Methods: 270 patients with aggressive periodontitis were recruited through the European Periodontal Genetics (EPG) consortium. A reference control group was obtained through anonymous blood donors from European Caucasian descent with unknown periodontal status (n=360-720). Five SNP's in CARD4 were genotyped and 4 in CARD15. Three of 4 CARD15 SNP's are associated with the etiology of Crohn’s disease.
Results: Distribution of genotypes was in Hardy-Weinberg-Equilibrium. For the CARD4, the frequencies in the aggressive periodontitis patients of allele 1 were 55%, 46%, 2%, 46% and 95% for SNP's 2, 3, 4, 5 and 7 respectively. The corresponding frequencies for reference controls were 54%, 44%, 4%, 45% and 92%. For CARD15, the frequencies in patients of allele 1 prevalence were 52%, 11%, 6 %, and 4% for SNP's 5, 8, 12 and 13 respectively. The corresponding frequencies for reference controls were 47%, 8%, 3% and 8%. Neither allele frequencies nor genotypes were statistically different between patients and controls.
Conclusions: Although barrier function and host defence play a pivotal role in the pathophysiology of periodontitis, genetic variants that lead to mucosal inflammation in Crohn’s disease are not associated with aggressive periodontis. Further work will concentrate on a systematic evaluation of barrier defence factors including inflammatory cytokines.