Periodontal disease is a chronic inflammatory infection affecting the gingiva, and is associated with gingiva, periodontal ligament, and alveolar bone loss1. The etiology of periodontal disease as a bacterial infection is well established. Several subgingival bacteria including Porphyromonas gingivalis (P. gingivalis), Prevotella intermedia, Tannerella forsythia, Aggregatibacter actinomycetemcomitans, and spirochetes are leading candidates as etiologic agents in periodontal disease2. Some form of periodontal disease affects 75% of the population; severe forms affect 14% of adults of all ages and 30% of older adults3. Direct treatment costs due to dental diseases including periodontal disease worldwide were estimated at US$298 billion yearly, corresponding to an average of 4.6% of global health expenditure billion yearly4. P. gingivalis is one of the main pathogenic factors of common periodontal disease in adults and is widely recognized as the black pigment producing anaerobic gram-negative bacteria involved in the initial progression of periodontal disease5–8. Furthermore, the burden that P. gingivalis infections place on the body may be larger than previous estimates, as periodontal disease is also associated with an increased risk of systematic symptoms, such as coronary heart disease and diabetes6, 9, 10.