ArticleJBMR plus2019
The Fracture Callus Is Formed by Progenitors of Different Skeletal Origins in a Site-Specific Manner.
Article in JBMR plus, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Chewing loads alter TMJ metabolism and Zn homeostasis via PIEZO1/ TRPV4.Journal of biological engineering · 2025Article
- Participation of the Periosteum, Endosteum, and Hematogenous Marrow in the Early Osseointegration of a Titanium Implant Inserted in Contact with the Hematogenous Marrow.Medicina (Kaunas, Lithuania) · 2025Article
- Fracture healing: cellular mechanisms and impact of parathyroid hormone and its analogs.Frontiers in endocrinology · 2025Review
- Periosteal Skeletal Stem Cells and Their Response to Bone Injury.Frontiers in cell and developmental biology · 2022Review
- Ablation of Ephrin B2 in Col2 Expressing Cells Delays Fracture Repair.Endocrinology · 2020Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
We evaluated repair following a mid-diaphyseal fracture of the tibia in 3-month-old mice. We observed differences in the repair process at three different sites of the callus. Site 1: bone developing from the outer layer of the periosteum of the cortex; site 2: bone developing within the bridge/central region of the fracture; and site 3: bone developing within the marrow of the ends of broken bones. We characterized these sites by correlating datasets from X-ray CT and histology. Correlated data demonstrated the involvement of different cells and different rates of mineralization. The origin of the progenitors and mechanism of progenitor differentiation involved at these sites was then evaluated using lineage tracing of cells expressing Prx1 and Col.2. The Prx1 progeny contributed to intramembranous bone formation (IBF) at site 1 and endochondral bone formation (EndoBF) at site 2 but not to intramedullary bone formation (IMBF) at site 3. IBF at site 1 was confirmed without a chondrocyte intermediate unlike EndoBF at site 2. Additionally, the presence of Col.2 progeny contributed to EndoBF in site 2 and IMBF in site 3 but not to IBF in site 1. However, the Col.2 progeny in IMBF in site 3 appeared to come from Col.2-expressing osteocytes originating in the cortices of the ends of the fractured bone. In conclusion we have identified three sites of bone fracture repair that differ in their origin of cells and their mechanisms of bone formation. © 2019 The Authors JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.
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