Abstract

Cleft palate is a common birth defect, requiring interventions that must be timed according to maxillary growth and patients often require multiple procedures to repair an alveolar cleft defect. Mechanical variables, such as pre‐surgical defect shape and size, have been suggested to affect the success of surgical repair, but the biomechanical consequences of these variables are not well understood. We hypothesize that mechanical performance of bony craniofacial structures will vary with cleft morphology.3D surface models of alveolar cleft defects were created from cone‐bean (CB) CT scans of adolescent and young adult patients (n=36; IRB: 201601711). Surface semilandmarks were used to conduct a cluster analysis, identifying common axes of variation which broadly differentiated between defects that are mediolaterally wider from those that are superoinferiorly taller.The centroid cleft defect shape from Cluster I was selected for preliminary biomechanical analysis. To isolate the mechanical effects of a defect of this shape/size, we used a previously published human cranial finite element model (FEM) as a baseline for model construction and comparison of performance. Patient CBCT was scaled and registered to the FEM and used to reconstruct the defect in the maxilla of the baseline model. Identical boundary conditions (material properties, muscle forces and joint and bite constraints) were applied to the cleft and non‐cleft FE models, to simulate biting on different teeth.Our results reveal notable and unexpected differences in deformation and strain regimes of the cleft and non‐cleft models. Although both models show characteristic regions of elevated strain on the biting‐side, the cleft‐model experiences a marked reduction (50‐90%) in strain on the balancing (non‐biting) side, due to the cleft disrupting the transmission of internal forces across the maxilla and palate from the biting to the balancing side. Importantly, regions that experience diffuse low‐level shear strains in our baseline model drop to nearly undetectable levels in the cleft model.We conclude that it is possible that the reduction of strain below this critical threshold could impede osteogenic mechanical signaling. This has important clinical implications for alveolar cleft defect repair and the development of novel scaffold‐based methods that both survive in vivo and restore functional orofacial load paths.

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