From bacterial origins to multifactorial complexity: Tracing the evolution of periodontitis pathogenesis from early era to 2017: A review article

The traditional model of periodontal disease pathogenesis primarily emphasized microbial infection as the central cause. However, a growing body of research has shifted this view toward a more complex interplay between microbial factors, host response, and environmental influences. The paradigm shift in the pathogenesis of periodontal disease reflects a transition from a bacterial-centric model to a multifactorial perspective. Emerging evidence highlights the role of dysbiosis, where a shift in microbial homeostasis due to host and environmental factors contributes significantly to disease progression. The host immune response, genetics, and systemic conditions such as diabetes now play critical roles in modulating periodontal health. Furthermore, lifestyle factors such as smoking exacerbate inflammatory responses, creating a prodestructive environment. This newer understanding emphasizes the dynamic relationship between host susceptibility and microbial virulence rather than solely focusing on bacterial infection. The evolving paradigm in periodontal disease pathogenesis emphasizes a holistic approach, recognizing the contributions of systemic health, genetics, and environmental factors alongside microbial influences. This shift necessitates updated diagnostic, preventive, and therapeutic strategies. This paradigm shift informs more personalized treatment plans, focusing on controlling inflammation, modifiable risk factors, and maintaining microbial balance rather than targeting bacteria alone.