Polymorphisms of pro-inflammatory cytokine genes and the risk for acute suppurative or chronic nonsuppurative apical periodontitis in a Colombian population.
OBJECTIVE
To determine the association of functional single nucleotide polymorphisms in genes of the pro-inflammatory cytokines tumour necrosis factor-α, interleukin-1β, interleukin-8 and interleukin-12B with the development of two clinical forms of apical periodontitis (AP): acute suppurative and chronic nonsuppurative.


METHODS
The study included 120 patients from Bucaramanga City, Colombia, 63 diagnosed with acute suppurative AP (ASAP) and 57 diagnosed with chronic nonsuppurative AP (CNAP). Genotyping for IL1B +3954 (rs1143634), IL8 / CXCL8 -251 (rs4073), IL12B +1188 (rs3212227) and TNFA -308 (rs1800629) was performed by the PCR-restriction fragment length polymorphisms method. The statistical analysis was performed using STATA 10.0 and PLINK V1.07 software.


RESULTS
Significant differences in the distribution of IL8 / CXCL8 -251 A allele (P adjusted = 0.041; OR adjusted = 0.41, CI adjusted = 0.31-0.97) and IL8 / CXCL -251 TT genotype (P adjusted = 0.04; OR adjusted = 2.24, CI adjusted = 1.04-4.84) were observed comparing patients diagnosed with ASAP and CNAP. No association was observed in genotype and allele distribution for other genetic polymorphisms analysed.


CONCLUSIONS
This study provides molecular epidemiological evidence that suggests in the present cohort that IL8 / CXCL8 -251 T allele, which is associated with higher production of IL8/CXCL8, is also associated with a higher risk of developing acute suppurative form of AP, whereas IL8 / CXCL8 -251 A allele, which is associated with lower production of IL8/CXCL8, is associated with chronic nonsuppurative form of AP. This suggests a pivotal role for IL-8/CXCL8 in periapical disease because of its ability to induce chemotaxis and modulating the directed migration of neutrophils to the site of inflammation in response to microbial infection of pulp.
Postgrado de Endodoncia, Facultad de Odontología, Universidad Santo Tomas, Bucaramanga, Colombia.
M P
MP
Amaya
L
L
Criado
B
B
Blanco
M
M
Gómez
O
O
Torres
L
L
Flórez
C I
CI
González
O
O
Flórez
D000225:Adenine; D000293:Adolescent; D000328:Adult; D000483:Alleles; D002634:Chemotaxis, Leukocyte / Q000235:genetics; D015331:Cohort Studies; D003105:Colombia; D016207:Cytokines / Q000235:genetics*; D005260:Female; D005838:Genotype; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology*; D053762:Interleukin-12 Subunit p40 / Q000235:genetics; D053583:Interleukin-1beta / Q000235:genetics; D016209:Interleukin-8 / Q000235:genetics; D008297:Male; D008875:Middle Aged; D020556:Neutrophil Infiltration / Q000235:genetics; D010482:Periapical Abscess / Q000276:immunology*; D010484:Periapical Granuloma / Q000276:immunology*; D012150:Polymorphism, Restriction Fragment Length / Q000235:genetics; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D013941:Thymine; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D055815:Young Adult
D016207:Cytokines; D018836:Inflammation Mediators; D053762:Interleukin-12 Subunit p40; D053583:Interleukin-1beta; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D000225:Adenine; D013941:Thymine