The long-term subjective and functional results after acute patellar dislocation are satisfactory in most patients. Initial operative repair of the medial structures combined with lateral release did not improve the long-term outcome, despite the very high rate of recurrent instability. A positive family history is a risk factor for recurrence and for contralateral patellofemoral instability. Routine repair of the torn medial stabilizing soft tissues is not advocated for the treatment of acute patellar dislocation in children and adolescents.

Objective. To profile the expression of all known members of the matrix metalloproteinase (MMP), ADAMTS, and tissue inhibitor of metalloproteinases (TIMP) gene families in normal cartilage and cartilage from patients with osteoarthritis (OA).Methods. Human cartilage was obtained from femoral heads at joint replacement for OA or following fracture to the femoral neck. Total RNA was purified, and gene expression was assayed using quantitative real-time polymerase chain reaction.Results. Several members of the above gene families were regulated in OA. Genes that showed increased expression in OA were MMP13, MMP28, and ADAMTS16 (all at P < 0.001), MMP9, MMP16, ADAMTS2, and ADAMTS14 (all at P < 0.01), and MMP2, TIMP3, and ADAMTS12 (all at P < 0.05). Genes with decreased expression in OA were MMP1, MMP3, and ADAMTS1 (all at P < 0.001), MMP10, TIMP1, and ADAMTS9 (all at P < 0.01), and TIMP4, ADAMTS5, and ADAMTS15 (all at P < 0.05). Correlation analysis revealed that groups of genes across the gene families were coexpressed in cartilage.Conclusion. This is the first comprehensive expression profile of all known MMP, ADAMTS, and TIMP genes in cartilage. Elucidation of patterns of expression provides a foundation with which to understand mechanisms of gene regulation in OA and potentially to refine the specificity of antiproteolytic therapies.Osteoarthritis (OA) is a debilitating disease that affects ϳ80% of people over the age of 65 (1). Given the current demographic trend toward an older population, OA, for which age is an important risk factor (2), will be an increasing health and economic burden on society.Degradation of articular cartilage is a major feature of OA. Cartilage is made up of 2 main extracellular matrix (ECM) macromolecules, type II collagen and aggrecan, a large aggregating proteoglycan (3,4). The type II collagen scaffold endows the cartilage with its tensile strength, while the aggrecan, by virtue of its high negative charge, swells against the collagen network as it draws water into the tissue, enabling it to resist compression. Quantitatively more minor components (e.g., types IX, XI, and VI collagen, biglycan, decorin, cartilage oligomeric matrix protein, etc.) also have important roles in controlling matrix structure and organization (5).Normal cartilage ECM is in a state of dynamic equilibrium, with a balance between synthesis and degradation. For the degradative process there is a balance between proteinases that degrade the ECM and their inhibitors. It is generally believed that in OA, a disruption of this balance, in favor of proteolysis, leads to pathologic cartilage destruction.The matrix metalloproteinases (MMPs) are a family of 23 enzymes in humans which facilitate ECM turnover and breakdown under normal and disease conditions (6). The MMP family contains the only mammalian proteinases that can specifically degrade triple-helical collagens at neutral pH. These so-called collagenases specifically cleave a single locus in all 3 collagen chains at a point three-quarters from the N-terminus of...

Objective. To use an in vitro model of chondrogenesis to identify microRNAs (miRNAs) with a functional role in cartilage homeostasis.Methods. The expression of miRNAs was measured in the ATDC5 cell model of chondrogenesis using microarray and was verified using quantitative reverse transcription-polymerase chain reaction. MicroRNA expression was localized by in situ hybridization. Predicted miRNA target genes were validated using 3-untranslated region-Luc reporter plasmids containing either wild-type sequences or mutants of the miRNA target sequence. Signaling through the Smad pathway was measured using a (CAGA) 12 -Luc reporter.Results. The expression of several miRNAs was regulated during chondrogenesis. These included 39 miRNAs that are coexpressed with miRNA-140 (miR-140), which is known to be involved in cartilage homeostasis and osteoarthritis (OA). Of these miRNAs, miR-455 resides within an intron of COL27A1 that encodes a cartilage collagen. When human OA cartilage was compared with cartilage obtained from patients with femoral neck fractures, the expression of both miR-140-5p and miR-455-3p was increased in OA cartilage. In situ hybridization showed miR-455-3p expression in the developing limbs of chicks and mice and in human OA cartilage. The expression of miR-455-3p was regulated by transforming growth factor ␤ (TGF␤) ligands, and miRNA regulated TGF␤ signaling. ACVR2B, SMAD2, and CHRDL1 were direct targets of miR-455-3p and may mediate its functional impact on TGF␤ signaling.Conclusion. MicroRNA-455 is expressed during chondrogenesis and in adult articular cartilage, where it can regulate TGF␤ signaling, suppressing the Smad2/3 pathway. Diminished signaling through this pathway during the aging process and in OA chondrocytes is known to contribute to cartilage destruction. We propose that the increased expression of miR-455 in OA exacerbates this process and contributes to disease pathology.Osteoarthritis (OA) is a degenerative joint disease characterized by degradation of articular cartilage, thickening of subchondral bone, and formation of osteophytes (1). The etiology of OA is complex, with the contribution of genetic, developmental, biochemical, and biomechanical factors. Chondrocytes are the only cells in cartilage and are responsible for the synthesis and turnover of extracellular matrix (ECM), which is crucial to tissue function.During development, mesenchymal cells aggregate and differentiate into chondrocytes, which undergo a series of differentiation events: proliferation, hypertrophy, terminal differentiation, mineralization, and programmed cell death. Blood vessels penetrate the calcified matrix, bringing in osteoblasts that build new bone. The cartilage model grows by rounds of chondrocyte cell

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We performed two independent, randomised, controlled trials in order to assess the potential benefits of immediate weight-bearing mobilisation after rupture of the tendo Achillis. The first trial, on operatively-treated patients showed an improved functional outcome for patients mobilised fully weight-bearing after surgical repair. Two cases of rerupture in the treatment group suggested that careful patient selection is required as patients need to follow a structured rehabilitation regimen. The second trial, on conservatively-treated patients, provided no evidence of a functional benefit from immediate weight-bearing mobilisation. However, the practical advantages of immediate weight-bearing did not predispose the patients to a higher complication rate. In particular, there was no evidence of tendon lengthening or a higher re-rupture rate. We would advocate immediate weight-bearing mobilisation for the rehabilitation of all patients with rupture of the tendo Achillis.