This 1998 narrative review by Einhorn synthesizes experimental data from standardized rat and mouse closed fracture models. It maps the cellular sequence, gene expression patterns, and extracellular matrix events of fracture healing from hematoma formation through bone remodeling. The central question: which cell types act, which genes are expressed, and precisely when does each event occur?
Fracture healing recapitulates growth plate biology — but on a temporal rather than a spatial scale. This single insight is why knowledge of physeal development directly translates to understanding fracture repair at any age.
When a fracture is rigidly fixed (plating), the periosteal response is suppressed and primary cortical healing must occur via cutting cones. When some motion is preserved (intramedullary nail, cast), secondary healing with callus formation dominates. Choosing fixation strategy means choosing which healing pathway you invoke.
Hypertrophic chondrocytes die by apoptosis, not transdifferentiation. This matters for understanding nonunion biology: disruption of the programmed removal sequence (by ischemia, NSAIDs, or metabolic derangement) can arrest the endochondral process and leave persistent cartilage at the fracture site.
BMP expression shifts from mesenchymal cells to chondrocytes to osteoblasts in sequence. This is the biological rationale for recombinant BMP use in challenging fractures. Exogenous BMP2 supplements a signal that normally emerges from the tissue itself.
This 1998 narrative review by Einhorn synthesizes experimental data from standardized rat and mouse closed fracture models. It maps the cellular sequence, gene expression patterns, and extracellular matrix events of fracture healing from hematoma formation through bone remodeling. The central question: which cell types act, which genes are expressed, and precisely when does each event occur?
Fracture healing recapitulates growth plate biology — but on a temporal rather than a spatial scale. This single insight is why knowledge of physeal development directly translates to understanding fracture repair at any age.
When a fracture is rigidly fixed (plating), the periosteal response is suppressed and primary cortical healing must occur via cutting cones. When some motion is preserved (intramedullary nail, cast), secondary healing with callus formation dominates. Choosing fixation strategy means choosing which healing pathway you invoke.
Hypertrophic chondrocytes die by apoptosis, not transdifferentiation. This matters for understanding nonunion biology: disruption of the programmed removal sequence (by ischemia, NSAIDs, or metabolic derangement) can arrest the endochondral process and leave persistent cartilage at the fracture site.
BMP expression shifts from mesenchymal cells to chondrocytes to osteoblasts in sequence. This is the biological rationale for recombinant BMP use in challenging fractures. Exogenous BMP2 supplements a signal that normally emerges from the tissue itself.