This study is the first to explore the influence of different vertebral growth patterns on AIS progression using state-of-the-art biomechanical modeling techniques. This research utilizes the "vicious cycle" notion of scoliotic progression under different spinal growth rates (accelerated AIS and normal). Simulation results of the finite element models, which were reaffirmed via sensitivity analyses, suggest that when an initial deformity is present, a faster AIS growth profile significantly encourages scoliotic progression in the coronal plane and decreases kyphosis in the sagittal plane. This result is consistent with the observations made between the height and angle velocities in AIS patients  and agrees with the tendency for scoliotic patients to adopt a reduced kyphosis [9, 10]. Result from Case 2 also suggests that the presence of a small kyphosis angle cannot lead to scoliosis exclusive of an initial coronal deformity. Therefore, results suggest that the abnormal growth pattern of the anterior spine may play a secondary instead of a primary role in the development of AIS.
To investigate if the spinal deformity was incurred by the axial rotate on of each vertebral body, axial rotation angle of every vertebral body, with respect to a fixed global reference plane, was analyzed. Minor axial rotation (less than 5 degrees) was measured. This observation is consistent with the simulation results reported in the literature [21, 38]. Therefore, it is perceivable that other mechanisms are involved in transverse plane deformations that include vertebral rotation, axial torsion, and rib hump.
A potential limitation of this analysis resides with the mere modeling of anterior spine growth. However, in a preceding study , it was shown that pedicle growth rate asymmetry (neuro-central growth plate) was neither able to independently generate a scoliosis nor to act in conjunction with other deformations to initiate scoliotic spinal curves. In addition, the cylindrical shape used to model the vertebral bodies may influence local stress distributions over the growth plates. However, this study seeks to draw comparative conclusions utilizing identical platforms while altering a single variable of interest (i.e. the growth rate) and, for the purpose of this analysis, such a factor was not deemed important. Moreover, assumptions that were considered to have important influence on the reported results were explored under complementing sensitivity analyses. Therefore, although the implemented numerical approach contains simplifications, sensitivity analyses suggest that adopted numerical techniques do not interfere with relative conclusion reported herein. Finally, as always in biomechanics, finite element modeling is a technique for simulating a mechanism of interest performed under logical assumptions rather than completely reconstructing reality. Therefore, results and conclusions of this study should be interpreted within the prescribed conditions. These modeling simplifications are not able to fully account for the functional limitations of the posterior elements and the coupling between loads in the different directions. However, resulting contact forces on facet joints might be more important in loading modes such as torsion, flexion/extension, and lateral bending as compared to compression, which may modify transmitted spinal loads. Thus, although not explored, these contact forces might potentially play a role in the scoliosis deformation process.
In the growth modulation equation, G
represents the growth rate (result of growth profile), β is the sensitivity factor and may be linked with the biological influences, and σ reflects mechanical factors (asymmetrical stress distribution). This is the first study that isolated and quantified the impact of growth profile (G
) on scoliotic progression, showing that the augmented Gm, combined with an initial coronal deformity, will lead to progression of coronal deformity as well as decreasing the kyphosis angle in the spine.
The magnitude of the adopted parameters used in the analyses may have influenced the simulations results and therefore the conclusion. More specifically, although the sensitivity factor β was held constant between the explored cases, β may vary with the patient age . Moreover, AIS patients' progression is mostly concentrated immediately prior to puberty, which may be related to circulatory hormones  (i.e., estrogen and melatonin). Such notions feed the speculation that, due to a variation in biological factors, the sensitivity factor β may be influenced by the disturbed growth plate mechanotransduction. For this reason, a sensitivity analysis exploring the influence of this variable was performed. The outcome of such study was encouraging and demonstrated that the identified association between scoliotic progression and increased growth velocity was robust. Although the current modeling settings were determined according to existing literature, one must recognize the possibility of inter-patient variability. Nevertheless, the developed finite element platform effectively allowed for the isolation of growth rate influence to implicitly explore its impact on the progressive profiles of scoliotic patients.