Morphologic changes on magnetic resonance imaging mainly corresponded to clinical outcomes but tended to lag behind improvement of leg pain. Disappearance of herniate nucleus pulposus was seen frequently in the cases of migrating disc herniation, and it was presumed that exposure to the vascular supply had a lot to do with this phenomenon.
Intervertebral disc herniation is a major cause of low back pain and sciatica. Spontaneous resorption of herniated disc (HD) is frequently detected by magnetic resonance imaging (MRI). Marked infiltration by macrophages and neo-vascuIarizatiol1~tioii are observed upon histogical exainiiiatioii of HD.
Intervertebral disc herniation (HD) is one of the most common orthopaedic conditions. MRI analysis of H D has revealed a spontaneous resorption mechanism related with neo-vascularization. It appears that the interaction of activated macrophages with disc tissues leads to the generation of inflammatory cytokines. Moreover, inflammatory cytokines such as tumor necrosis factor-a (TNF-a) is required for the induction of angiogenesis inducing factors such as vascular endothelial growth factor (VEGF) or matrix degrading enzymes such as MMP-3, MMP-7 and plasmin. We hypothesized that these molecules play a crucial role during spontaneous H D resorption. In this study, we have examined the sequential expression of these molecules using a co-culture system which is composed of the interaction of activated macrophages and disc tissues as a model of the acute response of inflammation occurred in HD. We have also considered the mechanism of activating latent MMPs during H D resorption process. Current our results indicate that upregulation of both TNF-cl mRNA and protein expressions occur first in the inflammation induced by HD. VEGF upregulation follows the increased level of TNF-a expression. Both plasmin and MMP-3 are upregulated at later time points. We also demonstrate that both TNF-a and VEGF induce upregulated expression of urokinase-type plasminogen activator (u-PA). Our previous work has demonstrated that TNF-(r could upregulate the expression of VEGF, MMP-3 and MMP-7 in the co-culture system. It has been reported that plasmin could affect to activate latent MMPs. Based on these findings, we suggest that TNF-a acts as the initiator of inflammation following contact between macrophages and disc chondrocytes and that plasmin and u-PA play a crucial role in activation of MMPs. We propose a spontaneous H D resorption cascade. Further understanding of the resorption process may provide future novel therapies for HD.
It has been suggested that matrix metalloproteinase-3 (MMP-3, stromelysin-1) has an important role in the degeneration of intervertebral discs (IVDs). A human MMP-3 promoter 5A/6A polymorphism was reported to be involved in the regulation of MMP-3 gene expression. We suggest that IVD degeneration is associated with 5A/6A polymorphism.We studied 54 young and 49 elderly Japanese subjects. Degeneration of the lumbar discs was graded using MRI in the younger group and by radiography in the elderly. 5A/6A polymorphism was determined by polymerase-chain reaction-based assays. We found that the 5A5A and 5A6A genotype in the elderly was associated with a significantly larger number of degenerative IVDs than the 6A6A (p < 0.05), but there was no significant difference in the young. In the elderly, the IVD degenerative scores were also distributed more highly in the 5A5A and 5A6A genotypes (p = 0.0029).Our findings indicate that the 5A allele is a possible risk factor for the acceleration of degenerative changes in the lumbar disc in the elderly. Low back pain (LBP) is one of the most common musculoskeletal disabilities, affecting from 70% to 80% of all people at some time. The annual prevalence ranges from 15% to 45%, with point prevalence averaging 30%.
1Degenerative changes in IVDs contribute to the development of LBP and the acute lumbar radiculopathy associated with herniation of a disc.2,3 These changes are a part of the normal ageing process. In a study of lumbar IVDs using MRI, the prevalence of degenerative IVDs was shown to increase linearly with age and 80% of all lumbar discs were abnormal at 70 years of age. 4 The exact physiopathological mechanism is, however, still unclear. Heavy physical loading, injury, vibration, infection and smoking have been reported to be risk factors. 5 Genetic factors also affect the degeneration and herniation of IVDs. 6 Recently, the relationship between IVD degeneration and polymorphism of genes such as the vitamin-D receptor, 7 type-IX collagen, 8 and aggrecan 9 has been investigated and the identification of such genetic factors may aid in the prediction and prevention of disc degeneration and LBP.
Segmental instability influences the whole lumbar motion in patients with degenerative spondylolisthesis. The patients with chronic low back pain did not show a significant difference when compared with the volunteers.
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