Efecto de la Porphyromonas gingivalis sobre células pre-osteoblásticas MC3T3-E1

Muriel Rios, Mariana

Efecto de la Porphyromonas gingivalis sobre células pre-osteoblásticas MC3T3-E1

dc.contributor.advisor	Vargas Sánchez, Paula
dc.contributor.advisor	Castillo Perdomo, Diana
dc.contributor.author	Muriel Rios, Mariana
dc.date.accessioned	2024-12-13T17:28:23Z
dc.date.available	2024-12-13T17:28:23Z
dc.date.issued	2024-11
dc.description.abstract	Antecedentes: La periodontitis es una enfermedad inflamatoria crónica, multifactorial, que afecta los tejidos de soporte dental, además es el resultado de la interacción de factores ambientales, bacterianos y del hospedador. Porphyromonas gingivalis es una de las bacterias más frecuentemente asociada con la periodontitis, entender los cambios que suceden cuando entra en contacto con los osteoblastos puede darnos bases para comprender los mecanismos de la progresión de esta enfermedad. La literatura reporta algunos estudios mostrando el efecto de P. gingivalis sobre los tejidos blandos, pero no se encuentran datos concluyentes sobre su efecto en las células óseas. Objetivo: Evaluar el efecto de dos cepas de P. gingivalis en la diferenciación de las células pre-osteoblásticas MC3T3-E1 subclón 14. Materiales y Métodos: Cepas de P. gingivalis ATCC 33277 y W83 fueron sembradas en agar Brucella suplementado durante 4 días en condiciones anaeróbicas a 37°C, pasado el tiempo se ajustaron inóculos en medio de cultivo celular sin antibiótico a 1 x 108, a partir de estos se ajustó cada MOI. Se cultivaron las células MC3T3-E1 subclón 14 (ATCC) y se colocaron en contacto durante 12 horas con las cepas de P. gingivalis previamente descritas (Control +, MOI 50, MOI 100, MOI 150 y Control -), cumplido este periodo de tiempo se evaluó la viabilidad celular con el ensayo de resarzurina. Posteriormente se evaluó la formación de nódulos mineralizados a los 14 y 17 días mediante el ensayo de rojo de alizarina para las concentraciones (MOI 50 y MOI 100). Los datos obtenidos se analizaron mediante ANOVA y post test de Tukey con un nivel de confianza del 95%. Resultados: La viabilidad celular de las células MC3T3-E1 disminuyó significativamente (p<0,0001) ante la exposición a las cepas P. gingivalis W83 y P. gingivalis 33277 MOI 50 y MOI 100. El ensayo de rojo de alizarina para P. gingivalis 33277 a los 14 y 17 días de exposición no mostró diferencias significativas entre los grupos (p=0,8672 y p=0,6950, respectivamente). Para la cepa P. gingivalis W83 hubo una disminución estadísticamente significativa a los 14 y 17 días de evaluación (p=0,0423 y p=0,0321 respectivamente). Conclusiones: Las células MC3T3-E1 expuestas a cepas de P. gingivalis W83 y P. gingivalis 33277 tuvieron una disminución de la viabilidad celular, pero solo las expuestas a la cepa P. gingivalis W83 presentaron disminución en la formación de matriz mineralizada.
dc.description.abstractenglish	Background: Periodontitis is an inflammatory, multifactorial disease that affects the dental support tissues, it is the result of the environmental, bacterial and host factors interaction. Porphyromonas gingivalis is one of the bacteria most frequently associated with periodontitis, understanding the changes that occur when it comes into contact with osteoblasts can give us a basis for understanding the progression mechanisms of this disease. Literature reports some studies about the effect of P. gingivalis on soft tissues, but there is no conclusive data on its effect on bone cells. The objective of this work was to evaluate the effect of two strains of Porphyromonas gingivalis on the differentiation of MC3T3-E1 subclone 14 pre-osteoblastic cells. Aim: To evaluate the effect of two strains of P. gingivalis on the differentiation of MC3T3-E1 subclone 14 pre-osteoblastic cells. Methods: P. gingivalis strains ATCC 33277 and W83 were sown on Brucella agar supplemented for 4 days under anaerobic conditions at 37°C. After that time, the inoculum was adjusted in cell culture medium without antibiotics to 1 x 108, from each MOI. MC3T3-E1 subclone 14 (ATCC) cells were cultured and placed in contact for 12 hours with the previously described P. gingivalis strains (Control +, MOI 50, MOI 100, MOI 150, and Control -), after this period, cell viability was evaluated with the resazurin assay. Subsequently, the formation of mineralized nodules was evaluated at 14 and 17 days using the alizarin red test for concentrations (MOI 50 and MOI 100). The data obtained were analyzed using ANOVA and Tukey's post-test with a confidence level of 95%. Results: The cell viability of MC3T3-E1 cells decreased significantly (p<0.0001) upon exposure to strains P. gingivalis W83 and P. gingivalis 33277 MOI 50 and MOI 100. The alizarin red assay for P. gingivalis 33277 at 14 and 17 days of exposure did not show significant differences between the groups (p=0.8672 and p=0.6950, respectively). For the P. gingivalis W83 strain, there was a statistically significant decrease at 14 and 17 days of evaluation (p=0.0423 and p=0.0321 respectively). Conclusions: MC3T3-E1 cells exposed to strains P. gingivalis W83 and P. gingivalis 33277 had a decrease in cell viability, and only those exposed to strain P. gingivalis W83 showed a decrease in the formation of mineralized matrix.
dc.description.degreelevel	Pregrado	spa
dc.description.degreename	Odontólogo	spa
dc.description.sponsorship	Grupo de Investigación UIBO – Unidad de Investigación Básica Oral
dc.format.mimetype	application/pdf
dc.identifier.instname	instname:Universidad El Bosque	spa
dc.identifier.reponame	reponame:Repositorio Institucional Universidad El Bosque	spa
dc.identifier.repourl	repourl:https://repositorio.unbosque.edu.co
dc.identifier.uri	https://hdl.handle.net/20.500.12495/13708
dc.language.iso	es
dc.publisher.faculty	Facultad de Odontología	spa
dc.publisher.grantor	Universidad El Bosque	spa
dc.publisher.program	Odontología	spa
dc.relation.references	1. Papanou P, Saenz M, Buduneli N, Dietrich T, Feres M, Fine D, Fleming T, Garcia R, Glannobile W, Graziani F, Greenwell H, Herrera D, Kao R, Kebschull M, Kinane D, Kirkwood K, Kocher T, Kornman K, Kumar P, Loos B, Machtei E, Meng H, Mombelli A, Needleman I, Offenbacher S, Seymour G, Teles R, Toneti M. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of periodontal and peri-implant Diseases and Conditions. Journal of clinical periodontology. 2018. Disponible en: https://pubmed.ncbi.nlm.nih.gov/29926490/
dc.relation.references	2. Nocca G, Filetici P, Bugli F, Mordente A, D'Addona A, Dassatti L. Permeability of P. gingivalis or its metabolic products through collagen and dPTFE membranes and their effects on the viability of osteoblast-like cells: an in vitro study. Odontology. 2022;110(4):710-718. doi:10.1007/s10266-022-00705-9
dc.relation.references	3. Lee SK, Ji MK, Jo YJ, Park C, Cho H, Lim HP. Effect of Non-Thermal Plasma Treatment of Contaminated Zirconia Surface on Porphyromonas gingivalis Adhesion and Osteoblast Viability. Materials (Basel). 2022;15(15):5348. Published 2022 Aug 3. doi:10.3390/ma15155348
dc.relation.references	4. Le XK, Laflamme C, Rouabhia M. Porphyromonas gingivalis decreases osteoblast proliferation through IL-6-RANKL/OPG and MMP-9/TIMPs pathways. Indian J Dent Res. 2009;20(2):141-149. doi:10.4103/0970-9290.52884
dc.relation.references	5. Akira S, Takeda K, Kaisho T. Toll-like receptors: critical proteins linking innate and acquired immunity. Nat Immunol. 2001;2(8):675-680. doi:10.1038/90609
dc.relation.references	6. Arancibia SA, Beltrán CJ, Aguirre IM, et al. Toll-like receptors are key participants in innate immune responses. Biol Res. 2007;40(2):97-112. doi:10.4067/s0716-97602007000200001
dc.relation.references	7. Sorsa T, Ingman T, Suomalainen K, et al. Identification of proteases from periodontopathogenic bacteria as activators of latent human neutrophil and fibroblast-type interstitial collagenases. Infect Immun. 1992;60(11):4491-4495. doi:10.1128/iai.60.11.4491-4495.1992
dc.relation.references	8. McCauley LK, Nohutcu RM. Mediators of periodontal osseous destruction and remodeling: principles and implications for diagnosis and therapy. J Periodontol. 2002;73(11):1377-1391. doi:10.1902/jop.2002.73.11.1377
dc.relation.references	9. Di Benedetto A, Gigante I, Colucci S, Grano M. Periodontal disease: linking the primary inflammation to bone loss. Clin Dev Immunol. 2013;2013:503754. doi:10.1155/2013/503754
dc.relation.references	10. Yucel-Lindberg T, Båge T. Inflammatory mediators in the pathogenesis of periodontitis. Expert Rev Mol Med. 2013;15:e7. Published 2013 Aug 5. doi:10.1017/erm.2013.8
dc.relation.references	11. Kinane DF. Causation and pathogenesis of periodontal disease. Periodontol 2000. 2001;25:8-20. doi:10.1034/j.1600-0757.2001.22250102
dc.relation.references	12. Zaidi M, Blair HC, Moonga BS, Abe E, Huang CL. Osteoclastogenesis, bone resorption, and osteoclast-based therapeutics. J Bone Miner Res. 2003;18(4):599-609. doi:10.1359/jbmr.2003.18.4.599
dc.relation.references	13. Ebersole JL, Dawson DR 3rd, Morford LA, Peyyala R, Miller CS, Gonzaléz OA. Periodontal disease immunology: 'double indemnity' in protecting the host. Periodontol 2000. 2013;62(1):163-202. doi:10.1111/prd.12005
dc.relation.references	14. Trindade E , Carvalho R, Machado V, Chambrone L, Mendes JJ, Botelho J. Prevalence of Periodontitis in dentate people between 2011 and 2020: A systematic review and meta-analysis of epidemiological studies. 2023. Disponible en: https://pubmed.ncbi.nlm.nih.gov/36631982/
dc.relation.references	15. Faddy MJ, Cullinan MP, Palmer JE, Westerman B, Seymour GJ. Ante-dependence modeling in a longitudinal study of periodontal disease: the effect of age, gender, and smoking status. J Periodontol. 2000 Mar;71(3):454-9. doi: 10.1902/jop.2000.71.3.454. PMID: 10776934
dc.relation.references	16. Wirth, R., Pap, B., Maróti, G., Vályi, P., Komlósi, L., Barta, N., Strang, O., Minárovits, J., & Kovács, K. L. (2021). Toward Personalized Oral Diagnosis: Distinct Microbiome Clusters in Periodontitis Biofilms. Frontiers in cellular and infection microbiology, 11, 747814. https://doi.org/10.3389/fcimb.2021.747814
dc.relation.references	17. Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis: Framework and proposal of a new classification and case definition. J Periodontol. 2018 Jun;89 Suppl 1:S159-S172. doi: 10.1002/JPER.18-0006. Erratum in: J Periodontol. 2018 Dec;89(12):1475. doi: 10.1002/jper.10239. PMID: 29926952
dc.relation.references	18. Herrera D, Retamal-Valdes B, Alonso B, Feres M. Acute periodontal lesions (periodontal abscesses and necrotizing periodontal diseases) and endo-periodontal lesions. J Periodontol. 2018 Jun;89 Suppl 1:S85-S102. doi: 10.1002/JPER.16-0642. PMID: 29926942
dc.relation.references	19. Bonfim, M., Mattos, F. F., Ferreira e Ferreira, E., Campos, A. C., & Vargas, A. M. (2013). Social determinants of health and periodontal disease in Brazilian adults: a cross-sectional study. BMC oral health, 13, 22. https://doi.org/10.1186/1472-6831-13-22
dc.relation.references	20. Delgado-Angulo, E. K., Bernabé, E., & Marcenes, W. (2016). Ethnic inequalities in periodontal disease among British adults. Journal of clinical periodontology, 43(11), 926–933. https://doi.org/10.1111/jcpe.12605
dc.relation.references	21. Eke, P. I., Thornton-Evans, G. O., Wei, L., Borgnakke, W. S., Dye, B. A., & Genco, R. J. (2018). Periodontitis in US Adults: National Health and Nutrition Examination Survey 2009-2014. Journal of the American Dental Association (1939), 149(7), 576–588.e6. https://doi.org/10.1016/j.adaj.2018.04.023
dc.relation.references	22. Kwon, T., Lamster, I. B., & Levin, L. (2021). Current Concepts in the Management of Periodontitis. International dental journal, 71(6), 462–476. https://doi.org/10.1111/idj.12630
dc.relation.references	23. Richards D. (2014). Review finds that severe periodontitis affects 11% of the world population. Evidence-based dentistry, 15(3), 70–71. https://doi.org/10.1038/sj.ebd.6401037
dc.relation.references	24. Page, R. C., & Eke, P. I. (2007). Case definitions for use in population-based surveillance of periodontitis. Journal of periodontology, 78(7 Suppl), 1387–1399. https://doi.org/10.1902/jop.2007.060264
dc.relation.references	25. Eke, P. I., Page, R. C., Wei, L., Thornton-Evans, G., & Genco, R. J. (2012). Update of the case definitions for population-based surveillance of periodontitis. Journal of periodontology, 83(12), 1449–1454. https://doi.org/10.1902/jop.2012.110664
dc.relation.references	26. Serrano, C., & Suarez, E. (2019). Prevalence of Severe Periodontitis in a Colombian Adult Population. Journal of the International Academy of Periodontology, 21(2), 53–62
dc.relation.references	27. Ministerio de Salud y Protección Social. ENSAB IV. 2014. Colombia. Disponible en: https://www.minsalud.gov.co/sites/rid/Lists/BibliotecaDigital/RIDE/VS/PP/ENSAB-IV-Situacion-Bucal-Actual.pdf
dc.relation.references	28. Sanz M, Herrera D, Kebschull M, et al; On behalf of the EFP Workshop Participants and Methodological Consultants. Treatment of stage I–III periodontitis—The EFP S3 level clinical practice guideline. J Clin Periodontol. 2020;47:4–60. https://doi.org/10.1111/jcpe.13290
dc.relation.references	29. Herrera, D., Sanz, M., Kebschull, M., Jepsen, S., Sculean, A., Berglundh, T., Papapanou, P. N., Chapple, I., Tonetti, M. S., & EFP Workshop Participants and Methodological Consultant (2022). Treatment of stage IV periodontitis: The EFP S3 level clinical practice guideline. Journal of Clinical Periodontology, 49(Suppl. 24), 4–71. https:// doi.org/10.1111/jcpe.13639
dc.relation.references	30. Wirth, R., Pap, B., Maróti, G., Vályi, P., Komlósi, L., Barta, N., Strang, O., Minárovits, J., & Kovács, K. L. (2021). Toward Personalized Oral Diagnosis: Distinct Microbiome Clusters in Periodontitis Biofilms. Frontiers in cellular and infection microbiology, 11, 747814. https://doi.org/10.3389/fcimb.2021.747814
dc.relation.references	31. Sundqvist G, Figdor D, Hanstrom L, Sorlin S, Sandstrom G. Phagocytosis and Virulence of Different Strains of Porphyromonas gingivalis. 1991. Disponible en: https://pubmed.ncbi.nlm.nih.gov/2052893/
dc.relation.references	32. Xu W, Zhou W, Wang H, Liang S. Roles of Porphyromonas gingivalis and its virulence factors in periodontitis. Adv Protein Chem Struct Biol. 2020;120:45-84. doi:10.1016/bs.apcsb.2019.12.001
dc.relation.references	33. Olsen I, Singhrao SK. Importance of heterogeneity in Porhyromonas gingivalis lipopolysaccharide lipid A in tissue specific inflammatory signalling. J Oral Microbiol. 2018;10(1):1440128. Published 2018 Feb 26. doi:10.1080/20002297.2018.1440128
dc.relation.references	34. AlQranei MS, Chellaiah MA. Osteoclastogenesis in periodontal diseases: Possible mediators and mechanisms. J Oral Biosci. 2020;62(2):123-130. doi:10.1016/j.job.2020.02.002
dc.relation.references	35. Kuramitsu H. K. (1998). Proteases of Porphyromonas gingivalis: what don't they do?. Oral microbiology and immunology, 13(5), 263–270. https://doi.org/10.1111/j.1399-302x.1998.tb00706.x
dc.relation.references	36. Imamura T. The role of gingipains in the patogenesis of periodontal disease. J Periodontol 74: 111-118. 2003
dc.relation.references	37. Potempa J, Sroka A, Imamura T, Travis J. Gingipains, the major cysteine proteinases and virulence factors of Porphyromonas gingivalis: structure, function and assembly of multidomain protein complexes. Curr Protein Pept Sci 4:397-407; 2003
dc.relation.references	38. Seers, C. A., Mahmud, A., Huq, N. L., Cross, K. J., & Reynolds, E. C. (2020). Porphyromonas gingivalis laboratory strains and clinical isolates exhibit different distribution of cell surface and secreted gingipains. Journal of oral microbiology, 13(1), 1858001. https://doi.org/10.1080/20002297.2020.1858001
dc.relation.references	39. Dashper, S. G., Mitchell, H. L., Seers, C. A., Gladman, S. L., Seemann, T., Bulach, D. M., Chandry, P. S., Cross, K. J., Cleal, S. M., & Reynolds, E. C. (2017). Porphyromonas gingivalisUses Specific Domain Rearrangements and Allelic Exchange to Generate Diversity in Surface Virulence Factors. Frontiers in microbiology, 8, 48. https://doi.org/10.3389/fmicb.2017.00048
dc.relation.references	40. Wilensky, A., Polak, D., Houri-Haddad, Y., & Shapira, L. (2013). The role of RgpA in the pathogenicity of Porphyromonas gingivalis in the murine periodontitis model. Journal of Clinical Periodontology, 40(10), 924–932. https://doi.org/10.1111/jcpe.12139
dc.relation.references	41. Jia, L., Han, N., Du, J., Guo, L., Luo, Z., & Liu, Y. (2019). Pathogenesis of Important Virulence Factors of Porphyromonas gingivalis via Toll-Like Receptors. Frontiers in cellular and infection microbiology, 9, 262. https://doi.org/10.3389/fcimb.2019.00262
dc.relation.references	42. Nemoto, T. K., & Ohara-Nemoto, Y. (2016). Exopeptidases and gingipains in Porphyromonas gingivalis as prerequisites for its amino acid metabolism. The Japanese dental science review, 52(1), 22–29. https://doi.org/10.1016/j.jdsr.2015.08.002
dc.relation.references	43. Pathirana, R. D., O'Brien-Simpson, N. M., Brammar, G. C., Slakeski, N., & Reynolds, E. C. (2007). Kgp and RgpB, but not RgpA, are important for Porphyromonas gingivalis virulence in the murine periodontitis model. Infection and immunity, 75(3), 1436–1442. https://doi.org/10.1128/IAI.01627-06
dc.relation.references	44. Castillo DM, Lafaurie GI, Romero-Sánchez C, et al. The Interaction Effect of Anti-RgpA and Anti-PPAD Antibody Titers: An Indicator for Rheumatoid Arthritis Diagnosis. J Clin Med. 2023;12(8):3027. Published 2023 Apr 21. doi:10.3390/jcm12083027
dc.relation.references	45. Nagano K, Hasegawa Y, Yoshida Y, Yoshimura F. A Major Fimbrilin Variant of Mfa1 Fimbriae in Porphyromonas gingivalis. J Dent Res.94:1143–1148; 2021
dc.relation.references	46. Pérez-Chaparro PJ, Lafaurie GI, Gracieux P, Meuric V, Tamanai-Shacoori Z, Castellanos JE, Bonnaure-Mallet M. Distribution of Porphyromonas gingivalis fimA genotypes in isolates from subgingival plaque and blood simple during bacteremia. Biomédica; 29: 298-306. 2009
dc.relation.references	47. Nagano K, Abiko Y, Yoshida Y, Yoshimura F. Genetic and antigenic analyses of Porphyromonas gingivalis FimA fimbriae. Mol Oral Microbiol. 28: 392–403; 2013
dc.relation.references	48. Holt SC, Kesavalu L, Walker S, Genco CA. Virulence Factors of P. gingivalis. Periodontol 2000: 168-238. 1999
dc.relation.references	49. Bélanger M, Kozarov E, Song H, Whitlock J, Progulske-Fox A. Both the unique and repeat regions of the Porphyromonas gingivalis hemagglutin A are involved in adhesionand invasion of host cells. Anaerobe. 18:128-134; 2012
dc.relation.references	50. Chen, T., Hosogi, Y., Nishikawa, K., Abbey, K., Fleischmann, R. D., Walling, J., & Duncan, M. J. (2004). Comparative whole-genome analysis of virulent and avirulent strains of Porphyromonas gingivalis. Journal of bacteriology, 186(16), 5473–5479
dc.relation.references	51. Genco, C. A., Cutler, C. W., Kapczynski, D., Maloney, K., & Arnold, R. R. (1991). A novel mouse model to study the virulence of and host response to Porphyromonas (Bacteroides) gingivalis. Infection and immunity, 59(4), 1255–1263
dc.relation.references	52. Baker, P. J., Dixon, M., Evans, R. T., & Roopenian, D. C. (2000). Heterogeneity of Porphyromonas gingivalis strains in the induction of alveolar bone loss in mice. Oral microbiology and immunology, 15(1), 27–32
dc.relation.references	53. Eick, S., Reissmann, A., Rödel, J., Schmidt, K. H., & Pfister, W. (2008). Porphyromonas gingivalis survives within KB cells and modulates inflammatory response. Oral microbiology and immunology, 21(4), 231–237
dc.relation.references	54. Bélanger, M., Reyes, L., von Deneen, K., Reinhard, M. K., Progulske-Fox, A., & Brown, M. B. (2008). Colonization of maternal and fetal tissues by Porphyromonas gingivalis is strain-dependent in a rodent animal model. American journal of obstetrics and gynecology, 199(1), 86.e1–86.e867
dc.relation.references	55. Xu, W., Pan, Y., Xu, Q., Wu, Y., Pan, J., Hou, J., Lin, L., Tang, X., Li, C., Liu, J., & Zhang, D. (2018). Porphyromonas gingivalis ATCC 33277 promotes intercellular adhesion molecule-1 expression in endothelial cells and monocyte-endothelial cell adhesion through macrophage migration inhibitory factor. BMC microbiology, 18(1), 16
dc.relation.references	56. Ho, M. H., Guo, Z. M., Chunga, J., Goodwin, J. S., & Xie, H. (2016). Characterization of Innate Immune Responses of Human Endothelial Cells Induced by Porphyromonas gingivalis and Their Derived Outer Membrane Vesicles. Frontiers in cellular and infection microbiology, 6, 139
dc.relation.references	57. American Type Culture Collection (ATCC). MC3T3-E1 SUBCLON 14 Characteristics. Disponible en: https://www.atcc.org/products/crl-2594
dc.relation.references	58. Wang D, et al. Isolation and characterization of MC3T3-E1 preosteoblast subclones with distinct in vitro and in vivo differentiation/mineralization potential. J. Bone Miner. Res. 14: 893-903, 1999. PubMed: 10352097
dc.relation.references	59. Sanz M, Herrera D, Kebschull M, et al; On behalf of the EFP Workshop Participants and Methodological Consultants. Treatment of stage I–III periodontitis—The EFP S3 level clinical practice guideline. J Clin Periodontol. 2020;47:4–60. doi.org/10.1111/jcpe.13290
dc.relation.references	60. Di Benedetto A, Gigante I, Colucci S, Grano M. Periodontal disease: linking the primary inflammation to bone loss. Clin Dev Immunol. 2013;2013:503754. doi:10.1155/2013/503754
dc.relation.references	61. Ebersole JL, Dawson DR 3rd, Morford LA, Peyyala R, Miller CS, Gonzaléz OA. Periodontal disease immunology: 'double indemnity' in protecting the host. Periodontol 2000. 2013;62(1):163-202. doi:10.1111/prd.12005
dc.relation.references	62. Zainal Ariffin SH, Megat Abdul Wahab R, Abdul Razak M, et al. Evaluation of in vitro osteoblast and osteoclast differentiation from stem cell: a systematic review of morphological assays and staining techniques. PeerJ. 2024;12:e17790. Published 2024 Jul 25. doi:10.7717/peerj.17790
dc.relation.references	63. Hayashi JI, Ono K, Iwamura Y, et al. Suppression of subgingival bacteria by antimicrobial photodynamic therapy using transgingival irradiation: A randomized clinical trial. J Periodontol. 2024;95(8):718-728. doi:10.1002/JPER.23-0328
dc.relation.references	64. Castillo, Y., Castellanos, J. E., Lafaurie, G. I., & Castillo, D. M. (2022). Porphyromonas gingivalis outer membrane vesicles modulate cytokine and chemokine production by gingipain-dependent mechanisms in human macrophages. Archives of oral biology, 140, 105453. https://doi.org/10.1016/j.archoralbio.2022.105453
dc.relation.references	65. Ministerio de Salud y Protección Social. 1993. Colombia. Resolución 008430 de 1993 por la que se establecen las normas científicas, técnicas y administrativas para la investigación en salud Título IV. Capítulo 1. Disponible en: https://www.minsalud.gov.co/sites/rid/Lists/BibliotecaDigital/RIDE/DE/DIJ/RESOLUCION-8430-DE-1993.PDF
dc.relation.references	66. Zhang W, Swearingen EB, Ju J, Rigney T, Tribble GD. Porphyromonas gingivalis invades osteoblasts and inhibits bone formation. Microbes Infect [Internet]. 2010;12(11):838–45. Disponible en: http://dx.doi.org/10.1016/j.micinf.2010.05.011
dc.relation.references	67. Wen Y, Dong H, Lin J, et al. Response of Human Gingival Fibroblasts and Porphyromonas gingivalis to UVC-Activated Titanium Surfaces. J Funct Biomater. 2023;14(3):137. Published 2023 Feb 28. doi:10.3390/jfb14030137
dc.relation.references	68. Xu LN, Yu XY, Chen WQ, Zhang SM, Qiu J. Biocorrosion of pure and SLA titanium surfaces in the presence of Porphyromonas gingivalis and its effects on osteoblast behavior. RSC Adv. 2020;10(14):8198-8206. Published 2020 Feb 25. doi:10.1039/d0ra00154f
dc.rights	Attribution-NonCommercial-ShareAlike 4.0 International	en
dc.rights.accessrights	https://purl.org/coar/access_right/c_abf2
dc.rights.accessrights	info:eu-repo/semantics/openAccess
dc.rights.local	Acceso abierto	spa
dc.rights.uri	http://creativecommons.org/licenses/by-nc-sa/4.0/
dc.subject	Osteoblastos
dc.subject	Porphyromonas gingivalis
dc.subject	Viabilidad celular
dc.subject	Mineralización celular
dc.subject.keywords	Osteoblasts
dc.subject.keywords	Porphyromonas gingivalis
dc.subject.keywords	Cell viability
dc.subject.keywords	Cell mineralization
dc.subject.nlm	WU 100
dc.title	Efecto de la Porphyromonas gingivalis sobre células pre-osteoblásticas MC3T3-E1
dc.title.translated	Effect of Porphyromonas gingivalis on pre-osteoblastic cells MC3T3-E1
dc.type.coar	https://purl.org/coar/resource_type/c_7a1f
dc.type.coarversion	https://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.driver	info:eu-repo/semantics/bachelorThesis
dc.type.hasversion	info:eu-repo/semantics/acceptedVersion
dc.type.local	Tesis/Trabajo de grado - Monografía - Pregrado	spa