Biology of Fracture Healing

2.1 Secondary Indirect Fracture Healing

The healing process The natural course of fracture healing is secondary and indirect via the fracture hematoma to callus formation. This healing process takes place in four stages:

Inflammatory phase
Soft callus phase (approximately 2–3 weeks)
Hard callus phase (3–4 months)
Remodeling phase, consolidation (months–years)

The fracture gap is bridged by intramembranous and enchondral ossification in 3 to 4 months.

With fresh fractures, this healing process is started by the interplay of physiological, biochemical, immunological, and molecular biological factors. Besides the patient’s age and sex, the fracture type (geometry and fracture gap), therapeutic immobilization (internal and/or external), and the subsequent loading influence fracture healing. Through dynamic osteogenesis, the bone mass, bone density, and bone structure adapt, under mechanical strain, to fit the situation. This means that dosed loading, adjusted to healing progress, must be exerted on the fracture during healing.

Mechanotransduction leads to the necessary molecular biological reaction, either through the macro- and micro-architecture (tensegrity theory) or alternatively proceeding from molecular and micromolecular structures to the macromolecular reaction (mechanosome theory). In each case, mechanotransfer leads to a molecular chemical reaction on loading, which is mediated through the three-dimensional network of the osteocytes. The healing process is thereby initiated (mechanocoupling, biochemical coupling, signal transduction from the sensor cells to the reactive cell, and its response—osteoblasts and osteoclasts) and regulated by cytokines, growth factors, hormones, and many other biochemical molecular substances. Mesenchymal cells from the bone marrow, along with induced angiogenesis, also play an important part in the healing process.

Note

Relative stability is a precondition for secondary fracture healing. This is achieved by external and/or internal immobilization.

Influencing factors Both fixation of the fracture and the type of loading can be influenced, but not the geometry of the fracture. This means that compression forces occur in a transverse fracture on axial loading and more additional shear forces in an oblique fracture. Moreover, transverse forces, bending forces, and rotational forces can act on a fracture.

In mechanobiological terms, well-dosed interfragmentary movement in the early phase leads to faster fracture healing and hastens the transition from soft connective tissue callus to bridging, solidifying bony callus. In the later healing phase, however, tolerance to stress loading by interfragmentary movement diminishes considerably. Overloading then results in hypertrophic pseudarthrosis.

In comminuted fractures, stress movement is distributed to many fracture planes, so the individual movements diminish at cellular level. For this reason, stress movements are better tolerated in comminuted fractures (strain theory, Perren 2008).

In general, compression forces have a positive effect on fracture healing, especially if they occur in a cyclical manner. By contrast, shear, torsional, bending, and transverse forces delay healing.

A further important factor in healing is the size of the fracture gap. Even dosed distraction forces improve bridging of a fracture gap through the mechanism of intramembranous ossification.

Fractures in trabecular bone structures, such as carpal bones and juxta-articular metaphysial areas, heal mainly by enchondral ossification or combined with intramembranous ossification; bone healing is protracted. It must be distinguished from cortical fracture healing.