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Table 3 Target genotypes and study population in association with periodontal disease and smoking

From: Destructive effects of smoking on molecular and genetic factors of periodontal disease

Genotypes

Subjects

Main findings

Articles

IL-1A -889, IL-1B +3954 (originally described as +3953)

134 subjects, USA

The polymorphic IL-1 gene cluster was associated with severity of periodontitis only in non-smokers.

59

IL-1A -889, IL-1B +3954 (originally described as +3953)

28 African-American and 7 Caucasian-American families (early onset periodontitis affected and unaffected subjects), USA

IL-1ß disequilibrium with EOP was found both in smokers and non-smokers.

57

IL-1A -889

46 patients and 12 controls, UK

The carriage of allele 2 was associated with an increase in IL-l α protein levels, especially in non-smokers, while heavy smokers showed reduced levels of IL-lα protein, regardless of genotype.

28

IL-1A -4845, IL-1B -3954

295 Caucasians, Australia

A relationship was observed between the IL-1-positive genotype and increased mean probing pocket depth in non-smokers more than 50 years of age. IL-1 genotype-positive smokers had an increase in the number of probing depths ≥3.5 mm.

56

IL-1A +4845, IL-B +3954

90 patients (non- or former smokers), USA

IL-1 genotype-positive non-smokers or former light smokers were at increased odds of having moderate-to-severe periodontal disease compared to IL-1 genotype-negative patients. The presence of both former moderate smoking history and IL-1-positive genotype showed a lower likelihood of developing the disease when compared to those with presence of only one of the risk factors.

60

IL-1A -889, IL-1B +3954, IL-1RN

154 Caucasians, Germany

Severity of periodontitis was associated with the composite genotype of IL-1α/1β in smokers, while no differences were found in genotype-negative subjects, irrespective of their smoking status.

62

IL-1A -889, IL-1B +3954, IL-1B -511

1085 Caucasians, Germany

An increased risk of periodontal disease and tooth loss was observed for IL-1 genotype-positive smokers.

61, 63, 64

IL-1A -889 IL-1B +3954

330 patients and 101 controls, Chile

The association between positive genotype and periodontitis was independent of smoking status.

58

IL-6 -174

155 patients and 54 controls, Brazil

An association between the G-genotype and periodontal status was observed only in non-smokers.

65

IL-10 -1087

60 patients and 39 controls, Sweden

An association between the GG genotype and periodontal status was more conspicuous in non-smokers.

66

Vitamin D receptor -1056 Taq-I

303 patients and 231 controls, UK

Vitamin D receptor Taq-I TT polymorphism was moderately associated with both the presence and progression of periodontitis in smokers.

70

FcγRIIIb

164 subjects aged 70 years old, Japan

An association between smoking and periodontal disease progression in elderly people with FcγRIIIb-NA2 polymorphism.

68

FcγRIIa

422 Caucasians, USA

FcγRIIa-H/H131 genotype may be associated with chronic periodontitis risk in smokers.

69

FcγRIIIa -158V/F, FcγRIIIb -NA1/NA2

1083 Caucasians, Germany

Smokers show a significantly increased attachment loss in the presence of FcγRIIIb-NA2 allele. The different genotypes show no differences in non-smokers.

63

IFNGR1

62 patients and 56 controls, Norway

In combination with smoking, IFNGR1 was significantly associated with periodontitis.

67

NAT2 -T341C, -G590A, G857A MPO G-463ª

1083 Caucasians, Germany

Smokers with the high activity variant of NAT 2 and MPO are at an increased risk of periodontitis.

63

  1. IL: interleukin, FcγR: Fcγ receptor, IFNGR1: interferon gamma receptor 1, NAT: N-acetyltransferase, MPO: myeloperoxidase