ABSTRACT
The involvement of ‘‘endogenous’’ copper in inflammation was discovered in the second half of the last century when evidence was published that: (i) total serum copper markedly increased in aseptic and septic acute inflammation, such as turpentine edema, Staphylococcus aureus abscesses, and typhoid vaccine injection (1953); (ii) total serum copper and ceruloplasmin as well as the ceruloplasmin measured within the inflamed tissue significantly increased in patients suffering from acute periodontal disease (1967); (iii) total serum copper was found significantly elevated in rheumatoid arthritic patients (1968), and in adjuvant-induced arthritis (AA) in the rat (1972), still a very useful experimental model for that human disease (1-5). It was, however, only in 1976, i.e., about two millennia after the first
documented intuition by Celsus on this issue in pharmacology (6), that the researchers’ attention again addressed the role of ‘‘exogenous’’ copper as a potentially effective anti-inflammatory and antiarthritic drug. In fact, in that year, two major papers were published.
