Assessing The Effect of Non-Surgical Periodontal Therapy on Levels of Caspase 3 And 7 in Patients With Chronic And Aggressive Periodontitis - A Systematic Review Protocol
DOI:
https://doi.org/10.61841/3djrt969Keywords:
Chronic periodontitis, Aggressive Periodontitis, Apoptosis, caspasesAbstract
Background: Chronic periodontitis (CP) and Aggressive Periodontitis (AgP), are characterized by destruction of periodontal tissues in response to dental plaque. Both have localized and generalized presentations initiated by bacterial plaque, but they differ in the pattern of destruction; familial aggregation and the quantity of dental plaque. Apoptosis has been reported to be one of the mechanisms of tissue destruction in periodontitis, and a family of cysteine proteases, named caspases have been reported to mediate the process. Two mechanisms involved in apoptosis are intrinsic and caspase-dependent extrinsic pathways. These pathway results in the formation of a death-inducing signaling complex (DISC) which in turn causes activation of the executioner caspases-3,6&7 to start the process of cell-death or apoptosis. In subjects with chronic periodontitis, the probability of detection of Caspase-3 has been found to be greater in gingival crevicular fluid compared to serum and saliva. Additionally, detection of caspase-3&7 marked an early event prior to any overt morphological changes characteristic of apoptosis. Therefore, evaluation of Caspase levels may help in early detection of sites with periodontitis as well as probably determine the probability of an inactive site becoming active. Therefore, compositional changes in gingival crevicular fluid of site specific periodontal disease may help in correlating the level of disease activity and tissue destruction.Objectives: To assess the effect of non-surgical periodontal therapy on levels of caspase 3 and 7 in patients with chronic and aggressive periodontitis. Search Methods: We will search PUBMED and CENTRAL, EMBASE without language restrictions up to March 2019. We will also search for ongoing studies in trial registers, perform handsearching, check bibliographic references of relevant articles to seek potentially relevant research. We won’t apply any restrictions on language, date, or publication status. Selection Criteria: We will
include randomised controlled (parallel-group or cross-over) trials, case control studies, cohort studies, case reports comparing the levels of caspase3 and 7 before and after SRP in patients with AgP and CP.
Downloads
References
[1] Isaza-Guzmán DM, Medina-Piedrahíta VM, Gutiérrez-Henao C, Tobón-Arroyave SI. Salivary Levels of NLRP3 Inflammasome-Related Proteins as Potential Biomarkers of Periodontal Clinical Status. J Periodontol. 2017;88(12):1329–38.
[2] Classification of periodontal diseases.Armitage.pdf.
[3] Armitage GC, Cullinan MP. Comparison of the clinical features of chronic and aggressive periodontitis. :16.
[4] Aral K, Aral CA, Kapila Y. The role of caspase-8, caspase-9, and apoptosis inducing factor in periodontal disease. J Periodontol [Internet]. 2018 Oct 26 [cited 2018 Dec 22]; Available from: http://doi.wiley.com/10.1002/JPER.17-0716
[5] Urnowey S, Ansai T, Bitko V, Nakayama K, Takehara T, Barik S. Temporal activation of anti- and pro-apoptotic factors in human gingival fibroblasts infected with the periodontal pathogen, Porphyromonas gingivalis: potential role of bacterial proteases in host signalling. BMC Microbiol. 2006;6:26.
[6] Pradeep AR, Kumar MS, Ramachandraprasad MV, Shikha C. Gingival Crevicular Fluid Levels of Neopterin in Healthy Subjects and in Patients With Different Periodontal Diseases. J Periodontol. 2007 Oct;78(10):1962–7.
[7] Khalaf H, Lönn J, Bengtsson T. Cytokines and chemokines are differentially expressed in patients with periodontitis: Possible role for TGF-β1 as a marker for disease progression. Cytokine. 2014 May;67(1):29–35.
[8] Offenbaceer S, Odle BM, Dyke TE. The use of crevicular fluid prostaglandin E2 levels as a predictor of periodontal attachment loss. J Periodontal Res. 1986 Mar;21(2):101–12.
[9] Abuhussein H, Bashutski JD, Dabiri D, Halubai S, Layher M, Klausner C, et al. The Role of Factors Associated With Apoptosis in Assessing Periodontal Disease Status. J Periodontol. 2014 Aug;85(8):1086–95.
[10] Zaric S, Shelburne C, Darveau R, Quinn DJ, Weldon S, Taggart CC, et al. Impaired Immune Tolerance to Porphyromonas gingivalis Lipopolysaccharide Promotes Neutrophil Migration and Decreased Apoptosis. Infect Immun. 2010 Oct 1;78(10):4151–6.
[11] Gamonal J, Bascones A, Acevedo A, Blanco E, Silva A. Apoptosis in Chronic Adult Periodontitis Analyzed by In Situ DNA Breaks, Electron Microscopy, and Immunohistochemistry. J Periodontol. 2001;72(4):517–25.
[12] Bantel H, Beikler T, Flemmig TF, Schulze-Osthoff K. Caspase activation is involved in chronic periodontitis. FEBS Lett. 2005 Oct 24;579(25):5559–64.
[13] Kang SW, Kim SK, Chung JH, Ban JY. Assessment of CASP gene polymorphisms in periodontal disease. Genet Mol Res GMR. 2015;14(4):18069–77.
[14] Fujita T, Yoshimoto T, Matsuda S, Kajiya M, Kittaka M, Imai H, et al. Interleukin-8 induces DNA synthesis, migration and down-regulation of cleaved caspase-3 in cultured human gingival epithelial cells. J Periodontal Res. 2015 Aug;50(4):479–85.
[15] Behl Y, Siqueira M, Ortiz J, Li J, Desta T, Faibish D, et al. Activation of the acquired immune response reduces coupled bone formation in response to a periodontal pathogen. J Immunol Baltim Md 1950. 2008 Dec 15;181(12):8711–8.
[16] Lamkanfi M, Kanneganti T-D. Caspase-7: A protease involved in apoptosis and inflammation. Int J Biochem Cell Biol. 2010 Jan;42(1):21–4.
[17] Lamkanfi M, Moreira LO, Makena P, Spierings DCJ, Boyd K, Murray PJ, et al. Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival. Blood. 2009 Mar 19;113(12):2742–5.
[18] Ouzzani M, Hammady H, Fedorowicz Z, Elmagarmid A. Rayyan—a web and mobile app for systematic reviews. Syst Rev. 2016 Dec;5(1):210.
[19] Moher D, Liberati A, Tetzlaff J, Altman DG, for the PRISMA Group. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. BMJ. 2009 Jul 21;339(jul21 1):b2535–b2535.
[20] Balshem H, Helfand M, Schünemann HJ, Oxman AD, Kunz R, Brozek J, et al. GRADE guidelines: 3. Rating the quality of evidence. J Clin Epidemiol. 2011 Apr;64(4):401–6.
[21] Higgins JPT, Altman DG, Gotzsche PC, Juni P, Moher D, Oxman AD, et al. The Cochrane Collaboration’s tool for assessing risk of bias in randomised trials. BMJ. 2011 Oct 18;343(oct18 2):d5928–d5928.
[22] Elbourne DR, Altman DG, Higgins JP, Curtin F, Worthington HV, Vail A. Meta-analyses involving cross-over trials: methodological issues. Int J Epidemiol. 2002 Feb;31(1):140–9.
[23] Riley RD, Higgins JPT, Deeks JJ. Interpretation of random effects meta-analyses. BMJ. 2011 Feb 10;342(feb10 2):d549–d549.
[24] Derry S, Rice AS, Cole P, Tan T, Moore RA. Topical capsaicin (high concentration) for chronic neuropathic pain in adults. Cochrane Database Syst Rev. 2017 13;1:CD007393.
[25] Kumar, G. K., & Prasad, R. S. (2019). A non-linear kernel feature subset selection based semi-supervised framework for medical disease prediction. International Journal of Advanced Science and Technology, 28(17), 517-526. Retrieved from www.scopus.com
[26] Kumar, R., Pruthi, M., & Taneja, G. (2019). Inventory model for deteriorating products with life time and demand depending on price. International Journal of Advanced Science and Technology, 27(1), 48-52. Retrieved from www.scopus.com
[27] Kumar, S., & Bathla, R. K. (2019). Multimodal approach with face and iris to enhance the efficiency of biometric system using soft biometrics. International Journal of Advanced Science and Technology, 28(16), 1572-1581. Retrieved from www.scopus.com
[28] Lakshmi, P., Bharadwaj, A., & Kumar Srivastava, R. (2019). Microbial profile of bacteriuria in pregnant women and their antibiogram. International Journal of Advanced Science and Technology, 28(14), 337-344.
Retrieved from www.scopus.com
[29] Lee, S. -., Choi, A. -., Kim, S. -., Won, J. -., & Lee, K. -. (2019). Comparison of EMG activity using spectrum indices from biceps femoris muscle during treadmill walking. International Journal of Advanced Science and Technology, 28(3), 33-39. Retrieved from www.scopus.com
Downloads
Published
Issue
Section
License

This work is licensed under a Creative Commons Attribution 4.0 International License.
You are free to:
- Share — copy and redistribute the material in any medium or format for any purpose, even commercially.
- Adapt — remix, transform, and build upon the material for any purpose, even commercially.
- The licensor cannot revoke these freedoms as long as you follow the license terms.
Under the following terms:
- Attribution — You must give appropriate credit , provide a link to the license, and indicate if changes were made . You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use.
- No additional restrictions — You may not apply legal terms or technological measures that legally restrict others from doing anything the license permits.
Notices:
You do not have to comply with the license for elements of the material in the public domain or where your use is permitted by an applicable exception or limitation .
No warranties are given. The license may not give you all of the permissions necessary for your intended use. For example, other rights such as publicity, privacy, or moral rights may limit how you use the material.
