Pathogenesis of Periodontal Disease in Individuals With Psoriasis

The aim of this study is to evaluate the levels of Th17 cell-associated cytokines (IL-17, IL-21, IL-23) and the salivary stress biomarkers cortisol, dehydroepiandrosterone, and Chromogranin A in the pathogenesis of periodontal disease in individuals with psoriasis, thereby revealing immunological and neuroendocrine interactions. The fundamental question it aims to answer is: What are the biological mechanisms that may increase the risk of periodontal disease in individuals with psoriasis? In this context, the periodontal status of individuals with psoriasis will be clinically assessed, followed by analysis of the levels of Th17-associated cytokines and stress biomarkers in gingival crevicular fluid and saliva samples. Additionally, patients will be asked questions from the Social Appearance Anxiety Scale. The periodontal status of individuals with psoriasis will be determined cross-sectionally, and the resulting biomarker levels will be examined. In addition, the data obtained will be evaluated with statistical analysis in relation to disease severity and clinical parameters.

Psoriasis and periodontitis are chronic inflammatory diseases, and Th17 cells and their secreted cytokines, such as IL-17, IL-21, and IL-23, have been shown to play a significant role in the pathogenesis of both. Recent studies suggest a possible immunological link between these two diseases. Furthermore, in a stress-induced disease like psoriasis, the effects of chronic stress on the immune system are attracting increasing attention. The interaction of neuroendocrine markers, such as cortisol, dehydroepiandrosterone (DHEA), and chromogranin A (CgA), released via the hypothalamic-pituitary-adrenal axis, with immune responses and inflammatory processes may play a significant role in the development of periodontal disease. This project will jointly examine the immunological and neuroendocrine basis of periodontal disease in individuals with psoriasis. Cortisol, DHEA, and CgA levels will be measured in saliva samples, and the relationship between these biomarkers and periodontal parameters will be analyzed. Cytokine levels related to the Th17 pathways will be examined in gingival crevicular fluid to reveal the impact of psoriasis on periodontal tissue. The Social Appearance Anxiety Scale will also be administered. All data obtained will be statistically analyzed. In this context, this study aims to investigate the role of these two chronic and inflammatory diseases (periodontitis and psoriasis) in the Th17 axis based on stress biomarkers (IL-17, IL-21, and IL-23). Thus, we plan to evaluate the relationship between periodontitis and psoriasis biochemically using salivary stress markers (cortisol, DHEA, and CgA) and to evaluate the immunopathogenesis of Th17. The findings of this study may significantly contribute to clinical practice regarding the early diagnosis and management of periodontal disease in individuals with psoriasis. It also aims to encourage multidisciplinary approaches by providing a holistic understanding of the effects of stress on the immune system and periodontal health.