Mechanisms Underlying the Progression of Congenital Scoliosis Involving Bone Marrow Stromal Progenitors [BiSulfite-seq]

Meanwhile, scoliosis-inducing insults, such as proneurodegenerative and proinflammatory cytokines, influenced specific precursor cells/MSCs, leading to a fate switch toward gliogenesis, extracellular matrix synthesis, and osteogenesis. These processes, in turn, contributed to the development of scoliosis through neurodegeneration, fibrosis, and disruptions in bone homeostasis. we validated neurodegeneration, fibrosis, and disruptions in bone homeostasis in clinical CS patient samples through epigenomic and transcriptome analysis and histological testing.

In addition, excessive differentiation during MSC injury repair marked scoliosis progression in murine models, indicating that inflammatory and neurodegeneration are two underlying pathogenic factors contributing to spinal deformities in CS. Meanwhile, the decreased expression of Hmox1 and increased expression of SPP1 in murine models and clinical patients indicating perhaps they are potential diagnostic and therapeutic targets in CS early phase.