Assessment of the Level of Interleukin-12 in Gingival Crevicular Fluid of a Group of Patients with Aggressive Periodontitis and a Group of Healthy Subjects

Objective Aggressive periodontitis (AgP) is a type of periodontal disease that is relatively prevalent among Sudanese population. The disease generally affects younger individuals and might lead to tooth loss if undetected early, leading to costly and long periodontal treatment. Until today, no reliable detection tool is present, so diagnosis is confirmed only after periodontal tissue loss has already occurred. Interleukin-12 (IL-2) has both proinflammatory and immune-regulatory effects and it has been implicated in the pathogenesis of other inflammatory diseases such as rheumatoid arthritis. However, it was not studied extensively in Sudanese population. Therefore, the aim of this study was to measure and compare the level of IL-12 in the gingival crevicular fluid (GCF) of patients with AgP and healthy subjects without periodontitis. Materials and Methods In this study, 30 patients with AgP and 30 healthy subjects were recruited. The periodontal parameters included bleeding on probing (BOP), periodontal pocket depth (PPD), and clinical attachment level (CAL). GCF levels of IL-12 were measured. Results A total of 60 participants were enrolled in this study with female predominance of 83% and males comprising 17%. The results of this study showed slight elevation in the level of IL-12 in the GCF in AgP group with a mean value of (60.7) and a mean value of (52.7) in the healthy subjects group; however, the difference was not statistically significant (p-value = 0.120). Also, no statistically significant correlation was found between the level of this interleukin and periodontal parameters with slight elevation in AgP group. The p-value for BOP, PPD, and CAL was 0.369, 0.985, and 0.797, respectively. Conclusion The slight increase in the level of IL-12 in GCF of AgP patient and slight elevation in sites with attachment loss suggest a possible role of this cytokine in the pathogenesis of AgP. More studies are required to determine the exact role of this cytokine in AgP.