Die Immunpathogenese der Parodontitis – Heutiges Wissen ermöglicht neue diagnostische und therapeutische Wege bei Problempatienten

Das Verständnis um die Pathogenese der Parodontitis hat sich in den letzten 15 Jahren deutlich gewandelt. In der Vergangenheit ging man von einem rein mikrobiologischen und daher eher infektiologischem Geschehen aus (Plaquehypothese). Heute weiß man, dass die Parodontitis als chronisch entzündliche Erkrankung in ihrer Entstehung und Progression multifaktoriell bedingt und dass die Immunantwort des Organismus die entscheidende Stellgröße für die Krankheitsentstehung ist. Auch wenn die Plaquebildung neben exogenen Risikofaktoren wie Rauchen, Stress und mangelnder Mundhygiene weiterhin den wichtigsten Kausalfaktor darstellt, ist die individuelle Entzündungsantwort eines Patienten entscheidend dafür, welche Folgen dieser auslösende Reiz (Biofilm) für den Krankheitsprozess hat. Im vorliegenden Artikel sollen die genannten Kausalfaktoren, ihre labordiagnostischen Nachweisverfahren und die sich aus der Diagnostik ergebenden Therapieoptionen vorgestellt werden.

• 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 Erciyas K et al. Association between TNF-alpha, TGF-beta1, IL-10, IL-6 and IFN-gamma gene polymorphisms and generalized aggressive periodontitis. Clin Invest Med 2010; 33
• 8 Ferreira Jr SB et al. An interleukin-1beta (IL-1beta) single-nucleotide polymorphism at position 3954 and red complex periodontopathogens independently and additively modulate the levels of IL-1beta in diseased periodontal tissues. Infect Immun 2008; 76: 3725-3734
• 9 Feng RN et al. TNF 308 G/A polymorphism and type 1 diabetes: a meta-analysis. Diabetes Res Clin Pract 2009; 85: 4-7
• 10 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
• 11 Kornman KS et al. The interleukin-1 genotype as a severity factor in adult periodontal disease. J Clin Periodontol 1997; 1: 72-77
• 12 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
• 13 Kilpatrick DC. Mannan-binding lectin and its role in innate immunity. Transfusion Med 2002; 12: 335-351
• 14 Kishimoto T. Interleukin-6: discovery of a pleiotropic cytokine. Arthritis Res Ther 2006; (Suppl. 02)
• 15 McGuire MK, Nunn ME. 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 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
• 17 Nibali L et al. Association between periodontitis and common variants in the promoter of the interleukin-6 gene. Cytokine 2009; 45: 50-54
• 18 Nibali L et al. Interleukin-6 polymorphisms are associated with pathogenic bacteria in subjects with periodontitis. J Periodontol 2008; 79: 677-683
• 19 Nikolopoulos GK et al. Cytokine gene polymorphisms in periodontal disease: a meta-analysis of 53 studies including 4178 cases and 4590 controls. J Clin Periodontol 2008; 35: 754-767
• 20 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
• 21 Sorsa T et al. Matrix metalloproteinases: contribution to pathogenesis, diagnosis and treatment of periodontal inflammation. Ann Med 2006; 5: 306-321
• 22 Stashenko P et al. Synergistic interactions between interleukin 1, tumor necrosis factor, and lymphotoxin in bone resorption. J Immunol 1987; 5: 1464-1468
• 23 Szabó GV, Acsády G. Tumornecrosis-Factor-α 308 GA Polymorphism in Atherosclerotic Patients. Pathol Oncol Res 2011; 17: 853-857
• 24 Tsutsumi et al. Mannose binding lectin: Genetics and autoimmmun disease. Autoimmunity Reviews 2005; 4: 364-372
• 25 Wilson AG 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
• 26 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