Gingival expression of MMP-1, MMP-9, and HBD-3 in healthy individuals and patients with moderate to severe chronic periodontitis

Periodontitis arises from dysregulated host-microbe interactions, driving progressive tissue degradation. Matrix metalloproteinases (MMPs) and antimicrobial peptides like human β-defensin-3 (HBD-3) serve as pivotal biomarkers in periodontal pathogenesis. This study quantified gingival mRNA expression of MMP-1, MMP-9, and HBD-3 across health, gingivitis, and chronic periodontitis to assess their diagnostic and therapeutic relevance. Gingival biopsies were collected from 23 healthy controls (probing depth [PD] < 3 mm), 18 gingivitis patients, and 19 moderate-to-severe chronic periodontitis patients (PD > 5 mm). RNA extraction utilized FavorPrep™ kits, followed by cDNA synthesis and quantitative real-time PCR (qRT-PCR) with GAPDH normalization. Gene expression was calculated via the 2^−ΔΔCt method. Statistical analyses included Kruskal-Wallis, Games-Howell post-hoc, and Spearman’s correlation (SPSS v20.0; α = 0.05). Chronic periodontitis exhibited significantly elevated MMP-1 expression (31.00 ± 7.1) versus healthy controls (21.26 ± 4.3; p = 0.001), with overall intergroup differences (p = 0.001). HBD-3 expression demonstrated significant variation across groups (p = 0.045), peaking in periodontitis (38.22 ± 9.6), though pairwise comparisons were non-significant. MMP-9 expression showed no intergroup differences (p = 0.688). Critically, HBD-3 expression correlated positively with clinical attachment loss (CAL) in periodontitis (ρ = 0.497; p = 0.030). MMP-1 overexpression in chronic periodontitis underscores its role as a primary mediator of tissue destruction and potential diagnostic biomarker. The HBD-3/CAL correlation suggests compensatory antimicrobial responses during disease progression. These findings nominate MMP-1 as a promising therapeutic target for mitigating periodontal breakdown. Longitudinal validation is warranted for clinical translation.