AbstractThis study tested the hypothesis that in vitro cleavage of C3 could be triggered with similar ease in serum samples from patients with adult periodontitis (n= 26) as in samples from periodontally healthy subjects (n= 13). A lipoteichoic acid, a lipopolysaccharide and an aggregated IgG served as activators of complement. On the average, the periodontitis group generated significantly (p<0.01) more C3d activation fragments than did the healthy group, as judged from rocket immunoelectrophoresis measurements. Cleavage of C4 and factor B were then assayed through immunoblotting, without prior purification of the sera. C4c fragments were seen in all activated samples, the healthy group causing significantly (p<0.05) more C4 conversion than did the periodontitis group. Cleavage of factor B, taken as a measure of soluble amplification convertase formation, was about equal between the groups. We inferred therefore that the 2 groups produced comparable amounts of C3b. The results suggested, however, that periodontitis sera favour breakdown of the opsonin C3b, most likely by activating the regulatory proteins factor H and I. Lipoteichoic acid, causing moderate depletion of C4 and factor B. produced significantly (p<0.01) more C3d fragments than the other two activators examined. It may be that complement activation is down‐regulated in periodontitis sera, perhaps at the expense of adequate local opsonic functio