TGFß1-Induced Transglutaminase-2 Triggers Catabolic Response in Osteoarthritic Chondrocytes by Modulating MMP-13.

BACKGROUND: Transforming growth factor beta 1 (TGFß1) plays an essential role in maintaining cartilage homeostasis. TGFß1 is known to upregulate anabolic processes in articular cartilage, but the role of TGFß1 in chondrocyte catabolism remains unclear. Thus, we examined whether TGFß1 increases catabolic processes in the osteoarthritic joint via transglutaminase 2 (TG2). In this study, we investigated whether interplay between TGFß1 and TG2 mediates chondrocyte catabolism and cartilage degeneration in osteoarthritis. METHODS: To investigate the role of TGFß1 and TG2 in osteoarthritis, we performed immunostaining to measure the levels of TGFß1 and TG2 in 6 human non-osteoarthritic and 16 osteoarthritic joints. We conducted quantitative reverse transcription polymerase chain reaction and western blot analysis to investigate the relationship between TGFß1 and TG2 in chondrocytes and determined whether TG2 regulates the expressions of matrix metalloproteinase (MMP)-13, type II, and type X collagen. We also examined the extent of cartilage degradation after performing anterior cruciate ligament transection (ACLT) and destabilization of the medial meniscus (DMM) surgery in TG2 knock-out mice. RESULTS: We confirmed the overexpression of TGFß1 and TG2 in human osteoarthritic cartilage compared with non-osteoarthritic cartilage. TGFß1 treatment significantly increased the expression of TG2 via p38 and ERK activation. TGFß1-induced TG2 also elevated the level of MMP-13 and type X collagen via NF-κB activation in chondrocytes. Cartilage damage after ACLT and DMM surgery was less severe in TG2 knock-out mice compared with wild-type mice. CONCLUSION: TGFß1 modulated catabolic processes in chondrocytes in a TG2-dependent manner. TGFß1-induced TG2 might be the therapeutic target for treating cartilage degeneration and osteoarthritis.

Supplemental Method for Reduction of Irreducible Mallet Finger Fractures by the 2-Extension Block Technique: The Dorsal Counterforce Technique.

PURPOSE: We suggest a method to achieve anatomical reduction in mallet finger fractures that are insufficiently treated by the 2-extension block wire technique. METHODS: We performed a retrospective review of 18 patients who were found to have an irreducible dorsal fragment and distal interphalangeal joint incongruence owing to rotation of the dorsal fragment in the sagittal plane. In these cases, we additionally employed a dorsal counterforce technique to supplement the 2-extension block technique. An additional K-wire was used to apply counterforce against the distal part of the dorsal fragment and control rotation in the sagittal plane. RESULTS: All 18 fractures united. Congruent joint surfaces and anatomical reduction were seen in all cases. The mean active flexion of the distal interphalangeal joints was 83.8° (range, 79°-88°) and the mean extension loss was 0.4° (range, 0°-4°). CONCLUSIONS: We believe that the dorsal counterforce technique effectively supplements the 2-extension block K-wire technique and aids control of dorsal fragment rotation in the sagittal plane. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic IV.

One-Barrel Microsurgical Fibula Flap for Reconstruction of Large Defects of the Femur.

Various methods for reconstructing large femur bone defects after tumor resection have been introduced. In this study, we reviewed the clinical outcomes of using a 1-barrel free vascularized fibular graft (FVFG) protected by a lateral locking plate for large femoral defects not involving the knee joint.Between August 2007 and August 2013, we treated 7 patients with large femoral bone defects after tumor resection. The mean age of the patients was 19 years (range, 12-36 years), and 3 were women. All defects were free of infection before the procedure. Femoral bone defects were reconstructed using a 1-barrel FVFG protected by a lateral locking plate. The mean bone defect size was 10.5 cm (range, 6-16 cm). We reviewed clinical outcomes at the last follow-up.All patients survived beyond the last follow-up; the mean follow-up period was 54 months (range, 26-100 months). Two patients sustained stress fractures of the FVFG, but the lateral locking plate protected the fractured graft until in situ bone healing obtained. Mean time to bone union of both host-graft junctions was 24 months (range, 18-31 months). The mean Musculoskeletal Tumor Society score (%) was 85.8% (range, 80-95%).A 1-barrel FVFG protected by a lateral locking plate maintained a stable graft-host bone construct, successfully leading to bone healing, even in cases of stress fractures of the graft, and appears to be a good option for large femur bone defects.

A modified deltoid splitting approach with axillary nerve bundle mobilization for proximal humeral fracture fixation.

INTRODUCTION: The deltopectoral and the deltoid splitting approach are commonly used for the treatment of proximal humeral fractures. While the deltopectoral approach requires massive soft tissue devascularization, the deltoid splitting approach needs an additional skipped incision to avoid axillary nerve injury. The purpose of this study was to describe a modified anterolateral deltoid splitting approach with axillary nerve bundle mobilization in the treatment of proximal humeral fractures and to assess its radiologic and clinical outcomes. PATIENTS AND METHODS: Twenty-two consecutive patients with proximal humeral fractures were treated with minimally invasive plate osteosynthesis by using a modified anterolateral deltoid splitting approach with axillary nerve bundle mobilization. The patients were divided into two groups: 10 patients of Neer type 2 or 3 fractures vs. 12 patients of Neer type 4 fractures. The mean age of the study population was 63.5 years (range: 30-80 years). Six patients had valgus impacted fractures, and nine had fractures with medial comminution. RESULTS: Fracture union was achieved in all cases. The mean time to union was 8.6 weeks (range: 6-12 weeks). Major complications, such as avascular necrosis of the humeral head and varus collapse at the fracture site, were not observed. No patients had clinically detectable sensory deficits in the axillary nerve distribution or paralysis of the anterior deltoid muscle. The mean neck-shaft angle at the final follow-up was 136.9° (range, 115°-159°). The mean visual analog score for patient satisfaction was 9.1 (range, 6-10), and the mean Neer scores were 93.5 (range, 84-100). There were no significant differences between the two groups with respect to radiologic and clinical outcomes except Neer scores: 95.8 (range: 86-100) in Neer type 2 or 3 fractures and 91.7 (range: 84-99) in Neer type 4 fractures. CONCLUSION: The use of a modified anterolateral deltoid splitting approach with axillary nerve bundle mobilization in the treatment of proximal humeral fractures yielded excellent outcomes. This approach is a useful alternative to the deltopectoral or the deltoid splitting approaches in the treatment of proximal humeral fractures.