Contribution of macrophage subpopulations to the pathogenesis of chronic periodontitis in humans and perspectives for study. Review of the literature
DOI:
https://doi.org/10.14739/2310-1210.2019.1.155863Keywords:
chronic periodontitis, macrophagesAbstract
The role of macrophages in chronic periodontitis (CP) is essential, but not well understood.
The purpose was a thematic analysis of the literature on contribution of M1/M2 macrophage subpopulations to the pathogenesis of chronic periodontitis, and methodology for macrophages study in order to define directions and approaches for further investigations.
Our own research findings as well as papers for the topic by searching the electronic databases (the Google Scholar, PMC, PubMed) were analyzed.
M1 macrophages can contribute to CP exacerbation, systemic inflammation enhancement, destruction of periodontal ligament, and inhibition of osteoclastogenesis. M2 macrophages are able both to develop tolerance influenced by LPS of periodontopathogens, and to enhance proinflammatory abilities. Experimental depletion of macrophages using clodronate liposomes can prevent the bone resorption. Influences on M1/M2 in CP with the purpose of treatment are not adequately investigated.
Polarization of macrophages is regulated by a wide spectrum of recognizing receptors, cytokines, specific signaling pathways and genetic programs, some of which are used as phenotype markers of certain macrophages. The unique molecules for M1/M2 are absent. Phenotypic markers of M1 and M2 show overlap, so markers combinations are used depending on a purpose and type of macrophages or profile/combination of expressed genes. The article lists markers used in various studies for M1/M2 identification.
Conclusions. Most of the data on the role of M1/M2 in CP was obtained using monocyte-derived macrophages in vitro and in animal models. This paper highlights the important role of M1 and M2 subpopulations of macrophages in the pathogenesis of CP in humans. The identification of predominant macrophage phenotypes remains elusive, as well as consequences of influences on them. Immunohistochemical methods are indispensable for human studies at the present stage due to availability of biopsy.
A prospect for further scientific research is to study the role of M1 and M2 macrophages in CP pathogenesis in humans.
References
Shinkevich, V. I., & Kaĭdashev, I. P. (2012) Rol' kletochnykh faktorov immuniteta v remodelirovanii tkanej desny pri khronicheskom generalizovannom parodontite [The role of immune cells factors in the remodeling of gingiva at chronic generalized periodontal disease]. Stomatologiya, 91(1), 23–7. [in Russian].
Silva, N., Abusleme, L., Bravo, D., Dutzan, N., Garcia-Sesnich, J., Vernal, R., et al. (2015). Host response mechanisms in periodontal diseases. Journal of Applied Oral Science, 23(3), 329–355. doi: 10.1590/1678-775720140259.
Chapple, C., Srivastava, M., & Hunter, N. (1998). Failure of macrophage activation in destructive periodontal disease. The Journal of Pathology, 186(3), 281–286. doi: 10.1002/(SICI)1096-9896(1998110)186:3<281::AID-PATH200>3.0.CO;2-7.
Kayal, R. (2013). The Role of Osteoimmunology in Periodontal Disease. BioMed Research International, 2013, 639368. doi: 10.1155/2013/639368.
Yang, Z., & Ming, X. (2014). Functions of Arginase Isoforms in Macrophage Inflammatory Responses: Impact on Cardiovascular Diseases and Metabolic Disorders. Frontiers in Immunology, 5, 533. doi: 10.3389/fimmu.2014.00533.
Harris, R. (2014). Spatial, Temporal, and Functional Aspects of Macrophages during “The Good, the Bad, and the Ugly” Phases of Inflammation. Frontiers In Immunology, 5, 612. doi: 10.3389/fimmu.2014.00612.
Rath, M., Müller, I., Kropf, P., Closs, E. I., & Munder, M. (2014) Metabolism via arginase or nitric oxide synthase: two competing arginine pathways in macrophages Front. Immunol., 5,532. doi: 10.3389/fimmu.2014.00532.
Murray, P. J., Allen, J. E., Biswas, S. K., Fisher, E. A., Gilroy, D. W., Goerdt, S., et al. (2014). Macrophage activation and polarization: nomenclature and experimental guidelines. Immunity, 41(1), 14–20. doi: 10.1016/j.immuni.2014.06.008.
Italiani, P., & Boraschi, D. (2014) From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation. Frontiers in Immunology, 5, 514. doi: 10.3389/fimmu.2014.00514.
Ambarus, C. A., Krausz, S., van Eijk, M., Hamann, J., Radstake, T. R., Reedquist, K. A., Tak, P. P. & Baeten, D. L. (2012) Systematic validation of specific phenotypic markers for in vitro polarized human macrophages. J Immunol Methods, 375(1–2), 196–206. doi: 10.1016/j.jim.2011.10.013.
Gordon, S., Plüddemann, A. & Estrada, F. M. (2014) Macrophage heterogeneity in tissues: phenotypic diversity and functions. Immunol Rev, 262(1), 36–55. doi: 10.1111/imr.12223.
Chávez-Galán, L., Olleros, M. L., Vesin, D., & Garcia, I. (2015) Much More than M1 and M2 Macrophages, There are also CD169+ and TCR+ Macrophages. Frontiers in Immunology, 6, 263. doi: 10.3389/fimmu.2015.00263.
Mills, C. D., Thomas, A. C., Lenz, L. L., & Munder, M. (2014) Macrophage: SHIP of Immunity. Frontiers in Immunology, 5, 620. doi: 10.3389/fimmu.2014.00620.
Champaiboon, C., Poolgesorn, M., Wisitrasameewong, W., Sa-Ard-Iam, N., Rerkyen, P., & Mahanonda, R. (2014) Differential inflammasome activation by Porphyromonas gingivalis and cholesterol crystals in human macrophages and coronary artery endothelial cells. Atherosclerosis, 235(1), 38–44. doi: 10.1016/j.atherosclerosis.2014.04.007.
Foey, A. D, Habil, N., Al-Shaghdali, K., & Crean, S. (2017) Porphyromonas gingivalis-stimulated macrophage subsets exhibit differential induction and responsiveness to interleukin-10. Arch Oral Biol, 73, 282–288. doi: 10.1016/j.archoralbio.2016.10.029.
Shinkevich, V., & Каidashev, I. (2010) Rol Toll-retseptoriv u patohenezi zakhvoriuvan slyzovoi obolonky porozhnyny rota [The role of toll-receptors in oral mucosa disease process]. Problemy ekolohii ta medytsyny, 14(3–4), 12–16. [in Ukrainian].
Yu, T., Zhao, L., Huang, X., Ma, C., Wang, Y, Zhang, J., & Xuan, D. (2016) Enhanced Activity of the Macrophage M1/M2 Phenotypes and Phenotypic Switch to M1 in Periodontal Infection. J Periodontol, 87(9), 1092–102. doi: 10.1902/jop.2016.160081.
Pourgonabadi, S., Müller, H. D., Mendes, J. R., & Gruber, R. (2017) Saliva initiates the formation of pro-inflammatory macrophages in vitro. Arch Oral Biol, 73, 295–301. doi: 10.1016/j.archoralbio.2016.10.012.
Yang, J., Zhu, Y., Duan, D., Wang, P., Xin, Y., Bai, L., et al. (2017). Enhanced activity of macrophage M1/M2 phenotypes in periodontitis. Arch Oral Biol., 96, 234–242. doi: 10.1016/j.archoralbio.2017.03.006.
Yamaguchi, T., Movila, A., Kataoka, S., Wisitrasameewong, W., Ruiz Torruella, M., Murakoshi, M., et al. (2016). Proinflammatory M1 Macrophages Inhibit RANKL-Induced Osteoclastogenesis. Infection and Immunity, 84(10), 2802–2812. doi: 10.1128/IAI.00461-16.
Dundar, S., Eltas, A., Hakki, S., Malkoc, S., Uslu, M., Tuzcu, M., et al. (2016) Dietary arginine silicate inositol complex inhibits periodontal tissue loss in rats with ligature-induced periodontitis. Drug Design, Development and Therapy, 10, 3771–3778. doi: 10.2147/DDDT.S115088.
Zheng, X., Cheng, X., Wang, L., Qiu, W., Wang, S., Zhou, Y, et al. (2015) Combinatorial Effects of Arginine and Fluoride on Oral Bacteria. Journal of Dental Research, 94(2), 344–353. doi: 10.1177/0022034514561259.
Tarique, A. A., Logan, J., Thomas, E., Holt, P. G., Sly, P. D., & Fantino, E. (2015) Phenotypic, functional, and plasticity features of classical and alternatively activated human macrophages. Am J Respir Cell Mol Biol, 53(5), 676–88. doi: 10.1165/rcmb.2015-0012OC.
Tedesco, S., Bolego, C., Toniolo, A., Nassi, A., Fadini, G., Locati, M., & Cignarella, A. (2015) Phenotypic activation and pharmacological outcomes of spontaneously differentiated human monocyte-derived macrophages. Immunobiology, 220(5), 545–554. doi: 10.1016/j.imbio.2014.12.008.
Wang, N., Liang, H., & Zen, K. (2014) Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance. Frontiers in Immunology, 5, 614. doi: 10.3389/fimmu.2014.00614.
Barros, M. H., Hauck, F., Dreyer, J. H., Kempkes, B., & Niedobitek, G. (2013) Macrophage polarisation: an immunohistochemical approach for identifying M1 and M2 macrophages. PLoS One, 8(11), e80908. doi: 10.1371/journal.pone.0080908.
Chinetti-Gbaguidi, G., & Staels, B. (2011) Macrophage polarization in metabolic disorders: functions and regulation. Curr Opin Lipidol, 22(5), 365–372. doi: 10.1097/MOL.0b013e32834a77b4.
Freitas Lima, L., Braga, V., do Socorro de França Silva, M., Cruz, J., Sousa Santos, S., de Oliveira Monteiro, M., & Balarini, C. (2015) Adipokines, diabetes and atherosclerosis: an inflammatory association. Frontiers in Physiology, 6, 304. doi: 10.3389/fphys.2015.00304.
Erbel, C., Tyka, M., Helmes, C., Akhavanpoor, M., Rupp, G., Domschke, G., et al. (2015) CXCL4-induced plaque macrophages can be specifically identified by co-expression of MMP7+S100A8+ in vitro and in vivo. Innate Immunity, 21(3), 255–265. doi: 10.1177/1753425914526461.
Romanets-Korbut, O., Najakshin, A., Yurchenko, M., Malysheva, T., Kovalevska, L., Shlapatska, L., et al. (2015). Expression of CD150 in Tumors of the Central Nervous System: Identification of a Novel Isoform. PLOS ONE, 10(2), e0118302. doi: 10.1371/journal.pone.0118302.
Downloads
How to Cite
Issue
Section
License
Authors who publish with this journal agree to the following terms:- 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.
- 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.
- 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 (See The Effect of Open Access)
