Study and analysis of the correlation between lumbar spondylolisthesis and Modic changes.

Background: This study aimed to explore the risk factors of Modic changes in lumbar spondylolisthesis. Methods: The distribution of Modic changes in different types of lumbar spondylolisthesis, degree of spondylolisthesis, and degree of intervertebral disc degeneration in patients with lumbar spondylolisthesis was observed and analyzed. Statistical analysis was conducted to assess whether intervertebral disc degeneration, local mechanical changes, etc. affect the occurrence of Modic changes. The risk factors of Modic changes in lumbar spondylolisthesis were further illustrated. Results: The age in the lumbar spondylolisthesis with Modic changes group was younger than that in the lumbar spondylolisthesis without Modic changes group, and the bone mineral density was better in the lumbar spondylolisthesis with Modic changes group than that in the lumbar spondylolisthesis without Modic changes group, P < 0.05. The two groups statistically differed in intervertebral disc height (IDH) and disc angle on magnetic resonance imaging (MRI). In the classification of Modic changes, the incidence of type II was the highest. The incidence of Modic changes is higher in isthmic spondylolisthesis than in degenerative spondylolisthesis. With the aggravation of lumbar spondylolisthesis and intervertebral disc degeneration, the incidence of Modic changes gradually increased. Modic changes are most commonly seen in both the upper and lower endplates. Logistic regression analysis showed that the occurrence of Modic changes in lumbar spondylolisthesis was significantly correlated with IDH, disc angle on MRI, type of spondylolisthesis, degree of spondylolisthesis, and degree of intervertebral disc degeneration, P < 0.05. Conclusions: The occurrence of Modic changes is related to the type of spondylolisthesis, the degree of spondylolisthesis, the degree of disc degeneration, the decrease of intervertebral disc height, and local stress angulation.

Stromal cell-derived factor-1α promotes recruitment and differentiation of nucleus pulposus-derived stem cells.

BACKGROUND: Intervertebral disc (IVD) degeneration is a condition characterized by a reduction in the water and extracellular matrix content of the nucleus pulposus (NP) and is considered as one of the dominating contributing factors to low back pain. Recent evidence suggests that stromal cell-derived factor 1α (SDF-1α) and its receptor C-X-C chemokine receptor type 4 (CXCR4) direct the migration of stem cells associated with injury repair in different musculoskeletal tissues. AIM: To investigate the effects of SDF-1α on recruitment and chondrogenic differentiation of nucleus pulposus-derived stem cells (NPSCs). METHODS: We performed real-time RT-PCR and enzyme-linked immunosorbent assay to examine the expression of SDF-1α in nucleus pulposus cells after treatment with pro-inflammatory cytokines in vitro. An animal model of IVD degeneration was established using annular fibrosus puncture in rat coccygeal discs. Tissue samples were collected from normal control and degeneration groups. Differences in the expression of SDF-1α between the normal and degenerative IVDs were analyzed by immunohistochemistry. The migration capacity of NPSCs induced by SDF-1α was evaluated using wound healing and transwell migration assays. To determine the effect of SDF-1α on chondrogenic differentiation of NPSCs, we conducted cell micromass culture and examined the expression levels of Sox-9, aggrecan, and collagen II. Moreover, the roles of SDF-1/CXCR4 axis in the migration and chondrogenesis differentiation of NPSCs were analyzed by immunofluorescence, immunoblotting, and real-time RT-PCR. RESULTS: SDF-1α was significantly upregulated in the native IVD cells cultured in vitro with pro-inflammatory cytokines, such as interleukin-1ß and tumor necrosis factor-α, mimicking the degenerative settings. Immunohistochemical staining showed that the level of SDF-1α was also significantly higher in the degenerative group than in the normal group. SDF-1α enhanced the migration capacity of NPSCs in a dose-dependent manner. In addition, SDF-1α induced chondrogenic differentiation of NPSCs, as evidenced by the increased expression of chondrogenic markers using histological and immunoblotting analyses. Real-time RT-PCR, immunoblotting, and immunofluorescence showed that SDF-1α not only increased CXCR4 expression but also stimulated translocation of CXCR4 from the cytoplasm to membrane, accompanied by cytoskeletal rearrangement. Furthermore, blocking CXCR4 with AMD3100 effectively suppressed the SDF-1α-induced migration and differentiation capacities of NPSCs. CONCLUSION: These findings demonstrate that SDF-1α has the potential to enhance recruitment and chondrogenic differentiation of NPSCs via SDF-1/CXCR4 chemotaxis signals that contribute to IVD regeneration.