Background: The neurocentral junction often has been identified as a potential cause of adolescent idiopathic scoliosis (AIS). Disparate growth at this site has been thought to lead to pedicle asymmetry, which then causes vertebral rotation in the transverse plane and ultimately, the development of scoliotic curves.

Objectives:

To develop a model that incorporates pedicle growth and growth modulation into an existing finite element model of the thoracic and lumbar spine already integrating vertebral growth and growth modulation

Methods: The model was personalised to the geometry of a non-pathological subject and used as the reference spinal configuration. Left/right asymmetry of pedicle geometry (i.e. initial length) and left/right asymmetry of the pedicle growth rate alone or in combination with other AIS potential pathogenesis (anterior, lateral, or rotational displacement of apical vertebra) were simulated over a period of 24 months. The Cobb angle and local scoliotic descriptors (wedging angle, axial rotation) were assessed at each monthly growth cycle.

Results: Simulations with asymmetrical pedicle geometry did not produce significant scoliosis, vertebral rotation or wedging. Simulations with asymmetry of pedicle growth rate did not cause scoliosis independently and did not amplify the scoliotic deformity caused by other initial deformations tested by Villemure (2004).

Discussion and Conclusion: The results of this biomechanical model do not support the hypothesis that asymmetrical neurocentral junction growth is a cause of AIS. This concurs with recent animal experiments in which neurocentral junction growth was unilaterally restricted and no scoliosis, vertebral wedging or rotation was noted. With regards to addressing the aetiology of scoliotic curve development, biomechanical modelling represents a powerful tool to investigate cause and affect relationships since AIS patients typically present to the scoliosis clinic well after curves have manifested.

Contact person and Presenter: Carl-Éric Aubin, Ph.D., Canada Research Chair “CAD Innovations in Orthopedic Engineering”, Department of Mechanical Engineering, Ecole Polytechnique, Montreal, Canada, Tel: (514) 340-4711, ext. 4437; Fax: (514) 340-5867; E-mail: carl-eric.aubin@polymtl.ca

Introduction: Experimental pinealectomy in chickens shortly after hatch produces scoliosis with morphological characteristics similar to that of human idiopathic scoliosis (Coillard et al., 1996). The objective of this study was to develop a finite element model (FEM) incorporating vertebral growth to analyse how bone growth modulation by mechanical loading affects development of scoliosis in chicken.

Materials and Methods: We have adapted the experimental set-up of Bagnall et al. (1999) to study spine growth of pinealectomised chickens. Three groups were followed for a period of six weeks:

wild-type (controls) (n=25);

The experimental data was used to adapt a FEM previously developed to simulate the scoliosis deformation process in human (Villemure et al. 2002). The FEM consists of 7 thoracic vertebrae and the first lumbar, the intervertebral discs and the zygapophyseal joints. The geometry was measured on specimens using a calliper. The material properties of human spines were used as initial approximation. The growth process included a baseline growth (0.130 mm/day) and a growth modulation behaviour proportional to the stress and to a sensitivity factor. It was implemented through an iterative process (from the 14th to the 28th day). Asymmetric loads (2–14 Nmm) were applied to represent different paravertebral muscle abnormalities influenced by the induced melatonin defect.

Results: Within the pinealectomised group, 55% of the animals (n = 42) developed a scoliosis. In the FEM model, by varying the value of the applied moment, different scoliosis configurations were simulated. The resulting Cobb angle varied between 6° and 37°, while the maximal vertebral wedging appeared at T4 or T5 (range between 5° to 28°). A descriptive comparison of the simulation results with the experimental deformation patterns (n = 41; mean Cobb angle: 26°) was made as a preliminary validation. In 2 typical cases, the scoliotic shapes were quite similar to that seen in the scoliotic chickens.

Discussion and Conclusion: The basic mechanisms by which the metabolism of the growing spine is affected by mechanical factors remain not well known, and especially the role of tissue remodelling and growth adaptation in scoliosis. The agreement between the experimental study and preliminary simulation results shows the feasibility of the model to simulate the scoliotic deformation process in pinealectomised chickens. When completely developed and validated this modelling approach could help investigating the pathomechanisms involved in the scoliotic deformation process. Especially, computer simulations could be used to complement bio-molecular and mechanobiological studies concerning the neuroendocrinal hypothesis implicating melatonin signalling dysfunction, which could trigger a complex cascade of molecules and mechanoreceptors leading to an accumulation of specific factors in specialised tissues (Moreau et al. 2004), directly or indirectly implicated in proprioception, and which can be implicated in the pathomechanisms of scoliotic deformities.