Pathophysiological events in periodontal disease initiation involve microbial biofilm formation by pathogens like Porphyromonas gingivalis, leading to a host immune response characterized by the production of key pro-inflammatory cytokines, such as interleukin-1beta (IL-1β), produced by various immune and tissue-resident cells, including macrophages, oral fibroblasts, oral epithelial cells, and osteoblasts. Here, IL1B is linked to periodontal disorder.