TY  - JOUR
AB  - OBJECTIVES: Prompt diagnosis of giant cell arteritis (GCA) with ultrasound is crucial for preventing severe ocular and other complications, yet expertise in ultrasound performance is scarce. The development of an artificial intelligence (AI)-based assistant that facilitates ultrasound image classification and helps to diagnose GCA early promises to close the existing gap. In the projection of the planned AI, this study investigates the minimum image resolution required for human experts to reliably classify ultrasound images of arteries commonly affected by GCA for the presence or absence of GCA. METHODS: Thirty-one international experts in GCA ultrasonography participated in a web-based exercise. They were asked to classify 10 ultrasound images for each of 5 vascular segments as GCA, normal, or not able to classify. The following segments were assessed: (1) superficial common temporal artery, (2) its frontal and (3) parietal branches (all in transverse view), (4) axillary artery in transverse view, and 5) axillary artery in longitudinal view. Identical images were shown at different resolutions, namely 32 × 32, 64 × 64, 128 × 128, 224 × 224, and 512 × 512 pixels, thereby resulting in a total of 250 images to be classified by every study participant. RESULTS: Classification performance improved with increasing resolution up to a threshold, plateauing at 224 × 224 pixels. At 224 × 224 pixels, the overall classification sensitivity was 0.767 (95% CI, 0.737-0.796), and specificity was 0.862 (95% CI, 0.831-0.888). CONCLUSIONS: A resolution of 224 × 224 pixels ensures reliable human expert classification and aligns with the input requirements of many common AI-based architectures. Thus, the results of this study substantially guide projected AI development.
AU  - Bauer, C.J.*
AU  - Chrysidis, S.*
AU  - Dejaco, C.*
AU  - Koster, M.J.*
AU  - Kohler, M.J.*
AU  - Monti, S.M.*
AU  - Schmidt, W.A.*
AU  - Mukhtyar, C.B.*
AU  - Karakostas, P.*
AU  - Milchert, M.*
AU  - Ponte, C.*
AU  - Duftner, C.*
AU  - de Miguel, E.*
AU  - Hocevar, A.*
AU  - Iagnocco, A.*
AU  - Terslev, L.*
AU  - Døhn, U.M.*
AU  - Nielsen, B.D.*
AU  - Juche, A.*
AU  - Seitz, L.*
AU  - Keller, K.K.*
AU  - Karalilova, R.*
AU  - Daikeler, T.*
AU  - Mackie, S.L.*
AU  - Torralba, K.*
AU  - van der Geest, K.S.M.*
AU  - Boumans, D.*
AU  - Bosch, P.*
AU  - Tomelleri, A.*
AU  - Aschwanden, M.*
AU  - Kermani, T.A.*
AU  - Diamantopoulos, A.*
AU  - Fredberg, U.*
AU  - Inanc, N.*
AU  - Petzinna, S.M.*
AU  - Albarqouni, S.
AU  - Behning, C.*
AU  - Schäfer, V.S.*
C1  - 74927
C2  - 57748
CY  - Radarweg 29, 1043 Nx Amsterdam, Netherlands
TI  - Exploring the limit of image resolution for human expert classification of vascular ultrasound images in giant cell arteritis and healthy subjects: The GCA-US-AI project.
JO  - Ann. Rheum. Dis.
VL  - 84
IS  - 9
PB  - Elsevier
PY  - 2025
SN  - 0003-4967
ER  - 

TY  - JOUR
AB  - OBJECTIVES: Osteoarthritis is a complex disease with a huge public health burden. Genome-wide association studies (GWAS) have identified hundreds of osteoarthritis-associated sequence variants, but the effector genes underpinning these signals remain largely elusive. Understanding chromosome organisation in three-dimensional (3D) space is essential for identifying long-range contacts between distant genomic features (e.g., between genes and regulatory elements), in a tissue-specific manner. Here, we generate the first whole genome chromosome conformation analysis (Hi-C) map of primary osteoarthritis chondrocytes and identify novel candidate effector genes for the disease. METHODS: Primary chondrocytes collected from 8 patients with knee osteoarthritis underwent Hi-C analysis to link chromosomal structure to genomic sequence. The identified loops were then combined with osteoarthritis GWAS results and epigenomic data from primary knee osteoarthritis chondrocytes to identify variants involved in gene regulation via enhancer-promoter interactions. RESULTS: We identified 345 genetic variants residing within chromatin loop anchors that are associated with 77 osteoarthritis GWAS signals. Ten of these variants reside directly in enhancer regions of 10 newly described active enhancer-promoter loops, identified with multiomics analysis of publicly available chromatin immunoprecipitation sequencing (ChIP-seq) and assay for transposase-accessible chromatin using sequencing (ATAC-seq) data from primary knee chondrocyte cells, pointing to two new candidate effector genes SPRY4 and PAPPA (pregnancy-associated plasma protein A) as well as further support for the gene SLC44A2 known to be involved in osteoarthritis. For example, PAPPA is directly associated with the turnover of insulin-like growth factor 1 (IGF-1) proteins, and IGF-1 is an important factor in the repair of damaged chondrocytes. CONCLUSIONS: We have constructed the first Hi-C map of primary human chondrocytes and have made it available as a resource for the scientific community. By integrating 3D genomics with large-scale genetic association and epigenetic data, we identify novel candidate effector genes for osteoarthritis, which enhance our understanding of disease and can serve as putative high-value novel drug targets.
AU  - Bittner, N.
AU  - Shi, C.*
AU  - Zhao, D.*
AU  - Ding, J.*
AU  - Southam, L.
AU  - Swift, D.*
AU  - Kreitmaier, P.
AU  - Tutino, M.
AU  - Stergiou, O.
AU  - Cheung, J.T.S.*
AU  - Katsoula, G.
AU  - Hankinson, J.
AU  - Wilkinson, J.M.*
AU  - Orozco, G.*
AU  - Zeggini, E.
C1  - 70255
C2  - 55470
CY  - British Med Assoc House, Tavistock Square, London Wc1h 9jr, England
TI  - Primary osteoarthritis chondrocyte map of chromatin conformation reveals novel candidate effector genes.
JO  - Ann. Rheum. Dis.
PB  - Bmj Publishing Group
PY  - 2024
SN  - 0003-4967
ER  - 

TY  - JOUR
AB  - Background Despite recent advances in the understanding of the genetic architecture of osteoarthritis (OA), only two genetic loci have been identified for OA of the hand, in part explained by the complexity of the different hand joints and heterogeneity of OA pathology. Methods We used data from the Rotterdam Study (RSI, RSII and RSIII) to create three hand OA phenotypes based on clustering patterns of radiographic OA severity to increase power in our modest discovery genome-wide association studies in the RS (n=8700), and sought replication in an independent cohort, the Framingham Heart Study (n=1203). We used multiple approaches that leverage different levels of information and functional data to further investigate the underlying biological mechanisms and candidate genes for replicated loci. We also attempted to replicate known OA loci at other joint sites, including the hips and knees. Results We found two novel genome-wide significant loci for OA in the thumb joints. We identified WNT9A as a possible novel causal gene involved in OA pathogenesis. Furthermore, several previously identified genetic loci for OA seem to confer risk for OA across multiple joints: TGFa, RUNX2, COL27A1, ASTN2, IL11 and GDF5 loci. Conclusions We identified a robust novel genetic locus for hand OA on chromosome 1, of which WNT9A is the most likely causal gene. In addition, multiple genetic loci were identified to be associated with OA across multiple joints. Our study confirms the potential for novel insight into the genetic architecture of OA by using biologically meaningful stratified phenotypes.
AU  - Boer, C.G.*
AU  - Yau, M.S.*
AU  - Rice, S.J.*
AU  - de Almeida, R.C.*
AU  - Cheung, K.*
AU  - Styrkarsdottir, U.*
AU  - Southam, L.
AU  - Broer, L.*
AU  - Wilkinson, J.M.*
AU  - Uitterlinden, A.G.*
AU  - Zeggini, E.
AU  - Felson, D.*
AU  - Loughlin, J.*
AU  - Young, M.*
AU  - Capellini, T.D.*
AU  - Meulenbelt, I.*
AU  - van Meurs, J.B.J.*
C1  - 60428
C2  - 49453
CY  - British Med Assoc House, Tavistock Square, London Wc1h 9jr, England
SP  - 367–375
TI  - Genome-wide association of phenotypes based on clustering patterns of hand osteoarthritis identify WNT9A as novel osteoarthritis gene.
JO  - Ann. Rheum. Dis.
VL  - 80
IS  - 3
PB  - Bmj Publishing Group
PY  - 2021
SN  - 0003-4967
ER  - 

TY  - JOUR
AB  - OBJECTIVES: To determine how gene expression profiles in osteoarthritis joint tissues relate to patient phenotypes and whether molecular subtypes can be reproducibly captured by a molecular classification algorithm. METHODS: We analysed RNA sequencing data from cartilage and synovium in 113 osteoarthritis patients, applying unsupervised clustering and Multi-Omics Factor Analysis to characterise transcriptional profiles. We tested the association of the molecularly defined patient subgroups with clinical characteristics from electronic health records. RESULTS: We detected two patient subgroups in low-grade cartilage (showing no/minimal degeneration, cartilage normal/softening only), with differences associated with inflammation, extracellular matrix-related and cell adhesion pathways. The high-inflammation subgroup was associated with female sex (OR 4.12, p=0.0024) and prescription of proton pump inhibitors (OR 4.21, p=0.0040). We identified two independent patient subgroupings in osteoarthritis synovium: one related to inflammation and the other to extracellular matrix and cell adhesion processes. A seven-gene classifier including MMP13, APOD, MMP2, MMP1, CYTL1, IL6 and C15orf48 recapitulated the main axis of molecular heterogeneity in low-grade knee osteoarthritis cartilage (correlation ρ=-0.88, p<10-10) and was reproducible in an independent patient cohort (ρ=-0.85, p<10-10). CONCLUSIONS: These data support the reproducible stratification of osteoarthritis patients by molecular subtype and the exploration of new avenues for tailored treatments.
AU  - Steinberg, J.
AU  - Southam, L.
AU  - Fontalis, A.*
AU  - Clark, M.J.*
AU  - Jayasuriya, R.L.*
AU  - Swift, D.*
AU  - Shah, K.M.*
AU  - Brooks, R.A.*
AU  - McCaskie, A.W.*
AU  - Wilkinson, J.M.*
AU  - Zeggini, E.
C1  - 61876
C2  - 50494
CY  - British Med Assoc House, Tavistock Square, London Wc1h 9jr, England
SP  - 1070-1074
TI  - Linking chondrocyte and synovial transcriptional profile to clinical phenotype in osteoarthritis.
JO  - Ann. Rheum. Dis.
VL  - 80
IS  - 8
PB  - Bmj Publishing Group
PY  - 2021
SN  - 0003-4967
ER  - 

TY  - JOUR
AU  - Denis, M.C.*
AU  - Karagianni, N.*
AU  - Fuchs, H.
AU  - Gailus-Durner, V.
AU  - Hrabě de Angelis, M.
AU  - Ntari, L.*
AU  - Sakkou, M.*
AU  - Kollias, G.*
C1  - 52151
C2  - 43777
CY  - London
SP  - A49-A49
TI  - TNF delta ARE/+: A multimorbidity model of spondyorthropathies.
JO  - Ann. Rheum. Dis.
VL  - 76
PB  - Bmj Publishing Group
PY  - 2017
SN  - 0003-4967
ER  - 

TY  - JOUR
AU  - Denis, M.C.*
AU  - Ntari, L.*
AU  - Sakkou, M.*
AU  - Chouvardas, P.*
AU  - Prados, A.*
AU  - Fuchs, H.
AU  - Gailus-Durner, V.
AU  - Hrabě de Angelis, M.
AU  - Simic, B.*
AU  - Crucet, M.*
AU  - Lüscher, T.F.*
AU  - Mitchell, K.*
AU  - Schwarzwald, C.*
AU  - Karagianni, N.*
AU  - Kollias, G.*
C1  - 52349
C2  - 43904
CY  - London
SP  - 500-500
TI  - Cardiac, pulmonary and periodontal disease as comorbidities in TNF-driven models of chronic polyarthritis.
JO  - Ann. Rheum. Dis.
VL  - 76
PB  - Bmj Publishing Group
PY  - 2017
SN  - 0003-4967
ER  - 

TY  - JOUR
AB  - OBJECTIVES: The idiopathic inflammatory myopathies (IIMs) are a heterogeneous group of rare autoimmune diseases characterised by muscle weakness and extramuscular manifestations such as skin rashes and interstitial lung disease. We genotyped 2566 IIM cases of Caucasian descent using the Immunochip; a custom array covering 186 established autoimmune susceptibility loci. The cohort was predominantly comprised of patients with dermatomyositis (DM, n=879), juvenile DM (JDM, n=481), polymyositis (PM, n=931) and inclusion body myositis (n=252) collected from 14 countries through the Myositis Genetics Consortium. RESULTS: The human leucocyte antigen (HLA) and PTPN22 regions reached genome-wide significance (p<5×10(-8)). Nine regions were associated at a significance level of p<2.25×10(-5), including UBE2L3, CD28 and TRAF6, with evidence of independent effects within STAT4. Analysis of clinical subgroups revealed distinct differences between PM, and DM and JDM. PTPN22 was associated at genome-wide significance with PM, but not DM and JDM, suggesting this effect is driven by PM. Additional suggestive associations including IL18R1 and RGS1 in PM and GSDMB in DM were identified. HLA imputation confirmed that alleles HLA-DRB1*03:01 and HLA-B*08:01 of the 8.1 ancestral haplotype (8.1AH) are most strongly associated with IIM, and provides evidence that amino acids within the HLA, such as HLA-DQB1 position 57 in DM, may explain part of the risk in this locus. Associations with alleles outside the 8.1AH reveal differences between PM, DM and JDM. CONCLUSIONS: This work represents the largest IIM genetic study to date, reveals new insights into the genetic architecture of these rare diseases and suggests different predominating pathophysiology in different clinical subgroups.
AU  - Rothwell, S.*
AU  - Cooper, R.G.*
AU  - Lundberg, I.E.*
AU  - Miller, F.W.*
AU  - Gregersen, P.K.*
AU  - Bowes, J.*
AU  - Vencovsky, J.*
AU  - Danko, K.*
AU  - Limaye, V.*
AU  - Selva-O'Callaghan, A.*
AU  - Hanna, M.G.*
AU  - Machado, P.M.*
AU  - Pachman, L.M.*
AU  - Reed, A.M.*
AU  - Rider, L.G.*
AU  - Cobb, J.*
AU  - Platt, H.*
AU  - Molberg, O.*
AU  - Benveniste, O.*
AU  - Mathiesen, P.*
AU  - Radstake, T.*
AU  - Doria, A.*
AU  - de Bleecker, J.*
AU  - de Paepe, B.*
AU  - Maurer, B.*
AU  - Ollier, W.E.*
AU  - Padyukov, L.*
AU  - O'Hanlon, T.P.*
AU  - Lee, A.*
AU  - Amos, C.I.*
AU  - Gieger, C.
AU  - Meitinger, T.
AU  - Winkelmann, J.
AU  - Wedderburn, L.R.*
AU  - Chinoy, H.*
AU  - Lamb, J.A.*
C1  - 46793
C2  - 37810
CY  - London
SP  - 1558-1566
TI  - Dense genotyping of immune-related loci in idiopathic inflammatory myopathies confirms HLA alleles as the strongest genetic risk factor and suggests different genetic background for major clinical subgroups.
JO  - Ann. Rheum. Dis.
VL  - 75
IS  - 8
PB  - Bmj Publishing Group
PY  - 2016
SN  - 0003-4967
ER  - 

TY  - JOUR
AB  - Introduction Systemic sclerosis (SSc)-related pulmonary arterial hypertension (PAH) has emerged as a major mortality prognostic factor. Mutations of transforming growth factor beta (TGF beta) receptor genes strongly contribute to idiopathic and familial PAH. Objective To explore the genetic bases of SSc-PAH, we combined direct sequencing and genotyping of candidate genes encoding TGF beta receptor family members. Materials and methods TGF beta receptor genes, BMPR2, ALK1, TGFR2 and ENG, were sequenced in 10 SSc-PAH patients, nine SSc and seven controls. In addition, 22 single-nucleotide polymorphisms (SNP) of these four candidate genes were tested for association in a first set of 824 French Caucasian SSc patients (including 54 SSc-PAH) and 939 controls. The replication set consisted of 1516 European SSc (including 219 SSc-PAH) and 3129 controls from the European League Against Rheumatism Scleroderma Trials and Research group network. Results No mutation was identified by direct sequencing. However, two repertoried SNP, ENG rs35400405 and ALK1 rs2277382, were found in SSc-PAH patients only. The genotyping of 22 SNP including the latter showed that only rs2277382 was associated with SSc-PAH (p=0.0066, OR 2.13, 95% CI 1.24 to 3.65). Nevertheless, this was not replicated with the following result in combined analysis: p=0.123, OR 0.79, 95% CI 0.59 to 1.07. Conclusions This study demonstrates the lack of association between these TGF beta receptor gene polymorphisms and SSc-PAH using both sequencing and genotyping methods.
AU  - Koumakis, E.*
AU  - Wipff, J.*
AU  - Dieudé, P.*
AU  - Ruiz, B.*
AU  - Bouaziz, M.*
AU  - Revillod, L.*
AU  - Guedj, M.*
AU  - Distler, J.H.W.*
AU  - Matucci-Cerinic, M.*
AU  - Humbert, M.*
AU  - Riemekasten, G.*
AU  - Airo, P.*
AU  - Melchers, I.*
AU  - Hachulla, E.*
AU  - Cusi, D.*
AU  - Wichmann, H.-E.
AU  - Hunzelmann, N.*
AU  - Tiev, K.*
AU  - Caramaschi, P.*
AU  - Diot, E.*
AU  - Kowal-Bielecka, O.*
AU  - Cuomo, G.*
AU  - Walker, U.*
AU  - Czirják, L.*
AU  - Damjanov, N.*
AU  - Lupoli, S.*
AU  - Conti, C.*
AU  - Müller-Nurasyid, M.
AU  - Müller-Ladner, U.*
AU  - Riccieri, V.*
AU  - Cracowski, J.-L.*
AU  - Cozzi, F.*
AU  - Bournia, V.K.*
AU  - Vlachoyiannopoulos, P.*
AU  - Chiocchia, G.*
AU  - Boileau, C.*
AU  - Allanore, Y.*
C1  - 10874
C2  - 30376
SP  - 1900-1903
TI  - TGFβ receptor gene variants in systemic sclerosis-related pulmonary arterial hypertension: Results from a multicentre EUSTAR study of European Caucasian patients.
JO  - Ann. Rheum. Dis.
VL  - 71
IS  - 11
PB  - BMJ Publishing Group
PY  - 2012
SN  - 0003-4967
ER  - 

TY  - JOUR
AB  - The development of novel treatments for rheumatoid arthritis (RA) requires the interplay between clinical observations and studies in animal models. Given the complex molecular pathogenesis and highly heterogeneous clinical picture of RA, there is an urgent need to dissect its multifactorial nature and to propose new strategies for preventive, early and curative treatments. Research on animal models has generated new knowledge on RA pathophysiology and aetiology and has provided highly successful paradigms for innovative drug development. Recent focus has shifted towards the discovery of novel biomarkers, with emphasis on presymptomatic and emerging stages of human RA, and towards addressing the pathophysiological mechanisms and subsequent efficacy of interventions that underlie different disease variants. Shifts in the current paradigms underlying RA pathogenesis have also led to increased demand for new (including humanised) animal models. There is therefore an urgent need to integrate the knowledge on human and animal models with the ultimate goal of creating a comprehensive 'pathogenesis map' that will guide alignment of existing and new animal models to the subset of disease they mimic. This requires full and standardised characterisation of all models at the genotypic, phenotypic and biomarker level, exploiting recent technological developments in 'omics' profiling and computational biology as well as state of the art bioimaging. Efficient integration and dissemination of information and resources as well as outreach to the public will be necessary to manage the plethora of data accumulated and to increase community awareness and support for innovative animal model research in rheumatology.
AU  - Kollias, G.*
AU  - Papadaki, P.*
AU  - Apparailly, F.*
AU  - Vervoordeldonk, M.J.*
AU  - Holmdahl, R.*
AU  - Baumans, V.*
AU  - Desaintes, C.*
AU  - di Santo, J.*
AU  - Distler, J.*
AU  - Garside, P.*
AU  - Hegen, M.*
AU  - Huizinga, T.W.*
AU  - Jüngel, A.*
AU  - Klareskog, L.*
AU  - McInnes, I.*
AU  - Ragoussis, I.*
AU  - Schett, G.*
AU  - Hart, B.*
AU  - Tak, P.P.*
AU  - Toes, R.*
AU  - van den Berg, W.*
AU  - Wurst, W.
AU  - Gay, S.*
C1  - 6513
C2  - 28834
CY  - London, UK
SP  - 1357-1362
TI  - Animal models for arthritis: Innovative tools for prevention and treatment.
JO  - Ann. Rheum. Dis.
VL  - 70
IS  - 8
PB  - H.K. Lewis
PY  - 2011
SN  - 0003-4967
ER  - 

TY  - JOUR
AB  - OBJECTIVE: There is a pressing need to develop reliable molecular biomarkers in osteoarthritis. The aim of the study was to identify novel serum biomarkers for osteoarthritis using a metabolomics approach. METHODS: A two-stage study design was utilised. 123 knee osteoarthritis cases and 299 controls were selected from the TwinsUK cohort as a discovery sample. 76 knee osteoarthritis cases and 100 controls from the Chingford Study were used as replication. Knee osteoarthritis was defined as either radiographic, medically diagnosed or total knee joint replacement due to primary osteoarthritis. All the subjects were unrelated white women. Their serum samples were assessed for targeted metabolite profiling by electrospray ionisation tandem mass spectrometry using the AbsoluteIDQ kit. 163 serum metabolites were assessed and their concentrations obtained. The ratios of metabolite concentrations as proxies for enzymatic reaction rates were calculated and tested for the association with knee osteoarthritis. Significance was assessed after adjustment for multiple testing (Bonferroni method) and potential confounders. RESULTS: In the discovery stage, the authors identified 14 ratios significantly associated with knee osteoarthritis with p < or = 1.9 x 10(-6). Two of these 14 ratios were successfully confirmed in the replication stage-the ratios of valine to histidine and xleucine to histidine, with p=0.002. The significance remained after adjustment for age and body mass index. CONCLUSION: This is the first serum-based metabolomic study of osteoarthritis in humans. The branched-chain amino acids to histidine ratio has potential clinical use as an osteoarthritis biomarker and shows the clinical potential of metabolomics.
AU  - Zhai, G.*
AU  - Wang-Sattler, R.
AU  - Hart, D.J.
AU  - Arden, N.K.*
AU  - Hakim, A.J.*
AU  - Illig, T.
AU  - Spector, T.D.*
C1  - 1670
C2  - 27358
SP  - 1227-1231
TI  - Serum branched-chain amino acid to histidine ratio: A novel metabolomic biomarker of knee osteoarthritis.
JO  - Ann. Rheum. Dis.
VL  - 69
IS  - 6
PB  - BMJ Publishing Group
PY  - 2010
SN  - 0003-4967
ER  - 

TY  - JOUR
AB  - Background: Knowledge of the deformational behaviour of articular cartilage in vivo is required to understand the pathogenesis of osteoarthritis and the mechanical target environment of prospective cartilage transplant recipients.
      
      	Objectives: To study the in vivo deformational behaviour of patellar and femorotibial cartilage for different types of physiological activities; and to test the hypothesis that in vivo deformation of cartilage is modified by intense physical exercise.
      
      	Methods: Magnetic resonance imaging and 3D digital image analysis were used to determine cartilage volume before and after physical activity in the patella of 12 volunteers (knee bends, squatting, normal gait, running, cycling). Deformation of femorotibial cartilage was investigated in 10 subjects (knee bends, static compression, high impact loading). Patellar cartilage deformation after knee bends was compared in seven professional weight lifters, seven sprinters, and 14 untrained volunteers.
      
      	Results: Patellar cartilage deformation was −5.9% after knee bends, −4.7% after squatting, −2.8% after normal walking, −5.0% after running, and −4.5% after cycling. The pattern of patellar cartilage deformation corresponded to the range of motion involved in the particular activity. Tibial cartilage deformation was greatest under high impact loading (−7%), but small for other activities. No significant difference was found between athletes and non-athletic controls.
      
      	Conclusions: Patellar cartilage deformation shows a “dose dependent” response, where more intense loading leads to greater deformation. Relatively little deformation was observed in the femorotibial joint, except during high impact activities. The findings provide no evidence that adult human cartilage properties are amendable to training effects in vivo.
AU  - Eckstein, F.*
AU  - Lemberger, B.*
AU  - Gratzke, C.*
AU  - Hudelmaier, M.*
AU  - Glaser, C.*
AU  - Englmeier, K.-H.
AU  - Reiser, M.*
C1  - 5074
C2  - 22751
SP  - 291-295
TI  - In vivo cartilage deformation after different types of activity and its dependence on physical training status.
JO  - Ann. Rheum. Dis.
VL  - 64
PY  - 2005
SN  - 0003-4967
ER  - 

TY  - JOUR
AB  - Objective: To study the correlation between ankle and knee cartilage morphology to test the hypothesis that knee joint cartilage loss in gonarthritis can be estimated retrospectively using quantitative MRI analysis of the knee and ankle and established regression equations; and to test the hypothesis that sex differences in joint surface area are larger in the knee than the ankle, which may explain the greater incidence of knee osteoarthritis in elderly women than in elderly men.
      
      	Methods: Sagittal MR images (3D FLASH WE) of the knee and hind foot were acquired in 29 healthy subjects (14 women, 15 men; mean (SD) age, 25 (3) years), with no signs joint disease. Cartilage volume, thickness, and joint surface area were determined in the knee, ankle, and subtalar joint.
      
      	Results: Knee cartilage volumes and joint surface areas showed only moderate correlations with those of the ankle and subtalar joint (r = 0.33 to 0.81). The correlations of cartilage thickness between the two joints were weaker still (r = −0.05 to 0.53). Sex differences in cartilage morphology at the knee and the ankle were similar, with surface areas being −17.5% to −23.5% lower in women than in men.
      
      	Conclusions: Only moderate correlations in cartilage morphology of healthy subjects were found between knee and ankle. It is therefore impractical to estimate knee joint cartilage loss a posteriori in cross sectional studies by measuring the hind foot and then applying a scaling factor. Sex differences in cartilage morphology do not explain differences in osteoarthritis incidence between men and women in the knee and ankle.
AU  - Eckstein, F.*
AU  - Siedek, V.*
AU  - Glaser, C.*
AU  - Al-Ali, D.*
AU  - Englmeier, K.-H.
AU  - Reiser, M.*
AU  - Graichen, H.*
C1  - 1120
C2  - 22750
SP  - 1490-1495
TI  - Correlation and sex differences between ankle and knee cartilage morphology determined by quantitative magnetic resonance imaging.
JO  - Ann. Rheum. Dis.
VL  - 63
PY  - 2004
SN  - 0003-4967
ER  - 

TY  - JOUR
AB  - Objective-To ascertain the incidence and prevalence of juvenile arthritis in a German urban population. Methods-All 766 paediatricians, orthopaedists, and rheumatologists working in practices or outpatient clinics in 12 south German towns were asked to report all patients who consulted them for juvenile arthritis during the year 1995. Patients with continuing symptoms were followed up for 9-12 months to obtain a final diagnosis. Extended measures of quality control were taken to control for known biases. Results-Of 457 reported cases, 294 were diagnosed with para-/postinfectious arthritis (PPA), 78 with juvenile chronic arthritis (ICA), and IS with other forms of arthritis. Half of the PPA cases were classified as transient synovitis of the hip (SH). For JCA the reported annual incidence was 6.6 and the prevalence 14.8 per 100 000 subjects under 16 years of age. For PPA the reported incidence was 76 and the prevalence 4.4 per 100 000 subjects under 16. The incidence of rheumatic fever was clearly below 1 per 100 000 people under 16. A correction model was used to control for known biases and to adjust the estimates accordingly. Conclusions-The results of this first prospective study on the incidence and prevalence of juvenile arthritis in Germany are consistent with a retrospective study performed in the Berlin area. Based on these results it was estimated that the annual frequency of juvenile arthritis in Germany is as follows: 750-900 incident JCA cases, 21 000 incident SH cases, and 21 000 incidence cases of other forms of PPA a year. The number of incidence cases of rheumatic fever is expected to be markedly lower than 150 a year. The total prevalence is expected to be 3600-4350 JCA cases, 2250-3000 SH cases, and the same number of other forms of PPA.
AU  - von Koskull, St.*
AU  - Truckenbrodt, H.*
AU  - Holle, R.
AU  - Hörmann, A.
C1  - 22169
C2  - 20868
SP  - 940-945
TI  - Incidence and prevalence of juvenile arthritis in an urban population of Southern Germany : A prospective study.
JO  - Ann. Rheum. Dis.
VL  - 60
IS  - 10
PB  - British Med. Journal Publ. Group
PY  - 2001
SN  - 0003-4967
ER  -