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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.