Background: Chronic recurrent multifocal osteomyelitis (CRMO) in children is a chronic non-suppurative inflammation involving multiple sites. Some children affected by chronic non-bacterial osteomyelitis (CNO) do not have multiple lesions or a recurrent course. Objective: To characterise the long term outcome of children with the full spectrum of CNO. Methods: 30 children diagnosed with CNO were followed up for a mean of 5.6 years and their disease assessed using a clinical score, multiple imaging, and a diagnostic biopsy, including extensive microbial analysis. Results: 9 patients had unifocal non-relapsing disease, 3 unifocal lesions with relapses, 9 multifocal lesions without relapses, and 9 multifocal lesions with relapses (CRMO). Granulocytes were present significantly more often in CRMO than in unifocal and non-recurrent lesions. Pustulosis was more common in multifocal cases regardless of recurrence. Mean duration of treatment in 15 children with a single occurrence was 9.2 months. Naproxen treatment was generally effective. Naproxen treatment in 12 patients with relapses lasted 25 months. However, 7 of these were not effectively treated with naproxen alone. Five were treated with oral glucocorticoids for 27 days in addition to naproxen, which induced remission in four, lasting for at least 1.5 years. Longitudinal growth of affected bones was not altered, except for the development of hyperostosis. Conclusion: CNO is a spectrum of inflammatory conditions, with CRMO being the most severe. Most children with CNO have a favourable outcome of the disease. Oral glucocorticoids may be necessary in severe recurrent cases.
Objective. To investigate the efficacy and safety of , an antiinflammatory and analgesic agent that acts by selective cyclooxygenase 2 (COX-2) inhibition and is not expected to cause the typical gastrointestinal (GI), renal, and platelet-related side effects associated with inhibition of the COX-1 enzyme.Methods. Four phase I1 trials were performed a 2-week osteoarthritis efficacy trial, a 4-week rheumatoid arthritis efficacy trial, a l-week endoscopic study of GI mucosal effects, and a l-week study of effects on platelet function.Results. The 2 arthritis trials identified SC-58635 dosage levels that were consistently effective in treating the signs and symptoms of arthritis and were distinguished from placebo on standard arthritis scales. In the upper GI endoscopy study, 19% of subjects receiving naproxen (6 of 32) developed gastric ulcers, whereas no ulcers occurred in subjects receiving SC-58635 or placebo. The study of platelet effects revealed no meaningful effect of SC-58635 on platelet aggregation or thromboxane B, levels, whereas aspirin caused significant decreases in 2 of 3 platelet aggregation measures and
Objective. This study was undertaken to test the hypothesis that abnormalities of the subchondral bone can result in osteoarthritis (OA).Methods. We used a knockin model of human osteogenesis imperfecta, the Brittle IV (Brtl) mouse, in which defective type I collagen is expressed in bone. OA in individual mice was documented by micro-magnetic resonance imaging (micro-MRI) and micro-computed tomography (micro-CT). Alterations in the knee joints were confirmed by histopathologic and immunohistochemical analysis. In addition, atomic force microscopy (AFM) was used to assess the ultrastructure of the articular cartilage and subchondral bone matrix.Results. Brtl mice had decreased integrity of bone but initially normal articular cartilage. However, by the second month of life, Brtl mice developed alterations of the cartilage that were characteristic of OA, as documented by micro-CT, micro-MRI, and histologic evaluation. In addition, chondrocyte loss and breakdown of the collagen matrix in the residual cartilage were demonstrated using AFM.Conclusion. The Brtl mouse model demonstrates that progressive destruction of articular cartilage characteristic of OA may be secondary to altered architecture of the underlying subchondral bone.
The development of reactive arthritis, a sterile inflammatory polyarthropathy that primarily affects HLA–B27 positive individuals, has been associated with previous enteric infections caused by various gram‐negative bacteria. The possibility that a common bacterial epitope triggers the disease was investigated by screening a panel of documented arthritogenic Shigella strains as well as 2 epidemic‐associated nonarthritogenic Shigella controls. A 2‐Md plasmid specific to the arthritogenic strains was identified and sequenced. The plasmid encodes a number of small peptides that could be related to the development of reactive arthritis. Within 1 of these is a stretch of 5 consecutive amino acids, inferred from the DNA sequence and contained within an open reading frame, that is homologous to amino acid residues 71–75 of the polymorphic region of the α1 domain of HLA–B27. The data indicate that there is a bacterial plasmid common to arthritogenic Shigella strains that may play a role in triggering reactive arthritis. The finding that this plasmid encodes an epitope shared with HLA–B27 suggests that molecular mimicry may play a role in the induction of this disease.
Objective. To determine whether Shigellaflexneri strains that cause enteric infection and are associated with reactive arthritis (ReA) carry a 2-Md plasmid, pHS-2, which encodes an HLA-B27 mimetic epitope.Methods. Plasmid DNA from Shigella isolates was characterized by DNA-DNA hybridization, restriction endonuclease digestion, and sequencing.Results. S jlexneri strains associated with ReA carried a 2-Md plasmid homologous to pHS-2.Conclusion. The finding of pHS-2 in additional Shigella strains associated with ReA underscores its potential importance in the etiology of the disease.The association between certain enteric bacterial infections and the subsequent development of reactive arthritis (ReA) in HLA-B27 positive subjects has been well documented (1). The temporal relationship between enteric infection and the onset of arthritis symptoms strongly suggests that the infecting microorganism triggers the disease in genetically susceptible individuals. However, the responsible pathogenic mechanism remains elusive. Several hypotheses have been proposed to account for the association of HLA-B27 and bacterially induced ReA. Among them are heightened inflammatory responsiveness in HLA-
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