Human spinal biomechanics are profoundly complex and not well understood, especially in terms of the dynamic spine function. Translation of biomechanics to disease is difficult, particularly since cause must be separated from effect. Primary dynamics predisposing to the onset of chronic spinal disorders, e.g., adolescent idiopathic scoliosis (AIS) or ankylosing spondylitis (AS), must clearly be differentiated from secondary alterations. This commentary addresses primary biomechanics that may predispose to these idiopathic diseases. A novel hypothesis is proposed, based upon inferences regarding their contrasting muscular dynamics. The hypothesis postulates opposing inherent muscle tonicity in AIS versus AS. Converse degrees of spinal stability may predispose to the respective curvature deformities of AIS and the enthesopathy lesions of AS. One condition is suspected to counter-oppose the other, within a polymorphic spectrum of spinal stability.