Comparison of double chevron-cut and biplanar distal femoral osteotomy techniques: A biomechanical study.

OBJECTIVE: This study aimed to compare the stability and mechanical properties of the double chevron-cut (DCC) and biplanar (BP) distal femoral osteotomy (DFO) techniques, along with analyzing their respective contact surface areas. METHODS: Biomechanical testing was performed using sawbone and 3D modeling techniques to assess axial and torsional stability, torsional stiffness, and maximum torque of both osteotomy configurations. Additionally, 3D models of the sawbone femur were created to calculate and compare the contact surface area of the DCC, BP, and conventional single-plane DFO techniques. RESULTS: Axial stiffness and maximum strength did not significantly differ between the two osteotomy techniques. However, in terms of torsional properties, the DCC technique exhibited superior torsional stiffness compared to the BP group (27 ± 7.7 Nm/° vs. 4.5 ± 1.5 Nm/°, p = 0.008). Although the difference in maximum torque did not reach statistical significance (63 ± 10.6 vs. 56 ± 12.1, p = 0.87), it is noteworthy that the DCC group sawbone model exhibited fracture in the shaft region instead of at the osteotomy site. Therefore, the actual maximum torque of the DCC construct may not be accurately reflected by the numerical values obtained in this study. The contact surface area analysis revealed that the BP configuration had the largest contact surface area, 111% larger than that of the single-plane configuration. but 60% of it relied on the less reliable axial cut. Conversely, the DCC osteotomy offered a 31% larger contact surface area than the single-plane configuration, with both surfaces being weight-bearing. CONCLUSION: The DCC osteotomy exhibited superior mechanical stability, showing improved rotational stiffness and maximum torque when compared to the BP osteotomy. Although the BP osteotomy resulted in a larger contact surface area than the DCC osteotomy, both were larger than the conventional single-plane configuration. In clinical practice, both the DCC and BP techniques should be evaluated based on patient-specific characteristics and surgical goals.

The Impact of Cage and End plate-Related Factors on Cage Subsidence in Oblique Lateral Interbody Fusion.

OBJECTIVES: To identify cage and end plate factors of cage subsidence (CS) in patients who underwent oblique lateral interbody fusion (OLIF) and their association with patient-reported outcomes. METHODS: Sixty-one patients (43 women and 18 men), with a total of 69 segments (138 end plates) which underwent OLIF at a single academic institution between November 2018 and November 2020, were included. All the end plates were separated into CS and nonsubsidence groups. Cage-related parameters (cage height, cage width, cage insertion level, and cage position) and end plate-related parameters (position of end plate, Hounsfield unit value of the vertebra, end plate concave angle [ECA], end plate injury, and angular mismatch measured with cage/end plate angle [C/EA]) were compared and analyzed using logistic regression to predict CS. Receiver operating characteristic curve analysis was used to determine the cutoff points of the parameters. RESULTS: Postoperative CS was identified in 50 of the 138 end plates (36.2%). The CS group had significantly lower mean Hounsfield unit values of the vertebra, higher rate of end plate injury, lower ECA, and higher C/EA than the nonsubsidence group. ECA and C/EA were identified as independent risk factors for developing CS. The optimal cutoff points for ECA and C/EA were 176.9° and 5.4°, respectively. CONCLUSIONS: An ECA greater than 176.9° and a cage/end plate angular mismatch greater than 5.4° were found to be independent risk factors of postoperative CS after the OLIF procedure. These findings aid in preoperative decision-making and intraoperative technical guidance.

Apoptosis in chondrogenesis of human mesenchymal stem cells: effect of serum and medium supplements.

Apoptosis is an inevitable process during development and is evident in the formation of articular cartilage and endochondral ossification of growth plate. Mesenchymal stem cells (MSCs) can serve as alternative sources for cell therapy in focal chondral lesions or diffuse osteoarthritis. But there are few, if any, studies investigating apoptosis during chondrogenesis by MSCs. The aim of this study was to find the better condition to prevent apoptosis during chondrogenesis by MSCs. Apoptosis were evaluated in MSCs induced in different chondrogenic media by the use of Annexin V, TUNEL staining, lysosomal labeling with lysotracker and immunostaining of apoptotic markers. We found apparent apoptosis was demonstrated by Annexin V, TUNEL staining and lysosomal labeling during chondrogenesis. Meanwhile, the degree of apoptosis was related to the reagents of the defined chondrogenic medium. Adding serum in medium increased apoptosis, however, TGF-beta1 inhibited apoptosis. The apoptosis was associated with the activation of caspase-3, the increase in the Bax/Bcl-2 ratio, the loss of lysosomal integrity, and the increase of PARP-cleavage. Pro-inflammatory cytokines, IL-1alpha, IL-1beta and TNFalpha did not induce any increase in apoptosis. Interestingly, the inhibition of apoptosis by serum free medium supplemented with ITS was also associated with an increase in the expression of type II collagen, and a decrease in the expression of type X collagen, Runx2, and other osteogenic genes, while TGF-beta1 increased the expression of Sox9, type II and type X collagen and decreased the expression of osteogenic genes. These data suggest apoptosis occurs during chondrogenesis by MSCs by cell death intrinsic pathway activation and this process may be modulated by culture conditions.

Impacts of Green Tea on Joint and Skeletal Muscle Health: Prospects of Translational Nutrition.

Osteoarthritis and sarcopenia are two major joint and skeletal muscle diseases prevalent during aging. Osteoarthritis is a multifactorial progressive degenerative and inflammatory disorder of articular cartilage. Cartilage protection and pain management are the two most important strategies in the management of osteoarthritis. Sarcopenia, a condition of loss of muscle mass and strength, is associated with impaired neuromuscular innervation, the transition of skeletal muscle fiber type, and reduced muscle regenerative capacity. Management of sarcopenia requires addressing both skeletal muscle quantity and quality. Emerging evidence suggests that green tea catechins play an important role in maintaining healthy joints and skeletal muscle. This review covers (i) the prevalence and etiology of osteoarthritis and sarcopenia, such as excessive inflammation and oxidative stress, mitochondrial dysfunction, and reduced autophagy; (ii) the effects of green tea catechins on joint health by downregulating inflammatory signaling mediators, upregulating anabolic mediators, and modulating miRNAs expression, resulting in reduced chondrocyte death, collagen degradation, and cartilage protection; (iii) the effects of green tea catechins on skeletal muscle health via maintaining a dynamic balance between protein synthesis and degradation and boosting the synthesis of mitochondrial energy metabolism, resulting in favorable muscle homeostasis and mitigation of muscle atrophy with aging; and (iv) the current study limitations and future research directions.

Mesenchymal stem cell-conditioned medium facilitates angiogenesis and fracture healing in diabetic rats.

The most critical factor for fracture union is the blood supply to the fracture site, which is usually impaired in patients with diabetes. Recently, mesenchymal stem cells-derived conditioned medium (MSC-CM) has shown significantly higher levels of angiogenic factors, such as VEGF and IL-6. We demonstrate in this report that MSC-CM delivered in gelatin sponges stimulates angiogenesis and promotes fracture healing in a diabetic rat model. Subcutaneous implantation of gelatin sponges soaked in MSC-CM demonstrated better tissue ingrowth and higher capillary densities at 2 and 3 weeks than gelatin sponges in minimal essential medium (MEM) or 293 cell-derived conditioned medium (293-CM). Implantation of fibular defects with gelatin sponges soaked in MSC-CM enhanced bone ingrowth and fracture healing rates compared to 293-CM and MEM groups at 8 weeks. Micro-computed tomography analysis further indicated a higher new bone volume in the MSC-CM group compared to the other diabetic groups. Histological analysis with CD31 immunostaining also revealed that MSC-CM increased endothelial cell counts compared to the other groups. Together, these results indicated that gelatin sponges used to deliver MSC-CM promote angiogenesis and fracture healing in a diabetic model and may be an alternative strategy for treating fracture non-union in patients with diabetes.

Type I collagen promotes proliferation and osteogenesis of human mesenchymal stem cells via activation of ERK and Akt pathways.

Biomaterials not only serve as scaffolds for bone regeneration, but may also exhibit inductive capability for bone growth. The goal of this study was to identify the best extracellular matrix protein for enhancing osteogenesis by hMSCs (human mesenchymal stem cells) and to investigate the underlying mechanism. Coating with collagen I, but not fibronectin, laminin, gelatin, and poly-L-lysine, enhanced late cell proliferation and promoted osteogenesis by hMSCs, as evidenced by an increase in Alizarin Red S staining, alkaline phosphatase activity and mRNA levels of Runx2 and osteocalcin. Coating with collagen I induced activation of ERK and Akt but not FAK, and treatment with PD98059 and LY294002 blocked the activation of ERK and Akt, respectively. Interestingly, LY294002 also blocked ERK activation, indicating the activation of PI3K/ERK pathway upon contact with collagen I. Furthermore, PD98059 or LY294002 abolished collagen I-induced promotion of osteogenesis by hMSCs. However, blocking antibodies against alpha2beta1 integrins did not inhibit collagen I-induced osteogenesis by hMSCs. These data demonstrate that collagen I promotes proliferation and osteogenesis of hMSCs via activation of ERK and Akt pathways.