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Despite its low incidence septic arthritis remains a serious problem in orthopaedic practice. General or local immunosuppression predisposes for septic arthritis. Thus we see an increasing incidence in elderly patients, in patients suffering from rheumatic diseases and after alloplastic arthroplasty of the hip and of the knee. In septic arthritis the first line of host defense mechanisms is overwhelmed and bacterial multiplication proceeds within the joint. The pathogens found are in 50% to 75% of cases Staphylococci and in 15% to 20% Streptococci. Histologically we initially find an edema of the synovial membrane and a dramatic polymorph-nuclear-cell infiltration. After developing all signs of inflammation, a persistent purulent effusion accumulates and cartilage and bone destruction ensues as a result of proteolytic enzyme activity released from the bacteria and the polymorph nuclear leukocytes. Modern therapy consists of early surgical intervention (synovectomy, debridement) combined with local and systemic antibiotic treatment. The early intervention is one of the main factors for successful management. Thus the interest of early detection of septic arthritis is obvious. The production of neopterin can be related to the activity of the specific antibacterial cell mediated immune response. In the current, study weexamined neopterin levels in 12 patients with septic arthrits and in 8 patients with an infected prosthesis. The results were related to a new inflammation marker (PMN-elastase) and to 4 other 'classical' inflammation markers (ESR, leukocytes, fibrinogen and C-reactive protein). All markers showed a high sensitivity in the detection of septic arthritis. 10 patients with septic arthritis and 5 patients with an infected prosthesis showed pathological neopterin levels > 10 nmol/l.

Similar to other chronic inflammatory diseases such as rheumatoid arthritis the distribution of macrophage subtypes seems to be disturbed in post-traumatic osteomyelitis. This atypical distribution is clearly locally restricted in osteomyelitis. 27E10-positive macrophages found only during the acute phase of inflammation were reduced in 39%, the 25F9-positive subtype, predominating in the late stage of inflammation, was missing in 33%. The antiinflammatory macrophage RM3/1 was decreased in 40% of the osteomyelitis biopsies. Local suppression of macrophage subsets has to be discussed as one of the reasons for the persistence of chronic inflammatory processes in osteomyelitis.

In patients with chronic post-traumatic osteomyelitis, several deficits in immunological response were demonstrated. In a prospective trial of 20 patients with proven osteomyelitis, histological analysis of lymphocyte subsets in peripheral blood and in the infected bone tissue was performed. The effects of chronic osteomyelitis on lymphocyte subsets in the peripheral blood and in inflamed tissue were only slight. The T4/T8 ratio was diminished in only two patients and had no relationship to the clinical course. Interleukin 2 receptor determination was negative in 83% of biopsies of infected tissue. Osteomyelitis may possibly cause a defect in lymphocyte/macrophage cooperation.

Investigations in patients with chronic post-traumatic osteomyelitis could demonstrate several deficits in immunologic response: Phagocytic activity of phagocytes is lowered accompanied by a functional deminution of leukocyte receptors for C3. Intracellular killing is diminished. Investigations concerning T lymphocyte subpopulations verified a decrease in total T cells and helper/inducer T cells. Dysfunctions in specific humoral immune response are still debatable.

PMN elastase, a proteolytic enzyme, is a biochemical marker for pathologic granulocyte stimulation. In the presence of sepsis, excessive neutrophil stimulation occurs and significant amounts of PMN elastase are released into the plasma and serve as an indicator for the severity of the disease and the prognosis. PMN elastase is also a useful parameter for preoperative diagnostic management and postoperative follow-up of bone and joint infections. In patients with osteomyelitis and joint empyema (n = 48) PMN elastase had a sensitivity of 77%, which was only exceeded by that of the unspecific erythrocyte sedimentation rate (sensitivity 89%). Sensitivities of other inflammation parameters were lower: C-reactive protein (CRP) 67%, fibrinogen 50%, neopterin 32% and leukocyte count 21%. Determination of PMN elastase levels was also helpful in postoperative follow-up of patients with bone and joint infections. In the early postoperative period PMN elastase levels normalized more quickly than the other parameters unless patients actually developed complications. At the first postoperative determination (day 2-4 after surgery) 38% of the patients (n = 24) already had PMN elastase levels within the normal range (less than or equal to 40 micrograms/l) (CRP 13%). After 10 days PMN elastase was normal in 57% and CRP in 30% of the patients. Later on both parameters reacted similarly: by the time of discharge from hospital levels of PMN elastase were normal in 70% and CRP levels in 74%.