As one of the first arriving immune cells after dental implantation, Mϕs own the abilities to polarize into to a spectrum of diverse phenotypes, from “classically activated” M1 Mϕs to “alternatively activated” M2 Mϕs. Herein, it was hypothesized that Mϕ phenotypes dynamically adapt after dental implantation, and the changes ensue a cascade of coordinated interplay with the bone-forming osteoblast and the bone-resorbing osteoclast. Results showed that the remodelling process after dental implantation was similar with the standard response to tissue injury (exampled by tooth extraction models), only with the delay of bone regeneration phases. Additionally, Mϕ activation in both groups underwent a transition from M1 Mϕs dominated to M2-type dominated stage, but the persistence of M1 Mϕs occurred in rat model of dental implantation. Further research in vitro showed that M1 Mϕs are involved in osteoclast activities via secreting the highest levels of TNF-α and IL-1β, as well as being the potential precursor of osteoclasts. Besides, they also recruited BMSCs by secreting the highest levels of chemoattractants, CCL2 and VEGF. M2 Mϕs accelerated osteogenesis in the subsequent stage via their capability to secrete osteogenesis-related proteins, BMP-2 and TGF-β1. However, the osteogenic differentiation of BMSCs was inhibited when cultured in a high concentration of conditioned media from each Mϕ phenotype, meaning that the immune strategies should be controlled within the proper ranges. These results suggest that coordinated efforts by both M1 and M2 Mϕs for bone remodelling, which may highlight an optimization strategy for tissue engineering implants.

中文翻译：

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巨噬细胞 M1/M2 极化动态适应微环境变化并调节牙种植后牙槽骨重塑

作为植牙后首批到达的免疫细胞之一，Mϕs 拥有极化成一系列不同表型的能力，从“经典激活”M1 Mϕs 到“替代激活”M2 Mϕs。在这里，假设 Mφ 表型在牙科植入后动态适应，并且这些变化导致与成骨成骨细胞和骨吸收破骨细胞的协调相互作用的级联反应。结果表明，种植牙后的重塑过程与组织损伤的标准反应相似（以拔牙模型为例），只是骨再生阶段延迟。此外，两组中的 Mϕ 激活都经历了从 M1 Mϕs 主导到 M2 型主导阶段的转变，但 M1 Mϕs 的持续存在发生在大鼠牙种植模型中。进一步的体外研究表明，M1 Mϕs 通过分泌最高水平的 TNF-α 和 IL-1β 参与破骨细胞活动，并且是破骨细胞的潜在前体。此外，他们还通过分泌最高水平的化学引诱物 CCL2 和 VEGF 来招募 BMSC。M2 Mϕs 通过其分泌成骨相关蛋白 BMP-2 和 TGF-β1 的能力加速了后续阶段的成骨。然而，BMSCs 的成骨分化在来自每个 Mφ 表型的高浓度条件培养基中培养时受到抑制，这意味着免疫策略应控制在适当的范围内。这些结果表明 M1 和 M2 Mϕ 对骨重塑的协调努力，这可能突出了组织工程植入物的优化策略。