part by endoplasmic reticulum stress through nitric oxide production

Cyclic stretch-induced apoptosis in rat annulus fibrosus cells is mediated in part by endoplasmic reticulum stress through nitric oxide production

Staying connected: structural integration at the intervertebral disc–vertebra interface of human lumbar spines

The vertebral endplate: disc degeneration, disc regeneration

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