Association of ficolin-2 gene polymorphisms and susceptibility to systemic lupus erythematosus in Egyptian children and adolescents: a multicenter study.

BACKGROUND: Pediatric-onset SLE (pSLE) is a multisystem autoimmune disease. Recently, the ficolin-2 (FCN2) gene has emerged as a potential candidate gene for susceptibility to SLE. OBJECTIVES: The objective of this study was to evaluate the association of the FCN2 gene polymorphisms at positions -986 (G/A), -602 (G/A), -4 (A/G) and SNP C/T (rs3124954) located in intron 1, with susceptibility to pSLE in Egyptian children and adolescents. METHODS: This was a multicenter study of 280 patients diagnosed with pSLE, and 280 well-matched healthy controls. The FCN2 promoter polymorphisms at -986 G/A (rs3124952), -602 G/A (rs3124953), -4 A/G (rs17514136) and SNP C/T (rs3124954) located in intron 1 were genotyped by polymerase chain reaction, while serum ficolin-2 levels were assessed using enzyme-linked immunosorbent assay. RESULTS: The frequencies of the FCN2 GG genotype and G allele at -986 and -602 positions were significantly more represented in patients with pSLE than in controls (p < 0.001). Conversely, the FCN2 AA genotype and A allele at position -4 were more common in patients than in controls (p < 0.001). Moreover, patients carrying the FCN2 GG genotype in -986 position were more likely to develop lupus nephritis (odds ratio: 2.6 (95% confidence interval: 1.4-4.78); p = 0.006). The FCN2 AA genotype at position -4 was also identified as a possible risk factor for lupus nephritis (odds ratio: 3.12 (95% confidence interval: 1.25-7.84); p = 0.024). CONCLUSION: The FCN2 promoter polymorphisms may contribute to susceptibility to pSLE in Egyptian children and adolescents. Moreover, the FCN2 GG genotype at position -986 and AA genotype at position -4 were associated with low serum ficolin-2 levels and may constitute risk factors for lupus nephritis in pSLE.

Influence of smoking on clinical parameters and gingival crevicular fluid volume in patients with chronic periodontitis.

BACKGROUND: Tobacco smoking is regarded as one of the most significant risk factors for the development and progression of periodontal disease. In particular, studies have shown an alteration in Gingival Crevicular Fluid (GCF) volume and its components in smokers. OBJECTIVE: The purpose of this study was to compare the GCF volume in smoking and non-smoking Saudi subjects with chronic periodontitis. METHODS: In this study, 30 smoking patients and 30 non-smoking patients with chronic periodontitis were enrolled. Periodontal Probing Depth (PPD), Clinical Attachment Level (CAL), Plaque Index (PI), and Bleeding on Probing (BOP) were measured to assess the pattern of periodontal destruction for each patient at six sites in selected teeth. Gingival inflammation was registered at six sites, where Gingival Crevicular Fluid (GCF) was also collected. The GCF volume was measured with a Periotron 8000®. Comparisons were made between smoking and non-smoking groups with periodontitis. RESULTS: Smokers demonstrated significantly deeper periodontal pockets (4.64±0.30 mm) than non-smokers (4.24±0.38 mm). Smoking subjects also presented significantly greater attachment loss (3.08±0.28 mm) than non-smoking subjects (2.74±0.42 mm), whereas the GCF volume was found to be significantly lower in smokers (0.25±0.04 µl) than in non-smokers (0.31±0.05 µl) (P<0.01). Among smoking subjects, lingual sites showed reduced GCF levels compared to facial sites (0.22±0.03 µl vs. 0.25±0.03 µl). CONCLUSION: Smoking appears to have considerable adverse effects on the inflammatory process, thereby promoting the progression of periodontal disease in smokers. CLINICAL SIGNIFICANCE: The adverse effect of smoking on the initiation and progression of periodontal disease is highlighted in this study. In particular, estimation of the GCF volume may serve as an indicator to assess the severity as well as the prognosis of periodontitis in smokers.