Introduction: Adolescent Idiopathic Scoliosis (AIS) is a multifactorial disorder that has been linked to genetic, hormonal, neurological, microbial and environmental cues. Eventually, however, AIS is a mechanical deformation of the spine, so an adequate theory of etiopathogenesis must provide an explanation for this and address the forces involved. Objective: In previous research with a physical model of the spine we showed that restrained differential growth, a mismatch of growth in mutually attached tissues, can result in the typical sequence of three-dimensional deformations seen in AIS.[1] Here we aim to identify the mechanobiological principles that may underlie this phenomenon and explain the deformities observed. Methods: We performed a literature study in Pubmed using the keywords growth, spine, tensegrity, muscle strength, vertebral body, growth plate, Hueter-Volkmann Law, intervertebral disc height, ligament, notochordal cells, and osmosis. Relevant information was gathered and combined for a comprehensive theory of etiopathogenesis for AIS. Results and Discussion: The human body is a tensegrity-like structure, in which muscles, ligaments and fasciae stabilize the skeleton. As the child grows, bone and cartilage elongate the muscles, ligaments and fasciae and induce their remodeling and growth. Considering the literature, we suggest the following scenario for the etiopathogenesis of AIS. During the growth spurt, there is a delay in muscular maturation, resulting in lowered prestress and decreased stability of the skeleton. According to Hueter-Volkmann, reduced axial compression enhances the growth of bones, which is indeed observed in AIS patients. Decreased spinal compression further results in lower vertebral bone density and increased disc height. Reduced dynamic loading also preserves the notochordal cells in the nucleus pulposus, which stimulates the production of proteoglycans and the assembly of the osmotic extracellular matrix. This intradiscal pressure increases intervertebral disc height to its limits, rendering the longitudinal ligaments and the annulus fibrosus under excessive tension (Figure 1). Under these conditions, spinal ligaments cannot remodel and therefore not grow with the intervertebral discs. The enhanced intradiscal pressure and locked ligamental remodeling embody the differential growth of the spine that results in scoliotic bending and rotation. Conclusion and Significance: AIS has been related to many physiological cues, yet the deformations observed remain essentially unexplained. The suggested differential growth mechanism fits well with the timing and speed of scoliotic deformations during the adolescent growth spurt. The identification of increased intradiscal pressure as the driving force of scoliotic deformities may be helpful to design prevention and treatment strategies for AIS.
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