Clinical and radiographic evaluation of cervical disk replacement: a retrospective study.

Studies have shown the effectiveness of cervical disk replacement. However, clinical outcomes, particularly by radiographic assessment during the 36-month follow-up visit, have not been reported for cervical disk replacement with Mobi-C (LDR, Austin, Texas) disk prostheses. A retrospective study was conducted at 10 centers across China and included 65 patients who underwent single-level Mobi-C disk prosthesis replacement from October 2009 to July 2010. Clinical and radiographic data were collected before replacement, 7 days postoperatively, and 1, 3, 6, 12, 24, and 36 months postoperatively. Clinical and neurologic outcomes were assessed by the Japanese Orthopaedic Association (JOA) score, visual analog scale (VAS), Neck Disability Index (NDI), and Odom's criteria. Static and dynamic radiographs were measured to determine intervertebral height and range of motion (ROM) of the cervical spine, the functional spinal unit, the treated segment, and adjacent segments. JOA, VAS, and NDI scores showed statistically significant improvement 36 months after replacement (P<.05). The ROM of the cervical spine, functional spinal unit, treated segment, and adjacent segments did not show a significant difference before and after replacement (P>.05). The intervertebral height of the treated segment increased significantly, and the intervertebral height of adjacent segments showed no statistical significance between time points and at follow-up. Clinical outcomes indicated that Mobi-C artificial cervical disk replacement is reliable. Radiographic data showed that it plays a role in reconstruction or maintenance of intervertebral height and ROM of the cervical spine, functional spinal unit, treated segment, and adjacent segments after Mobi-C cervical disk replacement.

Mechanisms of anti-inflammatory property of conserved dopamine neurotrophic factor: inhibition of JNK signaling in lipopolysaccharide-induced microglia.

Microglia are important resident immune cells in the central nervous system (CNS) and involved in the neuroinflammation caused by CNS disorders, including brain trauma, ischemia, stroke, infections, inflammation, and neurodegenerative diseases. Our study explores the hypothesis that conserved dopamine neurotrophic factor (CDNF), a secretory neurotrophic factor, may provide a novel therapy for associated with neuroinflammation related to the microglia. We observed that CDNF was upregulated in rat primary microglia treated with 1 µg/mL lipopolysaccharide, an inflammatory inducer, for 24 h. Thus, we hypothesize that CDNF may play a role, mediator or inhibitor, in regulating the inflammation in microglial cells induced by LPS. Finally, our data showed that CDNF significantly attenuated the production of proinflammatory cytokines (PGE2 and IL-1ß) and remarkably alleviated the cytotoxicity (percentage of lactate dehydrogenase released) in the LPS-induced microglia by suppressing the phosphorylation of JNK, but not the P38 or ERK pathways. These results demonstrate the anti-inflammatory property of CDNF by inhibition of JNK signaling in LPS-induced microglia, suggesting that CDNF may be a potential novel agent for the treatment of neuroinflammation in the CNS disorders.

CCL20 Secretion from the Nucleus Pulposus Improves the Recruitment of CCR6-Expressing Th17 Cells to Degenerated IVD Tissues.

BACKGROUND: Studies elucidated that Th17 cells are important contributors to the pathogenesis of many immune-mediated diseases, and IL-17A is present in pathologic intervertebral disc (IVD) tissues. However, the mechanisms, how these cells traffic into the degenerate discs are not clear. MATERIALS AND METHODS: The samples collected from 53 patients had been divided into 3 groups: Group P (annulus fibrosus was intact), Group E (annulus fibrosus was reptured) and normal control. Immunohistochemistry was used to detect the expression of CCL20, CCR6, IL-17A, TNF-α and CD4 in IVD tissues. Moreover, nucleus pulposus (NP) cells had been cultured in the presence and absence of Th17 associated cytokines. The supernatants were detected for CCL20 concentrations by ELISA, and the NP cells for the expression of CCL20 mRNA. Additionally, peripheral blood (PB) samples had undergone detection for the expression of CCR6 mRNA and the proportion of IL-17-producing cells, including the surface expression of CCR6. RESULTS: Immunohistochemistry revealed that CCL20 and TNF-α were expressed in degenerated NP cells. Double-labeled immunofluorescence elaborated, IL-17-producing cells (CD4(+)IL-17A(+) and CD4(+)CCR6(+)) appeared in the Group E samples, but no traces or expression in Group P and normal control. IL-17A and TNF-α, alone or combined, could enhance CCL20 secretion in a dose-dependent manner, which was obtained through RT-PCR results. There was a notable difference of CCR6 mRNA expression between patients and normal controls. In comparison to controls, flow cytometry data indicated that the proportion of IL-17-producing cells and the CCR6 expression in PB were significantly increased. CONCLUSION: Our results provide a potential explanation for involvement of the CCL20-CCR6 system in the trafficking of IL-17-producing cells to degenerated IVD tissues. Additionally, our results explain the contribution of Th17 associated cytokines to the development of degenerated discs via the up-regulation of CCL20 secretion from NP cells, which forms a positive chemotactic feedback loop.