The intervertebral disc is an important component of the spine, of which there are 23 in the body. It is not only the main structure that connects and supports the vertebral body, but is also a key structure for spinal motion and weight-bearing. It consists of a hyaline cartilage plate, a fibrous annulus and a nucleus pulposus. The fibrous ring consists of multiple layers of fibrous tissue gathered around the nucleus pulposus, which is firmly attached to both ends of the vertebral body, arranged at a certain level, and forming a certain angle to pull the upper and lower vertebral bodies. The outer fibrous ring is in direct contact with the vertebral body and the medullary ring, and 90% of the fibrous ring tissue is attached between the medullary ring and the hyaline cartilage ring. The nucleus pulposus is in a semi-colloid state, containing 80% water, in addition to collagen and polyprotein-bound mucopolysaccharide acid, which is mainly a large molecule of chondroitin sulfate complex and small amounts of hyaluronate and keratin sulfate. (1) The nucleus pulposus cannot be compressed and is located in the posterior 1/3 of the intervertebral disc. The pressure on the fibrous ring and cartilage plate at all points is comparable, and a relative equilibrium is maintained between the intervertebral disc and the two small joints behind it. It is generally accepted that the nucleus pulposus of the intervertebral disc is at fluid rest, with an internal pressure equivalent to 1.3-1.5 times the interaxial compression load. Although the nucleus pulposus cannot be compressed, the composite structure composed of it and the fibrous ring and cartilage plate, etc., is compressible. This compressibility is closely related to time. When the disc is loaded for a long time, due to the interaction between the nucleus pulposus and the annulus fibrosus, the nucleus pulposus can transmit the load evenly in all directions and redistribute the stress so that the vertebral body is not damaged by excessive changes in stress and strain. This process does not involve fluid exchange, except for nucleus pulposus degeneration. The intervertebral disc has no blood supply but relies on the osmotic balance of water, solutes, glucosamine, proteins and collagen. Some tolerances enter through the cartilage plate or the fibrous ring. Throughout the process, it is the junction between the nucleus pulposus and the fibrous ring that is most deprived of nutrients. This is where the earliest cracking occurs when the intervertebral disc degenerates. From a biochemical and biomechanical analysis, these fissures, which are radial in shape, penetrate the annulus fibrosus, the cartilage and reach the ligament. Biochemically, the annulus fibrosus becomes hypertrophic and the fibers separate from each other, and the arrangement of the annulus surroundings becomes disturbed. The disc begins to narrow, the collagen fibers tilt and twist, and resistance to load, especially to twisting forces, is reduced. With age, the demarcation between the nucleus pulposus and the annulus fibrosus becomes unclear, the cellular component of the nucleus pulposus decreases, the fibrous component increases, and the nucleus pulposus dehydrates, while vacuoles are formed. (2) Due to the atrophy of the nucleus pulposus, the fibrous rings of the inner layer contract inward, while the fibrous rings of the outer and middle layers are pushed outward. As a result, the alignment of the fiber bundles between the inner and middle layers is reversed. In this way, the fibrous ring is herniated by external forces. From a biomechanical analysis: degeneration of the intervertebral disc is accompanied by causing instability of the intervertebral joint. The disc is in relative equilibrium with the two small joints behind it. This undoubtedly increases the load on the posterior articular eminence, increases the intra-articular pressure, changes in the intra-articular stress and increases the pressure and friction between the upper and lower articular eminences, which may cause minor damage to the articular surface, to swelling, necrosis, until degenerative changes, hyperplasia and even subluxation, leading to narrowing of the root canal and intervertebral foramen and compression of the nerve roots. In addition, the change in the mode of transmission of the vertebral body load, i.e., from central to peripheral, can cause clinical symptoms due to osteophytes, although a new balance can be achieved. Degeneration of the intervertebral disc begins with a whorl-like cracking of the posterior lateral fibrous ring. The posterior portion of the annulus fibrosus is weaker and its proteoglycan, collagen and water metabolic cycles are different from those of the anterolateral annulus. Of course, the degeneration is accompanied by a low metabolic activity of the nucleus pulposus and fibro-ring cells. (3) The initial stage of this degeneration may not produce clinical symptoms. The formation of degenerative tears is accompanied by a decrease in intravertebral disc pressure and biomechanical equilibrium, especially in the functioning of the spinal motor units and biological subtleties. If the imbalance in the intervertebral joint continues repeatedly, the synovium may develop an inflammatory response and pain. The whorl-like fissures of the posterior intervertebral disc fibrous ring continuously expand posteriorly and laterally. The fissures are interconnected to form radial fissures. If the internal pressure of the disc rises. The nucleus pulposus moves in the direction of the fissure, resulting in a herniated nucleus pulposus. At the beginning of the herniated nucleus pulposus, there is no significant change in the internal pressure of the disc, and narrowing of the vertebral space is uncommon from the x-ray features. Soon, the degenerative cracking of the intervertebral disc fibrous ring expands anteriorly and laterally, the fibrous ring protrudes from the inner side to the outer side, the cells of the nucleus pulposus and intervertebral tissues undergo degenerative necrosis, the water content of the nucleus pulposus decreases significantly, the internal pressure of the disc decreases, and the vertebral space narrows significantly. This creates an impairment in the mutual movement and support of the vertebral bodies. This causes an imbalance in the intervertebral joints and subsequently produces degeneration of the cartilage of the intervertebral joints, loosening of the joint capsule, and the formation of posterior joint subluxation. X-ray features include narrowing of the intervertebral space and hypertrophy and deformation of the intervertebral joints and arches. Long-term intervertebral imbalance and abnormal motion induce hypertrophy of the ligamentum flavum. Hypertrophic degeneration of the vertebral body, arch, and intervertebral joints produces spinal stenosis. The spine is an intact structure that cooperates and supports each other. If the structural integrity or functional role of the intervertebral disc is disrupted or altered, it inevitably affects the surrounding tissues and structures. The discs and synovial joints are the basis of spinal motion, and the tension of the disc nucleus pulposus and the pressure of the synovial joints and surrounding ligaments are in balance with each other to keep the intervertebral joints stable when the spine is in any position, forming the intrinsic balance of the spine. The anterior, posterior and lateral muscles of the spine are important tissues that control the movement of the spine and allow the spine to maintain coordination and stability in all positions. It is the extrinsic balance of the spine. The coordination of the internal and external balance of the spine is essential for the body to perform various functional activities. A herniated disc disrupts the intrinsic balance of the spine, resulting in a relative change in the position of the intervertebral joints. Since the vertebral body, articular eminence and spinous process are one, the position of the spinous process is bound to change, manifesting itself as a deviation of the spinous process. When the nucleus pulposus protrudes, it pushes on the fibrous ring and the posterior longitudinal ligament, causing it to compress the spinal nerve roots, thus changing the tension of the posterior longitudinal ligament. The inflammatory response resulting from the imbalance is transmitted to the center through the posterior spinal nerve branches and the cerebrospinal reentrant branches, and the psoas muscle produces protective spasm as well as protecting the sensitive intervertebral ligaments, which, however, causes scoliosis or kyphosis. The lumbar muscle spasm also plays a role in maintaining a new balance between the imbalanced spine and vertebrae, and in order to maintain the new spine and intervertebral balance, the spine can produce mild displacement (anterior tilt, retroversion, right rotation, left rotation, tilt rotation, and supination). The herniated intervertebral space shows flattening of the adjacent vertebral body edge, posterior width of the herniated space, lateral deviation or narrowing, and lip-like growth or bone spine formation at the posterior edge of the vertebral body above and below the herniated space. In this way, the spinous process of the affected vertebrae also changes, resulting in the affected vertebrae upper and lower spinal gaps becoming one wide and one narrow (the affected vertebrae are wide at the top and narrow at the bottom in supination and narrow at the bottom in Xi rotation); in addition, the change in the relative position of the vertebral body often leads to injury, swelling or hypertrophy of the intervertebral ligaments (yellow ligament, interspinous ligament, supraspinous ligament, etc.).