Comparing the Interleukin-1ß and Prostaglandin E2Levels During Fixed Orthodontic Treatment in Smokers Versus Non-Smokers

Abstract

Aim: The present study aimed to compare prostaglandin E2 PGE2 and interleukin-1ß IL1ß levels, which are the indicators of bone resorption and found in the gingival crevicular fluid GCF , between smokers and nonsmokers who were under fixed orthodontic treatment. Material-Method: A total of 30 subjects 15 smokers mean age: 21,07 ± 5,934 years and 15 nonsmokers mean age: 18,53 ± 3,662 years , who had different types of dental malocclusion and applied to the Yüzüncü Yıl University Faculty of Dentistry, Department of Orthodontics for treatment, were enrolled in the study. The periodontal status of individuals was evaluated by plaque index, gingival index, bleeding on probing and probing depth of the periodontal pocket measurements using a periodontal probe. After placing orthodontic brackets, leveling stage was completed using 0.12, 0.14 and 0.16 Ni-ti arch wires. In the stage where 16x22 steel arch wires have been used, GCF samples were collected from the distal aspects of maxillar incisors using periopaper. IL1β and PGE2 levels in GCF were analyzed by ELISA method. Results: It was determined that gingival index and bleeding on probing parameters were lower but pocket depth was higher in smokers as compared to nonsmokers. The difference between the groups was statistically not significant. Total and concentration levels of IL-1ß and PGE2 were higher in smokers versus nonsmokers. However, the difference between the groups was not found statistically significant. Conclusion: The results of the study revealed no statistically significant difference between smokers and nonsmokers in terms of GCF cytokine levels during orthodontic treatment. Further studies that investigate GCF cytokine levels during orthodontic treatment performed with different forces in larger series are required dex, gingival index, bleeding on probing and probing depth of the periodontal pocket measurements using a periodontal probe. After placing orthodontic brackets, leveling stage was completed using 0.12, 0.14 and 0.16 Ni-ti arch wires. In the stage where 16x22 steel arch wires have been used, GCF samples were collected from the distal aspects of maxillar incisors using periopaper. IL1β and PGE2 levels in GCF were analyzed by ELISA method. Results: It was determined that gingival index and bleeding on probing parameters were lower but pocket depth was higher in smokers as compared to nonsmokers. The difference between the groups was statistically not significant. Total and concentration levels of IL-1ß and PGE2 were higher in smokers versus nonsmokers. However, the difference between the groups was not found statistically significant. Conclusion: The results of the study revealed no statistically significant difference between smokers and nonsmokers in terms of GCF cytokine levels during orthodontic treatment. Further studies that investigate GCF cytokine levels during orthodontic treatment performed with different forces in larger series are required

Keywords

• Cigarette, Orthodontic Treatment, Gingival Crevicular Fluid, IL-1ß, PGE2

SİGARA İÇEN VE İÇMEYEN BİREYLERİN SABİT ORTODONTİK TEDAVİLERİ SIRASINDAKİ İNTERLÖKİN-1ß VE PROSTAGLANDİN E2 SEVİYELERİNİN KARŞILAŞTIRILMASI

Abstract

Amaç: Bu araştırmada sigara içen ve içmeyen sabit ortodontik tedavi gören bireylerin dişeti oluğu sıvısındaki DOS kemik rezorpsiyonunu gösteren belirteçlerden prostaglandin E2 PGE2 ve interlökin-1ß IL-1ß seviyelerinin karşılaştırılması amaçlanmıştır Materyal-Metod: Araştırmaya Yüzüncü Yıl Üniversitesi Diş Hekimliği Fakültesi Ortodonti Anabilim Dalı’na tedavi amacıyla başvuran farklı dişsel maloklüzyona sahip sigara içen 15 yaş ortalaması: 21,07 ± 5,934 yıl ve sigara içmeyen 15 yaş ortalaması: 18,53 ± 3,662 yıl olmak üzere toplam 30 birey dahil edilmiştir. Bireylerin periodontal durumları periodontal sondla plak indeks, gingival indeks, sondlamada kanama ve cep derinliği ölçümleri yapılarak değerlendirilmiştir. Ortodontik braket uygulamasını takiben 0.12, 0.14 ve 0.16 Ni-ti ark telleri ile seviyeleme aşaması tamamlanmıştır. 16x22 çelik ark tellerinin kullanıldığı aşamada DOS örnekleri üst keser dişlerin distal bölgelerinden periopaper kullanılarak toplanmıştır. DOS’daki IL-1β ve PGE2 seviyelerinin incelenmesinde ise ELISA yönteminden faydalanılmıştır. Bulgular: Sigara içen bireylerdeki gingival indeks ve sondlamada kanama parametrelerinin içmeyenlere göre daha düşük, cep derinliği’nin ise daha yüksek olduğu saptanmıştır. Her iki grup arasındaki farkın istatistik olarak anlamlı olmadığı tespit edilmiştir. IL-1ß total ve konsantrasyon, PGE2 total ve konsantrasyon seviyelerinin sigara içen bireylerde içmeyen bireylere oranla daha fazla olduğu görülmüştür. Ancak iki grup arasındaki fark istatistik olarak anlamlı bulunmamıştır. Sonuçlar: Araştırmanın sonuçlarına göre sigara içen ve içmeyen gruplar arasında ortodontik tedavi sırasındaki DOS sitokin seviyelerinde istatistik olarak anlamlı bir fark çıkmamıştır. Konu ile ilgili daha fazla sayıda bireyi kapsayan ve farklı kuvvetlerin uygulandığı ortodontik tedavi aşamalarındaki DOS sitokin seviyelerinin incelendiği gelecek çalışmalara ihtiyaç olduğu düşünülmektedir.

Keywords

• Sigara, Ortodontik Tedavi, Dişeti Oluğu Sıvısı, IL-1ß, PGE2

References

1. 1. Buttke TM, Proffit WR. Referring adult patients for orthodontic treatment. J Am Dent Assoc 1999;130(1):73–9.
2. 2. Ertas N. Factors associated with stage of cigarette smoking among Turkish youth. Eur j Public Health 2007;17(2):155-61.
3. 3. Substance Abuse and Mental Health Services Administration. Results from the 2004 National Survey on Drug Use and Health: National Findings. DHHS 2005; Pub No SMA 05: 4062.
4. 4. Sodagar A, Donyavi Z, Arab S, Kharrazifard MJ. Effect of nicotine on orthodontic tooth movement in rats. Am J Orthod Dentofacial Orthop 2011;139(3):261-5.
5. 5. Shintcovsk RL, Knop L, Tanaka OM, Maruo H. Nicotine effect on bone remodeling during orthodontic tooth movement: histological study in rats. Dental Press J Orthod 2014;19(2):96-107.
6. 6. Henneman S, Von den Hoff JW, Maltha JC. Mechanobiology of tooth movement. Eur J Orthod 2008;30(3):299-306.
7. 7. McCormack SW, Witzel U, Watson PJ, Fagan MJ, Gröning F. The biomechanical function of periodontal ligament fibers in orthodontic tooth movement. Plos One 2014;9(7):1-13.
8. 8. Nakao S, Ogata Y, Sugiya H. Nicotine stimulates the expression of cyclooxygenase-2 mRNA via NKκB activation in human gingival fibroblasts. Arch Oral Biol 2009; 54(3):251-7.

9. 9. Hapidin H, Faizah H, Soelaiman IN, Shuid AN, Luke DA, Mohamed N. Negative effects of nicotine on bone-resorbing cytokines and bone histomorphometric parameters in rates. J Bone Miner Metab 2007;25(2):93-8.
10. 10. Wu L, Zhou Y, Zhou Z, Liu Y, Bai Y, Xing X et al. Nicotine induces the production of IL-1ß and IL8 via the α7 nAChR/NF-kB pathway in human periodontal ligament cells: an in vitro study. Cell Physiol Biochem 2004;34:423-31.
11. 11. Hallmon WW, Carranza FA, Drisko CL, Rapley JW, Robinson P. Periodontal Literature Reviews: a summary of current knowledge. Chicago: American Academy of Periodontology 1996;39-40.
12. 12. Mahanonda R, Sa-Ard-Lam N, Eksomtramate M, Rerkyen P, Phairat B, Schaecher KE et al. Cigarette smoke extract modulates human beta- defensin-2 and interleukin-8 expression in human gingival epithelial cells. J Periodontal Res 2009;44(4):557-64.
13. 13. Tipton DA, Dabbous MK. Effects of nicotine on proliferation and extracellular matrix production of human gingival fibroblasts in vitro. J Periodontol 1995;66(12):1056-64.
14. 14. Shchipkova AY, Nagaraja HN, Kumar PS. Subgingival microbial profiles of smokers with periodontitis. J Dent Res 2010;89(11):1247-53.
15. 15. Mavropoulous A, Aars H, Brodin P. Hyperaemic response to cigarette smoking in healty gingiva. J Clin Periodontol 2003;30(3):214-21.
16. 16. Pejcic A, Obradovic R, Kesic L, Kojovic D. Smoking and periodontal disease a review. Med and Biol 2007;14(2):53-9.
17. 17. Hanes PJ, Schuster GS, Lubas S. Binding, uptake, and release of nicotine by human gingival fibroblasts. J Periodontol 1991;62(2):147–152.
18. 18. Henemyre CL, Scales DK, Hokett SD, Cuenin MF, Peacock ME, Parker MH et al. Nicotine stimulates osteoclast resorption in a porcine marrow cell model. J Periodontol 2003;74(10):1440–6.
19. 19. Kamer AR, El-Ghorab N, Marzec N, Margarone JE, Dziak R. Nicotine induced proliferation and cytokine release in osteoblastic cells. Int J Mol Med 2006;17(1):121-7.
20. 20. Wang X, Liu Y, Wang Q, Tsuruoka M, Ohta K, Wu S et al. Functional expression of alpha 7 nicotinic acetylcholine receptors in human periodontal ligament fibroblasts and rat periodontal tissues. Cell Tissue Res 2010;340(2):347–55.
21. 21. Malhotra R, Kapoor A, Grover V, Kaushal S. Nicotine and periodontal tissues. J Indian Soc Periodontol 2010;14(1):72–9.
22. 22. Kirschneck C, Proff P, Maurer M, Reicheneder C, Römer P. Orthodontic forces add to nicotine-induced loss of periodontal bone. J Orofacial Orthop 2015;76(3):195-212.
23. 23. Teitelbaum SL. Bone resorption by osteoclasts. Science 2000;289(5484):1504-8.
24. 24. Sandy JR, Farndale RW, Meikle MC. Recent advances in understanding mechanically induced bone remodeling and their relevance to orthodontic theory and practice. Am J Orthod Dentofacial Orthop 1993;103(3):212-22.
25. 25. Saito M, Saito S, Ngan PW, Shanfeld J, Davidovitch Z. Interleukin 1 beta and prostaglandin E are involved in the response of periodontal cells to mechanical stress in vivo and in vitro. Am J Orthod Dentofacial Orthop 1991;99(3):226-40.
26. 26. Saito S, Ngan P, Saito M, Lanese R, Shanfeld J, Davidovitch Z. Interactive effects between cytokines on PGE production by human periodontal ligament fibroblasts in vitro. J Dent Res 1990;69(8):1456-62.
27. 27. Chang YC, Tsai CH, Yang SH, Liu CM, Chou MY. Induction of cyclooxygenase-2 mRNA and protein expression in human gingival fibroblasts stimulated with nicotine. J Periodontal Res 2003;38 (5):496–501.
28. 28. Laxman VK, Annaji S. Tobacco use and its effects on the periodontium and periodontal therapy. J Contemp Dent Pract 2008;9(7):97–107.
29. 29. Liu YF, Wu LA, Wang J, Wen LY, Wang XJ. Micro-computerized tomography analysis of alveolar bone loss in ligature-and nicotine-induced experimental periodontitis in rats. J Periodontal Res 45(6):714–9.
30. 30. Meikle MC. The tissue, cellular, and molecular regulation of orthodontic tooth movement: 100 years after Carl Sandstedt. Eur J Orthod 2006;28(3):221–40.
31. 31. Römer P, Wolf M, Fanghänel J, Reicheneder C, Proff P. Cellular response to orthodontically-induced short-term hypoxia in dental pulp cells. Cell Tissue Res 2014;355(1):173–80.
32. 32. Li J, Wang X, Li N, Zheng D, Su Y, Zhang J. Short-term effects of nicotine on orthodontically induced root resorption in rats. Angle Orthod 2016;86(2):199-205.
33. 33. Ren Y, Maltha JC, Kuijpers-Jagtman AM. Optimum force magnitude for orthodontic tooth movement: a systematic literature review. Angle Orthod 2003;73(1):86–92.