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Objective: Total knee arthroplasty (TKA) is one of the most universal and effective means for treating terminal stage osteoarthritis (OA) of knee. Accurate intramedullary guide of femur is the basis for the distal femoral cuts. Determining the surgical transepicondylar axis (sTEA) is the key to reconstruction of the femoral rotational alignment, because the correct rotational alignment can place the femoral component in the right position, balance the flexion gap so that the inner and outer tension is equal, get stability during the flexion process of the knee, and enhance the quality of life of patients. With the development of three-dimensional printing (3DP) technology in the medical domain, the application of patient-specific instrumentation (PSI) in arthroplasty has become more common. The aim of this study was to evaluate the accuracy of a novel 3D-printed patient-specific intramedullary guide to control femoral component rotation in TKA.Methods: Eighty patients (65 females and 15 males) with knee OA were included in this prospective randomized study. The patients were divided into two groups by random number table method, 40 in each group. TKA assisted by PSI (PSI group) and conventional TKA (conventional group) was performed respectively. Clinical outcomes [operation time, postoperative drainage volume, duration of drainage, Hospital for Special Surgery knee score (HSS), American Knee Society knee score (AKS)] and radiological outcomes [hip-knee-ankle angle (HKA), posterior condylar angle (PCA), patella transverse axis-femoral transepicondylar axis angle (PFA), depth of intramedullary guide] were compared between and within the two groups.Results: PSI group had less postoperative drainage volume but longer operation time than the conventional group (P < 0.05). The AKS and HSS scores after surgery were improved compared with those before surgery in each group (P < 0.05). However, there was no significant difference in the duration of drainage and range of motion (ROM) after surgery between the two groups. For the radiological results, the HKA and PFA were improved after surgery in both groups (P < 0.05).The postoperative PFA and PCA of the PSI group were closer to 0 , which was better than that of the conventional group (P < 0.05). The depth of intramedullary guide in the PSI group was less than the conventional group (P < 0.05). But there was no significant difference in HKA before and after surgery between the two groups as well as the preoperative PFA. Conclusion:The short-term clinical efficacy of TKA assisted by PSI was similar to the conventional TKA. Although TKA assisted by PSI spent more time during operation, it could assist in intramedullary guide and align femoral rotation more accurately.

Background: Osteoarthritis (OA), the most common joint disorder, is characterized by a progressive degradation of articular cartilage. Increasing evidence suggests that OA is closely associated with cartilage pathologies including chondrocyte hypertrophy and fibrosis. Methods: In this study, we showed that asiatic acid (AA) treatment reduced chondrocyte hypertrophy and fibrosis. First, the cytotoxicity of AA (0, 5, 10, and 20 μM) to chondrocytes was evaluated, and 5 μM was selected for subsequent experiments. Then, we detected the gene and protein level of chondrocyte hypertrophic markers including type X collagen (COL-X), matrix metalloproteinase-13 (MMP-13), alkaline phosphatase (ALP), and runtrelated transcription factor 2 (Runx2); chondrocyte fibrosis markers including type I collagen (COL-Ι) and alphasmooth muscle actin (α-SMA); and chondrogenic markers including SRY-related HMG box 9 (SOX9), type II collagen (COL-II), and aggrecan (ACAN). Further, we tested the mechanism of AA on inhibiting chondrocyte hypertrophy and fibrosis. Finally, we verified the results in an anterior cruciate ligament transection (ACLT) rat OA model. Results: We found that AA treatment inhibited the hypertrophic and fibrotic phenotype of chondrocytes, without affecting the chondrogenic phenotype. Moreover, we found that AA treatment activated AMP-activated protein kinase (AMPK) and inhibited phosphoinositide-3 kinase/protein kinase B (PI3K/AKT) signaling pathway in vitro. The results in an ACLT rat OA model also indicated that AA significantly attenuated chondrocyte hypertrophy and fibrosis. Conclusion: AA treatment could reduce hypertrophic and fibrotic differentiation and maintain the chondrogenic phenotype of articular chondrocytes by targeting the AMPK/PI3K/AKT signaling pathway. Our study suggested that AA might be a prospective drug component that targets hypertrophic and fibrotic chondrocytes for OA treatment.

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