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The authors describe three patients in whom septic arthritis of the sternoclavicular joint (SCJ) occurred, drug addiction and human immunodeficiency virus (HIV) infection representing the predisposing conditions. Infectious arthritis is well known in intravenous drug users, but it is rare in HIV positive patients, who are prone to bacterial infections from usual or unusual microorganisms. In one case, staphylococcus aureus methicillin sensitive was responsible for septic arthritis. In another case, SCJ infection was associated with pneumonitis.

Summary Using a double marking technique of peripheral blood lymphocyte (PBL) from 23 patients suffering from rheumatoid arthritis (RA) and 12 normal healthy subjects (NHS), the authors were able to demonstrate that there was no alteration in the OKT8 + ve population of RA patients, when compared with NHS. On the contrary, an increased percentage of the subpopulation of lymphocytes OKT4 + ve was detected. Finally, the presence of a subpopulation of T cells carrying both the receptors for monoclonal antibodies OKT4 and OKT8 has been detected.

<it>Objective</it>. We aimed to investigate the expression of nerve growth factor (NGF) and high affinity NGF receptor (p140 TrkA) on chondrocytes from human healthy and osteoarthritic cartilage. <it>Methods</it>. We recruited 12 patients with osteoarthritis (OA) undergoing surgical knee replacement. Articular cartilage was split into two zones showing macroscopically and histologically the lowest (MIN) and highest (MAX) degree of osteoarthritic damage. Additional specimens of cartilage were obtained from three healthy donors. Chondrocytes were isolated by enzymatic digestion and freshly processed for NGF protein, Trk A detection and mRNA extraction. NGF‐β mRNA was determined by a reverse transcriptase–polymerase chain reaction (RT–PCR). NGF‐β and TrkA expression was evaluated by immunofluorescence and flow cytometry analysis. <it>Results</it>. NGF‐β‐specific mRNA was detected in normal and osteoarthritic chondrocytes. NGF‐β protein levels were low in normal chondrocytes, increased in MIN osteoarthritic cartilage and further enhanced in MAX osteoarthritic cartilage. Likewise, TrkA was scarcely expressed on normal chondrocytes and progressively increased on osteoarthritic chondrocytes based on the extent of anatomic damage. <it>Conclusions</it>. This is the first study showing that human chondrocytes synthesize NFG‐β and express on their surface the high affinity NGFR (p140 TrkA). Of note, NGF‐β and TrkA were upregulated in osteoarthritic chondrocytes suggesting a role of NGF in the pathophysiology of OA. We can speculate that NGF, like other growth factors, stimulates chondrocyte metabolism in the osteoarthritic process.