Macrophages and bone inflammation

Abstract

SummaryBone metabolism is tightly regulated by the immune system. Accelerated bone destruction is observed in many bone diseases, such as rheumatoid arthritis, fracture, and particle-induced osteolysis. These pathological conditions are associated with inflammatory responses, suggesting the contribution of inflammation to bone destruction. Macrophages are heterogeneous immune cells and are polarized into the proinflammatory M1 and antiinflammatory M2 phenotypes in different microenvironments. The cytokines produced by macrophages depend on the macrophage activation and polarization. Macrophages and macrophage-derived cytokines are important to bone loss in inflammatory bone disease. Recent studies have shown that macrophages can be detected in bone tissue and interact with bone cells. The interplay between macrophages and bone cells is critical to bone formation and repair. In this article, we focus on the role of macrophages in inflammatory bone diseases, as well as discuss the latest studies about macrophages and bone formation, which will provide new insights into the therapeutic strategy for bone disease.

Healing differences in narrow diameter implants submitted to immediate and conventional loading in mandibular overdentures: A randomized clinical trial

“…At week 12, the IML group released significantly more IL‐10 (+45.74%) than the CL group suggesting the need to inhibit the more active remodeling process in the IML group. This suggests the anti‐inflammatory action of IL‐10 and its action as a suppressor in the osteoclastic differentiation, finalizing the bone resorption process . The positive correlation between IL‐10 and TNF‐α and IL‐1β biomarkers in both groups at week 8 evidences the inhibiting role of IL‐10 in the final phase of osseointegration, reducing the pro‐inflammatory response of the other cytokines …”

Biomaterial‐induced multinucleated giant cells express proinflammatory signaling molecules: A histological study in humans

“…In response to microenvironmental stimuli, they can polarize to either proinflammatory (M1) or anti‐inflammatory (M2) cells . Consequently, the proinflammatory type is involved in the inflammation process and phagocytosis in the early phase of wound healing and releases signaling molecules such as TNF‐α, IL‐1β, and C‐C chemokines that can promote angiogenesis and recruit further inflammatory cells . The M2 type is related to wound healing and releases signaling molecules such as transforming growth factor‐β and IL‐10 that are involved in tissue regeneration .…”

“…Consequently, the proinflammatory type is involved in the inflammation process and phagocytosis in the early phase of wound healing and releases signaling molecules such as TNF‐α, IL‐1β, and C‐C chemokines that can promote angiogenesis and recruit further inflammatory cells . The M2 type is related to wound healing and releases signaling molecules such as transforming growth factor‐β and IL‐10 that are involved in tissue regeneration . MNGCs, similar to their precursors (macrophages), were suggested to be able to polarize to M1 or M2 subtypes and may therefore demonstrate contribution to the biomaterial‐based regeneration process .…”

“…It was previously shown that MNGCs can release vascular endothelial growth factor that is a main progenitor of angiogenesis . In addition, the fact that MNGCs preserve a proinflammatory phenotype presupposes their ability to release IL‐1β and TNF‐α, which are also involved in angiogenesis . A high level of angiogenesis might be important to support biomaterial degradation in a highly active microenvironment.…”

“…27 The M2 type is related to wound healing and releases signaling molecules such as transforming growth factor-β and IL-10 that are involved in tissue regeneration. 27 MNGCs, similar to their precursors (macrophages), were suggested to be able to polarize to M1 or M2 subtypes and may therefore demonstrate contribution to the biomaterial-based regeneration process. 3 In this context, an in vivo study evaluated the inflammatory pattern of the MNGCs induced by the subcutaneous implantation of silk fibrion in CD-1 mice.…”