Coronal deformity in ankylosing spondylitis with concomitant thoracolumbar kyphosis: patterns, manifestations and surgical strategies.

PURPOSE: To evaluate different patterns of coronal deformity secondary to ankylosing spondylitis (AS), to propose relevant treatment strategies, and to assess efficacy of asymmetrical pedicle subtraction osteotomy (APSO). METHODS: Coronal deformity was defined as coronal Cobb angle over 20º or coronal balance distance (CBD) more than 3 cm. 65 consecutive AS patients with concomitant coronal and sagittal deformity who underwent PSO were included. The average follow-up time was 40.4 months. Radiographic evaluation included coronal Cobb angle and CBD. Furthermore, sagittal parameters were used to assess magnitude and maintenance of kyphosis correction. RESULTS: Based on curve characteristics, coronal deformity caused by AS included four different radiologic patterns: Pattern I: lumbar scoliosis; Pattern II: C-shaped thoracolumbar curve; Pattern III: trunk shift without major curve; Pattern IV: proximal thoracic scoliosis. APSO was performed for patients in Pattern I to III while conventional PSO was applied for patients in Pattern IV. Significant improvement in all the sagittal parameters were noted in 65 patients without obvious correction loss at the last follow-up. Besides, significant and sustained correction of coronal mal-alignment was identified in 59 APSO-treated patients. Rod fracture occurred in four cases and revision surgery was performed for one case. CONCLUSION: According to radiologic manifestations, coronal deformity caused by AS could be categorized into four patterns. APSO proved to be a feasible and effective procedure for correction of Pattern I to III patients. Coronal deformity pattern, apex location, sagittal profile of lumbar spine and preoperative hip function should be considered for osteotomy level selection in APSO.

Nrf-2/ROS/NF-κB pathway is modulated by cynarin in human mesenchymal stem cells in vitro from ankylosing spondylitis.

Ankylosing spondylitis (AS) is an immune chronic inflammatory disease, resulting in back pain, stiffness, and thoracolumbar kyphotic deformity. Based on the reported anti-inflammatory and antioxidant capacities of cynarin (Cyn), this study explored its protective role and molecular mechanisms in mesenchymal stem cells (MSCs) from AS. The target pathways and genes were verified using Western blotting, quantitative real-time polymerase chain reaction, and immunofluorescent staining, while molecular docking analysis was conducted. In AS-MSCs, we found that the expression levels of p-NF-κB, IL-6, IL-1ß, and TNF-α were higher and IκB-α, Nrf-2, and HO-1 were lower compared with healthy control (HC)-MSCs. With molecular docking analysis, the biding affinities between Cyn and Keap1-Nrf-2 and p65-IκB-α were predicted. The mRNA and protein expression of p-NF-κB, IL-6, IL-1ß, and TNF-α and the reactive oxygen species (ROS) generation were downregulated following Cyn administration. Meanwhile, the expression level of IκB-α, Nrf-2, and HO-1 were significantly increased after Cyn pretreatment. The results suggested that the protective mechanisms of Cyn in AS-MSCs were based on enhancing the antioxidation and suppression of excessive inflammatory responses via Nrf-2/ROS/NF-κB axis. Our findings demonstrate that Cyn is a potential candidate for alleviating inflammation in AS.