The periodontal disease-associated bacterium Porphyromonas gingivalis primarily uses FimA fimbriae for adhesion to and colonization in the gingival tissues. The fimbriae show a filamentous structure that is composed of polymer of FimA encoded by the fimA gene. FimC, FimD and FimE are associated with the fimbriae as minor components. FimB anchors the fimbriae to the bacterial surface and regulates their length. The N terminus of FimA is digested in a maturation process, then mature FimA proteins are polymerized to form fimbriae in the outer membrane. Transcription of the fimA gene is regulated by the two-component regulatory system of FimS/R. In addition, expression of FimA is influenced by many environmental factors such as nutrients, environmental stresses, and other bacterial products. The fimA gene shows a genetic polymorphism and it is proposed that there are six genotypes (types I-V and Ib). Types II and IV are frequently isolated from severe periodontal patients. Therefore, they are predicted to be high virulent types, but the molecular mechanisms remain unclear. FimA fimbriae also exhibit a heterogenic antigenicity that is basically consistent with the fimA genotype. The fimbriae interact with many molecules such as surface molecules of host cells, extracellular matrix, salivary components, and bacterial components. Many reports argue binding of FimA residues in the fimbriae to the target molecules, but it is reported that accessory components of FimCDE critically function as an adhesin. Elucidation of adherent mechanism of P. gingivalis through the FimA fimbriae could lead to a development of prophylaxis against the bacterial infection.