Rabbit Anti-Human IVD Polyclonal antibody

Purpose To assess the MRI modifications of the intervertebral disc (IVD) treated by chemiodiscolysis using T2 mapping sequences. Methods Thirty sciatica patients (17 males, 13 females, mean age 47.52 years) were enrolled for percutaneous CT-guided O-2-O-3 chemiodiscolysis treatment. As a control group, we enrolled 30 patients who were treated by CT-guided periradicular injections. All patients were submitted to clinical (using VAS and Oswestry Disability index (ODI)) and imaging studies to evaluate the intervertebral disc area (IDA) and T2 mapping values of the IVD before and at 1-month follow-up. Results In the study group, pre-treatment IDA mean values were 20.47 +/- 1.62 cm(2), with significant reduction at the follow-up (P < 0.05). Mean pre-treatment T2 relaxation time values were 38.80 +/- 4.51 ms, 44.05 +/- 0.91 ms, and 45.45 +/- 14.11 ms for anterior annulus fibrosus, nucleus pulposus (NP), and posterior annulus fibrosus, respectively, with significant increase at the level of the NP (P < 0.05) at the follow-up. Mean pre-treatment ODI and VAS scores were 21.5 +/- 10.6 and 8.5 +/- 0.57, with significant improvement at the post-treatment follow-up (P < 0.05). In the control group, despite clinical improvement, we did not find significant IVA reduction nor significant T2 values change after treatment. Correlation analysis of T2 mapping relaxation time values showed significant correlation of NP T2 mapping value with both the reduction of IDA (0.81, P < 0.001) and the improvement of VAS and ODI scores (0.86, P < 0.001) at 1 month. In the control group, we did not find any statistically significant correlation. Conclusions T2 mapping may be a useful indicator to predict disc shrinkage and the clinical response to CT-guided O-2-O-3 injection.

The intervertebral disc (IVD) degeneration is thought to be closely related to ingrowth of new blood vessels. However, the impact of anti-angiogenic factors in the maintenance of IVD avascularity remains unknown. Tenomodulin (Tnmd) is a tendon/ligament-specific marker and anti-angiogenic factor with abundant expression in the IVD. It is still unclear whether Tnmd contributes to the maintenance of IVD homeostasis, acting to inhibit vascular ingrowth into this normally avascular tissue. Herein, we investigated whether IVD degeneration could be induced spontaneously by the absence of Tnmd. Our results showed that Tnmd was expressed in an age-dependent manner primarily in the outer annulus fibrous (OAF) and it was downregulated at 6 months of age corresponding to the early IVD degeneration stage in mice. Tnmd knockout (Tnmd(-)(/)(-)) mice exhibited more rapid progression of age-related IVD degeneration. These signs include smaller collagen fibril diameter, markedly lower compressive stiffness, reduced multiple IVD- and tendon/ligament-related gene expression, induced angiogenesis, and macrophage infiltration in OAF, as well as more hypertrophic-like chondrocytes in the nucleus pulposus. In addition, Tnmd and chondromodulin I (Chm1, the only homologous gene to Tnmd) double knockout (Tnmd(-)(/)(-)Chm1(-)(/)(-)) mice displayed not only accelerated IVD degeneration, but also ectopic bone formation of IVD. Lastly, the absence of Tnmd in OAF-derived cells promoted p65 and matrix metalloproteinases upregulation, and increased migratory capacity of human umbilical vein endothelial cells. In sum, our data provide clear evidences that Tnmd acts as an angiogenic inhibitor in the IVD homeostasis and protects against age-related IVD degeneration. Targeting Tnmd may represent a novel therapeutic strategy for attenuating age-related IVD degeneration.