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.
Full Text
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call