Abstract
Chronic periodontitis (CP) is one of the most common chronic inflammatory diseases and cytokines play a pivotal role in the regulation of immune response. Interleukin-4 (IL-4) and interleukin-13 (IL-13) are anti-inflammatory cytokines and several polymorphisms of them have been proved involved in periodontal disease. This study aimed to evaluate whether three single nucleotide polymorphisms (SNPs), rs2070874 and rs2243248 from IL4 and rs1800925 from IL13, are associated with CP in a Han Chinese population consisting of 440 moderate or severe CP patients and 324 healthy controls. Genomic DNA extracted from buccal epithelial cells of the included participants were genotyped using a matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry method. No significant association between rs2070874 or rs1800925 and CP was found, while the frequencies of rs2243248 and two haplotypes C-G-T and C-T-T showed significant differences between the two groups. The results suggest that the polymorphism rs2243248 and haplotypes C-G-T and C-T-T may be associated with CP susceptibility in the present Han Chinese population.
Highlights
As a major cause of tooth loss in adults and one of the most common chronic inflammatory diseases, Chronic periodontitis (CP) is initiated by dental microbial plaque accumulation and characterized by progressive destruction of teeth supporting structures [1]
Since it has been shown that attachment loss in periodontitis is induced by Gram-negative bacteria and mediated by inflammatory activation, candidate genes have frequently been selected from proinflammatory and regulatory cytokines which play an important part in immune response regulations [4]
The study was conducted in accordance with the Declaration of Helsinki (1964), and the protocol was approved by the Ethics Committee of Shanghai Stomatological Disease Center (Project identification code: 2009-005)
Summary
As a major cause of tooth loss in adults and one of the most common chronic inflammatory diseases, CP is initiated by dental microbial plaque accumulation and characterized by progressive destruction of teeth supporting structures [1]. It has been well accepted that CP is initiated by bacterial flora, the dental microbial factor is necessary but not sufficient for the disease onset. Studies of humans and animals indicated that genetic factors could influence inflammatory and immune responses in periodontitis [4,5,6,7]. Since it has been shown that attachment loss in periodontitis is induced by Gram-negative bacteria and mediated by inflammatory activation, candidate genes have frequently been selected from proinflammatory and regulatory cytokines which play an important part in immune response regulations [4]. Soluble proteins secreted by cells, could transmit signals to other cells as a messenger. They initiate, mediate, and control immune and inflammatory responses [5]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
