Buradasınız

AGRESİF PERİODONTİTİS Lİ BİREYLERDE NÜKLEER FAKTÖR KAPPA B AKTİVASYONUN İMMUN OHİSTOKİMYASAL OLARAK İNCELENMESİ: STEREOLOJİK ÇALIŞMA

IMMUNOHISTOCHEMICAL EXAMINATION OF NUCLEAR FACTOR KAPA B ACTIVATION IN INDIVIDUALS WITH AGGRESSIVE PERIODONTITIS: STEREOLOGIC STUDY

Journal Name:

Publication Year:

Abstract (2. Language): 
he purpose of this study was immunohistochemical and stereologic investigation of nuclear and cytoplasmic expression of p50 and p65 subunits of Nuclear Factor kappa B (NF-KB) and the cytoplasmic expression of Inhibitor kappa B (IKB), the inhibitor of NF-KB, in the gingival tissues of subjects with aggressive periodontitis. The study population was consisted of 30 individuals (15 aggressive periodontitis and 15 control) which were referred with different complaints to Ataturk University, Faculty of Dentistry between 2006 and 2007 years. 1 to 2 mm of gingival tissue was biopsied from the buccal side of the teeth of all individuals. Tissues were immediately transferred to 10% neutral buffered formalin and were then sent to immunohistochemical staining. The sections were examined under electron microscope and the numerical values of the stained cells were computed using stereologic method. One-way analysis of variance (ANOVA) and Multiple Range least significant difference (LSD) was used for intergroup comparison (p=0.05). According to the findings of this study, statistically significant differences were found in the number of cytoplasmic and nuclear positive stained cells with p65 and p50 in aggressive periodontitis group compared to control group (p<0.01). However, statistically significant positive correlations were found between laboratory findings and clinical scores (probing depth and clinical attachment level) in aggressive periodontitis group. In conclusion, it was found that NF-KB activation was highly important in patients with aggressive periodontitis. The present study forms the basis for future strategies that will generate specific inhibitors for using NF-KB inhibition to prevent the progressing of periodontitis.
Abstract (Original Language): 
Bu çalışmanın amacı; agresif periodontitisli bireylerin diş eti dokularında Nükleer Faktör kappa B (NF-KB) proteinlerinden p50 ve p65 alt ünitelerinin çekirdek ve sitoplazmik ekspresyonunun ve NF-KB inhibitörü olan İnhibitör kappa B'nin (IKB) sitoplazmik ekspresyonunun immunohistokimyasal ve stereolojik olarak araştırılmasıdır. Çalışma popülasyonunu, Atatürk Üniversitesi Diş Hekimliği Fakültesine 2006-2007 yılları arasında değişik nedenlerle müracaat eden 30 birey (15'i agresif periodontitisli ve 15'i periodontal olarak sağlıklı) oluşturdu. Tüm bireylerden lokal anestezi altında dişlerin bukkal dişeti bölgesinden biyopsi ile 1-2 mm diş eti dokusu alındı. Alınan dişeti dokuları hemen % 101uk nötral tamponlu formalin içerisine konuldu ve sonra immunohistokimyasal boyamaya gönderildi. Elde edilen kesitler elektron mikroskobu altında incelendi ve stereolojik yöntem kullanılarak boyanan hücre sayısal değerleri hesaplandı. Grupların birbirleri ile karşılaştırmalarında Tek Yönlü Varyans Analizi ve Çoklu karşılaştırmalı en küçük önemli fark (LSD) testi (p=0.05) kullanıldı. Çalışma sonuçlarına göre p50 ve p65 ile hem çekirdek hem de sitoplazmada pozitif boyanan hücre sayısı açısından agresif periodontitis grubu ile kontrol grubu arasında istatistiksel olarak anlamlı fark bulundu (p<0.01). Bunun yanı sıra agresif periodontitisli grupta tüm immunohistokimyasal bulgular ile klinik skorlar (Sondalanabilir cep derinliği ve klinik ataşman seviyesi) arasında istatistiksel olarak anlamlı pozitif korelasyonlar tespit edildi. Sonuç olarak, NF-KB aktivasyonu agresif periodontitisli bireylerde oldukça anlamlı bulunmuştur. Bu çalışma periodontitisin ilerleyişini önlemek için NFKB inhibisyonunda kullanılmak üzere spesifik inhibitörlerin üretileceği gelecek stratejilere temel oluşturmaktadır.
84-91

REFERENCES

References: 

1. American Academy of Periodontology: Parameter on aggressive periodontitis. J Periodontal., 2000; 71 (Suppl.): 867-869.
2. Barrington EP, Nevins M. Diagnosing periodontal diseases. J Am Dent Assoc 1990; 121: 460-464.
3. Tonetti MS, Mombelli A. Early-onset periodontitis.
Ann Periodontol 1999; 4: 39-52.
4. American Academy of Periodontology. The new classification for periodontal disease and conditions. Ann Periodontol 1999; 4: 1-108.
5. Darveau hP, Tanner A, Page hC. The microbial challenge in periodontitis. Periodontol 2000 1997;
14: 12-32.
89
Atatürk Üniv. Diş Hek. Fak. Derg.
J Dent Fac Atatürk Uni
Cilt:20, Sayı: 2, Yıl: 2010, Sayfa: 84-91
6. Daniel MA, Van Dyke TE. Alterations in phagocyte function and periodontal infection. J Periodontol
1996; 67: 1070-1075.
7. Yoshie H, Kobayashi T, Tai H, Galicia JC. The role of
genetic polymorphisms in periodontitis. Periodontol
2000 2007; 43: 102-132.
8. Li Q, Verma IM. NF-kB regulation in the immun system. Nature heviews 2002; 2: 725- 735.
9. Verma IM, Stevenson JK, Schwarz EM, Van Antwerp
D, Miyamoto S. hel/NF-kB/IkB family: intimate tales of association and dissociation. Genes Dev
1995; 9: 2723-2735.
10. Triphati P, Aggarwal A. NF-kB transcription factor: a key player in the generation of immune response. Current Science 2006; 90: 519-531.
11. Sen h, Baltimore D. Inducibility of immunoglobulin enhancer-binding protein NF-KB by a posttranslational mechanism. Cell 1986;47: 921¬928.
12. Baeuerle PA, Henkel T. Function and activation of NF-k/B in the immune system. Annu hev Immunol
1994; 12: 141-179.
13. Grimm S, Baeuerle PA. The inducible transcription factor NF-kB: structure-function relationship of its protein subunits. Biochem J 1999; 290: 297-308.
14.
Yıldı
z OG, Soyuer S, Soyuer I, Uçar K, Gundoğ M, Kaplan B, Özkan M. Gastrektomi sonrası adjuvan kemoradyoterapi uygulanan mide karsinomlu olgularda NF-kB'nin prognostik önemi. Türk Onkoloji Dergisi 2007; 22: 69-73.
15. imler JL, Hoffmann JA. Toll and Toll-like proteins: an ancient family of receptors family signaling infection. hev. immunogenet. 2000; 2: 294-304.
16. Ghosh S, May MJ, Koop EB. NF-kB and hel proteins: evolutionarily conserved mediators of immune responses. Annu hev Immunol 1998; 16:
225-260.
17. Barnes PJ, Karin M. NF-kB. A pivotal transcription factor in chronic inflammatory diseases. N Engl J
Med 1997; 336: 1066-1071.
18. Celancy hM, Amin Ah, Abromson SB. The role of nitric oxide in inflammation and immunity. Arthritis&hheumatism 1998; 41:1141-1151.
19. informational paper. Modulation of host response in periodontal therapy. J Periodontol 2002; 73:460¬470.
AhABACI, ÇİÇEK,
ALBAYhAK, KELEŞ
20. Ataoğlu H, Alptekin NO, Haliloğlu S, Gürsel M, Ataoğlu T, Serpek B, Durmuş E. interleukin 1p, tumor necrosis factor-a levels and neutrophil elastase activity in peri-implant crevicular fluid. Clin Oral impl hes 2002; 13: 470-476.
21. Erdemir EO, Duran i, Haliloğlu S. Effects of smoking on clinical parameters and the gingival crevicular fluid levels of IL-6 and TNF-a in patients with chronic periodontitis. J Clin Periodontol 2004;
31: 99-104.
22. Pahl HL. Activators and target genes of hel/NF-kB transcription factors. Oncogene 1999; 18: 6853¬6866.
23. Milward Mh, Chapple ILC, Wright HJ, Millard JL, Matthews JB, Cooper Ph. Differantial activation of NF-kB and gene expression in oral epithelial cells by periodontal pathogens. Clinical and Experimental immunology 2007; 148: 307-324.
24. Pihlstrom BL, Michalowicz BS, Jhonson NW. Periodontal diseases. Lancet 2005; 366: 1809¬1820.
25. Sillness J, Löe H. Periodontal disease in pregnancy II. Correlation of between oral hygiene and periodontal condition. Acta Odontol Scand. 1964;
22: 121-135.
26. Löe H, Sillness J. Periodontal disease in pregnancy I. Prevalance and severity. Acta Odontol Scand.
1963; 21: 531-551.
27. West MJ. The new stereological tools: Disector, Fractionator, nucleator, and point sampled intercepts and their use in pathological research and diagnosis. APMIS, 1988; 96: 857-881.
28. international Workshop for a Classification of Periodontal Diseases and Conditions. Consensus report on aggressive periodontitis. Ann. Periodontol., 4: 53, 1999.
29. Zadeh HH, Nichols FC, Miyasaki KT. The role of the cell-mediated immune response to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in periodontitis. Periodontol. 2000 1999; 20: 239-288.
30. Ambili h, Santhi WS, Janam P, Nandakumar K, Pillai hM. Expression of activated transcription factor Nuclear Factor-kB in periodontally diseased tissues. J Periodontol 2005; 76: 1148-1153.
90
Atatürk Üniv. Diş Hek. Fak. Derg.
J Dent Fac Atatürk Uni
Cilt:20, Sayı: 2, Yıl: 2010, Sayfa: 84-91
31. Newman MG, Takei HH, Carranza FA. Carranza's clinical periodontology. Philedelphia London New York St Louis Sydney Toronto: W.B Saunders Company, 2002: 398-402.
32. Armitage GC. Development of a classification system for periodontal disease and conditions. Ann Periodontol 1999; 4: 1-6.
33. Flemmig TF. Periodontitis. Ann Periodontol 1999;
4: 32-37.
34. Chen HY, Cox SW, Eley BM, Mântylâ P, hönkâ H, Sorsa T. Matrix metalloproteinase- 8 levels and elastase activities in gingival crevicular fluid from chronic adult periodontitis patients. J Clin Periodontol 2000; 27: 366-369.
35. Vis M, Havaardsholm EA, Haugeberg G, Uhlig T, Voskuyl AE, van de Stadt hJ, Dijkmans BAC, Woolf AD, Kvien TK, Lems WF. Evaluation of bone mineral density, bone metabolism, osteoprotegerin and receptor activator of the NFkB ligand serum levels during treatment with infliximab in patients with rheumatoid arthritis. Ann hheum Dis 2006;
65: 1495-1499.
36. Steeve KT, Marc P, Sandrine T, Dominique H, Yannick F. IL-6, hANKL, TNF-alpha/IL-1: interrelations in bone resorption pathophysiology. Cytokine & Growth Factor heviews 2004; 15: 49¬60.
37. Kawai T, Matsuyama T, Hosokawa Y, Makihira S, Seki M, Karimbux NY, Goncalves hB, Valverde P, Dibart S, Li YP, Miranda LA, Ernst CWO, izumi Y, Taubman MA. B and T lymphocytes are the primary sources of hANKL in the bone resorptive lesion of periodontal disease. The American Journal of Pathology 2006; 169: 987-998.
38. Ferrer I, Marti E, Lopez E, Tortosa A. NF-kB immunoreactivity is observed in association with PA4 diffuse plaques in patients with Alzheimer's disease. Neuropathology and Applied Neurobiology
1998; 24: 271-277.
39. Aggarwal BB. Nuclear factor-kB: The enemy within. Cancer Cell 2004; 6: 203-208.
40. Belibasakis G.N., Johansson A., Wang Y, Chen C, Lagergard T, Kalfas S, Lerner U.H. Cytokine responses of human gingival fibroblasts to Actinobacillus actinomycetemcomitans cytolethal distending toxin. Cytokine 2005; 30: 56-63.
AhABACI, ÇİÇEK,
ALBAYhAK, KELEŞ
41. Epinat JC, Gilmore TD. Diverse agents act at multiple levels to inhibit the hel/NF-KB signal transduction pathway. Oncogene 1999; 18: 6896¬6909.
42. Yin MJ, Yamamoto Y, Gaynor hB. The antiinflammatory agents aspirin and salicylate inhibit the activity of IKB kinase-p. Nature 1998; 396: 77¬80.
43. Makarov S. NF-KB as a therapeutic target in chronic inflammation: hecent advances. Mol Med
Today 2000; 6: 441-448.
44. Hirasawa M, Takada K, Makimura M, Otake S. improvement of periodontal status by green tea catechin using a local delivery system: A clinical pilot study. J Periodont hes 2002; 37: 433-438.
45. May MJ, D'Acquisto F, Madge LA, Glockner J, Pober JS, Ghosh S. Selective inhibition of NF-kappa B activation by a peptide that blocks the interaction of NEMO with the I kappa B kinase complex. Science 2000; 289: 1550-1554.

Thank you for copying data from http://www.arastirmax.com