Introduction: Enterococcus faecalis, a dominant pathogen in pulpal and periapical diseases, induces an inflammatory response leading to increased interleukin 1 beta (IL-1). Studies have implicated the role of Porphyromonas gingivalis and elevated levels of human Nucleotide Oligomerizing Domain Like Receptor Protein Pyrin 3 (NLRP3) inflammasome in addition to IL-1. But due to the dominant role of E. faecalis in retreatment endodontic cases, the purpose of this systematic review was to prove that E faecalis is responsible for the activation of NLRP3 inflammasome and caspase-1 leading to increased levels of IL-1.