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The alveolar ridge splitting technique enables reconstruction of atrophied alveolar ridges prior implantation. However, in cases of severe atrophy, there is an unpredictable risk of fracturing the buccal lamella during the expansion. Currently, there is no preoperative assessment to predict the maximum distraction of the lamella. The aim of this study was to develop a biomechanical model to mimic the alveolar ridge splitting and a finite element (FE) model to predict the experimental results. The biomechanical testing was conducted on porcine mandibles. To build the FE model high resolution peripheral quantitative computer tomography scans of one specimen was performed after the osteotomy outline, but before the lamella displacement. A servo-electric testing machine was used for the axial tension test to split the lamellae. Results showed, in line with clinical observations, that the lamellae broke primarily at the base of the splits with a median displacement of 1.27 mm. The FE model could predict fracture force and fracture displacement. Fracture force showed a nonlinear correlation with the height of the bone lamella. In conclusion, good correspondence between mechanical testing and virtual FE analysis showed a clinically relevant approach that may help to predict maximum lamella displacement to prevent fractures in the future.

The alveolar ridge splitting technique (ARST) offers an alternative to classic ridge augmentation techniques for successful insertion of dental implants. However, the buccal lamella is at risk of fracturing during ARST distraction. To better understand the fracture mechanisms and displacement limits of the split lamella, this study conducted biomechanical tests on human cadaveric maxilla specimens having extremely atrophied alveolar ridges treated with ARST. A total of 12 standardized alveolar splits were prepared on the maxillae of 3 elderly female donors using an oscillating piezoelectric saw. Mimicking the surgical distraction process of the lamella, each split was tested to failure using a dental osteotome attached to the crosshead of an electromechanical testing system. All specimens were scanned by means of high-resolution peripheral quantitative computed tomography prior to and post testing to evaluate split geometries and failure modes. Split stiffness, failure force, and displacement were 27.4 ± 18.7 N/mm, 12.0 ± 8.4 N, and 0.97 ± 0.31 mm, with no significant differences between anatomical sides and split locations ( p ≥ 0.17 ). Stiffness correlated significantly with failure force ( R 2 = 0.71 , p < 0.01 ). None of the alveolar split widths correlated significantly with the outcomes from biomechanical testing ( p ≥ 0.10 ). The results suggest that simple geometrical measures do not predict the allowed extent of lamella distraction prior to failure. More sophisticated methods are required for surgical planning to optimize the ARST outcomes. Still, the present study may advocate a clinical protocol for the maxilla where the implant site is prepared directly after osteotomy setting and immediately before full lamella dislocation, when the lamella is still stable, resistant to mechanical stress, and bone loss caused by the abrasion of the burr is minimized.

In bone tissue engineering (TE) endothelial cell-osteoblast cocultures are known to induce synergies of cell differentiation and activity. Bone marrow mononucleated cells (BMCs) are a rich source of mesenchymal stem cells (MSCs) able to develop an osteogenic phenotype. Endothelial progenitor cells (EPCs) are also present within BMC. In this study we investigate the effect of EPCs present in the BMC population on MSCs osteogenic differentiation. Human BMCs were isolated and separated into two populations. The MSC population was selected through plastic adhesion capacity. EPCs (CD34+and CD133+) were removed from the BMC population and the resulting population was named depleted MSCs. Both populations were cultured over 28 days in osteogenic medium (Dex+) or medium containing platelet lysate (PL). MSC population grew faster than depleted MSCs in both media, and PL containing medium accelerated the proliferation for both populations. Cell differentiation was much higher in Dex+medium in both cases. Real-time RT-PCR revealed upregulation of osteogenic marker genes in depleted MSCs. Higher values of ALP activity and matrix mineralization analyses confirmed these results. Our study advocates that absence of EPCs in the MSC population enables higher osteogenic gene expression and matrix mineralization and therefore may lead to advanced bone neoformation necessary for TE constructs.