Periodontal disease remains a significant global health concern, characterized by chronic inflammation and destruction of the tooth-supporting structures. While microbial dysbiosis is a well-established factor in its pathogenesis, emerging evidence suggests that epigenetic modifications play a crucial role in the initiation and progression of periodontal disease. This narrative review aims to synthesize current knowledge on the intricate interplay between epigenetics and periodontal disease progression. Epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNAs, regulate gene expression patterns without altering the underlying DNA sequence. Dysregulation of these mechanisms can disrupt inflammatory and immune responses, exacerbating periodontal tissue damage. Various studies have highlighted specific epigenetic alterations associated with periodontal disease, such as aberrant DNA methylation patterns in promoter regions of key inflammatory genes and dysregulated microRNA expression profiles implicated in tissue remodeling processes. Moreover, environmental factors, such as smoking, diet, and stress, can modulate epigenetic signatures, further influencing periodontal disease susceptibility and severity. Understanding the epigenetic landscape of periodontal disease offers new avenues for therapeutic interventions and personalized treatment strategies. Targeting epigenetic regulators may provide innovative approaches to mitigate inflammation, promote tissue regeneration, and ultimately improve clinical outcomes in patients with periodontal disease. In conclusion, epigenetics plays a significant role in periodontal disease progression by regulating inflammatory and tissue remodeling pathways. Future research should continue to elucidate the complex epigenetic mechanisms underlying periodontal disease pathogenesis, paving the way for novel therapeutic interventions and personalized management strategies.