Şiddetli Kronik Periodontitisli Hastalarda Başlangıç Periodontal Tedavinin Kardiyovasküler Risk Belirteçleri Üzerindeki Etkisi

Amaç: Bu çalışmanın amacı, şiddetli kronik periodontitisli hastalarda kardiyovasküler hastalık ile ilişkili enflamatuvar belirteçler üzerinde başlangıç periodontal tedavinin etkisini belirlemektir. Gereç ve Yöntemler: Bu çalışmaya, sistemik olarak sağlıklı, şiddetli kronik periodontitisli 40 hasta (29’u kadın, 11'i erkek) (test grubu) ve periodontal olarak sağlıklı 40 birey (21 kadın, 19 erkek) (kontrol grubu) olmak üzere toplam da 80 sigara içmeyen birey dahil edildi. Sondalama derinliği, klinik ataşman seviyesi, plak indeksi, gingival indeks ve kan örnekleri tedavi öncesinde ve tedaviden sonraki 3. ayda toplandı ve asimetrik dimetilarginin (ADMA), endotelyal nitrik oksit sentaz (eNOS), homosistein (Hcy) ve monosit kemoatraktan protein-1 (MCP-1) serum seviyeleri enzim-bağlı immünosorbent analiziyle belirlendi. Bulgular: Başlangıçta, tüm klinik periodontal parametreler kronik periodontitisli grupta periodontal olarak sağlıklı gruba göre anlamlı derecede yüksek bulundu (p

Effect of Initial Periodontal Treatment on Cardiovascular Risk Markers in Patients with Severe Chronic Periodontitis

Objective: The aim of the study was to determine the influence of initial periodontaltreatment in patients with severe chronic periodontitis on inflammatory markersrelated to risk for cardiovascular diseases.Materials and Methods: A total of 80 non-smokers with systemically healthy,including 40 patients (29 female, 11 male) with severe chronic periodontitis(test group) and 40 periodontally healthy participants (21 female, 19 male)(control group) were included into the present study. The probing depth, clinicalattachment level, plaque index, gingival index and blood samples were collected atbaseline and at the 3rd months after treatment and the serum levels of asymmetricdimethylarginine (ADMA), endothelial nitric oxide synthase (eNOS), homocysteine(Hcy), monocyte chemoattractant protein-1 (MCP-1) were determined withenzyme-linked immunosorbent assay.Results: At baseline, all clinical periodontal parameters were significantly higher inthe chronic periodontitis group than in the periodontally healthy group (p

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  • Tatakis DN, Kumar PS. Etiology and pathogenesis of periodontal diseases. Dent Clin North Am 2005; 49: 491-516.
  • Beck JD, Offenbacher S. Systemic effects of periodontitis: epidemiology of periodontal disease and cardiovascular disease. J Periodontol 2005; 76: 2089-100.
  • Heitzer T, Schlinzig T, Krohn K, Meinertz T, Münzel T. Endothelial dysfunction, oxidative stress, and risk of cardiovascular events in patients with coronary artery disease. Circulation 2001; 104: 2673-8.
  • Khader YS, Albashaireh ZS, Alomari MA. Periodontal diseases and the risk of coronary heart and cerebrovascular diseases: a meta-analysis. J Periodontol 2004; 75: 1046-53.
  • Loos BG, Craandijk J, Hoek FJ, Wertheim-van Dillen PM, van der Velden U. Elevation of systemic markers related to cardiovascular diseases in the peripheral blood of periodontitis patients. J Periodontol 2000; 71: 1528-34.
  • Lalla E, Lamster IB, Hofmann MA, Bucciarelli L, Jerud AP, Tucker S, et al. Oral infection with a periodontal pathogen accelerates early atherosclerosis in apolipoprotein E-null mice. Arterioscler Thromb Vasc Biol 2003; 23: 1405-11.
  • Hansson GK, Robertson AK, Söderberg-Nauclér C. Inflammation and atherosclerosis. Annu Rev Pathol 2006; 1: 297-329.
  • Tonetti MS, Van Dyke TE; working group 1 of the joint EFP/AAP workshop. Periodontitis and atherosclerotic cardiovascular disease: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Periodontol 2013; 84: 24-9.
  • Jeftha A, Holmes H. Periodontitis and cardiovascular disease. SADJ 2013; 68: 60, 62-3.
  • Bartova J, Sommerova P, Lyuya-Mi Y, Mysak J, Prochazkova J, Duskova J, et al. Periodontitis as a risk factor of atherosclerosis. J Immunol Res 2014; 2014: 636893.
  • Bokhari SA, Khan AA, Butt AK, Azhar M, Hanif M, Izhar M, et al. Non-surgical periodontal therapy reduces coronary heart disease risk markers: a randomized controlled trial. J Clin Periodontol 2012; 39: 1065-74.
  • Teeuw WJ, Slot DE, Susanto H, Gerdes VE, Abbas F, D’Aiuto F, et al. Treatment of periodontitis improves the atherosclerotic profile: a systematic review and meta-analysis. J Clin Periodontol 2014; 41: 70-9.
  • Carnicer R, Crabtree MJ, Sivakumaran V, Casadei B, Kass DA. Nitric oxide synthases in heart failure. Antioxid Redox Signal 2013; 18: 1078-99.
  • Böger RH. Asymmetric dimethylarginine: understanding the physiology, genetics, and clinical relevance of this novel biomarker. Proceedings of the 4th International Symposium on ADMA. Pharmacol Res 2009; 60: 447.
  • Wang BR, Ou Z, Jiang T, Zhang YD, Zhao HD, Tian YY, et al. Independent Correlation of Serum Homocysteine with Cerebral Microbleeds in Patients with Acute Ischemic Stroke due to Large- Artery Atherosclerosis. J Stroke Cerebrovasc Dis 2016; 25: 2746- 51.
  • Zhang HP, Wang YH, Cao CJ, Yang XM, Ma SC, Han XB, et al. A regulatory circuit involving miR-143 and DNMT3a mediates vascular smooth muscle cell proliferation induced by homocysteine. Mol Med Rep 2016; 13: 483-90.
  • Cioni G, Marcucci R, Gori AM, Valente S, Giglioli C, Gensini GF, et al. Increased homocysteine and lipoprotein(a) levels highlight systemic atherosclerotic burden in patients with a history of acute coronary syndromes. J Vasc Surg 2016; 64: 163-70.
  • Lin J, Kakkar V, Lu X. Impact of MCP-1 in atherosclerosis. Curr Pharm Des 2014; 20: 4580-8.
  • Silness J, Löe H. Periodontal disease in pregnancy. II. Correlation between oral hygiene and periodontal condition. Acta Odontol Scand 1964; 22: 121-35.
  • Löe H, Silness J. Periodontal disease in pregnancy. I. Prevalence and severity. Acta Odontol Scand 1963; 21: 533-51.
  • Vallance P, Leiper J. Cardiovascular biology of the asymmetric dimethylarginine:dimethylarginine dimethylaminohydrolase pathway. Arterioscler Thromb Vasc Biol 2004; 24: 1023-30.
  • Saitoh M, Osanai T, Kamada T, Matsunaga T, Ishizaka H, Hanada H, et al. High plasma level of asymmetric dimethylarginine in patients with acutely exacerbated congestive heart failure: role in reduction of plasma nitric oxide level. Heart Vessels 2003; 18: 177-82.
  • Sydow K, Schwedhelm E, Arakawa N, Bode-Böger SM, Tsikas D, Hornig B, et al. and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins. Cardiovasc Res 2003; 57: 244-52.
  • Landim MB, Casella Filho A, Chagas AC. Asymmetric dimethylarginine (ADMA) and endothelial dysfunction: implications for atherogenesis. Clinics (Sao Paulo) 2009; 64: 471- 8.
  • Krzyzanowska K, Mittermayer F, Shnawa N, Hofer M, Schnabler J, Etmüller Y, et al. Asymmetrical dimethylarginine is related to renal function, chronic inflammation and macroangiopathy in patients with Type 2 diabetes and albuminuria. Diabet Med 2007; 24: 81-6.
  • Fickling SA, Williams D, Vallance P, Nussey SS, Whitley GS. Plasma concentrations of endogenous inhibitor of nitric oxide synthesis in normal pregnancy and pre-eclampsia. Lancet 1993; 342: 242-3.
  • Cai H, Harrison DG. Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress. Circ Res 2000; 87: 840-4.
  • Antoniades C, Tousoulis D, Marinou K, Vasiliadou C, Tentolouris C, Bouras G, et al. Asymmetrical dimethylarginine regulates endothelial function in methionine-induced but not in chronic homocystinemia in humans: effect of oxidative stress and proinflammatory cytokines. Am J Clin Nutr 2006; 84: 781-8.
  • Cooke JP. ADMA: its role in vascular disease. Vasc Med 2005; 1: 11-7.
  • De Gennaro Colonna V, Bianchi M, Pascale V, Ferrario P, Morelli F, Pascale W, et al. Asymmetric dimethylarginine (ADMA): an endogenous inhibitor of nitric oxide synthase and a novel cardiovascular risk molecule. Med Sci Monit 2009; 15: 91-101.
  • Welch GN, Loscalzo J. Homocysteine and atherothrombosis. N Engl J Med 1998; 338: 1042-50.
  • Dillon MC, Opris DC, Kopanczyk R, Lickliter J, Cornwell HN, Bridges EG, et al. Detection of homocysteine and C-reactive protein in the saliva of healthy adults: comparison with blood levels. Biomark Insights 2010; 5: 57-61.
  • Joseph R, Nath SG, Joseraj MG. Elevated plasma homocysteine levels in chronic periodontitis: a hospital-based case-control study. J Periodontol 2011; 82: 439-44.
  • Gerard C, Rollins BJ. Chemokines and disease. Nat Immunol 2001; 2: 108-15.
  • Charo IF, Taubman MB. Chemokines in the pathogenesis of vascular disease. Circ Res 2004; 95: 858-66.
  • Gemmell E, Marshall RI, Seymour GJ. Cytokines and prostaglandins in immune homeostasis and tissue destruction in periodontal disease. Periodontol 2000 1997; 14: 112-43.
  • Tonetti MS, Imboden MA, Gerber L, Lang NP, Laissue J, Mueller C. Localized expression of mRNA for phagocyte-specific chemotactic cytokines in human periodontal infections. Infect Immun 1994; 62: 4005-14.
  • Kurtiş B, Tüter G, Serdar M, Akdemir P, Uygur C, Firatli E, et al. Gingival crevicular fluid levels of monocyte chemoattractant protein-1 and tumor necrosis factor-alpha in patients with chronic and aggressive periodontitis. J Periodontol 2005; 76: 1849-55.