The current paradigm of etiopathogenesis for periodontitis suggests that though periodontal diseases are pathogen and site specific, the host- microbial interactions leading to overproduction of destructive enzymes and pro-inflammatory mediators which determine the extent and severity of tissue destruction.This shift in paradigm has led to better understanding of the underlying host immune responses and to development of novel treatment strategies that may improve therapeutic outcomes and overall clinical management of periodontitis patients.