Cage subsidence after instrumented lumbar spinal fusion surgery remains a significant cause of treatment failure, specifically for posterior or transforaminal lumbar interbody fusion. Recent advancements in computational techniques and additive manufacturing, have enabled the development of patient-specific implants and implant optimization to specific functional targets. This study aimed to introduce a novel full-scale topology optimization formulation that takes the structural response of the adjacent bone structures into account in the optimization process. The formulation includes maximum and minimum principal strain constraints that lower strain concentrations in the adjacent vertebrae. This optimization approach resulted in anatomically and mechanically conforming spinal fusion cages. Subsidence risk was quantified in a commercial finite element solver for off-the-shelf, anatomically conforming and the optimized cages, in two representative patients. We demonstrated that the anatomically and mechanically conforming cages reduced subsidence risk by 91% compared to an off-the-shelf implant with the same footprint for a patient with normal bone quality and 54% for a patient with osteopenia. Prototypes of the optimized cage were additively manufactured and mechanically tested to evaluate the manufacturability and integrity of the design and to validate the finite element model. 

Anatomically and mechanically conforming patient-specific spinal fusion cages designed by full-scale topology optimization

Kashin–Beck disease is an endemic joint disease characterized by deep chondrocyte necrosis, and T-2 toxin exposure has been confirmed its etiology. This study investigated mechanism of T-2 toxin inducing mitochondrial dysfunction of chondrocytes through p53-cyclophilin D (CypD) pathway. The p53 signaling pathway was significantly enriched in T-2 toxin response genes from GeneCards. We demonstrated the upregulation of the p53 protein and p53-CypD complex in rat articular cartilage and ATDC5 cells induced by T-2 toxin. Transmission electron microscopy showed the damaged mitochondrial structure of ATDC5 cells induced by T-2 toxin. Furthermore, it can lead to overopening of the mitochondrial permeability transition pore (mPTP), decreased mitochondrial membrane potential, and increased reactive oxygen species generation in ATDC5 cells. Pifithrin-α, the p53 inhibitor, alleviated the increased p53-CypD complex and mitochondrial dysfunction of chondrocytes induced by T-2 toxin, suggesting that p53 played an important role in T-2 toxin-induced mitochondrial dysfunction. Mechanistically, T-2 toxin can activate the p53 protein, which can be transferred to the mitochondrial membrane and form a complex with CypD. The increased binding of p53 and CypD mediated the excessive opening of mPTP, changed mitochondrial membrane permeability, and ultimately induced mitochondrial dysfunction and apoptosis of chondrocytes. 

T-2 toxin induces mitochondrial dysfunction in chondrocytes via the p53-cyclophilin D pathway.

Clinical and radiographic features of the atlantoaxial dislocation that is associated with Kashin-Beck disease.

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Clinical and radiographic features of the atlantoaxial dislocation that is associated with Kashin-Beck disease.