Esperimental and clinical study on spontaneous regression mechanisms of lumbar disc herniation

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In the experimental study, adult mongrel dogs were used. Under general anesthesia, the caudal vertebral disc was removed and divided into nucleus pulposus and annulus fibrosus. After laminectomy at L6, the L7nerve root was exposed and the previously harvested nucleus pulposus tissue was placed on in while avoiding mechanical pressure. The animals were sacrificed 1 week and 3 weeks later. Nucleus pulposus samples removed from the caudal vertebrae were used as a control. At 1 and 3 weeks after surgery, the nucleus pulposus tissue showed involution and there was angiogenesis from the surrounding tissue along with the appearance of T cells and macrophages. Within the nucleus pulposus, the notochordal cells, chondrocytes, and macrophages were positive for IL-1 β,TNF-α,i-NOS, and MMP-3. Degeneration of nerve fibers or the appearance of inflammatory cells, including T cells and macrophages, was not observed in the nerve root.In the clinical study, we examined surgical lumbar disc herniation specimens by light microscopy, and investigated the localization and function of macrophages using immunohistochemical techniques. Vascularization and macrophage infiltration of the hernia tissue were evident in 21.7% from subligamentous extrusion hernias. In all of the patients with trasligamentous extrusion and sequestration hernias, macrophages were seen inside the hernia tissue, with many being present around newly formed blood vessels. Examination of serial sections confirmed that macrophages were positive for IL-1βi-NOS, and MMP-3. The macrophages that infiltrate herniated tissue play an important role in the breakdown and removal of extracellular matrix by producing various chemical mediators. In conclusion, inflammatory changes induced by nucleus pulposus tissue are considered to be an important factor in reducing herniation and resolving radiculopathy, while it seems unlikey that chemical factors produced within the inflammatory zone are the principal cause of radiculopathy.