Die Parodontitis ist eine chronisch entzündliche Erkrankung, deren Entstehung und
Progression durch unterschiedliche Faktoren bedingt wird. Neben exogenen Risikofaktoren,
wie Rauchen, Stress und mangelnde Mundhygiene, gilt allgemein eine Verschiebung des
mikrobiellen Keimspektrums in der Mundhöhle und die damit einhergehende steigende
Pathogenität des Biofilms als wichtigster initialer Faktor einer Parodontitis. Ausmaß
und Verlauf der Erkrankung wird dann aber durch die körpereigene Entzündungsreaktion
des Patienten bestimmt. Bereits 1997 wies Kornman [21] darauf hin, dass man dem auslösenden Reiz (Biofilm) auch immer die individuelle
inflammatorische Wirtsreaktion gegenüberstellen muss. Die individuelle Entzündungskompetenz
eines jeden Patienten wird durch genetische Varianten (Polymorphismen) in den für
die Immunantwort relevanten Genen bestimmt und erklärt den genetischen Faktor als
einen entscheidenden Risikofaktor für die Progression der Parodontitis [Abb. 1].
Abb. 1 Die individuelle Entzündungsantwort auf pathogene Bakterien wird u. a. durch genetische
Varianten in den für die Immunantwort relevanten Genen bestimmt.
Literatur
- 1
Assuma R et al..
IL-1 and TNF antagonists inhibit the inflammatory response and bone loss in experimental
periodontitis.
J Immunol.
1998;
160
403-409
- 2
Bouma G et al..
Distribution of four polymorphisms in the tumour necrosis factor (TNF) genes in patients
with inflammatory bowel disease (IBD).
Clin Exp Immunol.
1996;
103
391-396
- 3
Claudino M et al..
The broad effects of the functional IL-10 promoter-592 polymorphism: modulation of
IL-10, TIMP-3, and OPG expression and their association with periodontal disease outcome.
J Leukoc Biol.
2008;
84
1565-1573
- 4
Cominelli F, Pizarro TT.
Interleukin-1 and interleukin-1 receptor antagonist in inflammatory bowel disease.
Aliment Pharmacol Ther.
1996;
2
49-53
- 5
Crawley E et al..
Polymorphic haplotypes of the interleukin-10 5' flanking region determine variable
interleukin-10 transcription and are associated with particular phenotypes of juvenile
rheumatoid arthritis.
Arthritis Rheum.
1999;
42
1101-1108
- 6
D'Aiuto F et al..
Gene polymorphisms in pro-inflammatory cytokines are associated with systemic inflammation
in patients with severe periodontal infections.
Cytokine.
2004;
28
29-34
- 7
Fox SW et al..
Activation of osteoclasts by interleukin-1: divergent responsiveness in osteoclasts
formed in vivo and in vitro.
J Cell Physiol.
2000;
3
334-340
- 8
Fuller K et al..
TNFalpha potently activates osteoclasts, through a direct action independent of and
strongly synergistic with RANKL.
Endocrinology.
2002;
3
1108-1118
- 9
Galbraith GM et al..
Tumor necrosis factor alpha production by oral leukocytes: influence of tumor necrosis
factor genotype.
J Periodontol.
1998;
69
428-433
- 10
Gu W et al..
Identification of interleukin-6 promoter polymorphisms in the Chinese Han population
and their functional significance.
Crit Care Med.
2008;
36
1437-1443
- 11
Kishimoto T.
Interleukin-6: discovery of a pleiotropic cytokine.
Arthritis Res Ther.
2006;
(S 02)
- 12
Kornman S K et al..
The interleukin-1 genotype as a severity factor in adult periodontal disease.
J Clin Periodontol.
1997;
1
72-77
- 13
Laine ML et al..
Polymorphisms of the interleukin-1 gene family, oral microbial pathogens, and smoking
in adult periodontitis.
J Dent Res.
2001;
8
1695-1699
- 14
Le XK et al..
Porphyromonas gingivalis decreases osteoblast proliferation through IL-6-RANKL/OPG
and MMP-9/TIMPs pathways.
Indian J Dent Res.
2009;
2
141-149
- 15
McGuire K M, Nunn E M.
Prognosis versus actual outcome. IV. The effectiveness of clinical parameters and
IL-1 genotype in accurately predicting prognoses and tooth survival.
J Periodontol.
1999;
1
49-56
- 16
Michalowicz BS et al..
Evidence of a substantial genetic basis for risk of adult periodontitis.
J Periodontol.
2000;
11
1699-1707
- 17
Moreira PR et al..
Interleukin-6 expression and gene polymorphism are associated with severity of periodontal
disease in a sample of Brazilian individuals.
Clin Exp Immunol.
2007;
148
119-126
- 18
Nibali L et al..
Interleukin-6 polymorphisms are associated with pathogenic bacteria in subjects with
periodontitis.
J Periodontol.
2008;
79
677-683
- 19
Nibali L et al..
Vitamin D receptor polymorphism (-1056 Taq-I) interacts with smoking for the presence
and progression of periodontitis.
J Clin Periodontol.
2008;
35
561-567
- 20
Nibali L et al..
Association between periodontitis and common variants in the promoter of the interleukin-6
gene.
Cytokine.
2009;
45
50-54
- 21
Page RC, Kornman KS.
The pathogenesis of human periodontitis: an introduction.
Periodontol 2000.
1997;
14
9-11
- 22
Shirodaria S et al..
Polymorphisms in the IL-1A gene are correlated with levels of interleukin-1alpha protein
in gingival crevicular fluid of teeth with severe periodontal disease.
J Dent Res.
2000;
11
1864-1869
- 23
Sorsa T et al..
Matrix metalloproteinases: contribution to pathogenesis, diagnosis and treatment of
periodontal inflammation.
Ann Med.
2006;
5
306-321
- 24
Stashenko P et al..
Synergistic interactions between interleukin 1, tumor necrosis factor, and lymphotoxin
in bone resorption.
J Immunol.
1987;
5
1464-1468
- 25
Tachi Y et al..
Vitamin D receptor gene polymorphism is associated with chronic periodontitis.
Life Sci.
2003;
73
3313-3321
- 26
Trevilatto C P et al..
Polymorphism at position -174 of IL-6 gene is associated with susceptibility to chronic
periodontitis in a Caucasian Brazilian population.
J Clin Periodontol.
2003;
30
438-442
- 27
van der Velden U et al..
The effect of sibling relationship on the periodontal condition.
J Clin Periodontol.
1993;
9
683-690
- 28
Wilson G A et al..
Effects of a polymorphism in the human tumor necrosis factor alpha promotor on transcriptional
activation.
Proc Natl Acad Sci.
1997;
94
3195-3199
- 29
Woo P.
Cytokine polymorphisms and inflammation.
Clin Exp Rheumatol.
2000;
6
767-771
- 30
Zhang X, Teng YT.
Interleukin-10 inhibits gram-negative-microbe-specific human receptor activator of
NF-kappaB ligand-positive CD4+-Th1-cell-associated alveolar bone loss in vivo.
Infect Immun.
2006;
8
4927-4931
Korrespondenzadresse
Dr. Sabine Schütt
Institut für Medizinische Diagnostik
Nicolaistraße 22
12247 Berlin-Steglitz
eMail: s.schuett@IMD-Berlin.de