The purpose of this study was to investigate whether the location of the hinge affects the incidence of hinge fracture during medial closing-wedge distal femoral varus osteotomy (DFVO). Twenty knees from 10 fresh-frozen human cadavers (mean age, 75 ± 17 years) were used to perform uniplanar medial closing-wedge DFVO with a 7-mm wedge. Each specimen was randomly assigned to either group A (supracondylar hinge) or group B (lateral condylar hinge). The incidence of hinge fracture and stability was compared between both groups after uniplanar medial closing-wedge DFVO. In group A, 8 of 10 knees had a lateral cortex fracture during closure of the osteotomy gap, and all fractured knees were unstable. Two knees with an intact lateral cortical hinge showed stability under manual valgus and varus forces. After intentional breakage of the lateral cortical hinge, both knees were found to be unstable under the same force. In group B, 2 of 10 knees had a lateral cortex fracture, and 8 knees had no fractures. All specimens were found to be stable under manual valgus and varus forces. After intentional breakage of the lateral cortical hinge in group B, 2 knees were unstable, while 8 knees remained stable. This study showed a significantly higher incidence of lateral cortical hinge fracture and instability in group A than in group B during closure of the osteotomy gap.
PurposeHigh Outerbridge grade lesions of the articular cartilage have been associated with poor outcomes of high tibial osteotomy (HTO). However, there has been no report on the efficacy of HTO in the presence of kissing lesions. The purpose of this study was to compare clinical and radiographic outcomes of HTO between kissing lesion and non-kissing lesion groups.Materials and MethodsOf the patients with medial compartment osteoarthritis and varus deformity treated with HTO between 2007 and 2012, 21 cases with kissing lesions and 22 cases without kissing lesions were selected. Clinical outcomes were assessed using the Lysholm knee scoring scale score, visual analogue scale score, Hospital for Special Surgery score, Western Ontario and McMaster Universities score, and Tegner activity score. Radiographic outcomes were assessed using the femoral-tibial angle, mechanical axis deviation, medial proximal tibial angle, posterior tibial slope angle, and joint space width.ResultsClinical outcomes were improved in both groups from the postoperative assessment to the final follow-up, which showed no statistically significant difference between groups at the final follow-up. No statistically significant differences were observed with regard to radiographic assessment.ConclusionsSince both groups showed favorable short-term clinical and radiographic outcomes, HTO might be an alternative treatment option for degenerative osteoarthritis with kissing lesions in relatively young patients.
Background Muscle atrophy, leading to muscular dysfunction and weakness, is an adverse outcome of sustained period of glucocorticoids usage. However, the molecular mechanism underlying this detrimental condition is currently unclear. Pyruvate dehydrogenase kinase 4 (PDK4), a central regulator of cellular energy metabolism, is highly expressed in skeletal muscle and has been implicated in the pathogenesis of several diseases. The current study was designed to investigated and delineate the role of PDK4 in the context of muscle atrophy, which could be identified as a potential therapeutic avenue to protect against dexamethasone-induced muscle wasting. Methods The dexamethasone-induced muscle atrophy in C2C12 myotubes was evaluated at the molecular level by expression of key genes and proteins involved in myogenesis, using immunoblotting and qPCR analyses. Muscle dysfunction was studied in vivo in wild-type and PDK4 knockout mice treated with dexamethasone (25 mg/kg body weight, i.p., 10 days). Body weight, grip strength, muscle weight and muscle histology were assessed. The expression of myogenesis markers were analysed using qPCR, immunoblotting and immunoprecipitation. The study was extended to in vitro human skeletal muscle atrophy analysis. Results Knockdown of PDK4 was found to prevent glucocorticoid-induced muscle atrophy and dysfunction in C2C12 myotubes, which was indicated by induction of myogenin (0.3271 ± 0.102 vs 2.163 ± 0.192, ****P < 0.0001) and myosin heavy chain (0.3901 ± 0.047 vs. 0.7222 ± 0.082, **P < 0.01) protein levels and reduction of muscle atrophy F-box (10.77 ± 2.674 vs. 1.518 ± 0.172, **P < 0.01) expression. In dexamethasone-induced muscle atrophy model, mice with genetic ablation of PDK4 revealed increased muscle strength (162.1 ± 22.75 vs. 200.1 ± 37.09 g, ***P < 0.001) and muscle fibres (54.20 ± 11.85% vs. 84.07 ± 28.41%, ****P < 0.0001). To explore the mechanism, we performed coimmunoprecipitation and liquid chromatography-mass spectrometry analysis and found that myogenin is novel substrate of PDK4. PDK4 phosphorylates myogenin at S43/T57 amino acid residues, which facilitates the recruitment of muscle atrophy F-box to myogenin and leads to its subsequent ubiquitination and degradation. Finally, overexpression of non-phosphorylatable myogenin mutant using intramuscular injection prevented dexamethasone-induced muscle atrophy and preserved muscle fibres. Conclusions We have demonstrated that PDK4 mediates dexamethasone-induced skeletal muscle atrophy. Mechanistically, PDK4 phosphorylates and degrades myogenin via recruitment of E3 ubiquitin ligase, muscle atrophy F-box. Rescue of muscle regeneration by genetic ablation of PDK4 or overexpression of non-phosphorylatable myogenin mutant indicates PDK4 as an amenable therapeutic target in muscle atrophy.
Purpose The purpose of this study was to evaluate the wear and survival rates of third-generation ceramic heads on a conventional ultra-high molecular weight polyethylene liner. Materials and Methods A total of 160 hips (147 patients with a mean age of 55.9 years) who underwent total hip arthroplasty using the third-generation ceramic head on a conventional polyethylene liner from March 1998 to August 2003 were reviewed retrospectively. Evaluation of the wear rate for 56 hips (49 patients) followed-up for at least 15 years was performed using the PolyWare program version 8 (Draftware Developers, USA). The Kaplan–Meier survivorship was also evaluated. Results Linear wear and volumetric wear rates were 0.11±0.47 mm/year and 32.75±24.50 mm 3 /year, respectively. Nine revisions were performed during the follow-up period because of cup or stem loosening. The Kaplan–Meier survival rate, using cup revision or total revision total hip arthroplasty (THA) as the endpoint of analysis, was 93.7% at 15 years and 73.6% at 20 years. Conclusion Because all revisions were performed between 15 and 20 years in our study, surgeons should pay greater attention to patients who underwent THA with ceramic-on-polyethylene bearing from 15 years postoperatively. Contemporary alumina ceramic on highly cross-linked polyethylene could certainly be a good alternative bearing couple providing better longevity.
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