January 2012

Our understanding of the etiology and pathogenesis of periodontitis has dramatically improved over the last three decades. The primary etiological role of dental biofilm has been well established; a number of periodontal pathogens have been identified and characterized; and wide arrays of virulence factors and pathogenic mechanisms have been determined. It has also become clear that tissue damage in periodontitis is mostly the result of destructive host immune responses rather than a direct bacterial assault, and many of these have been elucidated. To our disappointment, however, this seems to have little clinical significance so far as periodontitis continues to be treated as a non-specific infection, and to impose a high level of morbidity and an economic burden to societies (Loesche and Grossman, 2001).