The relationships between image type and resorption of giant lumbar disc herniation are shown in Table 3. The associations between resorption of protrusions and Komori typing, MSU typing, Iwabuchi typing, "bull’s eye” sign, and Modic changes were evaluated for the study patients. The numbers of Komori type 1, 1, Iwabuchi type 4, and MSU Modic types I and III were insufficient for statistical analysis. Chi-square tests showed non-significant differences (P > 0.05) between Komori types 2 and 3, and between MSU types 2 and 3. Apparent absorption was seen in 22/35 (62.86%) Iwabuchi type 1 cases, 2/15 (13.33%) type 2 cases, no type 3 or 4 cases, and 1 (25.00%) type 5 case. Iwabuchi type 2 and type 1 and type 3 by chi-square test P < 0.01, significant statistical significance on the difference between the remaining parting compare the chi-square (P > 0.05, no significant statistical significance, Iwabuchi classification is illustrated in the projection type 1 component of nucleus pulposus, the more the higher water content, resorption is more likely to occur. Obvious resorption was found in 22/47 (46.81%) cases with a positive bull’s eye sign and 3/17 (17.65%) cases with a negative bull’s eye sign, with the difference being statistically significant (chi-square test, P < 0.01), indicating that a protrusion surrounded by an active inflammatory reaction with new vascular growth and a positive bull’s eye sign were more likely to show resorption. Modic type II with Modic changes in patients with absorption by chi-square test, P > 0.05 difference is not significant.
A typical case description (Fig. 8) A 30-year-old woman presented at the hospital in January 2018 with lumbago and pain in both lower extremities but no symptoms of cauda equina compression. Physical examination indicated L4/L5 and L5/S1 bilateral paracanth tenderness radiating to both lower limbs. A straight leg elevation test was performed at 50° (+) on the left side and 50° (+) on the right side. The skin sensation and muscle strength of both lower limbs were normal. The first MRI examination showed an L4/L5 giant protrusion of Komori improved type 3, MSU type 3-AB, Iwabuchi type 1, positive bull’s eye sign, and no Modic changes, and an L5/S1 herniated disc of Komori modified type 2, MSU type 2-A, Iwabuchi type 2, no bull’s eye sign, and no Modic changes. Eight months later, the symptoms of lumbago and leg pain were mostly relieved. The straight leg elevation test showed 80° (-) on the left side and 80° (-) on the right side, and the JOA score was 22 points. The first MRI review shown in Fig. 8B showed partial resorption of the L4/L5 type huge disc herniation. The patient was followed up 18 months later, and the symptoms of lumbago and leg pain were completely resolved, with a straight leg elevation test result of 80° (-) on the left side and 90° (-) on the right side, and a JOA score of 26 points. The second MRI review shown in Fig. 8C showed that the L4/L5 herniated disc had disappeared, the bull's eye sign had disappeared on contrast-enhanced MRI, and the L5/S1 herniated disc was not changed from before.
Possible mechanisms for the resorption of intervertebral discs include the following.
(1) Phagocytosis of inflammatory cells: intervertebral disc herniation after chemical inflammation and vascular proliferation may contribute to mononuclear macrophage inflammatory cell infiltration and prominence and heavy this change more apparent, caused by inflammatory cells phagocytosis of the outstanding intervertebral disc tissue absorption [8]. Kobayashi et al. [26] performed light and electron microscopy observations on disc herniation tissues from 73 patients undergoing lumber disc herniation surgery, and found that new microvessels grew around the intervertebral disc tissue that entered the epidural space, with there also being local inflammatory reactions and high infiltration of macrophages at the same time. Tsuru et al. [27] observed human intervertebral disc surgical specimens at the cell level with electron microscopy, and found a large number of infiltrated macrophages in the herniated intervertebral disc tissue. They believed that these infiltrating macrophages were the mechanism for the spontaneous resorption of the herniated disc, with there being fragments of intervertebral disc tissue present. Minamide et al. [28] studied the resorption of intervertebral disc herniation in rabbits, and found that when the nucleus pulposus was free in the spinal canal, peripheral capillary proliferation increased, accompanied by infiltration of macrophages, lymphocytes, and fibroblasts.
(2) The body's own immune function: in free, after longitudinal ligament, protrusions longitudinal ligament into epidural, worn out after exposure to blood circulation of intervertebral disc tissue to become the body of the antigen, which can lead to autoimmune reaction, and the resulting autoantibodies or self-sensitization lymphocyte immune to outstanding intervertebral disc tissue dissolution [8]. Through the immunohistochemical staining of specimens from 49 cases of lumbar disc herniation, Arai et al. [29] found that the inflammatory cell infiltration at the site of disc herniation comes mainly from T lymphocytes and macrophages, which play an important role in the resorption of disc herniation. It is suggested [30] that antigens and antibodies in the medullary nucleus form immune complexes to activate complement, attracting inflammatory cells such as neutrophils that produce inflammatory transmitters, thereby causing local inflammation. Inflammatory transmitters can increase vascular permeability, promote macrophage phagocytosis of antigen and antibody complexes, release lysosomal proteases, break down proteoglycan, break collagen balance, degrade collagen molecules, and make the fiber ring crack and fracture. All these processes have specific effects on lumbar disc resorption. As an immune response develops, the rapid cellular immune response is weakened or even disappears, whereas the delayed humoral immune response is gradually strengthened until the antigens are completely digested and decomposed.
(3) Growth of new blood vessels: vascularization is a very important indicator of resorption of herniated disc tissue, and the presence and progression of vascularization is greatly related to the degree of reduction of the absorption of the protrusion and the prognosis [31]. Grang et al. [32] found that 57% of large and free herniated tissues had capillary infiltration, a rate much higher than that found in other types of herniated disc tissues. In addition, vascular endothelial growth factor, an important vascular growth stimulator, can induce the growth of new capillaries from the edge of the intervertebral disc and promote resorption. Toru et al. [33] analyzed macrophages produced by rat tail discs, studying interleukin 1 (IL 1), vascular endothelial growth factor (VEGF), and expression of matrix metalloproteinases (MMPs) in the role of intervertebral disc heavy absorption, and found they were all positively expressed in the intervertebral disc, under the condition of women within the intervertebral disc tissue to form the new blood vessels, IL − 1, VEGF, MMPs further contribute to the formation of new blood vessels, heavy absorption. It can be seen that herniated intervertebral disc has the possibility of resorption and shrinkage after making contact with tissue with an abundant blood supply, and that the nucleus pulposus tends to shrink or disappear.
(4) Degradation imbalance of matrix metalloproteinases (MMPs): recent studies have shown that disc herniation is closely related to matrix metabolism imbalance, with matrix metalloproteinases (MMPs) and tissue inhibitors of matrixmetalloproteinase (TIMPs) playing important roles [34]. Le Maitre et al. [35] found that the MMP-3-positive cell rate in tissue from human herniated discs was significantly higher than that in a normal control group, and that it was closely related to the degree of herniation. Haro [5] 36 etc by reverse transcription polymerase chain reaction (PT - PCR) technology to find the chondrocytes culture alone makes a small amount of MMP-3, macrophages and cultivate the expression of MMP-3 increased significantly after, MMP-3 in addition to direct degradation of protein, polysaccharide, also induced macrophage chemotactic factor, may be the intervertebral disc cells express monocytes chemical affect protein 1 (MCP 1), make the protein dissolved macrophage infiltration in the activity, lead to highlight the absorption of intervertebral disc tissue. Iwabuchi et al. [38] used low-intensity pulsed ultrasound to stimulate rat intervertebral disc tissue in vitro, and found that it increased the content of MMP-3 and promoted the absorption of intervertebral disc tissue.
(5) The involvement of various cytokines: Interleukin-1 (IL-1) is a common inflammatory factor that shows high activity in herniated disc tissue [39]. Yoshida et al. [40] suggested that at the time of intervertebral disc herniation, intervertebral disc tissue cells begin to produce pre-inflammatory factors such as tumor necrosis factor (TNF-) and IL-1. The transfer of these cytokines from the intracellular to extracellular environment leads to the accumulation of macrophages in the herniated disc, and the material in the disc is gradually absorbed because of the strong phagocytic activity of the aggregated macrophages and the neutral metalloproteinases released by them. Tumor necrosis factor TNF-A can stimulate cytokine secretion, promote macrophage aggregation, play a strong role in phagocytic activity, release a large amount of interleukin, and absorb the herniated intervertebral disc tissue. TNF alpha is an important component of inflammation; it can strengthen the function of neutrophils and eosinophils, directly affect nerves and blood vessels, and stimulate cells to produce other pathogenic substances that also effect inflammatory cells and the organization of the nerve sheath cells, thereby leading to more TNF alpha generation and promoting heavy absorption of outstanding intervertebral disc.