Pathogenic mechanisms of adult degenerative scoliosis

Adult degenerative scoliosis (ADS) is not merely a unidimensional sagittal decompensation, but rather a three-dimensional pathological process driven by asymmetric degeneration of intervertebral discs, endplates, facet joints, and paraspinal muscles, wherein coronal scoliosis, sagittal imbalance, and vertebral axial rotation mutually couple and amplify one another. Endplate tilting and nucleus pulposus displacement convert segmental mechanics to an asymmetric pattern, representing the initiating event; all three axes are reciprocally driven through facet joints and ligamentous tension, forming a self-amplifying progression loop; paraspinal muscles on the convex and concave sides exhibit opposing degenerative patterns that exacerbate instability; facet joint sagittalization transitions scoliosis from a compensable to a structurally fixed state; bone density loss and genetic susceptibility modulate individual progression rates. This review systematically synthesizes the above mechanisms and proposes a Three-Axis Reciprocal Coupling Pathogenic Model as a conceptual, hypothesis-generating framework, and discusses potential mechanism-informed intervention directions together with the limitations of the current evidence base. ADS is best understood as a systemic musculoskeletal syndrome involving multiple tissue systems, and this conceptualization may carry implications for early identification and precision intervention pending further validation.