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      Intradiscal platelet-rich plasma (PRP) injections for discogenic low back pain: an update

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          Most cited references 29

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          The prevalence and clinical features of internal disc disruption in patients with chronic low back pain.

          This was a cross-sectional analytic study of patients with chronic low back pain. To investigate whether the criteria for internal disc disruption, as adopted by the International Association for the Study of Pain, could be satisfied in patients with chronic low back pain and to test whether there were any conventional clinical features that could identify this condition. Internal disc disruption has been postulated as an important cause of low back pain. To diagnose this condition, the International Association for the Study of Pain taxonomy requires that pain be reproduced on provocation discography and that computed tomography discography reveal internal disc disruption, provided that as a control, stimulation of at least one other disc fails to reproduce pain. Ninety-two consecutive patients with chronic low back pain and no history of previous lumbar surgery were studied. Each patient underwent a standard physical examination. Computed tomography discography was performed at a minimum of two levels. The diagnostic criteria for internal disc disruption were fully satisfied in 39% of patients, most commonly at L5-S1 and L4-L5. None of the clinical tests used could differentiate between those patients with internal disc disruption and other patients. A diagnosis of internal disc disruption can be made in a significant proportion of patients with chronic low back pain, but no conventional clinical test can discriminate patients with internal disc disruption from patients with other conditions.
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            Histology and pathology of the human intervertebral disc.

            The intervertebral disc is a highly organized matrix laid down by relatively few cells in a specific manner. The central gelatinous nucleus pulposus is contained within the more collagenous anulus fibrosus laterally and the cartilage end plates inferiorly and superiorly. The anulus consists of concentric rings or lamellae, with fibers in the outer lamellae continuing into the longitudinal ligaments and vertebral bodies. This arrangement allows the discs to facilitate movement and flexibility within what would be an otherwise rigid spine. At birth, the human disc has some vascular supply within both the cartilage end plates and the anulus fibrosus, but these vessels soon recede, leaving the disc with little direct blood supply in the healthy adult. With increasing age, water is lost from the matrix, and the proteoglycan content also changes and diminishes. The disc-particularly the nucleus-becomes less gelatinous and more fibrous, and cracks and fissures eventually form. More blood vessels begin to grow into the disc from the outer areas of the anulus. There is an increase in cell proliferation and formation of cell clusters as well as an increase in cell death. The cartilage end plate undergoes thinning, altered cell density, formation of fissures, and sclerosis of the subchondral bone. These changes are similar to those seen in degenerative disc disease, causing discussion as to whether aging and degeneration are separate processes or the same process occurring over a different timescale. Additional disorders involving the intervertebral disc can demonstrate other changes in morphology. Discs from patients with spinal deformities such as scoliosis have ectopic calcification in the cartilage end plate and sometimes in the disc itself. Cells in these discs and cells from patients with spondylolisthesis have been found to have very long cell processes. Cells in herniated discs appear to have a higher degree of cellular senescence than cells in nonherniated discs and produce a greater abundance of matrix metalloproteinases. The role that abnormalities play in the etiopathogenesis of different disorders is not always clear. Disorders may be caused by a genetic predisposition or a tissue response to an insult or altered mechanical environment. Whatever the initial cause, a change in the morphology of the tissue is likely to alter the physiologic and mechanical functioning of the tissue.
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              Investigation of the role of IL-1 and TNF in matrix degradation in the intervertebral disc.

              To establish if IL-1 or TNF regulates matrix degradation in the non-degenerate or degenerate intervertebral disc (IVD). In situ zymography (ISZ) has been used to investigate the role of IL-1 and TNF in the matrix degradation characterizing symptomatic IVD degeneration. ISZ employed three substrates (gelatin, collagen II, casein) and four different challenges, IL-1beta, IL-1 receptor antagonist (IL-1Ra), TNF-alpha and anti-TNF. We have shown for the first time that whilst IL-1beta will stimulate and IL-1 receptor antagonist will inhibit matrix degradation in intact human IVD tissue, neither TNF-alpha nor anti-TNF have any measurable effect on degradation of these matrices. This study has addressed a current area of controversy in IVD biology, namely, whether either IL-1 or TNF or both are involved in driving matrix degradation. Our data indicate that IL-1 is a key cytokine mediating matrix degradation in the IVD and therefore a therapeutic target.
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                Author and article information

                Journal
                International Orthopaedics
                International Orthopaedics (SICOT)
                Springer Nature
                0341-2695
                1432-5195
                June 2016
                April 12 2016
                : 40
                : 6
                : 1321-1328
                Article
                10.1007/s00264-016-3178-3
                © 2016

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