Relationship between cervical curvature and spinal cord drift distance after laminectomy via lateral mass screw fixation and its effect on clinical efficacy.

BACKGROUND: Laminectomy with lateral mass screw fixation (LCS) is considered an effective surgical procedure for cervical spondylotic myelopathy. However, varying degrees of loss of the cervical curvature were noted in some patients postoperatively. The aim of this study was to observe the relationship between cervical curvature and spinal drift distance after LCS and to determine its effect on neurological function, axial symptoms, and C5 palsy. METHODS: A total of 117 consecutive cervical spondylotic myelopathy patients with normal cervical curvature underwent LCS from April 2015 to May 2017 in our institution. Of these patients, 90 patients who accepted to undergo an integrated follow-up were enrolled in this study. The patients were divided into 3 groups based on their postoperative cervical curvature. In group A (28 patients), the cervical curvature became straight postoperatively (0°≤cervical spine angle≤5°); in group B (36 patients), the cervical curvature decreased (5°16.5°). Spinal drift distance, neurological recovery, axial symptoms, and C5 palsy in the patients were recorded and analyzed. RESULTS: Postoperative measurements showed that there was no significant difference in laminectomy width between the groups (P > .05). The cervical spine angle was 2.7°â€Š±â€Š0.5° in group A, 11.2°â€Š±â€Š2.6° in group B, and 20.8°â€Š±â€Š4.1° in group C (P < .05), while the spinal drift distance was 1.2 ±â€Š0.2 mm, 1.8 ±â€Š0.4 mm, and 3.0 ±â€Š0.5 mm, respectively (P < .05). The postoperative Japanese Orthopedic Association score was significantly increased in all groups (P < .05), and there was no significant difference between the groups at different time points (P > .05). However, significant differences were noted between the groups in axial symptoms (P < .05), which were analyzed via the visual analog scale score. The occurrence of C5 palsy in groups A, B, and C was 7.1% (2/28), 8.3% (3/36), and 11.5% (3/26), respectively (P > .05). CONCLUSION: In LCS, the cervical curvature should be maintained at the normal angle to obtain a good spinal cord drift distance and a lower incidence of axial symptoms.

Pentraxin 3 promotes the osteoblastic differentiation of MC3T3-E1 cells through the PI3K/Akt signaling pathway.

Osteoblast cells are responsible for synthesizing new bone tissue, and determining how to control osteoblastic differentiation is vital to the treatment of osteoporosis. In the present study, we show that pentraxin 3 (PTX3) signaling is involved in the regulation of osteoblastic differentiation in MC3T3-E1 cells. Our data reveal that PTX3 is abundantly expressed in MC3T3-E1 cells and that its expression is inducible by the introduction of osteogenic induction medium (OIM). Overexpression of PTX3 was observed to significantly increase the expression of four osteoblast signature genes, including Runt-related transcription factor 2 (RUNX2), alkaline phosphatase (ALP), osteocalcin (OCN) and osterix (OSX), suggesting that the overexpression of PTX3 promotes osteoblastic differentiation. The relative level of gene expression between OIM and OIM plus overexpressed PTX3 was evaluated using the Affymetrix Gene Chip® mouse gene microarray. PTX3-related differentially expressed genes (DEGs) were screened. Gene ontology (GO) functional and Kyoto Encyclopedia of Genes and Genomes database (KEGG) pathway enrichment analyses were performed, and the PI3K/Akt signaling pathway was primarily involved in the osteogenic differentiation of PTX3. Protein-protein interactions (PPIs) were also constructed, and the molecular complex detection (MCODE) plugin calculated modules of PPI networks. Moreover, we show that the effect of PTX3 is mediated by its induction of the PI3K/Akt signaling pathway. Mechanistically, we show that the action of PTX3 requires the activation of PI3K and Akt, and deactivation of PI3K by its inhibitor LY294002 weakens the PTX3-mediated induction of osteoblast signature genes, ALP and matrix mineralization. The present study revealed a new role played by PTX3 and suggest a potential mechanism governing the osteoblastic differentiation of MC3T3-E1 cells.