Metal block augmentation, which is used for the treatment of tibial bone defects in total knee arthroplasty, with high stiffness will cause significant alteration in stress distribution, and its solid structure is not suitable for osseointegration. This study aimed to design a porous block to reduce weight, promote bone ingrowth, and improve its biomechanical performance. The metal block augmentation technique was applied to finite element models of tibial bone defects. Minimum compliance topology optimization subject to volume fraction combined with the porous architecture was adopted to redesign the block. Biomechanical changes compared with the original block were analyzed by finite element analysis. The stress distribution of the block and proximal tibia was recorded. The strain energy density of the proximal tibia was obtained. The newly designed block realized 40% weight reduction. The maximum stress in the optimized block decreased by 11.6% when compared with the solid one. The maximum stress of the proximal tibia in the optimized group increased by 18.6%. The stress of the anterior, medial, and posterior parts of the proximal medial tibia in the optimized group was significantly greater than that in the original group (all p < 0.05). The optimized block could effectively improve the biomechanical performance between the block and the bone. The presented method might provide a reference for the design of customized three-dimensional printed prostheses.

Epithelial-mesenchymal transition (EMT) serves an important role in the formation and development of various types of cancer, including oral squamous cell carcinoma (OSCC). Metformin, used for treating type 2 diabetes, has been revealed to exert an anticancer effect in various types of cancer, including liver, breast and colorectal cancer. However, its role in the EMT of OSCC has been rarely reported. Therefore, the present study aimed to investigate the effects of metformin on EMT and to identify its underlying mechanism in OSCC. Firstly, EMT was induced in CAL-27 cells using CoCl 2 . Subsequently, the effects of metformin on cell viability, migration and xenograft growth were evaluated in vitro and in vivo . Reverse transcription-quantitative PCR was performed to detect the expression levels of E-cadherin, vimentin, snail family transcriptional repressor 1, mTOR, hypoxia inducible factor 1α, pyruvate kinase M2 and STAT3. The results demonstrated that metformin abolished CoCl 2 -induced cell proliferation, migration, invasion and EMT. Moreover, metformin reversed EMT in OSCC by inhibiting the mTOR-associated HIF-1α/PKM2/STAT3 signaling pathway. Overall, the present findings characterized a novel mechanism via which metformin modulated EMT in OSCC.

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