Retinoic Acid Therapy and Regulation of Salivary and Serum IL-1β, IL-8 and MCP-1 Levels

Vitamin A (isotretinoin, 13-cis-retinoic acid) and its metabolites are essential for various biological processes, including vision, development, and immune regulation. The periodontium, which consists of tissues supporting the teeth, can transition from health to disease due to multiple factors. The impact of retinoic acid (RA) on periodontal tissues has primarily been investigated in vitro; however, evidence suggests that it may reduce alveolar bone destruction and modulate cytokine expression, indicating potential anti-inflammatory properties. Nevertheless, there is a lack of studies examining the relationship between RA and periodontal health. This study aims to evaluate the potential association between systemic RA use and the periodontal tissue response in terms of inflammatory markers (cytokines: IL-1β, IL-8; chemokines: MCP-1) and to assess dental/periodontal status at different time intervals. The study hypothesizes that RA use will enhance the periodontal tissue response independently of the existing bacterial biofilm and its quantity in the oral cavity, thereby negatively affecting the maintenance of periodontal health through alterations in the periodontium's defense mechanisms. Saliva and serum samples from 24 participants were collected to assess inflammatory responses. The samples were obtained and stored at Istanbul Medipol University Mega Hospital, Turkey, and subsequently transferred to the University of Turku, Finland, for laboratory analyses. Serum and saliva samples were analyzed for inflammatory markers (IL-1β, IL-8, MCP-1) using multiplex immunoassay kits (Millipore; MILLIPLEX® Human Cytokine/Chemokine/Growth Factor Panel A-Immunology Multiplex Assay, #HCYTA-60K, Merck Millipore, Massachusetts, MA). Additionally, sociodemographic, dental, and periodontal data of each participant were analyzed. This study will contribute to understanding the potential relationship between RA and periodontal status, as well as the effects of RA on the inflammatory response of periodontal tissues.