Macrophage polarization in human gingival tissue in response to periodontal disease

Abstract

Objective Although accumulating evidence indicates that macrophages are central players in the destructive and reparative phases of periodontal disease, their polarization states at different stages of periodontal inflammation remain unclear. Methods We collected gingival biopsies from patients with chronic periodontitis (P group), gingivitis (G group), or periodontally healthy individuals (H group). Polarized macrophages were identified through immunofluorescence. M1‐ and M2‐related cytokines were detected by immunohistochemistry. Results Compared with the H group, the P group had more M1 cells (higher M1/M2 ratio) and significantly higher TNF‐α, IFN‐γ, IL‐6, and IL‐12 levels. Although the G group also exhibited higher TNF‐α and IL‐12 levels than the H group, they had similar M1/M2 ratios. The M1/M2 ratio and IFN‐γ and IL‐6 levels were significantly higher in the P than the G group. Among M2‐related cytokines, IL‐4 levels were significantly higher in the G than the H group. The M1/M2 ratio was positively correlated with clinical probing depth (PD), and both were positively correlated with IFN‐γ and IL‐6. PD was negatively correlated with IL‐4. Conclusion Macrophage polarization in gingival tissue may be responsible for the development and progression of inflammation‐induced tissue destruction, and modulating macrophage function may be a potential strategy for periodontal disease management.

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

“…Furthermore, our data showed that calcitriol intervention contributed to a decreased level of IL‐17 and increased levels of IL‐4 and IL‐10, suggesting a potential role for calcitriol in skewing Th cells toward Th2 and Treg polarization. Although the changes in cytokine levels may also result in the polarization of other immune cells, such as macrophages, the capacity of calcitriol to inhibit proinflammatory cytokines and stimulate anti‐inflammatory cytokine release during periodontitis underscores its therapeutic function. Calcitriol has also been confirmed to induce the downregulation of proinflammatory cytokines, including IL‐1β, IL‐6 and IL‐8, in inflammatory reactions; these molecules have the same role in osteoclastogenesis as in inflammatory reactions .…”

“…Periodontal pathogen‐induced tissue damage in periodontitis is mediated by immune response dysregulation, with the involvement of various immune cells, such as T cells, B cells, macrophages, and neutrophils . The immune response mediated by CD4 + T helper (Th) cells plays an especially crucial role in bone damage during this process …”

“…2 The immune response mediated by CD4 + T helper (Th) cells plays an especially crucial role in bone damage during this process. 3,4 The resorption/remodeling of periodontal tissue is believed to be largely mediated by polarized Th cells, such as the proinflammatory Th1 and anti-inflammatory Th2 subsets. 2,5,6 Generally, Th1 cells release cytokines that trigger the local inflammatory reaction and induce tissue injury, while Th2 cells secrete cytokines that promote reparative responses and facilitate periodontal repair.…”

Concise Review: Periodontal Tissue Regeneration Using Stem Cells: Strategies and Translational Considerations

“…Periodontal tissue regeneration is a complex healing cascade that arises from a coordinated interplay among stem cells, biomaterials, and the host immune system . In this concise review, we illustrate the possible approaches based on the therapeutic potential of stem cells that might enhance periodontal wound healing and regeneration and highlight the advantages and disadvantages of culture‐expanded and host‐mobilized cell populations in clinical translation.…”

The relationship between T‐helper cell polarization and the RANKL/OPG ratio in gingival tissues from chronic periodontitis patients

“…Therefore, periodontal bone resorption is closely linked to the host immune response to a microbial challenge (Díaz‐Zúñiga et al, ; Ghighi et al, ; Hienz, Paliwal, & Ivanovski, ; Pan et al, ; Takayanagi, ). During such pathological cascades, many immune cells polarize toward proinflammatory responses; for example, we previously reported increased levels of M1 phenotypes of macrophages in inflammatory gingival tissues (Zhou et al, ). Given the nature of the disease, it is essential to regulate the immune response involved in periodontal reparative events when designing new therapies for periodontitis (e.g., see Bi et al, ; He et al, ; Ni et al, ; Wu et al, ; Yu, Wu, Yin, & Chen, ).…”