The complement system is an important host response to invading bacteria. Activation leads to deposition on the bacterial surface of C3b and its' inactivation products and phagocytosis of the opsonised bacteria by host cells. Alternatively the entire complement pathway including terminal components C5b-9 may be activated on the cell surface which gives rise to generation and insertion of the membrane attack complex into the bacterial membrane and cell lysis. Bacterial resistance to complement may be by enzyme digestion of complement components or by the generation or acquisition from the host of cell surface molecules which allow the organism to adopt host complement control proteins. The involvement of surface polysaccharides can be deduced from the very strong association of resistance with the presence of capsule and extended or modified LPS O-antigens in several species. However, in many cases the mechanism is unclear. The proteases of Porphyromonas gingivalis breakdown C3 and C5 and prevent the deposition of C3b on the bacterial cell surface. Greater deposition of both C3b and C5b-9 occurs in protease deficient mutants but mutants do not show loss of resistance to complement mediated lysis. Instead, complement resistance in P. gingivalis is associated with the presence on the cell surface of an anionic branched mannan and appears independent of capsule serotype.