Signal-Transducing Adaptor Proteins in Periodontal Disease

Overview

This study will look at certain proteins in the gums, saliva, and gum fluid of people with healthy gums, gingivitis (mild gum inflammation), or periodontitis (more severe gum disease). The proteins to be studied called STAP-1, STAP-2, STAT3, STAT5A, NLRP3, and CASP3, are known to be involved in inflammation and cell health in other diseases, but their role in gum disease is not well understood. Seventy-five healthy adults will be grouped by their gum health status. Samples of saliva and gum fluid will be collected and tested, and gum tissue samples will be collected from a subset of participants during routine dental treatment. Researchers will measure the levels of these proteins and look for patterns linking them to the severity of gum disease. The results are expected to show whether these proteins are found at different levels in people with periodontitis compared to those with healthy gums, suggesting they may play a role in how gum disease develops and progresses. This information may help researchers better understand the biological processes behind periodontal disease and could eventually contribute to new ways of detecting or treating it.

Signal-transducing adaptor proteins (STAPs), particularly STAP-1 and STAP-2, are involved in intracellular signaling pathways that regulate cell growth, immune responses, and inflammatory processes, and have been implicated in the pathogenesis of several chronic inflammatory and malignant conditions. Their regulatory partners, STAT3 and STAT5A, are transcription factors known to modulate immune and inflammatory signaling, while NLRP3 (a key component of the inflammasome) and CASP3 (a central mediator of apoptosis) are closely linked to tissue destruction and programmed cell death in chronic inflammatory diseases. Although periodontal disease is fundamentally driven by a dysregulated host inflammatory and immune response to bacterial biofilm, the involvement of STAP-1, STAP-2, and their associated signaling molecules in this process has not previously been investigated. This study will enroll 75 systemically healthy adults, allocated into three groups of 25 participants each based on periodontal status: periodontally healthy, gingivitis, and periodontitis. Diagnosis and group allocation will be based on standard clinical periodontal parameters. From all 75 participants, gingival crevicular fluid (GCF) and unstimulated whole saliva samples will be collected. In addition, gingival tissue biopsies will be obtained from a subset of 60 systemically healthy participants (20 per group), collected during periodontal or extraction procedures that are independently clinically indicated. GCF and saliva samples will be analyzed for total levels of STAP-1, STAP-2, STAT3, STAT5A, NLRP3, and CASP3 using enzyme-linked immunosorbent assay (ELISA). Gingival tissue samples will be analyzed for relative gene expression of the same six molecules using real-time quantitative polymerase chain reaction (RT-qPCR). Clinical periodontal parameters (such as probing depth, clinical attachment level, bleeding on probing, and plaque index) will be recorded for all participants at the time of sampling. Statistical analyses will compare protein and gene expression levels across the three periodontal groups and will assess correlations among STAP-1, STAP-2, STAT3, STAT5A, NLRP3, and CASP3, as well as their relationships with clinical periodontal parameters, within GCF, saliva, and gingival tissue. The study aims to determine whether STAP family proteins and their related inflammatory/apoptotic signaling molecules are differentially expressed according to periodontal disease severity, and whether they may serve as biological indicators involved in the inflammatory and tissue-destructive processes underlying periodontitis.