Effectiveness of Epigallocatechin-3-Gallate (Green Tea Extract) as Adjunctive Locally Delivered Nanotherapeutic in the Treatment of Stage II Periodontitis (A Randomized Controlled Clinical Trial)Man

Introduction Periodontitis is a complex, chronic inflammatory disease affecting the gingiva and the periodontal tissues, ultimately leading to the destruction of the periodontal ligament and supporting bone. This condition is often triggered by a localized or generalized overgrowth of dysbiotic microorganisms within the dental biofilm. Their presence accelerates the formation of periodontal pockets and subsequent bone loss, ultimately leading to tooth loss. The presence of periodontal pockets acts as a biological niche, promoting the release of pro-inflammatory cytokines and proteolytic enzymes, which further enhance bone resorption and contribute to the progressive breakdown of the periodontal apparatus (1).

The initiation and progression of periodontitis are primarily driven by four interconnected events: periodontal pathogen infection, inflammation, oxidative stress, and autophagy (2). A critical pathogen-associated molecular pattern (PAMP) implicated in periodontitis pathogenesis is lipopolysaccharide (LPS), predominantly derived from Porphyromonas gingivalis. Upon exposure to P. gingivalis LPS, gingival epithelial cells release a spectrum of inflammatory mediators, including interleukin-1β (IL- 1β), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α), all of which exert significant immunomodulatory effects (3).

Crucially, the destructive processes observed in periodontal tissues are not directly caused by the pathogen itself. Instead, they are predominantly a consequence of the host's dysregulated immune response to the pathogenic challenge, compounded by damage induced by reactive oxygen species (ROS), resulting in oxidative protein damage and denaturation, as well as enzyme inhibition (2, 4, 5).

3 The first suggested method for managing periodontal disease is nonsurgical periodontal therapy (NSPT), which is the cornerstone of periodontal therapy (6). The primary goal of the initial phase of periodontal therapy is to reduce inflammation by eliminating local factors using scaling and root planing (SRP). Although, a new attachment is not frequently formed, this therapy reduces the probing pocket depth because of extended junctional epithelium growth or shrinking. The healing result appears to be sufficient currently but is susceptible to future disease progression (7).

While scaling and root planing (SRP) remains the gold standard for managing periodontitis, individuals with advanced forms of the disease may benefit from adjunctive therapeutic strategies. Systemic antibiotics are commonly employed as part of periodontal treatment to help suppress or eliminate residual pathogenic bacteria, serving as a complement to conventional mechanical debridement (8, 9).