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VOLUME 24 , ISSUE 10 ( October, 2023 ) > List of Articles

ORIGINAL RESEARCH

Soluble Receptor Activator of Nuclear Factor Ligand and Osteoprotegerin Levels in Gingival Crevicular Fluid among Cigarette Smokers and Non-smokers with and without Periodontitis

Salma Musa Adam Abduljalil, Nada Hashim, Muhammed Mustahsen Rahman, Nallan CSK Chaitanya, Moawia Mohamed Mukhtar, Bakri Gobara Gismalla

Keywords : Gingival crevicular fluid, Grading, OPG, Periodontitis, RANKL, Smoking, Staging

Citation Information : Abduljalil SM, Hashim N, Rahman MM, Chaitanya NC, Mukhtar MM, Gismalla BG. Soluble Receptor Activator of Nuclear Factor Ligand and Osteoprotegerin Levels in Gingival Crevicular Fluid among Cigarette Smokers and Non-smokers with and without Periodontitis. J Contemp Dent Pract 2023; 24 (10):771-778.

DOI: 10.5005/jp-journals-10024-3580

License: CC BY-NC 4.0

Published Online: 05-12-2023

Copyright Statement:  Copyright © 2023; The Author(s).


Abstract

Aim: This study aimed to measure and compare the levels of soluble receptor activator of nuclear factor ligand (RANKL) and osteoprotegerin (OPG) in the gingival crevicular fluid (GCF), as well as their ratio, in smokers and nonsmokers with periodontitis. Materials and methods: Gingival crevicular fluid samples were collected using PerioPaper strips, from 150 individuals, who were categorized into three groups: current smokers with periodontitis stage III grades C and B (n = 50), nonsmokers with periodontitis stages I and II grade A (n = 50), and control healthy individuals (n = 50). The concentrations (pg/mL) of sRANKL and OPG in the GCF were measured by enzyme-linked immunesorbent assays (ELISA). Result: The smokers’ group exhibited the highest sRANKL (pg/mL) concentration as a subsequent lead to a higher sRANKL/OPG ratio. The healthy control group exhibited higher OPG and lower sRANKL concentration, subsequently, the sRANKL/OPG ratio was reduced compared with the other study groups. However, there was no statistical significance of sRANKL and its relative ratio between periodontitis stage III grades C and B, periodontitis stages I and II grade A, and healthy control individuals. There was a statistically significant positive moderate correlation between smoking duration (years) and the sRANKL (pg/mL) concentration and a statistically significant negative moderate correlation between OPG (pg/mL) concentration and cigarettes smoked per day. Conclusion: As a result, compared to the other research groups, smokers with periodontitis stage III grades C and B had greater GCF concentrations of sRANKL, lower OPG, and a higher sRANKL/OPG ratio. The difference in OPG (pg/mL) level was statistically significant. However, there was no statistically significant difference in sRANKL (pg/mL) or its relative ratio, sRANKL/OPG, across the groups. Clinical significance: A characteristic that sets periodontitis apart is alveolar bone loss. Resorption is induced by RANKL and inhibited by OPG, resulting in a relative ratio. In light of this, the levels of RANKL and OPG may be helpful indicators for monitoring the activity of periodontal disease in both smokers and nonsmokers with and without periodontitis.


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  1. Newman MG, Takei H, Klokkevold PR, et al. Carranza's Clinical Periodontology: Elsevier Health Sciences; 2011.
  2. Flemmig TF. Periodontitis. Ann Periodontol 1999;4(1):32–38. DOI: 10.1902/annals.1999.4.1.32.
  3. Deo V, Bhongade M. Pathogenesis of periodontitis: Role of cytokines in host response. Dent Today 2010;29(9):60–62, 64–66. PMID: 20973418.
  4. Schätzle M, Faddy MJ, Cullinan MP, et al. The clinical course of chronic periodontitis: V. Predictive factors in periodontal disease. J Clin Periodontol 2009;36(5):365–371. DOI: 10.1111/j.1600-051X.2009.01391.x.
  5. Hanada R, Hanada T, Sigl V, et al. RANKL/RANK – Beyond bones. J Mol Med 2011;89(7):647–656. DOI: 10.1007/s00109-011-0749-z.
  6. Boyce BF, Xing L. Biology of RANK, RANKL, and osteoprotegerin. Arthritis Res Therapy 2007;9(Suppl 1):S1. DOI: 10.1186/ar2165.M.
  7. Mogi M, Otogoto J, Ota N, et al. Differential expression of RANKL and osteoprotegerin in gingival crevicular fluid of patients with periodontitis. J Dent Res 2004;83(2):166–169. DOI: 10.1177/154405910408300216.
  8. Gautam DK, Jindal V, Gupta SC, et al. Effect of cigarette smoking on the periodontal health status: A comparative, cross-sectional study. J Indian Soc Periodontol 2011;15(4):383–387. DOI: 10.4103/0972-124X.92575.
  9. Ojima M, Hanioka T. Destructive effects of smoking on molecular and genetic factors of periodontal disease. Tob Induc Dis 2010;8(1):1. DOI: 10.1186/1617-9625-8-4.
  10. Machuca G, Rosales I, Lacalle JR, et al. Effect of cigarette smoking on periodontal status of healthy young adults. J Periodontol 2000;71(1):73–78. DOI: 10.1902/jop.2000.71.1.73.
  11. Buduneli N, Kinane DF. Host-derived diagnostic markers related to soft tissue destruction and bone degradation in periodontitis. J Clin Periodontol 2011;38(Suppl 11):85–105. DOI: 10.1111/j.1600-051X.2010.01670.x.
  12. Kawai T, Paster B, Komatsuzawa H, et al. Cross-reactive adaptive immune response to oral commensal bacteria results in an induction of RANKL-dependent periodontal bone resorption in a mouse. Oral Microbiol Immunol 2007;22(3):208–215. DOI: 10.1111/j.1399-302X.2007.00348.x.
  13. WHO Global Report on Trends in the Prevalence of Tobacco Smoking 2000–2025, second edition. Geneva: World Health Organization.
  14. Pihlstrom BL. Periodontal risk assessment, diagnosis and treatment planning. Periodontology 2000 2001;25(1):37–58. DOI: 10.1034/j.1600-0757.2001.22250104.x.
  15. Khongkhunthian S, Kongtawelert P, Ongchai S, et al. Comparisons between two biochemical markers in evaluating periodontal disease severity: A cross-sectional study. BMC Oral Health 2014;14:107. DOI: 10.1186/1472-6831-14-107.
  16. Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis: Framework and proposal of a new classification and case definition. J Clin Periodontol 2018;45(Suppl S20):S149–S161. DOI: 10.1111/jcpe.12945.
  17. Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol 2018;89(Suppl 1):S173–S182. DOI: 10.1002/JPER.17-0721.
  18. Lang NP, Joss A, Orsanic T, et al. Bleeding on probing. A predictor for the progression of periodontal disease? J Clin Periodontol 1986;13(6):590–596. DOI: 10.1111/j.1600-051x.1986.tb00852.x.
  19. Glavind L, Löe H. Errors in the clinical assessment of periodontal destruction. J Periodontal Res 1967;2(3):180–184. DOI: 10.1111/j.1600-0765.1967.tb01887.x.
  20. Offenbaceer S, Odle BM, Van Dyke TE. The use of crevicular fluid prostaglandin E2 levels as a predictor of periodontal attachment loss. J Periodontal Res 1986;21(2):101–112. DOI: 10.1111/j.1600-0765.1986.tb01443.x.
  21. Guentsch A, Kramesberger M, Sroka A, et al. Comparison of gingival crevicular fluid sampling methods in patients with severe chronic periodontitis. J Periodontol 2011;82(7):1051–1060. DOI: 10.1902/jop.2011.100565.
  22. Mei JV, Alexander JR, Adam BW, et al. Use of filter paper for the collection and analysis of human whole blood specimens. J Nutrition 2001;131(5):1631S–1636S. DOI: 10.1093/jn/131.5.1631S.
  23. Albandar JM, Streckfus CF, Adesanya MR, et al. Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss. J Periodontol 2000;71(12):1874–1881. DOI: 10.1902/jop.2000.71.12.1874.
  24. Giannobile WV, Beikler T, Kinney JS, et al. Saliva as a diagnostic tool for periodontal disease: Current state and future directions. Periodontol 2000 2009;50:52–64. DOI: 10.1111/j.1600-0757.2008.00288.x.
  25. Takayanagi H. Inflammatory bone destruction and osteoimmunology. J Periodontal Res 2005;40(4):287–293. DOI: 10.1111/j.1600-0765.2005.00814.x.
  26. Tabari ZA, Azadmehr A, Tabrizi MA, et al. Salivary soluble receptor activator of nuclear factor kappa B ligand/osteoprotegerin ratio in periodontal disease and health. J Periodontal Implant Sci 2013;43(5):227–232. DOI: 10.5051/jpis.2013.43.5.227.
  27. Listgarten MA. Pathogenesis of periodontitis. J Clin Periodontol 1986;13(5):418–430. DOI: 10.1111/j.1600-051x.1986.tb01485.x.
  28. Page RC, Kornman KS. The pathogenesis of human periodontitis: An introduction. Periodontology 2000 1997;14(1):9–11. DOI: 10.1111/j.1600-0757.1997.tb00189.x.
  29. Costa PP, Trevisan GL, Macedo GO, et al. Salivary interleukin-6, matrix metalloproteinase-8, and osteoprotegerin in patients with periodontitis and diabetes. J Periodontol 2010;81(3):384–391. DOI: 10.1902/jop.2009.090510.
  30. Al-Sabbagh M, Alladah A, Lin Y, et al. Bone remodeling-associated salivary biomarker MIP-1α distinguishes periodontal disease from health. J Periodontal Res 2012;47(3):389–395. DOI: 10.1111/j.1600-0765.2011.01445.x.
  31. Tobon-Arroyave SI, Isaza-Guzman DM, Restrepo-Cadavid EM, et al. Association of salivary levels of the bone remodelling regulators sRANKL and OPG with periodontal clinical status. J Clin Periodontol 2012;39(12):1132–1140. DOI: 10.1111/jcpe.12012.
  32. Tanaka H, Tanabe N, Kawato T, et al. Nicotine affects bone resorption and suppresses the expression of cathepsin K, MMP-9 and vacuolar-type H(+)-ATPase d2 and actin organization in osteoclasts. PLoS One 2013;8(3):e59402. DOI: 10.1371/journal.pone.0059402.
  33. Tang TH, Fitzsimmons TR, and Bartold PM. Effect of smoking on concentrations of receptor activator of nuclear factor kappa B ligand and osteoprotegerin in human gingival crevicular fluid. J Clin Periodontol 2009;36(9):713–718. DOI: 10.1111/j.1600-051X.2009.01444.x.
  34. Bostanci N, Ilgenli T, Emingil G. Gingival crevicular fluid levels of RANKL and OPG in periodontal diseases: Implications of their relative ratio. J Clin Periodontol 2007;34(05):370–376. DOI: 10.1111/j.1600-051X.2007.01061.x.
  35. Frodge BD, Ebersole JL, Kryscio RJ, et al. Bone remodeling biomarkers of periodontal disease in saliva. J Periodontol 2008;79(10):1913–1919. DOI: 10.1902/jop.2008.080070.
  36. Miller CS, King CP Jr, Langub MC, et al. Salivary biomarkers of existing periodontal disease: A cross-sectional study. J Am Dent Assoc 2006;137(3):322–329. DOI: 10.14219/jada.archive.2006.0181.
  37. Buduneli N, Biyikoglu B, Sherrabeh S, et al. Saliva concentrations of RANKL and osteoprotegerin in smoker versus non-smoker chronic periodontitis patients. J Clin Periodontol 2008;35(10):846–852. DOI: 10.1111/j.1600-051X.2008.01310.x.
  38. Belibasakis GN, Bostanci N. The RANKL-OPG system in clinical periodontology. J Clin Periodontol 2012;39(3):239–248. DOI: 10.1111/j.1600-051X.2011.01810.x.
  39. Morrow M. Department of Gender and Women's Health; World Health Organization. Tobacco Free Initiative. Gender, Health and Tobacco 2003;2022.
  40. Giovannoni ML, Valdivia-Gandur I, de Luaces VL, et al. Betel and tobacco chewing habit and its relation to risk factors for periodontal disease. Oral Dis 2018;24(5):829–839. DOI: 10.1111/odi.12820.
  41. Akishima S, Matsushita S, Sato F, et al. Cigarette-smoke-induced vasoconstriction of peripheral arteries—Evaluation by synchrotron radiation microangiography. Circ J 2007;71(3):418–422. DOI: 10.1253/circj.71.418.
  42. Cekici A, Kantarci A, Hasturk H, et al. Inflammatory and immune pathways in the pathogenesis of periodontal disease. Periodontol 2000 2014;64(1):57–80. DOI: 10.1111/prd.12002.
  43. Song L, Dong G, Guo L, et al. The function of dendritic cells in modulating the host response. Mol Oral Microbiol 2018;33(1):13–21. DOI: 10.1111/omi.12195.
  44. Silva H. Tobacco use and periodontal disease—The role of microvascular dysfunction. Biology 2021;10(5):441. DOI: 10.3390/biology10050441.
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