Through clinical studies and animal experiments, it has been proposed that the degree of low back pain and pain in patients with lumbar disc herniation is not related to the type of herniated nucleus pulposus, and that nerve root inflammation induced by inflammatory mediators in the nucleus pulposus is an important factor in the production of pain. Hou Shuxun et al. studied 300 patients with lumbar disc herniation and found that 68 patients had significant congestion, edema, and adhesions in the nerve roots and nearby tissues. These tissues were extremely sensitive to surgical stimulation, and all 68 patients had severe preoperative low back and leg pain. In the remaining 232 patients, the dural sac, epidural fat, ligamentum flavum, posterior longitudinal ligament, and annulus fibrosus, which had no inflammatory reaction, were insensitive to mechanical stimulation by surgery. This result suggests that the level of pain in patients with lumbar disc herniation is not related to the type of nucleus pulposus protrusion and that the inflammatory response is an important factor in the production of pain. In addition, Hou Shuxun et al. measured the level of phospholipase A2 activity in the blood of 20 patients with lumbar disc herniation and the nucleus pulposus of the intervertebral discs obtained during surgery by using the microacid titration method and compared it with the level of the patient’s pain and the intraoperative pathology seen. Phospholipase A2 activity levels in the nucleus pulposus of lumbar disc herniation were found to be as high as 35-fold and 10-fold compared with those in own blood and healthy nucleus pulposus, respectively, and the phospholipase A2 activity levels were significantly correlated with the patient’s pain level. It was demonstrated that nerve root inflammation induced by inflammatory mediators in the nucleus pulposus was directly related to pain.