We all see fractures nearly every day in orthopedic practice. But why do we sometimes see abundant healing callus and sometimes not on the x-rays? Let's shed some light on the biology of fracture healing to answer this question.
Generally, there are three phases of bone healing after injury:
1. Inflammation (1-2 weeks): bleeding from the fracture results in vascular disruption followed by fracture hematoma, abundant with cells and growth factors to promote neovascularization (new blood vessel formation). Bone blood flow, initially disrupted by the fracture, is the major determinant of fracture healing, but recanalizes within 2 weeks and flow is escalated (hypervascular) until it returns to normal around 12 weeks.
2. Repair (2-12 weeks): primary “soft callus" (unmineralized cartilage) forms periosteally (around the bone), stimulated by motion at the fracture site… the more fracture mobility, the greater the callus. This is followed by “hard callus” (soft callus mineralizing, maturing into bone) as fracture motion ceases. This process is enchondral ossification… bone formation from a cartilage template. In addition, membranous ossification results from direct bone formation from the periosteal tissues and stem cells without a cartilage template.
3. Remodeling (8 weeks-2 years): New bone is slowly converted to mature bone through haversian “cutting cones”, removal of older bone and deposition of new bone.
The above process is defined as “secondary bone healing”. However, when a fracture is rigidly repaired (ie, with a plate and screw construct), there is minimal to no motion at the fracture site and thus, there is generally no stimulation for the soft/hard callus to bone formation processes above. Consequently, mostly “primary bone healing” occurs which essentially is the normal bone remodeling process (mostly just stage 3 above). Ironically, fractures treated with rigid internal fixation will take longer to biologically heal than those treated less rigid...non-surgically treated with just a cast. However, ORIF patients (patients who have had surgery with hardware to fix a fracture) clinically heal sooner, they feel better faster due to rigid internal fixation. But “skipping” the repair phase above in the primary bone healing pathway is why we generally do not see much callus after ORIF…there is minimal motion at the former fracture site and thus minimal to no fracture callus.
What about Bone stimulation??
1. Bio-electric: Application of an electromagnetic field to a fracture simulates mechanical stress on bone. This stress induces gene upregulation to release BMPs to stimulate bone remodeling.
2. Ultrasound: Application of a pulsed low intensity ultrasound stimulates gene upregulation to release other growth factors such as IGF and TGF-B. In addition, it directly stimulates chondrogenesis (new cartilage) and thus the formation of soft callus described above, followed by mineralization and then remodeling.
Available data favors ultrasound, but a head-to-head comparison has not been studied and both types of stimulation are considered acceptable adjunctive treatments if a fracture fails to show significant healing after 90 days.
In the end, most fractures heal uneventfully via the processes reviewed above, infrequently needing stimulation. Regardless, it’s our job as orthopedic providers to facilitate physiology and bone biology via various available treatments to best enable uneventful fracture healing with an eventual restoration of normal function.