Abstract
Investigations in patients with chronic post-traumatic bone infections show dysfunctions in non-specific host defense mechanisms. There is a decreased availability of complement-derived chemotactic serum factors vs. an increased alternate complement pathway activity. We suppose these dysfunctions are acquired during the development of an acute to a chronic infection. Further investigations will show if there are therapeutic measures which are able to improve host defense mechanisms. Then, the future treatment of chronic bone infections will hopefully be more successful.
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Schedule a callMore From: Archives of orthopaedic and traumatic surgery. Archiv fur orthopadische und Unfall-Chirurgie
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