The chapter discusses the inflammatory and immune pathways involved in the pathogenesis of periodontal diseases. Inflammation is a physiological response to injuries or infections, but when unresolved, it becomes chronic and involves adaptive immune responses. The etiology of periodontal diseases is primarily bacterial, with the oral cavity hosting a diverse microbial community. The severity of the disease depends on the ecological interactions between the host and microbes. Periodontal diseases are often mediated by the overgrowth of commensal organisms rather than exogenous pathogens. Understanding the regulation of immune mechanisms and inflammatory responses is crucial for comprehending periodontal disease pathogenesis. The initial inflammation in periodontal tissues is a physiological defense mechanism, but if unresolved, it progresses to pathology. The stages of gingivitis and periodontitis are described, highlighting the transition from initial to advanced lesions. The immune response involves both innate and adaptive mechanisms, with neuropeptides playing a significant role in vasodilation, immune cell recruitment, and regulation. Key immune cells and mediators, such as neutrophils, macrophages, T-cells, B-cells, and cytokines, are discussed, along with their roles in inflammation and tissue destruction. The chapter also delves into the role of toll-like receptors in recognizing pathogen-associated molecular patterns and initiating inflammatory responses. Antigen presentation and activation of acquired immunity are crucial for the progression of periodontal diseases. Cytokines and chemokines, such as interleukin-1beta, interleukin-6, and tumor necrosis factor alpha, play essential roles in inflammation and bone resorption. Lipid mediators like prostaglandins and lipid mediators derived from arachidonic acid are also discussed for their inflammatory effects. Finally, the destruction of periodontal tissues, particularly bone, is attributed to the disruption of the balance between osteoblast and osteoclast activities, influenced by bacterial products and inflammatory cytokines. The RANKL/RANK/osteoprotegerin pathway is highlighted as a key regulator of bone remodeling and osteoclastogenesis.The chapter discusses the inflammatory and immune pathways involved in the pathogenesis of periodontal diseases. Inflammation is a physiological response to injuries or infections, but when unresolved, it becomes chronic and involves adaptive immune responses. The etiology of periodontal diseases is primarily bacterial, with the oral cavity hosting a diverse microbial community. The severity of the disease depends on the ecological interactions between the host and microbes. Periodontal diseases are often mediated by the overgrowth of commensal organisms rather than exogenous pathogens. Understanding the regulation of immune mechanisms and inflammatory responses is crucial for comprehending periodontal disease pathogenesis. The initial inflammation in periodontal tissues is a physiological defense mechanism, but if unresolved, it progresses to pathology. The stages of gingivitis and periodontitis are described, highlighting the transition from initial to advanced lesions. The immune response involves both innate and adaptive mechanisms, with neuropeptides playing a significant role in vasodilation, immune cell recruitment, and regulation. Key immune cells and mediators, such as neutrophils, macrophages, T-cells, B-cells, and cytokines, are discussed, along with their roles in inflammation and tissue destruction. The chapter also delves into the role of toll-like receptors in recognizing pathogen-associated molecular patterns and initiating inflammatory responses. Antigen presentation and activation of acquired immunity are crucial for the progression of periodontal diseases. Cytokines and chemokines, such as interleukin-1beta, interleukin-6, and tumor necrosis factor alpha, play essential roles in inflammation and bone resorption. Lipid mediators like prostaglandins and lipid mediators derived from arachidonic acid are also discussed for their inflammatory effects. Finally, the destruction of periodontal tissues, particularly bone, is attributed to the disruption of the balance between osteoblast and osteoclast activities, influenced by bacterial products and inflammatory cytokines. The RANKL/RANK/osteoprotegerin pathway is highlighted as a key regulator of bone remodeling and osteoclastogenesis.