Preliminary analysis demonstrates altered immune response and identifies molecular markers in severe periodontitis patients.
Periodontitis is an inflammatory disease characterized by the destruction of the periodontal attachment apparatus, which includes alveolar bone, periodontal ligament, and cementum. This destruction is driven by a dysregulated host immune response to pathogenic subgingival biofilm. The present preliminary study aimed to evaluate immune-related gene expression patterns in patients with stage III/IV periodontitis utilizing the NanoString nCounter® platform. Unstimulated saliva samples were collected from twelve individuals: ten with severe periodontitis (stage III/IV) and two periodontally healthy controls. Total RNA was isolated and analyzed using the nCounter® Human Inflammation Panel, which profiles 249 inflammation-associated human genes. Data normalization and differential expression analysis were performed with nSolver™ software. Following quality control, genes with low expression (mean normalized counts < 20) were excluded, resulting in 89 genes available for comparison. Among these, 26 genes (29.2%) met a predefined effect-size threshold (|log2FC| ≥ 1), comprising 23 upregulated and 3 downregulated transcripts in the periodontitis group. Notably, the upregulated genes HLA-DRB1 (p = 0.003; FDR = 0.267) and CCR1 (p = 0.007; FDR = 0.312) exhibited relatively large log2 fold changes and the lowest unadjusted p-values; however, neither retained significance after FDR correction. These findings underscore the feasibility of salivary gene expression profiling as a method for identifying molecular markers associated with disease severity. Given their roles in immune activation and leukocyte recruitment, HLA-DRB1 and CCR1 emerge as potential biomarker candidates for detection, risk stratification, and therapeutic monitoring in periodontitis, necessitating validation in larger, well-characterized cohorts.
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Savina Hadjidekova (2025) studied this question.
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