An aseptic inflammation of the clavicle in a patient with Crohn's disease. A potential manifestation of the SAPHO syndrome.

A female patient with Crohn's disease developed an septic osteoarticular involvement of the left clavicle and sterno- and acromioclavicular regions. Repeated surgical revisions combined with a broad-spectrum antimicrobial treatment could not prevent the progress of the disease. However, the patient started to improve after the diagnosis of the SAPHO (synovitis, acne, pustulosis, hyperostosis and osteomyelitis) syndrome was made and the dose of her immunosuppressive therapy increased. This patient reminds of the existence of extraintestinal aseptic infections in association with inflammatory bowel disease (IBD). Moreover, it may provide further evidence on the significant association between SAPHO and IBD.

Activated monocytes induce arthritis-associated changes in mitochondria of cultured synovial fibroblasts.

We have recently shown that synovial fibroblasts cultured from patients with reactive or rheumatoid arthritis exhibit increased autofluorescence when compared with controls. Morphological studies suggested that this increase was related to the anomalous structure of mitochondria in cells cultured from rheumatoid or non-rheumatoid inflammatory synovial tissue. The present study describes attempts to find an explanation for these observations. The effects of conditioned media of cultured mononuclear cells were tested on normal synovial fibroblasts. Conditioned media of monocytes stimulated with lipopolysaccharide or poly-IC induced an increase in the cellular autofluorescence and changes in the morphology of mitochondria in normal fibroblasts. These changes were indistinguishable from those seen in synovial fibroblasts cultured from various arthritides. Indomethacin or gold salts did not abolish the effects of monocyte-conditioned media. Abnormal mitochondria could not be induced in the presence of cycloheximide. This study describes a new aspect of monocyte-fibroblast interactions during rheumatoid and non-rheumatoid inflammation of synovial tissue.