GFI-1 and Periodontal Disease

Periodontal disease encompasses a spectrum of inflammatory conditions, from gingivitis to more advanced periodontitis, that progressively damage the tooth-supporting tissues. Although its pathogenesis has been studied extensively, the molecular mechanisms driving the inflammatory response in periodontal tissues are not yet fully understood. Inflammasomes, multiprotein complexes known to regulate inflammatory processes, have been proposed to play a role in this pathogenesis, but the contribution of their regulatory proteins remains unclear. This study investigates the potential role of GFI-1, a regulator of inflammasome activity, in periodontal disease, along with its relationship to NLRP3, IL-1β, and NF-κB, structures known to be involved in inflammasome signaling and inflammatory regulation. The study consists of two complementary components. In the in vitro component, human gingival fibroblast cells will be stimulated with lipopolysaccharide (LPS) derived from Porphyromonas gingivalis and/or ATP to model bacterially driven inflammatory activation. Gene expression levels of GFI-1, NLRP3, IL-1β, and NF-κB will be measured using RT-PCR to characterize how these structures respond to bacterial and inflammatory stimuli. In the clinical component, gingival tissue samples will be collected from patients with periodontal disease as well as from periodontally healthy individuals during dental procedures they are already undergoing. Gene and protein expression levels of GFI-1, NLRP3, IL-1β, and NF-κB in these tissues will be assessed using RT-PCR and Western blotting, and IL-1β protein levels will additionally be quantified by ELISA. By comparing findings from the in vitro and clinical components, this study aims to determine whether GFI-1 is dysregulated at the gene and protein level in periodontal disease and to clarify its potential role in disease pathogenesis. These findings may contribute to a better understanding of the inflammatory mechanisms underlying periodontal disease and help inform future research into targeted therapeutic approaches.

Inclusion criteria

• Inclusion criteria for the Healthy Control group were: presence of ≥ 20 teeth in the mouth, probing pocket depth (PPD) ≤ 3 mm, the percentage of bleeding sites for the whole mouth < 10%, and, on radiographic examination, a distance of ≤ 3 mm between the cemento-enamel junction and the alveolar bone crest in 95% of all teeth. Inclusion criteria for the Gingivitis group were: presence of ≥ 20 teeth in the mouth, PPD ≤ 3 mm, % of bleeding sites for the whole mouth ≥ 10%, and, on radiographic examination, a distance of ≤ 3 mm between the cemento-enamel junction and the alveolar bone crest in 95% of all teeth. Inclusion criteria for the Stage 3 Periodontitis group were: presence of ≥ 15 teeth in the mouth, more than 30% of teeth affected by periodontal disease, affected teeth exhibiting probing depths of 6 mm or more and clinical attachment loss (CAL) of ≥ 5 mm, vertical bone loss of 3 mm or more, class 2 or 3 furcation involvement, and radiographic evidence of alveolar bone loss extending to the middle third and beyond (33%) in the relevant teeth

Exclusion criteria

Exclusion criteria

for all groups were defined as: presence of any systemic disease, regular use of any medication, smoking, pregnancy or lactation, periodontal treatment within the last 6 months, antibiotic use within the last 6 months, and the presence of prosthetic restorations on the teeth to be sampled