Preoperative Halo-Femoral Traction With Posterior Surgical Correction for the Treatment of Extremely Severe Rigid Congenital Scoliosis (Cobb Angle &gt;120°)

Zhang, Hongqi; Yang, Guanteng; Guo, Chaofeng; Deng, Ang; Xiao, Lairong

doi:10.5435/jaaos-d-21-01095

Cited by 2 publications

(2 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[ 20 ] However, although surgery is the only curative tool, it is very risky and costly. [ 3 , 21 ] Thus, it is important to reveal the pathology and mechanism of CS to explore better treatment options.…”

Section: Discussionmentioning

confidence: 99%

“…[ 1 , 2 ] Hemivertebra, or segmentation failure, is the most common manifestation of CS. [ 3 ] In addition, smaller vertebrae and low bone mineral density (BMD) have been reported. [ 4 ] The etiology of CS is still unclear, but it is widely believed that some genetic defects, such as the Notch pathway and TBX6 (T-box transcription factor 6) mutations, and environmental factors, such as gestational diabetes and anoxia, can lead to CS.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Promotion effect of FGF23 on osteopenia in congenital scoliosis through FGFr3/TNAP/OPN pathway

Zhang

Xiang

et al. 2023

Chinese Medical Journal

Self Cite

View full text Add to dashboard Cite

Background: Congenital scoliosis (CS) is a complex spinal malformation of unknown etiology with abnormal bone metabolism. Fibroblast growth factor 23 (FGF23), secreted by osteoblasts and osteocytes, can inhibit bone formation and mineralization. This research aims to investigate the relationship between CS and FGF23. Methods: We collected peripheral blood from two pairs of identical twins for methylation sequencing of the target region. FGF23 mRNA levels in the peripheral blood of CS patients and age-matched controls were measured. Receiver operator characteristic (ROC) curve analyses were conducted to evaluate the specificity and sensitivity of FGF23. The expression levels of FGF23 and its downstream factors fibroblast growth factor receptor 3 (FGFr3)/tissue non-specific alkaline phosphatase (TNAP)/osteopontin (OPN) in primary osteoblasts from CS patients (CS-Ob) and controls (CT-Ob) were detected. In addition, the osteogenic abilities of FGF23-knockdown or FGF23-overexpressing Ob were examined. Results: DNA methylation of the FGF23 gene in CS patients was decreased compared to that of their identical twins, accompanied by increased mRNA levels. CS patients had increased peripheral blood FGF23 mRNA levels and decreased computed tomography (CT) values compared with controls. The FGF23 mRNA levels were negatively correlated with the CT value of the spine, and ROCs of FGF23 mRNA levels showed high sensitivity and specificity for CS. Additionally, significantly increased levels of FGF23, FGFr3, OPN, impaired osteogenic mineralization and lower TNAP levels were observed in CS-Ob. Moreover, FGF23 overexpression in CT-Ob increased FGFr3 and OPN levels and decreased TNAP levels, while FGF23 knockdown induced downregulation of FGFr3 and OPN but upregulation of TNAP in CS-Ob. Mineralization of CS-Ob was rescued after FGF23 knockdown. Conclusions: Our results suggested increased peripheral blood FGF23 levels, decreased bone mineral density in CS patients, and a good predictive ability of CS by peripheral blood FGF23 levels. FGF23 may contribute to osteopenia in CS patients through FGFr3/TNAP/OPN pathway.

show abstract

Section: Discussionmentioning

confidence: 99%