Periodontal disease is a group of chronic inflammatory diseases affecting tooth-supporting tissues. The early stage is the presence of biofilm-associated gingival inflammation which, in patients having juvenile systemic lupus erythematosus (SLE), might function as a reservoir of anaerobic Gram-negative bacteria such as Porphyromonas gingivalis. Porphyromonas gingivalis has been associated with an increased level of anticardiolipin and anti-b2-glycoprotein antibodies in patients with SLE, which implies periodontal disease as a modifiable risk factor for SLE morbility1 . Besides, Porphyromonas gingivalis also express functional endogenous Peptidylarginine deiminase (PAD) enzymes, which catalyzes a citrullination reaction that can lead to formation of citrullinated peptides. PAD can frequently be recognized in sera of patients with rheumatoid arthritis, systemic lupus erythematosusand primary Sjögren syndrome2 . Laugisch et al. 3 reported that PAD secreted by Porphyromonas gingivalis (PPAD) from patients having rheumatoid arthritis and periodontal disease may exert its citrullinating activity in distant regions of the periodontium. Although the relevance of PADs to the pathogenesis of SLE has been wellreported4,5 to the best of our knowledge, no evidence for the presence of PPAD in patients having SLE has been reported