I. Intervertebral disc degeneration and pathogenesis Lower back pain is a common condition affecting human health. Degenerative changes of the intervertebral disc and its secondary pathological changes are the common causes of lower back pain. As human beings have evolved, science has developed, and living and working conditions have improved, spinal disorders have instead become more common, attracting clinical attention. Therefore, understanding the degenerative changes of the intervertebral disc is crucial to the proper understanding of lumbar disc herniation, and for this reason scholars at home and abroad have extensively discussed the pathogenesis of intervertebral disc degeneration. Below we provide a detailed description of the pathogenesis of intervertebral disc degeneration. Current studies have shown that the nucleus pulposus plays a critical role in maintaining the normal function of the intervertebral disc. Rupture of the annulus fibrosus rarely occurs in the absence of structural destruction of the nucleus pulposus. When the nucleus pulposus loses its inherent elasticity, the load capacity of the disc is reduced accordingly, and structural destruction of the disc can occur under the action of minor external injurious factors. (i) Decrease in cellular nutrition Changes in the cellular and matrix components of the intervertebral disc are closely related to changes in nutrition, and the survival of the cells in the disc depends on nutrients diffusing into the disc matrix from the outer layer of the annulus fibrosus and the internal vasculature of the vertebral body. The main factors affecting nutrient diffusion are the decrease in peripheral blood vessels of the disc, secondly the aggregation of degraded matrix macromolecules, and thirdly the decrease in the water content inside the disc. Further decreases in cellular nutrients are influenced by, firstly, low oxygen tension within the disc, secondly, decreased lactate clearance and decreased PH values. Third, impairment of cellular metabolism and biologic symmetric function. (ii) Decrease in the number of surviving cells As age adversely affects the cells of the intervertebral disc, nutrition of the intervertebral disc center and the decrease in PH value, the number of surviving cells gradually decreases. (iii) Cellular senescence Normally, despite the absence of nutritional changes, many normally differentiated cells gradually age with age, losing the ability to replicate DNA synthesis and other synthetic functions will also decline accordingly. (iv) Loss and decrease in concentration of aggregated proteoglycans Loss and decrease in concentration of aggregated proteoglycans reduces the ability of the disc to retain water, increases collagen content and aggregation of non-collagenous proteins, the disc becomes stiff due to fibrosis, the disc height cannot be maintained normally, and the ability to distribute load decreases. (v) Changes in matrix proteins The intervertebral disc tissue gradually loses its inherent elasticity and strength with age, and the loss of elasticity and strength may be due to changes in elastin, proteoglycans, and especially collagen components after synthesis. In addition, the products of glycosylation can stimulate cells, including chondrocytes, to release cytokines and proteases and cause degeneration of the disc. (vi) Aggregation of degraded matrix macromolecules Aggregation of degraded macromolecules can alter the biomechanical properties of the disc and the ability of nutrients and metabolites to disperse through the matrix. The increase in degradation products within the disc inhibits the ability of cells to synthesize new molecules and also affects the assembly of newly synthesized molecules. Aggregation of degradation products is most commonly seen in disc tissues that lack a blood supply. (vii) Matrix fatigue decline The disc normally has the ability to regain its normal shape after weight-bearing deformation, and the water within the disc is expelled from the disc matrix in the upright position, causing the height of the disc to decrease. In the recumbent position, the water returns to the disc and the shape and capacity of the disc are restored. The fatiguing decline of the matrix is manifested in the intervertebral disc by firstly the formation of fissures, secondly the fragmentation of the disc tissue and thirdly the mucoid degeneration of the disc. The loss of proteoglycan water in the disc increases the load on the collagen network. Changes in collagen, decrease in water content and aggregation of matrix degradation products make the collagen network more susceptible to damage. Decreased cellular nutrition, reduced number of viable cells, natural apoptosis and changes in matrix composition further impair the ability of cells to repair. (viii) Elevated phosphodiesterase A2 (PLA2) activity in degenerated discs Saal et al. measured PLA2 activity in surgically removed herniated disc tissue from five patients and first found abnormally elevated PLA2 activity, suggesting the presence of PLA2 chemical inflammatory mediators in the disc tissue and suggesting that PLA2 may play a role in initiating the inflammatory response in degenerated discs. The activation of PLA2 in the disc is associated with degeneration, PLA2 accumulates in the disc as a result of aging and degeneration, and each of these progressive biochemical changes could theoretically promote the activation of PLA2 in the disc. (ix) Assessment of disc degeneration Loss of intervertebral space height, altered disc bulge, decreased disc signal, Schmorl nodule formation, and endplate abnormalities can be seen by qualitative MRI assessment methods. Loss of intervertebral space height is the most common clinical imaging feature used to diagnose disc degeneration. Severe loss of intervertebral space height is a common sign of disc degeneration. Modic staging and presentation of endplate degeneration has been emphasized more in recent years. The endplate degeneration process is represented by Modic typing, which is based on MRI morphology and is divided into three types: (1) Type I (edema phase): T1 low signal and T2 high signal; suggesting a progressive degenerative process. (2) Type II (fatty infiltration phase): high signal in both T1 and T2 images, suggesting a stable process of chronic degeneration of bone marrow fat (3) Type III (adjacent vertebral fibrosis or calcification phase): low signal in both T1 and T2 images, suggesting subchondral osteosclerosis of the endplate. Modic changes are seen in 22-50% of patients with degenerative disc disease (DDD) and are clinically prevalent in the first two types. Single and multiple vertebral involvement is seen on MRI, but most are adjacent to each other. Sometimes two types of Modic changes are seen together in the same case, called mixed changes. This indicates that the individual is at different stages of the degenerative pathology process, indicating that Modic changes can change from one type to another. Modic changes are a manifestation of degeneration of the intervertebral disc that results in the weakening or loss of the protective effect of the endplate, causing edema of the adjacent vertebral cancellous bone and consequent pathological changes such as fatty infiltration, fibrosis and calcification.