Periodontal diseases are characterized by progressive inflammation that destroys the tooth-supporting tissues, leading to gum bleeding and tooth loss. Porphyromonas gingivalis is considered one of the main etiological agents responsible for the initiation and progression of chronic periodontitis. This gram-negative, anaerobic bacterium is a part of a multi-species oral biofilm. P. gingivalis does not have the full pathway of protoporphyrin IX synthesis, nor does it produce siderophores. Therefore, for survival and proliferation, it requires heme as a source of iron and protoporphyrin IX. In order to obtain heme, P. gingivalis uses a number of
mechanisms that affect the ability of this bacterium to initiate a pathological condition. This
review presents the current knowledge regarding the best-known and characterized systems
involved in heme acquisition by P. gingivalis. We focused on processes occurring in the initial
states of infection, where gingipain, hemagglutinins, and hemolysins play a crucial role. The
mechanisms encoded by hmu, iht and hus operons, including proteins with hemophore-like
properties, as well as TonB-dependent outer membrane receptors are described. We present
their function and participation in the progression of the infection. In addition, we describe
mechanisms produced by P. gingivalis and other periodontopathogens in synergistic processes
promoting the growth and virulence of P. gingivalis. We also describe processes regulating iron
and heme homeostasis, including the homolog of the Fur protein, the two-component system
HaeSR, as well as the OxyR, SigH, and PgDps proteins.