Fracture healing and Perren’s strain theory: absolute and relative stability

Two ways a fracture heals

Bone is unusual among tissues in healing with more of itself rather than with scar. It can do so by two routes, and which one it takes depends on the mechanical environment at the fracture — which is to say, on what the surgeon does.

Primary (direct) healing

Occurs only when the fragments are anatomically reduced and held rigidly under compression. Osteoclasts at the tip of cutting cones tunnel across the fracture line and osteoblasts behind them lay down new osteons, so the cortex is reconstituted by Haversian remodelling. No callus forms. Where the cortices are in direct contact this is contact healing; where a small stable gap remains, the gap is first filled with lamellar bone laid down perpendicular to the long axis and then remodelled by cutting cones — gap healing.

Secondary (indirect) healing

Occurs when some movement is allowed at the fracture. It proceeds through a cartilaginous intermediate — callus — and is the natural way fractures heal in a cast, on a nail, under a bridge plate or in an external fixator. It combines intramembranous ossification, mostly beneath the periosteum, with endochondral ossification in the fracture gap.

The stages of secondary healing

Blood supply underlies all of it. In an intact long bone the endosteal circulation from the nutrient artery supplies roughly the inner two-thirds of the cortex and the periosteal circulation the outer third. After a fracture the periosteal vessels become the dominant source of supply to the callus, which is why periosteal stripping — by the injury or by the surgeon — is so costly, and why reaming, which temporarily destroys the endosteal supply, is tolerated when the soft-tissue envelope is intact.

Perren’s strain theory

Stephan Perren’s insight was that a tissue can only form in a fracture gap if it can survive the deformation it experiences there. He defined interfragmentary strain as the movement of the fracture gap divided by the width of the gap — the change in length over the original length — and observed that each tissue of repair tolerates a different amount before it fails.

Secondary healing is therefore a cascade in which each tissue makes the gap stiff enough for the next: granulation tissue lowers strain enough for cartilage, cartilage lowers it enough for woven bone, and a wide callus — being far from the axis of the bone — is mechanically very effective at resisting bending. The three ranges that matter for the examination follow directly.

• Strain below about 2%: primary bone healing. This is the environment created by absolute stability.
• Strain between about 2% and 10%: secondary bone healing with callus. This is the environment created by relative stability.
• Strain persistently above about 10%: bone cannot form; the gap fills with fibrous tissue and a non-union results.

Absolute and relative stability

The choice is made by the fracture pattern and the bone, not by the surgeon’s preferred implant. Articular fractures need anatomical reduction and absolute stability so that the cartilage heals without a step and the joint can move early. Simple transverse or short oblique fractures of the forearm are treated in the same way because the forearm behaves as a joint. Multifragmentary shaft fractures are bridged: reducing every fragment would strip the blood supply for no mechanical gain.

Working length is the distance between the fixation points nearest the fracture on each side. Lengthening it — by leaving screw holes empty over the fracture zone of a bridge plate — makes the construct less stiff and distributes bending stress over a longer segment of the plate, which both lowers the strain concentration in the implant and permits the movement that callus formation needs. Too little stiffness is as harmful as too much: movement beyond what the tissues tolerate again leads to non-union.

When healing fails

A non-union is a fracture that will not heal without further intervention. Weber and Cech divided non-unions by their biological activity, and the division tells you the treatment.

Hypertrophic non-union

Abundant callus that fails to bridge — the ‘elephant’s foot’ appearance. The biology is good and the blood supply is adequate; the problem is too much movement. The treatment is to increase stability, for example by exchange nailing or compression plating. Bone graft is not usually needed.

Oligotrophic non-union

Little or no callus but vascular bone ends, typically where the fragments are displaced or distracted. It needs reduction and stable fixation, often with graft.

Atrophic non-union

No callus, with resorbed, sclerotic or tapered bone ends. The biology has failed: poor blood supply, periosteal stripping, bone loss or host factors. It needs both biological stimulation — debridement to bleeding bone and bone graft — and stable fixation. Infection must be excluded in any non-union, particularly after an open fracture or previous surgery.

Patient factors that impair healing include smoking, diabetes, malnutrition, vitamin D deficiency and drugs such as corticosteroids; non-steroidal anti-inflammatory drugs inhibit the prostaglandin-mediated early phase and are often avoided in fractures at risk. Injury factors include high energy, open wounds, bone loss, soft-tissue stripping and an unfavourable site such as the distal tibia, the scaphoid waist or the femoral neck.