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PERIODONTAL DOKU YIKIMINDA REAKTIF OKSİJEN TÜRLERİNİN ROLÜ

THE ROLE OF REACTIVE OXYGEN SPECIES IN PERIODONTAL TISSUE DESTRUCTION

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Abstract (2. Language): 
In periodontal diseases tissue destruction occurs in two ways; directly and indirectly. The bacteria colonized in gingival crevicular and periodontal pocket and enzymes derived from bacteria are resposible for directly destruction. Indirectly destruction is the tissue destruction caused as a response of host tissue against bacterial factors. Bacteria and bacterial metabolic enzymes causes polymorphonuclear leukocytes' migration as chemotatic agent and inflammatuar response occurs by the activation of immunologycal system. Activated polymorphonuclear leukocytes relaeses various reactive oxygen species to protect tissue from microorganisms. The aim of this review is looking at the mechanisms of periodontal tissue destruction and to show the role of the reactive oxygen species in periodontal tissue destruction.
Abstract (Original Language): 
Periodontal hastalıklarda doku yıkımı birkaç mekanizmanın ortak faaliyeti ile direkt ve indirekt olmak üzere iki şekilde gerçekleşir. Dişeti oluğunda ve periodontal cepte kolonize olan bakteriler ve bakterilerden kaynaklı çeşitli enzimler direkt yıkımdan sorumludur. İndirekt yıkım ise konak dokuda bakteriyel faktörlere karşı oluşan doku cevabının meydana getirdiği doku yıkımıdır. Bakteriler ve bakterilerin metabolik enzimleri, kemotaktik ajan olarak polimorfonükleer lökositlerin migrasyonuna yol açmakta, immünolojik sistem aktivasyonu ile enflamatuvar cevap oluşmaktadır. Aktive olmuş polimorfonükleer lökositler dokuyu mikroorganizmalardan korumak amacıyla çeşitli türde reaktif oksijen türlerini salarlar. Bu derlemede amacımız periodontal doku yıkım mekanizmalarına kısaca göz atmak ve reaktif oksijen türlerinin periodontal doku yıkımında oynadığı rolü sunmaktır.

REFERENCES

References: 

1. Lindhe J. Clinical periodontology and implant dentistry, 4th edition, Blackwell Pub Comp 2003; 209-214.
2. Barry M, Eley W, Stephen W. Proteolytic and hydrolytic enzymes from putative periodontal pathogens: characteriztions, moleculer genetics, effects on host defenses and tissues and detection in gingival crevice fluid. Periodontol 2000 2003; 31:
105-124.
3. Courant PR, Paunio I, Gibbons R.J. Infectivity and hyaluronidase activity of debris from healthy and diseased gingiva. Arc Oral Biol 1965; 10: 119-125.
4. Cowley G.C, Levine M. The effect of plaque on gingival epithelium. Oral Sci Rev 1972; 1: 103-127.
5. Fine DH, Tabak L, Oshrain H, Salkind A, Siegel K. Studies in plaque pathogenicity: I. Plaque collection and limulus lysate screening of adherent and loosely adherent plaque. J Periodont Res 1978; 13:
127-133.
259
Atatürk
Univ
. Diş Hek. Fak. Derg.
J Dent Fac Atatürk Uni
Cilt:21, Sayı: 3, Yıl: 2011, Sayfa: 255-261
ÖZCAN, ÖZDEMİR,
ÇANAKÇI
6. Ivanyi L, Lehner T. Stimulation of lymphocyte transformation by bacterial antigens in patients with periodontal disease. Arc Oral Biol 1970; 15:
1089-1096.
7. Genco RJ, Slots J. Host responses in periodontal disease. J Dent Res 1984; 63: 441-451.
8.
Vya
s S. P, Mishra S, Mishra V. Controlled and targeted drug delivery strategies towards intraperiodontal pocket diseases. J Clin Pharm
Therap 2000; 25: 21-42.
9. Schenkein H. A. Host responses in maintaining
periodonta
l health and determining periodontal disease. Periodontol 2000 2006; 40: 77-93.
10. Çanakçı C. F, Tatar A, Çanakçı V, Çiçek Y, Öztaş S, Orbak R. New evidence of premature oxidative DNA damage: mitochondrial DNA deletion in gingival tissue of patients with periodontitis. J Periodontol
2006; 77: 1894-1900.
11. Çanakçı CF, Çiçek Y, Çanakçı V. Reactive oxygen species and human inflammatory periodontal diseases. Biocem (Moscow) 2005; 70: 619-628.
12. Yokuş B, Çakır DU. İnvivo oksidatif DNA hasarı biyomarkerı; 8-hydroxy 2'-deoxyguanosine T Clin J
Med Sci 2002; 22: 535-543.
13. Su H, Gornitsky M, Velly AM, Yu H, Benarroch M, Scihipper HM. Salivary DNA, lipid, and protein oxidation in non-smokers with periodontal disease.
Free Radic Biol Med 2009; 46: 914-921.
14. Inoue T, Hayashi M, Takayanagi K, Morooka S. Oxidative DNA damage is induced by chronic cigarette smoking, but repaired by abstention. J
Health Sci 2003; 49: 217-220.
15. Aoshiba K, Nagai A. Oxidative stress, cell death, and other damage to alveolar epithelial cells induced by cigarette smoke. Tabacco Induc Dis
2003; 1: 219-226.
16. Miyasaki KT, Wilson ME, Brunetti AJ, Genco RJ. Oxidative and nonoxidative killing of Actinobacillus actinomycetemcomitans by human neutrophils. Infect Immun 1986; 53: 154-160.
17. Wu LL, Chiou CC, Chang P.Y, Wu JT. Urinary 8-OHdG: a marker of oxidative stress to DNA and a risk factor for cancer, atherosclerosis and diabetics, Clinica Chimica Acta 2004; 339: 1-9.
18. Ekuni D, Tomofuji T, Tamaki N, Sanbe T, Azuma T, Yamanaka R. Yamamato T, Watanabe T. Mechanical stimulation of gingiva reduces plasma 8-OHdG level in rat periodontitis. Arch Oral Biol 2008;
53: 324-329.
19. Çanakçı V, Yıldırım A, Çanakçı CF, Eltaş A, Çiçek Y, Çanakçı H. Total antioxidant capacity and antioxidant enzymes in serum, saliva, and gingival crevicular fluid of preeclamptic women with and without periodontal disease J Periodontol 2007; 78:
1-10.
20. Chen SS, Huang WJ, Chang LS, Wei YH. 8-hydroxy-2'-deoxyguanosine in leukocyte DNA of spermatic vein as a biomarker of oxidative stress in patients
with varicocele. J Urol 2004; 172: 1418-1421.
21.
Dinçe
r Y, Akçay T, Saygılı Eİ, Ersoy EY, Tortum O. Helicobacter pylori ile enfekte vakalarda clarithromycine + amoxicilline tedavisinin oksidatif DNA hasarı üzerine etkisi. Uluslararası Hematoloji-
Onkoloji Derg 2007; 17: 204-208.
22. Igishi T, Hitsuda Y, Kato K, Sako T, Burioka N, Yasuda K, Sano H, Shigeoka Y, Nakanishi H, Shimizu E. Elevated urinary 8-hydroxydeoxyguanosine, a biomarker of oxidative stress, and lack of association with antioxidant vitamins in chronic obstructive pulmonary disease. Respirol 2003; 8: 455-60.
23. Seki S, Kitada T, Sakaguchi H, Nakatani K, Wakasa K. Pathological significance of oxidative cellular damage in human alcoholic liver disease.
Histopathol 2003; 42: 365-71.
24. Wu LL, Chiou CC, Chang PY, Wu JT. Urinary 8-
OHdG: a marker of oxidative stress to DNA and a risk factor for cancer, atherosclerosis and diabetics. Clinica Chimica Acta 2004; 339: 1-9.
25. Fahn HJ, Wang LS, Kao SH, Chang SC, Huang MH,
Wei YH. Smoking-associated mitochondrial DNA mutations and lipid peroxidation in human lung tissue. Am J Respir Cell Mol Biol 1998; 19: 901-909.
26. Daiuto F, Nibali L, Parkar M, Patel K, Suvan J, Donos N. Oxidative stress, systemic inflammation, and severe periodontitis. J Dent Res 2010; 89:
1241-1246.
27. Jornot L, Petersen H, Junot AF. Hydrogen peroxide-induced DNA damage is independent of nuclear calcium but dependent on redox-active ions.
Biochem J 1998; 335: 85-94.
28. Thomas R, Richar PM, Chandraratna DS, Sendall TJ, Ryder E, Liu B, Lewis E, Rosahl T, Hider R, Camargo LM, Mark SS, Crowther DC, Lomas DA. Fenton chemistry and oxidative stress mediate the toxicity of the p-amiyloid peptide in a Drosophila model of Alzheimer's disease. Eur J Neurosci 2009;
29: 1335-1347.
260
Atatürk
Univ
. Diş Hek. Fak. Derg.
J Dent Fac Atatürk Uni
Cilt:21, Sayı: 3, Yıl: 2011, Sayfa: 255-261
ÖZCAN, ÖZDEMİR,
ÇANAKÇI
29. Kendall H.K, Marshall RI., Bartold PM. Nitric oxide and tissue destruction. Oral Dis 2001; 7: 2-10.
30. Lai C-H, Liou S-H, Lin H-C, Shih T-S, Tsai P-J, Chen J-S, Yang T, Jaagkola JJK, Strickland PT. Exposure to traffic exhautus and oxidative DNA damage. Occup Environ Med 2005; 62: 216-222.
31.
Burça
k G, Andican G. Oksidatif DNA hasarı ve yaşlanma. Cerrahpaşa J Med 2004; 35: 159-169.
32. Koppole JM, Lucassen PJ, Sakkee AN, Asten JG, Ravid R, Swaap DF, Bezooijen CF. 8-OHdG Levels in brain do not indicate oxidative DNA damage in Alzheimer's disease. Neurobiol Aging 2000; 17:
819-826.
33.
Baltacıoğl
u E, Akalın AF, Alver A, Balaban F, Unsal M, Karabulut E. Total antioxidant capacity and superoxide dismutase activity levels in serum and gingival crevicular fluid in post-menopausal women with chronic periodontitis. J Clin Periodontol 2006;
33: 385-392.
34. Fujita T, Fujimoto Y. Formation and removal of acvtive oxygen species and lipid peroxides in biological systems. Nippon Yakurigaku Zassi 1992;
99: 381-390.
35. Battino M, Bullon P, Wilson M, Newman H. Oxidative injury and inflammatory periodontal disease: the challenge of anti-oxidants to free radicals and reactive oxygen species. Crit Rev Oral
Biol Med 1999; 10 458-76.
36. Chapple L.C., Matthews J.B. The role of reactive oxygen and antioxidant species in periodontal tissue destruction. Periodontol 2000 2007; 43: 160¬232.
37. Krol K, Reactive oxygen species and antioxidant mechanisms in the pathogenesis of periodontitis. Ann Acad Med Stetin 2004; 50: 135-148.
38. Sulaiman AE, Shehadeh RM. Assesment of total antioxidant capacity and the use of vitamin C in the treatment of non-smokers with chronic periodontitis. J Periodontol 2010; 81: 1547-1554.
39. Mayne S.T. Antioxidant nutrients and chronic disease: use of biomarkers of exposure and oxidative stress status in epidemiologic research. J
Nutr 2003; 133: 933-940.
40. Shargorodsky M, Debby O, Matas Z, Zimlichman R. Effect of long-term treatment with antioxidants (vitamin C, vitamin E, coenzyme Q10 and selenium) on arterial comliance, humoral factors and inflammatory markers in patients with multiple cardiovascular risk factors. Nutr and Metabol 2010;
7: 1-8.
41. Tomofuji T, Ekuni D, Sanbe T, Irie K, Azuma T, Maruyama T, Tamaki N, Murakami J, Kokeguchi S, Yamamato S. Effects of vitamin C intake on gingival oxidative stress in rat periodonbtitis. Free Radic Biol
Med 2009; 15: 163-168.
42. Chul KS, Su OK, Joon OK, Joon YK, Chung HJ.
Antioxidant profile of whole saliva after scaling and root planning in periodontal disease. J Periodont
Implant Sci 2010; 40: 164-171.
43. Konopka T, Krol K, Kopec W, Gerber H. Total antioxidant status and 8-hydroxy-2-deoxyguanosine levels in gingival and peripheral blood of periodontitis patients. Arch Immunol Ther Exp
2007; 55: 1-7.
44. Sheikhi M, Bouhafs RKL, Hammarström KJ, Jarstrand C. Lipid peroxidation caused by oxygen radicals from Fusobacterium-stimulated neutrophils as a possible model for the emergence of periodontitis. Oral Dis 2001; 7: 41-46.
45. Peter ME, Heufelder AE, Hengartner M.O. Advanced in apoptosis research. Proc Natl Acad Sci 1997; 94:
12736-12737.
46. Guzik K, Potempa J. Friendly fire against neutrophils: proteolytic enzymes confuse the recognition of apopthotic cells by macrophages. Biochimie 2007; 90: 405-415.
47. Shi H, Hudson LG, Liu KJ. Oxidative stress and apoptosis in metal ion-induced carcinogenesis. Free
Radic Biol Med 2004; 37: 582-593.
48. Takane M, Sugano N, Iwasaki H, Iwano Y, Shimizu N, Ito K. New biomarker evidence of oxidative DNA damage in whole saliva from clinically healthy and periodontally diseased individualis. J Peridontol
2002; 73: 551-554.
49. Çanakçı CF, Çiçek Y, Yıldırım A, Sezer U, Çanakçı V. Increased levels of 8-hydroxydeoxyguanosine and malondialdehyde and its relationship with antioxidant enzymes in saliva of periodontitis patients. Eur J Dent 2009; 3: 100-106.
50. Bahar G, Feinmesser R, Shpitzer T, Popovtzer A, Nagler RM. Salivary analysis in oral cancer patients. Am Cancer Soc 2007; 109: 54-59.

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