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This study aimed to explore the effects on resorption of cervical disc herniation (CDH) and clinical outcomes of surgery. Cervical microendoscopic laminoplasty (CMEL), which is commonly preferable to anterior corpectomy and fusion, was applied to patients with 1- to 3-level degenerative cervical myelopathy (DCM). DCM patients with 1-3 levels DCM underwent either conservation treatment or CMEL. In conservation-treated patients (53 cases), CDH volume remained unchanged with no improvement in JOA and VAS scores. Conversely, 63 patients with 1-3 levels DCM were prospectively enrolled and exhibited a profound decrease in CDH volume: 89.1% of CDHs (123/138) regressed over 10%, 64.5% of CDHs (89/138) regressed over 25%, while 27.5% and 6.5% of CDHs (38/138 and 9/138) largely regressed over 50% and 75%, respectively. Meanwhile, the JOA and VAS scores were improved in different ways. Intriguingly, CDH volume changes correlated significantly with elevations in JOA scores, indicating an association of clinical CDH resolution with neurological recovery. We showed that CMEL induced clinically related diminishment of CDH and alleviation of clinical symptoms in patients with 1- to 3-level myelopathy and that it could help avoid anterior dissection of the disc to some extent.

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STUDY DESIGN: An algorithm was developed with MATLAB platform to automatically quantify the volume of cervical disc herniation (CDH) based on the sagittal magnetic resonance images. This automated program was used for CDH data set, and then compared with manual measurement results confirming its reliability. OBJECTIVE: The aim was to develop a new software for automated CDH volume measurement. SUMMARY OF BACKGROUND DATA: CDH compresses the spinal cord, regarding as the leading cause of cervical myelopathy. However, the CDH volume, of great value to clinical symptoms, can be only manually measured with no-excellent but acceptable interobserver reliability. This was due to the manual error of outlining CDH area and inclusion of structure posterior vertebra. No studies has proposed such an automated algorithm of CDH volume quantification which is standardised to quantify the accurate volume of CDH thus helping doctors easily evaluate CDH progressing. METHODS: The algorithm of CDH volume measurement was proposed. This program was then tested for 490 CDHs data set, from 185 patients with two repeated magnetic resonance imaging detections. Three individual observers manually measured the volumes of these CDHs, to justify the accuracy of this software. CDH volume was either in the classic way or the revised way excluding the influence of structure posterior vertebra. RESULTS: The automated software was successfully developed on MATLAB platform, with no difference found with manual measurements (average level) in CDH volume measurement. The change ratios in CDH volumes were profoundly consistent with manual observation, showing the error of 5.8% in median. The revised method elevated the absolute value of ratio by amplifying the percentage change. CONCLUSION: Our developed automated volumetry system was an standardized and accurate way, with selective removal module of structure posterior vertebra, replaceable for manual volume measurement of CDH, which was useful for spinal surgeons diagnosing and treating CDH disease.

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STUDY DESIGN: Retrospective study on 185 patients with 490 cervical disc herniation (CDH). OBJECTIVE: The aim of this study was to compare the changes in volumes of CDH in patients with degenerative cervical myelopathy (DCM) surgically treated by expansive open-door laminoplasty (EOLP) or cervical microendoscopic laminoplasty (CMEL). SUMMARY OF BACKGROUND DATA: Spontaneous resorption of CDH was shown in patients with DCM after conservation treatment, but very few in surgically treated patients. Our previous study identified the clinical efficiency of CMEL to treat DCM but how CDH sized postoperatively, as well as comparing to EOLP, was unknown. METHODS: Consecutive patients with DCM from December 2015 to December 2019, who underwent MRI evaluation, receiving CMEL or EOLP, and repeat MRI in follow-up were included. The volume of CDH were monitored using the picture archiving and communication system, further calculating the incidence of CDH with volume regression and the percentage changes of CDH volume. The correlations of possible determines with CDH volume changes were analyzed by Spearman rank correlation coefficient. RESULTS: A total of 89 patients (215 CDHs, EOLP-group) and 96 patients (275 CDHs, CMEL-group) was surveyed, respectively. Resultantly, volume of CDH was decreased postoperatively in both EOLP and CMEL cases. But this CDH volume regression was more profound in CMEL groups (incidence of 81.2% from 223/275, median volume change ratio of -26.7%, occurring from 1 month after CMEL), statistically different from EOLP group (50.2% from 108/215, median volume change ratio of -5.4%, none-appearance within 1 month). Patients information as sex, age, and follow-up time, not CDH significant, was significantly correlated with CDH volume changes. CONCLUSION: Patients who underwent CMEL developed a postoperative reduction of CDH volume, with more popularity, greater degree and earlier-staged than EOLP-patients. Young females with longer follow-up time were more likely occur.Level of Evidence: 4.

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Bone tissue engineering-based therapy for bone lesions requires the expansion of seeding cells, such as autologous mesenchymal stem cells (MSCs). A major obstacle to this process is the loss of the phenotype and differentiation capacity of MSCs subjected to passage. Recent studies have suggested that primary cilia, primordial organelles that transduce multiple signals, particularly hedgehog signals, play a role in senescence. Therefore, we explored the relationships among senescence, primary cilia, and hedgehog signaling in MSCs. Ageing of MSCs by expansion in vitro was accompanied by increased cell doubling time. The osteogenic capacity of aged MSCs at passage 4 was compromised compared to that of primary cells. P4 MSCs exhibited reductions in the frequency and length of primary cilia associated with decreased intensity of Arl13b staining on cilia. Senescence also resulted in downregulation of the expression of hedgehog components and CDKN2A. Suppression of ciliogenesis reduced the gene expression of both Gli1, a key molecule in the hedgehog signaling pathway and ALP, a marker of osteoblastic differentiation. This study demonstrated that the senescence of MSCs induced the loss of osteoblastic differentiation potency and inactivated hedgehog signaling associated with attenuated ciliogenesis, indicating that primary cilia play a mediating role in and are biomarkers of MSC senescence; thus, future antisenescence strategies involving manipulation of primary cilia could be developed.

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Osteoporosis is a common debilitating bone disease characterized by loss of bone mass and degradation of the bone architecture, which is primarily driven by dysregulated differentiation of mesenchymal stem cells into bone-producing osteoblasts. Osteoblasts contribute to bone formation by secreting various proteins that guide the deposition of bone extracellular matrix, such as alkaline phosphatase (ALP), osteocalcin (OCN), and osteopontin (OPN). The Wnt/ß-catenin pathway is widely recognized as a regulator of bone mass and is required to maintain bone homeostasis. Hormones have long been recognized as playing a key role in bone metabolism, and in recent years, growing evidence has shown that diabetes is a risk factor for osteoporosis. In the present study, we investigated the effects of the antidiabetic drug anagliptin on the differentiation and mineralization of osteoblasts induced by osteogenic medium. Anagliptin promotes insulin production via inhibition of dipeptidyl peptidase IV (DPP-4), an enzyme that targets the incretin hormone glucagon-like peptide 1 (GLP-1) for degradation. Our findings show that anagliptin significantly increases the differentiation of MSCs into osteoblasts via activation of RUNX2. Anagliptin significantly increased matrix deposition and mineralization by osteoblasts, as evidenced by elevated levels of ALP, OCN, OPN, and BMP-2. We further demonstrate that anagliptin activates the canonical and noncannonical Wnt signaling pathways and that silencing of Wnt/ß-catenin signaling completely abolished the effects of anagliptin. Thus, anagliptin might be a safe, effective therapy for type II diabetes that might show promise as a therapy against osteoporosis.

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