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. 2022 Apr 27;10:912133. doi: 10.3389/fbioe.2022.912133

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Copyright © 2022 Tan, Wang, Chen, Liu, Ma, Ma, Wang, Zeng, Xue, Yue and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Fibrous tissue formed and hindered the repair of necrotic areas in NONFH (A) Representative images of Sirius Red-stained sections from patients with different types and stages of NONFH. Scale bar, 2.5 mm (B,C) Collagen quantification in sections from patients with different types NONFH in Ficat Stage III (B) or Ficat stage IV (C), based on Sirius red staining (D–F) Schematic showing how macrophage M1/M2 imbalance participates in the formation of chronic inflammation and tissue fibrosis, and facilitates the progression of human NONFH: macrophages migrate to the local bone lesion and adopt the M1 phenotype, then secrete abundant IL-6, IL-1β and other inflammatory factors after bone necrotic (D). Those cytokines induce blood vessels formation and recruit monocytes into the local lesion. And then the monocyte/macrophages are polarized to M1 (avascular regions) and M2 (around blood vessel) subtype. The M1 subtype is dominating in local lesion and secreting the inflammatory cytokines to formation the inflammatory microenvironment (E). When osteonecrosis progresses to the base of the femoral head (end-stage), inflammation subsided, the number of macrophages M1 decreased, bone necrotic with bone formation (F).