An acute inflammatory process is the immediate result of the body’s recognition of and reaction to a foreign pathogen and the body’s attempt to eliminate the intruder . A prolonged chronic inflammatory process might depend on the persistence of the pathogens because of the nature of the invaders and/or the inability of the host to eliminate this intruder . The constant host-microbe interactions are exhausting to the host body . During an acute inflammatory response, the natural defensive reaction is more devastating to the body than the invasion itself. The contrary occurs during chronic inflammation, where the overgrowth of an otherwise hidden infection might cause septicemia, micro-circulatory defects, ischemia, and chronic organ failure . Chronic sepsis and multiple organ failure can be consequences of a prolonged chronic inflammatory process . In many cases, the source of inflammation is known, however with poor prospects of eliminating it. Bacteria in the planktonic shape might often be sensitive to immune responses and antibiotics, whereas the coexistence of bacteria in a biofilm makes them resistant to antibiotics. This also contributes to the development of new drug resistant strains [26, 27]. Therefore, it is most important to find out the reason why the infection succeeds in persisting, before it becomes invasive. As a model of chronic organ injury, we have investigated patients with chronic ulcers and have tried to clarify why some ulcers do not heal [28–31]. Periodontitis has been studied in our group with special focus on the role of P. gingivalis in chronic inflammatory diseases . We have shown that stimulation of lymphocytes from a patient who suffered from periodontitis with P. gingivalis caused maturation of cells into antibody secreting, CD38-expressing plasma cells, 2–3 weeks after stimulation. The results from SPR analysis of crevicular fluid samples from patients with periodontitis and controls correlated significantly with RT-PCR results (p >0.05) .