Microfracture Versus a Porcine-Derived Collagen-Augmented Chondrogenesis Technique for Treating Knee Cartilage Defects: Results at Midterm Follow-up.

Background: Damaged cartilage can be treated using the creation of microfractures (MFxs) or the porcine-derived collagen-augmented chondrogenesis technique (C-ACT).

Purpose: To provide the midterm results of a multicenter randomized controlled trial comparing MFx and C-ACT for knee cartilage defects.

Study Design: Randomized controlled trial; Level of evidence, 1.

Long-term Results of Partial Release Versus Nonrelease of the Posterior Cruciate Ligament at Cruciate-Retaining Total Knee Arthroplasty: Minimum 15-Year Follow-up.

The goal of this study was to compare the clinical and radiologic results of posterior cruciate ligament (PCL) partial release and PCL nonrelease in performing cruciate-retaining total knee arthroplasty (CR-TKA) for a long-term follow-up period of greater than 15 years. A total of 224 patients underwent CR-TKA in our hospital from June 1996 to April 2002 with greater than 15 years of follow-up. We divided the subjects into 2 groups based on release of the PCL.

PPARα-ACOT12 axis is responsible for maintaining cartilage homeostasis through modulating de novo lipogenesis.

Here, in Ppara mice, we found that an increased DNL stimulated the cartilage degradation and identified ACOT12 as a key regulatory factor. Suppressed level of ACOT12 was observed in cartilages of OA patient and OA-induced animal. To determine the role and association of ACOT12 in the OA pathogenesis, we generated Acot12 knockout (KO) (Acot12) mice using RNA-guided endonuclease.

Mechanoreceptors in Remnant Posterior Cruciate Ligament and Achilles Tendon Allografts After Remnant-Preserving Posterior Cruciate Ligament Reconstruction: Hematoxylin-Eosin and Immunohistochemical Assessments.

Background: Mechanoreceptor is a subtype of somatosensory receptor. It conveys extracellular stimuli through intracellular signal conduction via mechanically gated ion channel. It conveys not only kinetic stimuli but also pressure, stretching, touch, and even sound wave.

Quantitative assessment of neural elements in a rat model using nerve growth factor after remnant-preserving anterior cruciate ligament reconstruction: a histological and immunofluorescence pilot study.

Background: Immunofluorescence analyses of anterior cruciate ligament (ACL) allografts following remnant-preserving ACL reconstruction using Achilles tendon allografts have provided evidence for the presence of neural elements. In this study, we aimed to examine the expression of neural elements and quantify the presence of neural cells in ACL remnants and Achilles allografts using nerve growth factor (NGF) therapy after remnant-preserving ACL reconstruction.

Methods: Experiments were conducted on 5 pairs of rats (approximately 8 weeks old and weighing 320 g at the time of surgery).

Microfractures Versus a Porcine-Derived Collagen-Augmented Chondrogenesis Technique for Treating Knee Cartilage Defects: A Multicenter Randomized Controlled Trial.

Purpose: The purpose of this study was to evaluate the clinical efficacy and safety of treating patients with a cartilage defect of the knee with microfractures and porcine-derived collagen-augmented chondrogenesis technique (C-ACT).

Methods: One hundred participants were randomly assigned to the control group (n = 48, microfracture) or the investigational group (n = 52, C-ACT). Clinical and magnetic resonance imaging (MRI) outcomes were assessed 12 and 24 months postoperatively for efficacy and adverse events.

Correction to: MicroRNA-9 regulates survival of chondroblasts and cartilage integrity by targeting protogenin.

Following publication of the original article [1], the authors reported that Figs. 3 and 6 are incorrect.

Correction to: Fis1 depletion in osteoarthritis impairs chondrocyte survival and peroxisomal and lysosomal function.

In Fig. 1C, the wrong si-control image was used by mistake.

Tibial Tubercle Osteotomy vs the Extensile Medial Parapatellar Approach in Revision Total Knee Arthroplasty: Is Tibial Tubercle Osteotomy a Harmful Approach?

Background: As the frequency of total knee arthroplasty (TKA) is increasing, long-term follow-up of patients has become essential, and the frequency of revision total knee arthroplasty (R-TKA) due to the occurrence of various complications has also increased. There is controversy regarding which approach has minimal complications and an adequate visual field in R-TKA. Therefore, we compared the clinical and radiological results between the extensile medial parapatellar (EMP) approach and tibial tubercle osteotomy (TTO) for R-TKA.

Correction: HIF-1α:CRAT:miR-144-3p axis dysregulation promotes osteoarthritis chondrocyte apoptosis and VLCFA accumulation.

[This corrects the article DOI: 10.18632/oncotarget.20615.

Comparison of Modified Transtibial and Anteromedial Portal Techniques in Anatomic Single-Bundle ACL Reconstruction.

The purpose of this study was to compare the clinical, 3-dimensional computed tomography, magnetic resonance imaging, and second-look arthroscopic findings of the modified transtibial technique with those of the anteromedial portal technique in single-bundle anterior cruciate ligament reconstruction (SB-ACLR). Among patients who underwent SB-ACLR from February 2012 to May 2014, 95 patients with a minimum of 36 months of follow-up were included in this retrospective study. Forty-five patients underwent a reconstruction using the modified transtibial technique.

The CH25H-CYP7B1-RORα axis of cholesterol metabolism regulates osteoarthritis.

Osteoarthritis-the most common form of age-related degenerative whole-joint disease-is primarily characterized by cartilage destruction, as well as by synovial inflammation, osteophyte formation and subchondral bone remodelling. However, the molecular mechanisms that underlie the pathogenesis of osteoarthritis are largely unknown. Although osteoarthritis is currently considered to be associated with metabolic disorders, direct evidence for this is lacking, and the role of cholesterol metabolism in the pathogenesis of osteoarthritis has not been fully investigated.

RNA-binding protein ZFP36L1 regulates osteoarthritis by modulating members of the heat shock protein 70 family.

Osteoarthritis (OA) is a whole-joint disease characterized by cartilage destruction and other whole-joint pathological changes. There is currently no effective disease-modifying therapy. Here we investigate the post-transcriptional mRNA regulation of OA-modulating proteins in chondrocytes and show that the ZFP36 family member, ZFP36L1, is specifically upregulated in OA chondrocytes and OA cartilage of humans and mice.

Critical role for arginase II in osteoarthritis pathogenesis.

Objective: Osteoarthritis (OA) appears to be associated with various metabolic disorders, but the potential contribution of amino acid metabolism to OA pathogenesis has not been clearly elucidated. Here, we explored whether alterations in the amino acid metabolism of chondrocytes could regulate OA pathogenesis.

Methods: Expression profiles of amino acid metabolism-regulating genes in primary-culture passage 0 mouse chondrocytes were examined by microarray analysis, and selected genes were further characterised in mouse OA chondrocytes and OA cartilage of human and mouse models.

Pseudoaneurysm Formation due to Popliteal Artery Injury Caused by Drilling during Medial Opening Wedge High Tibial Osteotomy.

We report a case of 53-year-old woman with an injured popliteal artery due to excessive drilling with a drill bit during medial opening wedge high tibial osteotomy (MOWHTO). Pseudoaneurysm was diagnosed three days after surgery and confirmed by urgent computed tomography (CT) angiography. Open vascular surgery with resection of the perivascular hematoma and end-to-end anastomosis using ipsilateral saphenous vein interposition graft was performed.

Suppression of ABCD2 dysregulates lipid metabolism via dysregulation of miR-141:ACSL4 in human osteoarthritis.

Even though increasing evidence indicates the importance of peroxisomal lipid metabolism in regulating biological and pathological events, its involvement in cartilage development has not been well studied. Here, we identified the importance of peroxisomal function, particularly the functional integrity of ABCD2, in the pathogenesis of osteoarthritis (OA). Knockdown of ABCD2 in OA chondrocytes induced the accumulation of very long chain fatty acids (VLCFAs) and apoptotic cell death.

Dysregulation of the NUDT7-PGAM1 axis is responsible for chondrocyte death during osteoarthritis pathogenesis.

Osteoarthritis (OA) is the most common degenerative joint disease; however, its etiopathogenesis is not completely understood. Here we show a role for NUDT7 in OA pathogenesis. Knockdown of NUDT7 in normal human chondrocytes results in the disruption of lipid homeostasis.

Alleviation of Murine Osteoarthritis by Cartilage-Specific Deletion of IκBζ.

Objective: IκBζ, an atypical IκB family member, regulates gene expression in the nucleus as a transcriptional cofactor. Although IκBζ has been extensively studied in the immune system, its specific roles in osteoarthritis (OA) are currently unknown. The objective of this study was to investigate the potential role of IκBζ in chondrocyte catabolism and OA pathogenesis.

A case of bilateral revision total knee arthroplasty using distal femoral allograft-prosthesis composite and femoral head allografting at the tibial site with a varus-valgus constrained prosthesis: ten-year follow up.

Background: We report the successful use of allograft-prosthesis composite (APC) and structural femoral head allografting in the bilateral reconstruction of large femoral and tibial uncontained defects during revision total knee arthroplasty (RTKA).

Case Presentation: A 67-year-old female with degenerative arthritis underwent bilateral total knee arthroplasty (TKA) using the Press Fit Condylar (PFC) modular knee system at our clinic in March, 1996. At 8 years postoperatively, the patient presented with painful, bilateral varus knees, with swelling, limited passive range of motion (ROM), and severe instability.

Estrogen-related receptor γ causes osteoarthritis by upregulating extracellular matrix-degrading enzymes.

The estrogen-related receptor (ERR) family of orphan nuclear receptor is composed of ERRα, ERRβ, and ERRγ, which are known to regulate various isoform-specific functions under normal and pathophysiological conditions. Here, we investigate the involvement of ERRs in the pathogenesis of osteoarthritis (OA) in mice. Among ERR family members, ERRγ is markedly upregulated in cartilage from human OA patients and various mouse models of OA.

HIF-1α:CRAT:miR-144-3p axis dysregulation promotes osteoarthritis chondrocyte apoptosis and VLCFA accumulation.

The functional role(s) of peroxisomes in osteoarthritis remains unclear. We demonstrated that peroxisomal dysfunction in osteoarthritis is responsible for very-long-chain fatty acid (VLCFA) accumulation. Through gene-profiling analyses, we identified as the gene responsible for this event.