Low-field magnetic resonance imaging study on carpal arthritis in systemic sclerosis--low-grade erosive arthritis of carpal bones is an unexpected and frequent disease manifestation.

Introduction: The aim of the present study was to assess the prevalence and characteristics of subclinical arthritis of carpal and metacarpophalangeal joints in patients with systemic sclerosis (SSc).

Methods: Low-field (0.2 T) magnetic resonance imaging (MRI) was performed in consecutive patients with SSc attending our center between January 2010 and March 2011.

Endocardial and myocardial involvement in systemic sclerosis--is there a relevant inflammatory component?

Objectives: Myocardial manifestations of systemic sclerosis are mainly due to fibrotic remodeling. We report on two cases, where an endocardial and myocardial inflammation may be a relevant component of cardiac disease.

Case Series: Case 1 presented with fulminant tricuspid failure in the absence of pulmonary hypertension and with newly developing systemic sclerosis.

Update on the profile of the EUSTAR cohort: an analysis of the EULAR Scleroderma Trials and Research group database.

Objectives: Systemic sclerosis (SSc) is a rare disease requiring multicentre collaboration to reveal comprehensive details of disease-related causes for morbidity and mortality.

Methods: The European League Against Rheumatism (EULAR) Scleroderma Trials and Research (EUSTAR) group initiated a database to prospectively gather key data of patients with SSc using a minimal essential dataset that was reorganised in 2008 introducing new items. Baseline visit data of patients who were registered between 2004 and 2011 were analysed using descriptive statistics.

Arthritis in patients with systemic sclerosis.

Background: Systemic sclerosis (SSc) is a connective tissue diseases characterised by excessive thickening of the dermis in addition to affection of internal organs. Many patients experience musculoskeletal symptoms, but arthritis is still considered to be a rare manifestation. Therefore, we analysed a cohort of SSc patients in our department and related the findings to published data.

Antitumor necrosis factor-α antibody-coupled gold nanorods as nanoprobes for molecular optoacoustic imaging in arthritis.

Optoacoustic molecular imaging can provide spatially resolved information about the presence of molecular markers in vivo. We synthesized elongated gold nanorods having an absorption maximum in the range of 1064 nm modified with the antibodies infliximab and certolizumab for targeting TNF-α to detect inflammation in arthritic mouse knees. We showed an differential enhancement of optoacoustic signal amplitudes after the injection of infliximab-, but not certolizumab-modified and PEGylated control particles on arthritic and healthy control mice by using a fast-scanning optoacoustic imaging platform based on a pulsed Nd:YAG laser and a single focused ultrasound transducer.

Endogenous regeneration after collagenase-induced knee joint damage in the adult newt Notophthalmus viridescens.

Objectives: To determine whether adult newts (Notophthalmus viridescens) are able to repair experimentally-induced joint damage in order to generate a model system for the study of endogenous joint regeneration.

Methods: Joint instability and articular cartilage lesions of the knee joint of adult newts (N viridescens) were induced by intra-articular injection of collagenase. The changes over time were analysed clinically, by MRI, histologically and by reverse transcription PCR to detect selected relevant markers.

Synovial fibroblasts spread rheumatoid arthritis to unaffected joints.

Active rheumatoid arthritis originates from few joints but subsequently affects the majority of joints. Thus far, the pathways of the progression of the disease are largely unknown. As rheumatoid arthritis synovial fibroblasts (RASFs) which can be found in RA synovium are key players in joint destruction and are able to migrate in vitro, we evaluated the potential of RASFs to spread the disease in vivo.

Expression of Brachyury in mesenchymal progenitor cells leads to cartilage-like tissue that is resistant to the destructive effect of rheumatoid arthritis synovial fibroblasts.

Our objectives were to determine the chondrogenic potential of a murine Brachyury-transformed mesenchymal progenitor cell line in the presence of rheumatoid arthritis-activated synovial fibroblasts (RASFs). Brachyury-transformed mesenchymal progenitor cells were implanted alone or combined with RASFs isolated from diseased human joints in each of six immunodeficient SCID mice. De novo tissue formation was analysed by histology and immunohistochemistry after 60 days.

Animal models for arthritis.

Animal models for rheumatic diseases complement human investigations to study in detail pathogenic hypotheses and therapeutic strategies. An overview of animal studies in the last years shows examples for ideas taken from bench to bedside and from bedside to bench. Depending on the disease studied, progress includes a refinement of physiological and pathogenic thinking and a better definition of promising cellular and molecular therapeutic targets.

Expression of PSACH-associated mutant COMP in tendon fibroblasts leads to increased apoptotic cell death irrespective of the secretory characteristics of mutant COMP.

Objective: Pseudoachondroplasia (PSACH) is a dominantly inherited chondrodysplasia associated with mutations of cartilage oligomeric matrix protein (COMP), characterized clinically by disproportionate dwarfism and laxity of joints and ligaments. Studies in chondrocytes and cartilage biopsies suggest that the cartilage disease is caused by retention of mutant COMP in the endoplasmic reticulum of chondrocytes and by disruption of the collagen network of the extracellular matrix. The pathogenesis of the tendon disease remains unclear in the absence of a cell culture model, with available tendon biopsies leading to conflicting results with respect to the intracellular retention of mutant COMP.

Fibroblast activation protein is expressed by rheumatoid myofibroblast-like synoviocytes.

Fibroblast activation protein (FAP), as described so far, is a type II cell surface serine protease expressed by fibroblastic cells in areas of active tissue remodelling such as tumour stroma or healing wounds. We investigated the expression of FAP by fibroblast-like synoviocytes (FLSs) and compared the synovial expression pattern in rheumatoid arthritis (RA) and osteoarthritis (OA) patients. Synovial tissue from diseased joints of 20 patients, 10 patients with refractory RA and 10 patients with end-stage OA, was collected during routine surgery.

Disruption of extracellular matrix structure may cause pseudoachondroplasia phenotypes in the absence of impaired cartilage oligomeric matrix protein secretion.

Pseudoachondroplasia and multiple epiphyseal dysplasia are two dominantly inherited chondrodysplasias associated with mutations in cartilage oligomeric matrix protein (COMP). The rarely available patient biopsies show lamellar inclusions in the endoplasmic reticulum. We studied the pathogenesis of these chondrodysplasias by expressing several disease-causing COMP mutations in bovine primary chondrocytes and found that COMP-associated chondrodysplasias are not exclusively storage diseases.

Successful treatment of disseminated aspergillosis with the combination of voriconazole, caspofungin, granulocyte transfusions, and surgery followed by allogeneic blood stem cell transplantation in a patient with primary failure of an autologous stem cell graft.

The treatment of disseminated aspergillus infections in neutropenic patients remains a major challenge in spite of several new antifungal drugs. We report the case of a patient with multiple myeloma in prolonged neutropenia after primary failure of an autologous stem cell graft who developed invasive aspergillosis despite voriconazole monotherapy. He responded to a combination of voriconazole and caspofungin, supported by granulocyte transfusions and surgery.

Pseudoachondroplasia is caused through both intra- and extracellular pathogenic pathways.

Pseudoachondroplasia is a dominantly inherited chondrodysplasia associated with mutations in cartilage oligomeric matrix protein (COMP). Investigations into the pathogenesis of pseudoachondroplasia are hampered by its rarity. We developed a cell culture model by expressing mutant COMP in bovine primary chondrocytes using a gutless adenoviral vector.

Comparison of three dsDNA-ELISAs with regard to their efficiency in the diagnosis of systemic lupus erythematosus.

We compared the performance of three commercially available anti-double-stranded DNA antibody ELISA kits with respect to their precision, accuracy, linearity, and the detection limit. We tested six sets of patients (lupus erythematosus, scleroderma, rheumatoid arthritis, psoriatic arthritis, hepatitis C, malignancies) to assess specificity, sensitivity, and diagnostic efficiency of the three assays. The diagnostic efficiency of the Crithidia luciliae immunofluorescence test was analyzed as a reference.