Periodontal diseases are inflammatory chronic diseases characterized by the disruption of the complex and specific balance between pathogenic bacteria within the dental biofilm and the host defense system, leading to tissue destruction (Chapple et al., 2018). The primary etiological factor in the development of periodontal disease is microbial dental plaque. The main sources of tissue destruction in periodontal tissues are the pathogenic bacteria in the microbial dental plaque and the chemical mediators produced by host defense system cells. Additionally, the severity of tissue destruction varies according to the response of the host (Preshaw, 2008).

Early detection and treatment of periodontal diseases are important for preventing disease progression and preventing tooth/tissue loss. Recent research has demonstrated that the mediators found in the gingival crevicular fluid (GCF), which is the fluid in the periodontal pocket, play a valuable role in the diagnosis of periodontal diseases (Gürlek, Gümüş, Nile, Lappin, & Buduneli, 2017). Throughout the course of periodontal disease, changes in the content of GCF have been shown due to the effects of inflammatory processes. These changes can manifest as increases or decreases in the levels of biochemical substances called mediators. The most commonly investigated mediators include prostaglandins, cytokines, enzymes, and inflammatory markers (Ghallab, 2018).

The detection of these mediators can be used as a clinical tool to diagnose and determine the prognosis of periodontal diseases. For example, high levels of prostaglandins found in GCF can indicate the presence of inflammation and help predict the severity of periodontal disease (Basegmez, Yalcin, Yalcin, Ersanli, & Mijiritsky, 2012). Similarly, the levels of cytokines and enzymes can provide information about the intensity of the inflammatory process and the response to treatment. The biochemical analysis of GCF is a non-invasive method and can be an important step in the early detection and treatment of periodontal diseases (Barros, Hefni, Nepomuceno, Offenbacher, & North, 2018).

Presepsin is a protein used as an inflammatory marker. It is formed by the breakdown of pro-kallikrein 1, a precursor protein present in the bloodstream. Presepsin can be found at increased levels in systemic inflammatory conditions, especially septic shock and infections. Presepsin is being evaluated as a potential indicator for early diagnosis and prognosis (Dierikx et al., 2023). Clinically, measuring presepsin levels can be used to diagnose septic shock early and monitor the response to treatment. Therefore, presepsin can play an important role in the diagnosis and treatment process of many critical illnesses (Okamura, 2015).

Raftlin, also known as lipopolysaccharide-binding protein receptor (LPBRR), is a protein identified in humans and other mammals (Bilgen, Ural, Kurutas, & Bekerecioglu, 2019). It is primarily found in lipid raft domains, specialized regions of the cell membrane enriched with cholesterol and sphingolipids. Raftlin is believed to play a role in various cellular processes, including signal transduction and immune responses (Hursitoglu et al., 2023). One notable function attributed to raftlin is its role in innate immunity. It has been suggested that raftlin interacts with lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria, and may participate in the recognition and response to bacterial infections (Lee, Yoo, Ku, Kim, & Bae, 2014). Additionally, raftlin has been implicated in regulating Toll-like receptor signaling, which is crucial for initiating immune responses against pathogens. While the exact mechanisms and all functions of raftlin are still under investigation, it is considered an interesting protein with potential effects in immune-related processes (Watanabe et al., 2011). Additionally, Bayliss' findings revealed that raftlin is recruited by neuropilin-1 to the activated VEGFR2 complex, thus regulating proangiogenic signaling in endothelial cells (Bayliss, Sundararaman, Granet, & Mellor, 2020). Tatematsu's investigation showcased the role of raftlin in mediating LPS-induced TLR4 internalization and TICAM-1 signaling in human monocyte-derived dendritic cells and macrophages (Tatematsu et al., 2016). These collective results strongly indicate that raftlin contributes to the development of inflammation by participating in the activation of TLR3 and TLR4. Further research is needed to deepen our understanding of raftlin, its cellular biology, and its roles in human health.

The aim of this study is to investigate the relationship between Raftlin and Presepsin levels in periodontal diseases. We hypothesize that the levels of these markers will differ significantly between diseased and healthy conditions. This study seeks to determine whether these mediators can serve as potential indicators in the diagnosis of periodontal diseases.