Physiopathology of disc herniation I. Physiological degeneration of the lumbar disc Physiological degeneration is an age-related biological change, i.e., the aging process, which is not the same as the pathological process, but there is not a clear boundary between physiological degeneration and pathological process. The degeneration of the intervertebral disc starts at the age of 20-30 years and is most obvious after 30-40 years. 1, the degeneration of the fibrous ring type (1) type: edge type that is fibrous ring tear (2) type: annular tear (3) type: radial fissure 2, the degeneration of the cartilage end plate: adults about 1MM thick and the edge of its connection with the epiphyseal ring is about 10MM wide, the main degeneration performance is thinning, calcification, incomplete, and produce cartilage cystic degeneration and chondrocyte necrosis. The cartilage plate is not neurovascular so it cannot be regenerated and repaired. 3, the nucleus pulposus degeneration: the main manifestation is the reduction of water content type 2 loss of glial elements, that is, the reduction in the number of functional cells II, the pathology of herniated disc (a) the morphological changes of the herniated disc tissue fiber ring and nucleus pulposus tissue containing 70% to 80% water, these tissues are gradually lost after the protrusion of water and lack of nutrition and crumpled. Three types of disc calcification: receding cervical disc, dormant disc, and resting disc are not associated with signs and symptoms Three conditions of intervertebral space narrowing: lumbar 5 vertebral body anisotropy, due to rupture of the annulus fibrosus and protrusion of nucleus pulposus material into the vertebral body or into the spinal canal through the fissure of the annulus fibrosus.3 Due to disc dehydration and fibrosis, not associated with rupture of the annulus fibrosus or protrusion through the endplate of the cartilage. cartilage endplate protrusion is unrelated. (ii) SCHMORI’s nodule and transosseous protrusion (1) SCHMORI’s nodule is the vertical entry of the nucleus pulposus into the vertebral body either upward or downward through the cartilage plate. It occurs when the cartilage endplate is defective and the nucleus pulposus is still elastic, and the following changes can occur: 1. The vertebral body is locally fractured and necrotic, forming a cavity to accommodate the herniated nucleus pulposus, around which there is an inflammatory response to absorb the necrotic tissue. 2, the herniated nucleus pulposus may gradually or rapidly increase in size until the pressure of the herniation is balanced with the counter pressure. The herniated nucleus pulposus may be dehydrated and surrounded by myelinated chondrocytes or osteocytes, with increased density of surrounding trabeculae limiting its expansion. 4. Blood vessels regenerate around the herniated nucleus pulposus and enter the intervertebral disc through the cartilage plate fissure, leading to fibrosis, calcification and ossification of the nucleus pulposus. (2) Transosseous protrusion X-ray shows three forms: 1, ruptured nucleus pulposus type 2, post-absorptive proliferation type 3, lip type 3, pathological typing and clinical typing (a) pathological typing: the forties are divided into fixed and active types. Now divided into five types: 1, peripheral fibular ring bulge 2, limited fibular ring protrusion 3, disc protrusion 4, disc prolapse 5, disc free. (b) The relationship between clinical and pathological typing The three-type typing of bulging, ruptured and free is the unification of pathological and clinical concepts. IV. Neuropathology of lumbar disc herniation (a) Relationship between lumbar disc herniation and nerve roots, the relationship between the level of lumbar nerve root emanation and the intervertebral disc and the herniated disc 2 The site and mode of nerve root compression by the herniated disc 3 The relative position of the herniated disc and the nerve root (b) Mechanisms of nerve root compression by lumbar disc herniation: distraction mechanism, compression mechanism, relevant mechanisms for sciatica relief (c) Pathological changes of compressed nerve roots Classification of deformation of compressed nerve roots: local compression in the contact area, distraction local compression of nerve roots in the contact area is often mechanical, when the nerve root is compressed and deformed, all nerve fibers, adjacent tissues and intra-neural vessels are compressed and deformed. In the case of local compression, the nerve fibers can be divided into a central compression area and a marginal compression area, also known as the marginal effect. The nerve damage is most pronounced at the margin due to its greatest mechanical compression deformation. Two forms of functional alterations of nerve roots 1. reduction of nerve function: sensory impairment and reduced muscle strength, and diminished reflexes. 2, nerve root tissue hypersensitivity: (d) mechanism of neurological symptoms of lumbar disc herniation 1, mechanical compression theory 2, chemical radiculitis theory 3, autoimmune theory V. Secondary pathological changes of lumbar disc herniation 1, articular eminence joint 2, ligamentum flavum 3, degenerative lumbar spinal stenosis 4, degenerative lumbar spondylolisthesis 5 osteochondral formation (traction osteochondral outward flattening suggests instability, claw-type osteochondral arc outward. Divided into four degrees (1) bone edge for isolated proliferation point (2) bone superfluous larger with horizontal protrusion (3) beak-like (4) bone bridge formation. The bone floss is created as a response to enhance stability and counteract stress (reconstruction)