Magnetic resonance imaging identifies features in clinically unaffected knees predicting extension of arthritis in children with monoarthritis.

OBJECTIVE: A proportion of children with oligoarthritis have an aggressive disease course. Identifying these children at presentation would help guide prognosis and management. We examined if magnetic resonance imaging (MRI) of clinically unaffected joints is more sensitive than clinical assessment in identifying those at risk of developing arthritis in more than one joint. METHODS: Ten children were recruited; they had a mean age of 9.4 (range 5.2-14.2) years at presentation of a monoarthritis. MRI of a clinically unaffected knee was performed within 4 months of presentation, and was reported by 2 pediatric radiologists blinded to the clinical findings. All MR examinations included post-gadolinium sequences. Joints with clinically apparent arthritis were recorded regularly over a median of 37.0 (range 6.6-47.0) months by a median of 6.0 (range 2-8) pediatric rheumatologists blinded to the MR result. RESULTS: Four children developed arthritis in other joints over a median of 3.9 (range 3-6) months after the MRI scan; all had abnormal MRI scans at presentation. Three of these developed clinical features in the previously normal knee 4-11 months after MRI identified small joint effusions, synovial hypertrophy, and lymph node enhancement. One child developed a polyarthritis, but never developed clinical features in the imaged knee over 3.8 years of followup. Four other children had a persistent monoarthropathy with a median followup of 29.5 (range 6.6-42.0) months. All 4 had normal MRI. Two children had reactive arthritis. CONCLUSION: MRI distinguished between patients with a persistent monoarthritis and those who developed further clinical arthritis up to 1 year later. The results suggest a widespread inflammatory process may exist in children whose arthritis extends, and this has implications for our understanding of disease and the design and timing of therapeutic interventions.

Imaging of muscle disorders in children.

Muscle inflammation is a relatively common pathological process in childhood. The diagnosis of the underlying cause relies on an appreciation of the pattern of clinical features, as well as the results of biochemical, histological and radiological investigations. Often the clinical and biochemical features are non-specific and insensitive. Consequently, the radiological abnormalities are very important in establishing a diagnosis and an understanding of the imaging features of muscle inflammatory disorders in childhood is needed. Some of the imaging protocols needed to investigate a variety of muscle and soft-tissue inflammatory conditions in childhood are reviewed in this article. Those features that are helpful in narrowing the differential diagnosis are indicated and a logical approach to the investigation of affected children is provided. The value of MR imaging is highlighted.

T-cell activation without proliferation in juvenile idiopathic arthritis.

A study was done to determine if the differentiation and activation phenotype of T cells in synovial fluid (SF) from patients with juvenile idiopathic arthritis (JIA) is associated with T-cell proliferation in situ. Mononuclear cells were isolated from 44 paired samples of peripheral blood and SF. Differentiation and activation markers were determined on CD4 and CD8 T cells by flow cytometry. Cell-cycle analysis was performed by propidium iodide staining, and surface-marker expression was also assessed after culture of the T cells under conditions similar to those found in the synovial compartment. The majority of the T cells in the SF were CD45RO+CD45RBdull. There was greater expression of the activation markers CD69, HLA-DR, CD25 and CD71 on T cells from SF than on those from peripheral blood. Actively dividing cells accounted for less than 1% of the total T-cell population in SF. The presence or absence of IL-16 in T-cell cultures with SF or in a hypoxic environment did not affect the expression of markers of T-cell activation. T cells from the SF of patients with JIA were highly differentiated and expressed early and late markers of activation with little evidence of in situ proliferation. This observation refines and extends previous reports of the SF T-cell phenotype in JIA and may have important implications for our understanding of chronic inflammation.

An association between the acute phase response and patterns of antigen induced T cell proliferation in juvenile idiopathic arthritis.

The aim of this research was to determine whether all memory T cells have the same propensity to migrate to the joint in patients with juvenile idiopathic arthritis. Paired synovial fluid and peripheral blood mononuclear cell proliferative responses to a panel of antigens were measured and the results correlated with a detailed set of laboratory and clinical data from 39 patients with juvenile idiopathic arthritis. Two distinct patterns of proliferative response were found in the majority of patients: a diverse pattern, in which synovial fluid responses were greater than peripheral blood responses for all antigens tested; and a restricted pattern, in which peripheral blood responses to some antigens were more vigorous than those in the synovial fluid compartment. The diverse pattern was generally found in patients with a high acute phase response, whereas patients without elevated acute phase proteins were more likely to demonstrate a restricted pattern. We propose that an association between the synovial fluid T cell repertoire and the acute phase response suggests that proinflammatory cytokines may influence recruitment of memory T cells to an inflammatory site, independent of their antigen specificity. Additionally, increased responses to enteric bacteria and the presence of alphaEbeta7 T cells in synovial fluid may reflect accumulation of gut associated T cells in the synovial compartment, even in the absence of an elevated acute phase response. This is the first report of an association between the acute phase response and the T cell population recruited to an inflammatory site.