BackgroundRecently, medical rapid prototyping (MRP) models, fabricated with computer-aided design and computer-aided manufacture (CAD/CAM) techniques, have been applied to reconstructive surgery in the treatment of head and neck cancers. Here, we tested the use of preoperatively manufactured reconstruction plates, which were produced using MRP models. The clinical efficacy and esthetic outcome of using these products in mandibular reconstruction was evaluated.MethodsA series of 28 patients with malignant oral tumors underwent unilateral segmental resection of the mandible and simultaneous mandibular reconstruction. Twelve patients were treated with prebent reconstruction plates that were molded to MRP mandibular models designed with CAD/CAM techniques and fabricated on a combined powder bed and inkjet head three-dimensional printer. The remaining 16 patients were treated using conventional reconstruction methods. The surgical and esthetic outcomes of the two groups were compared by imaging analysis using post-operative panoramic tomography.ResultsThe mandibular symmetry in patients receiving the MRP-model-based prebent plates was significantly better than that in patients receiving conventional reconstructive surgery.ConclusionsPatients with head and neck cancer undergoing reconstructive surgery using a prebent reconstruction plate fabricated according to an MRP mandibular model showed improved mandibular contour compared to patients undergoing conventional mandibular reconstruction. Thus, use of this new technology for mandibular reconstruction results in an improved esthetic outcome with the potential for improved quality of life for patients.
Competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (the statins) that inhibit the synthesis of mevalonic acid are in wide use for treatment of hypercholesterolemia. Although antitumor effects on a variety of cell types have been reported for statins, the effect of simvastatin (one of the statins) on human melanoma cell lines is not known. Here, we report antitumor effects of simvastatin on human melanoma cell lines. We treated human melanoma cell lines, A375M, G361, C8161, GAK, and MMAc with simvastatin in various concentrations for 1 to 3 days. To investigate the antitumor effect of simvastatin, we analyzed cell viability, morphologic changes, reversibility of inhibition by geranylgeranyl pyrophosphate and farnesyl pyrophosphate, apoptosis and the cell cycle. Simvastatin treatment reduced cell viability in all five melanoma cell lines. The different melanoma cell lines, however, displayed different sensitivities to simvastatin. The addition of geranylgeranyl pyrophosphate to A375M and G361 cells in the presence of simvastatin completely restored the viability of cells, but the addition of farnesyl pyrophosphate did not. DNA fragmentation assay showed that simvastatin induced apoptosis in A375M and G361 cells. Simvastatin caused a G1 arrest in G361 and MMAc cells. Consistent with the cell cycle arrest, simvastatin caused an increase in the mRNA levels of p21 and p27 on G361 and MMAc cells. We conclude that simvastatin has an antitumor effect on human melanoma cells in vitro via apoptosis and cell cycle arrest. These results suggest that simvastatin may be an effective anticancer drug for malignant melanoma.
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