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We are analyzing https://link.springer.com/article/10.1007/s00586-006-0126-8.

Title:
Senescence in human intervertebral discs | European Spine Journal
Description:
Intervertebral discs demonstrate degenerative changes relatively early in life. Disc degeneration, in turn, is associated with back pain and disc herniation, both of which cause considerable clinical problems in the western world. Cell senescence has been linked to degenerative diseases of other connective tissues such as osteoarthritis. Thus we investigated the degree of cell senescence in different regions of discs from patients with different disc disorders. Discs were obtained from 25 patients with disc herniations; from 27 patients undergoing anterior surgery for either back pain due to degenerative disc disease (n = 25) or spondylolisthesis (n = 2) and from six patients with scoliosis. In addition, four discs were obtained post-mortem. Samples were classified as annulus fibrosus or nucleus pulposus and tissue sections were assessed for the degree of cell senescence (using the marker senescence-associated-β-galactosidase (SA-β-Gal)) and the number of cells present in clusters. There were significantly more SA-β-Gal positive cells in herniated discs (8.5% of cells) than those with degenerative disc disease, spondylolisthesis, scoliosis, or cadaveric discs (0.5% of cells; P < 0.001). There was more senescence of cells of the nucleus pulposus compared to those of the annulus fibrosus and in herniated discs a higher proportion of cells in cell clusters (defined as groups of three or more cells) were SA-β-Gal positive (25.5%) compared to cells not in clusters (4.2%, P < 0.0001). This study demonstrates an increased degree of cell senescence in herniated discs, particularly in the nucleus where cell clusters occur. These clusters have been shown previously to form via cell proliferation, which is likely to explain the increased senescence. These findings could have two important clinical implications: firstly, that since senescent cells are known to behave abnormally in other locations, they may lead to deleterious effects on the disc matrix and so contribute to the pathogenesis and secondly, cells from such tissue may not be ideal for cell therapy and repair via tissue engineering.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

article, cell, google, scholar, senescence, disc, pubmed, cells, intervertebral, discs, cas, spine, human, roberts, degeneration, clusters, access, privacy, cookies, content, journal, degenerative, osteoarthritis, tissue, proliferation, lumbar, res, chondrocyte, publish, research, search, eisenstein, patients, herniated, cellular, aging, eur, data, european, information, log, june, evans, kletsas, back, pain, herniation, degree, nucleus, saβgal,

Topics {✒️}

month download article/chapter pressure-induced cellular senescence sa-β-gal positive cells sa-β-gal positive full article pdf intervertebral disc herniation european economic area sa-β-gal intervertebral disc degeneration privacy choices/manage cookies lumbar disc degeneration human intervertebral discs related subjects intervertebral disc cells normal human cells lumbar intervertebral discs degenerative disc disease treating disc degeneration oxidative stress intervertebral disc aging journal finder publish considerable clinical problems cell clusters occur important clinical implications rabbit carotid arteries cell-based therapeutics cell cluster formation clin orthop 427s mrs janis menage mrs lynne murphy agnes hunt orthopaedic cellular senescence conditions privacy policy bone jt surg[ mammary cell proliferation back pain due low back pain article log accepting optional cookies disc herniation scope submit manuscript obtained post-mortem pereira-smith om author information authors limiting cartilage repair ageing disc degeneration article cite check access catabolism access

Schema {🗺️}

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         headline:Senescence in human intervertebral discs
         description:Intervertebral discs demonstrate degenerative changes relatively early in life. Disc degeneration, in turn, is associated with back pain and disc herniation, both of which cause considerable clinical problems in the western world. Cell senescence has been linked to degenerative diseases of other connective tissues such as osteoarthritis. Thus we investigated the degree of cell senescence in different regions of discs from patients with different disc disorders. Discs were obtained from 25 patients with disc herniations; from 27 patients undergoing anterior surgery for either back pain due to degenerative disc disease (n = 25) or spondylolisthesis (n = 2) and from six patients with scoliosis. In addition, four discs were obtained post-mortem. Samples were classified as annulus fibrosus or nucleus pulposus and tissue sections were assessed for the degree of cell senescence (using the marker senescence-associated-β-galactosidase (SA-β-Gal)) and the number of cells present in clusters. There were significantly more SA-β-Gal positive cells in herniated discs (8.5% of cells) than those with degenerative disc disease, spondylolisthesis, scoliosis, or cadaveric discs (0.5% of cells; P < 0.001). There was more senescence of cells of the nucleus pulposus compared to those of the annulus fibrosus and in herniated discs a higher proportion of cells in cell clusters (defined as groups of three or more cells) were SA-β-Gal positive (25.5%) compared to cells not in clusters (4.2%, P < 0.0001). This study demonstrates an increased degree of cell senescence in herniated discs, particularly in the nucleus where cell clusters occur. These clusters have been shown previously to form via cell proliferation, which is likely to explain the increased senescence. These findings could have two important clinical implications: firstly, that since senescent cells are known to behave abnormally in other locations, they may lead to deleterious effects on the disc matrix and so contribute to the pathogenesis and secondly, cells from such tissue may not be ideal for cell therapy and repair via tissue engineering.
         datePublished:2006-06-14T00:00:00Z
         dateModified:2006-06-14T00:00:00Z
         pageStart:312
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            Herniation
            Degeneration
            Cell clusters
            Stress-induced-premature-senescence (SIPS)
            Catabolism
            Surgical Orthopedics
            Neurosurgery
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      headline:Senescence in human intervertebral discs
      description:Intervertebral discs demonstrate degenerative changes relatively early in life. Disc degeneration, in turn, is associated with back pain and disc herniation, both of which cause considerable clinical problems in the western world. Cell senescence has been linked to degenerative diseases of other connective tissues such as osteoarthritis. Thus we investigated the degree of cell senescence in different regions of discs from patients with different disc disorders. Discs were obtained from 25 patients with disc herniations; from 27 patients undergoing anterior surgery for either back pain due to degenerative disc disease (n = 25) or spondylolisthesis (n = 2) and from six patients with scoliosis. In addition, four discs were obtained post-mortem. Samples were classified as annulus fibrosus or nucleus pulposus and tissue sections were assessed for the degree of cell senescence (using the marker senescence-associated-β-galactosidase (SA-β-Gal)) and the number of cells present in clusters. There were significantly more SA-β-Gal positive cells in herniated discs (8.5% of cells) than those with degenerative disc disease, spondylolisthesis, scoliosis, or cadaveric discs (0.5% of cells; P < 0.001). There was more senescence of cells of the nucleus pulposus compared to those of the annulus fibrosus and in herniated discs a higher proportion of cells in cell clusters (defined as groups of three or more cells) were SA-β-Gal positive (25.5%) compared to cells not in clusters (4.2%, P < 0.0001). This study demonstrates an increased degree of cell senescence in herniated discs, particularly in the nucleus where cell clusters occur. These clusters have been shown previously to form via cell proliferation, which is likely to explain the increased senescence. These findings could have two important clinical implications: firstly, that since senescent cells are known to behave abnormally in other locations, they may lead to deleterious effects on the disc matrix and so contribute to the pathogenesis and secondly, cells from such tissue may not be ideal for cell therapy and repair via tissue engineering.
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         Degeneration
         Cell clusters
         Stress-induced-premature-senescence (SIPS)
         Catabolism
         Surgical Orthopedics
         Neurosurgery
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