Evaluation of RANK induced periodontitis in rats previously exposed to Cyclosporine A
DOI:
https://doi.org/10.33448/rsd-v10i1.11108Keywords:
Cyclosporine A; Alveolar bone loss; Periodontitis; Osteoporosis; Receptor activator of nuclear factor-kappa B.Abstract
The aim of this study was to investigate the effect of previous exposure to CsA on the expression of RANK and bone loss in experimental periodontitis induced in rats. Forty rats were divided into four groups as follows: Control (CON); Cyclosporine A (CsA), with daily doses of 10 mg/Kg of CsA; Ligature (LIG), with a ligature around the upper right second molar on day 30; and Ligature + CsA (CsAL). Sixty days later, the animals were sacrificed and samples removed for histomorphometric and immunohistochemical analysis of bone resorption, bone density and RANK expression. There was no significant influence of bone resorption on the application of CsA. LIG Group (735.88 ± 121.82) had significantly higher bone resorption (p = 0.01) than CON Group (569.13 ± 89.76), and CsAL Group (759.38 ± 198.23) also had significantly higher bone resorption (P = 0.001) than CsA Group (410.90 ± 105.95). Bone density in the CsA Group (87.49 ± 4.07) was lower than that of CON Group (92.42 ± 2.27) and similar to that of LIG Group (91.85 ± 3.91). CsAL Group (79.41 ± 3.81) showed the lowest density compared to the other groups. RANK did not differ between the groups. The prior exposure to CsA had no influence on the expression of RANK or bone resorption.
References
Arboleya, L., & Castañeda, S. (2013). Osteoimmunology: the study of the relationship between the immune system and bone tissue. Reumatologia clinica, 9(5), 303–315. https://doi.org/10.1016/j.reuma.2013.02.008.
Boltchi, F. E., Rees, T. D., & Iacopino, A. M. (1999). Cyclosporine A-induced gingival overgrowth: a comprehensive review. Quintessence international (Berlin, Germany: 1985), 30(11), 775–783.
Cetinkaya, B. O., Acikgoz, G., Keles, G. C., Ayas, B., & Korkmaz, A. (2006). The effect of cyclosporin A on alveolar bone in rats subjected to experimental periodontal disease. Toxicologic pathology, 34(6), 716–722. https://doi.org/10.1080/01926230600826269
da Silva Peralta, F., Pallos, D., Silva Queiroz, C., & Ricardo, L. H. (2015). Previous exposure to Cyclosporine A and periodontal breakdown in rats. Archives of oral biology, 60(4), 566–573. https://doi.org/10.1016/j.archoralbio.2015.01.004
Fu, E., Hsieh, Y. D., Nieh, S., Wikesjö, U. M., & Liu, D. (1999). Effects of cyclosporin A on alveolar bone: an experimental study in the rat. Journal of periodontology, 70(2), 189–194. https://doi.org/10.1902/jop.1999.70.2.189
Fu, E., Hsieh, Y. D., Mao, T. K., & Shen, E. C. (2001). A histomorphological investigation of the effect of cyclosporin on trabecular bone of the rat mandibular condyle. Archives of oral biology, 46(12), 1105–1110. https://doi.org/10.1016/s0003-9969(01)00080-2
Goodman, G. R., Dissanayake, I. R., Bowman, A. R., Pun, S., Ma, Y., Jee, W. S., Bryer, H. P., & Epstein, S. (2001). Transforming growth factor-beta administration modifies cyclosporine A-induced bone loss. Bone, 28(6), 583–588. https://doi.org/10.1016/s8756-3282(01)00428-8
Hallmon, W. W., & Rossmann, J. A. (1999). The role of drugs in the pathogenesis of gingival overgrowth. A collective review of current concepts. Periodontology 2000, 21, 176–196. https://doi.org/10.1111/j.1600-0757.1999.tb00175.x
Jayasheela, M., & Mehta, D. S. (2013). The role of cyclosporine A on the periodontal tissues. Dental research journal, 10(6), 802–808.
Kawai, T., Matsuyama, T., Hosokawa, Y., Makihira, S., Seki, M., Karimbux, N. Y., Goncalves, R. B., Valverde, P., Dibart, S., Li, Y. P., Miranda, L. A., Ernst, C. W., Izumi, Y., & Taubman, M. A. (2006). B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease. The American journal of pathology, 169(3), 987–998. https://doi.org/10.2353/ajpath.2006.060180
Li, Y., Lu, Z., Zhang, X., Yu, H., Kirkwood, K. L., Lopes-Virella, M. F., & Huang, Y. (2015). Metabolic syndrome exacerbates inflammation and bone loss in periodontitis. Journal of dental research, 94(2), 362–370. https://doi.org/10.1177/0022034514561658
Liang, L., Yu, J. F., Wang, Y., & Ding, Y. (2008). Estrogen regulates expression of osteoprotegerin and RANKL in human periodontal ligament cells through estrogen receptor beta. Journal of periodontology, 79(9), 1745–1751. https://doi.org/10.1902/jop.2008.070437
Lin, D., Li, L., Sun, Y., Wang, W., Wang, X., Ye, Y., Chen, X., & Xu, Y. (2014). IL-17 regulates the expressions of RANKL and OPG in human periodontal ligament cells via TRAF6/TBK1-JNK/NF-κB pathways. Immunology, 144(3), 472–485. Advance online publication. https://doi.org/10.1111/imm.12395
Stanford, T. W., & Rees, T. D. Acquired immune suppression and other risk factores/indicators for periodontal disease progression. Periodontol 2000. 2003; 32:118-135.
Nassar, C. A., Nassar, P. O., Abi Rached, R. S., Holzhausen, M., Marcantonio, E., Jr, & Spolidorio, L. C. (2004). Effect of cyclosporin A on alveolar bone homeostasis in a rat periodontitis model. Journal of periodontal research, 39(3), 143–148. https://doi.org/10.1111/j.1600-0765.2004.00739.x
Nassar, P. O., Felipetti, F. A., Nassar, C. A., & Spolidorio, L. C. (2013). Evaluation of effect of cyclosporine A on the bone tissue with induced periodontal disease to ligature in rats. Transplantation proceedings, 45(2), 778–782. https://doi.org/10.1016/j.transproceed.2012.02.029
Ricardo, L. H., do Prado, R. F., Carvalho, Y. R., da Silva Peralta, F., & Pallos, D. (2019). Cyclosporine A - Induced gingival overgrowth and proliferating cell nuclear antigen expression in experimental periodontitis. Journal of oral biology and craniofacial research, 9(1), 86–90. https://doi.org/10.1016/j.jobcr.2018.10.004
Shen, E. C., Fu, E., & Hsieh, Y. D. (2001). Effects of cyclosporin A on dental alveolar bone: a histomorphometric study in rats. Journal of periodontology, 72(5), 659–665. https://doi.org/10.1902/jop.2001.72.5.659
Souza, P. P., & Lerner, U. H. (2013). The role of cytokines in inflammatory bone loss. Immunological investigations, 42(7), 555–622. https://doi.org/10.3109/08820139.2013.822766
Spahni, A. I., Schawalder, P., Rothen, B., Bosshardt, D. D., Lang, N., & Stoffel, M. H. (2009). Immunohistochemical localization of RANK, RANKL and OPG in healthy and arthritic canine elbow joints. Veterinary surgery: VS, 38(6), 780–786. https://doi.org/10.1111/j.1532-950X.2009.00566.x
Spolidório, L. C., Merzel, J., Villalba, H., Vargas, P. A., Coletta, R. D., & Almeida, O. P. (2001). Morphometric evaluation of gingival overgrowth and regression caused by cyclosporin in rats. Journal of periodontal research, 36(6), 384–389. https://doi.org/10.1034/j.1600-0765.2001.360606.x
Spolidorio, L. C., Spolidorio, D. M., & Holzhausen, M. (2004). Effects of long-term cyclosporin therapy on the periodontium of rats. Journal of periodontal research, 39(4), 257–262. https://doi.org/10.1111/j.1600-0765.2004.00734.x
Spolidorio, L. C., Marcantonio, E., Jr, Spolidorio, D. M., Nassar, C. A., Nassar, P. O., Marcantonio, R. A., & Rossa, C., Jr (2007). Alendronate therapy in cyclosporine-induced alveolar bone loss in rats. Journal of periodontal research, 42(5), 466–473. https://doi.org/10.1111/j.1600-0765.2007.00970.x
Takayanagi, H. (2005). Inflammatory bone destruction and osteoimmunology. Journal of periodontal research, 40(4), 287–293. https://doi.org/10.1111/j.1600-0765.2005.00814.x
Van Dyke, T. E. (2007). Cellular and molecular susceptibility determinants for periodontitis. Periodontology 2000, 45, 10–13. https://doi.org/10.1111/j.1600-0757.2007.00228.x
Wada, C., Kataoka, M., Seto, H., Hayashi, N., Kido, J., Shinohara, Y., & Nagata, T. (2006). High-turnover osteoporosis is induced by cyclosporin A in rats. Journal of bone and mineral metabolism, 24(3), 199–205. https://doi.org/10.1007/s00774-005-0672-x
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2021 Felipe da Silva Peralta; Lucilene Hernandes Ricardo; Hilson Fernando Resende Nogueira; Renata Falchete do Prado; Richardson Mondego Boaventura; Yeon Jung Kim; Debora Pallos
This work is licensed under a Creative Commons Attribution 4.0 International License.
Authors who publish with this journal agree to the following terms:
1) Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
2) Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
3) Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work.