Evaluation of TNF-α, IL-17A, and YKL-40 in GCF and Serum of Psoriasis Patients and Healthy Controls

Background: Psoriasis is a chronic inflammatory skin disease that affects 2-3% of the global population and is linked to immune dysregulation and systemic inflammation. Periodontitis, a chronic inflammatory gum disease, leads to the destruction of gum tissues and bone. Both conditions share common inflammatory pathways, with key immune mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-17A (IL-17A), and YKL-40 playing a role in tissue destruction and disease progression. However, the biological mechanisms linking psoriasis and periodontitis remain unclear, and few studies have examined localized inflammatory responses in the gums of psoriasis patients. Objectives and Methods: This study aims to evaluate the relationship between psoriasis and periodontitis by measuring TNF-α, IL-17A, and YKL-40 levels in both gingival crevicular fluid (GCF) and serum. A total of 100 participants will be recruited and categorized into three groups: Control (C): Healthy individuals without psoriasis or periodontitis. Gingivitis (G): Individuals diagnosed with gingivitis but without psoriasis. Periodontitis (P): Individuals diagnosed with periodontitis but without psoriasis. Psoriasis with gingivitis (PS+G): Individuals diagnosed with gingivitis but without psoriasis. Psoriasis with Periodontitis (PS+P): Individuals with both psoriasis and periodontitis. All participants will undergo periodontal examinations, including plaque index (PI), bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment level (CAL). GCF and blood samples will be collected, and biomarker levels will be analyzed using enzyme-linked immunosorbent assay (ELISA). Expected Outcomes and Clinical Relevance: The study will investigate whether systemic inflammation in psoriasis contributes to periodontal disease progression. If psoriasis patients show higher inflammatory biomarker levels, it may suggest a shared immunopathogenic mechanism. The results may contribute to: Early detection strategies for periodontitis in psoriasis patients. Targeted anti-inflammatory therapies for both conditions. Interdisciplinary collaboration between dermatologists and periodontists for better management. This study is the first to evaluate TNF-α and YKL-40 in the GCF of psoriasis patients, filling a critical gap in the literature regarding localized immune responses. The results could also help identify potential biomarkers that may be useful for monitoring disease progression and treatment responses in psoriasis and periodontitis patients. Conclusion: By investigating the inflammatory relationship between psoriasis and periodontitis, this study aims to uncover new insights into the immune system's role in chronic inflammatory diseases. Understanding these mechanisms could lead to improved diagnostic tools, prevention strategies, and personalized treatment approaches for patients affected by both conditions.

Psoriasis and periodontitis are chronic inflammatory diseases that share key immunopathological mechanisms. Psoriasis is primarily a dermatological condition, but it also exhibits systemic inflammatory characteristics that may contribute to comorbidities such as periodontitis. Periodontitis, a chronic immune-inflammatory condition of the supporting structures of the teeth, is similarly characterized by sustained inflammatory responses and tissue destruction. Emerging evidence suggests that these two diseases may be biologically linked through shared inflammatory pathways. Among the common mediators, tumor necrosis factor-alpha (TNF-α), interleukin-17A (IL-17A), and YKL-40 play prominent roles in the pathogenesis of both conditions. TNF-α contributes to immune activation, tissue breakdown, and bone resorption. IL-17A, associated with Th17-mediated responses, promotes keratinocyte proliferation and inflammatory cell infiltration in psoriasis, while driving extracellular matrix degradation and osteoclastogenesis in periodontitis. YKL-40, a glycoprotein involved in tissue remodeling and inflammation, has been proposed as a potential biomarker for chronic inflammatory diseases, including psoriasis and periodontitis. While elevated levels of these markers have been individually observed in serum or tissues of patients with either condition, limited data exist on their expression in both systemic and local environments-particularly within the gingival crevicular fluid (GCF) of psoriasis patients. This study will address this gap by assessing TNF-α, IL-17A, and YKL-40 levels in GCF and serum samples of individuals with and without psoriasis and periodontal disease. Through a cross-sectional, case-control study design, this research aims to investigate whether systemic inflammation associated with psoriasis correlates with increased periodontal inflammation and whether common biomarkers may indicate a shared pathogenic mechanism. Understanding this potential link could lead to improved interdisciplinary management strategies and earlier identification of periodontal risk in patients with psoriasis.