Fracture Healing

7.1 Introduction

This chapter describes what happens when bone is broken or cut, and how it joins again.

In plastic surgery we meet this in two ways:

• Fractures that we treat: facial fractures, hand fractures, and open tibial fractures that need flap cover.
• Osteotomies that we make ourselves: a Le Fort I osteotomy, a fibula flap cut into segments for the mandible, bone shortening in replantation. An osteotomy is a planned fracture. It heals by the same process.

Two things decide whether bone heals: stability (how much the bone ends move) and blood supply. This chapter is organized around these two.

7.2 Two types of bone healing

Bone can heal in two ways. Which one happens depends on how much movement there is between the bone ends.

7.2.1 Primary healing in detail

• Contact healing: occurs where the gap is less than about 0.01 mm and strain is under 2%. Cutting cones form at the ends of the osteons nearest the fracture. Osteoclasts at the tip of the cone cut a tunnel across the fracture line at about 50 to 100 µm per day. Osteoblasts behind them lay down lamellar bone. Union and remodeling happen at the same time.
• Gap healing: occurs where there is a stable gap of less than about 0.8 to 1 mm. The gap is first filled with lamellar bone laid across the gap, at right angles to the long axis. This bone is weak in that direction. From about 3 to 8 weeks, cutting cones cross it and replace it with osteons in the correct direction.
• Primary healing is not faster than secondary healing. Its advantage is that the fixation carries the load, so function can start early.
• Callus appearing under a compression plate means the fixation is moving ("irritation callus"). It is a warning sign.

Neither type is "better". Primary healing allows early movement because the fixation is rigid. Secondary healing is faster and stronger, but it needs the part to be protected, and it produces callus.

7.3 Stages of secondary healing

Most fractures that are not rigidly plated heal by secondary healing. It has four stages. The stages overlap.

1. Hematoma and inflammation (day 0 to 5). Blood clot forms at the fracture. Platelets and inflammatory cells release growth factors. These attract stem cells from the periosteum and the marrow.
2. Soft callus (day 5 to week 3). New vessels grow in. Cartilage and fibrous tissue form between the bone ends. The fracture becomes "sticky": it no longer moves easily.
3. Hard callus (week 3 to 12). The cartilage is replaced by woven bone. The fracture is now clinically united: no pain and no movement.
4. Remodeling (months to years). Woven bone is replaced by lamellar bone. Extra callus is removed.

7.3.1 Cellular and molecular events

Secondary healing repeats the steps of endochondral ossification in the embryo (Gerstenfeld 2003).

Source of the cells. The periosteum is the most important source of progenitor cells for callus. The endosteum and marrow contribute. Surrounding muscle also supplies cells and vessels, which is one reason why muscle cover helps fracture healing.

Angiogenesis and osteogenesis are coupled. Hypoxia stabilizes HIF-1α, which increases VEGF. New vessels bring oxygen, nutrients and osteoprogenitor cells. A specific type of bone capillary (type H) is linked to osteoprogenitors (Kusumbe 2014).

Times are for an adult long bone. Facial bones and children heal faster. (Einhorn and Gerstenfeld 2015)

7.4 Stability and strain

The amount of movement at the fracture decides the type of healing. The reason is strain.

Strain is the amount of movement at the fracture divided by the width of the gap:

strain = movement ÷ gap width

Each tissue tolerates a different amount of strain (Perren 2002):

• Bone: up to about 2%
• Cartilage: up to about 10%
• Granulation tissue: up to 100%

So if strain is under 2%, bone can form directly (primary healing). If strain is between 2% and 10%, cartilage forms first, makes the fracture stiffer, and then bone can form (secondary healing). If strain is too high, no tissue can bridge the gap and the result is nonunion. These numbers are a guide, not exact limits.

7.4.1 Other mechanobiology theories

• Some movement stimulates callus. In experimental osteotomies, axial movement of about 0.2 to 1 mm in a gap of 1 to 2 mm gave the best callus.
• Axial (compressive) movement is tolerated better than shear.
• Large gaps heal poorly even when they are stable. A gap over about 2 mm delays healing.
• Callus increases the diameter of the bone at the fracture. Bending stiffness rises with the fourth power of the radius, so a small amount of peripheral callus stabilizes the fracture efficiently.

Worked examples:

Evidence from fibula flap reconstruction

This rule has been measured in free fibula reconstruction of the jaw. On follow-up CT scans (Swendseid 2020):

• When there was a gap of 1 mm or more between bone ends, 79% did not unite completely.
• When the bone ends were in contact, only 8% did not unite completely.
• Nonunion on CT was followed by more wound complications (40% versus 19%).

The type of plate was less important. In 117 fibula flaps, miniplates and reconstruction plates had the same nonunion rate (14% and 13%) (Robey 2008). Good bone contact matters more than the plate.

7.5 Blood supply of bone

Stability is the first requirement. The second is blood supply. The cortex of a long bone has two blood supplies:

• The endosteal (medullary) supply from the nutrient artery. It supplies the marrow and the inner two-thirds of the cortex.
• The periosteal supply from the periosteum and attached muscle. It supplies the outer one-third of the cortex.

Injury and surgery can remove one or both. There are four possible situations:

(Rhinelander 1974)

7.6 Soft tissue cover

The periosteum and surrounding muscle supply blood to bone. In an open fracture this soft tissue is lost. Exposed bone without soft tissue cover does not heal, and it becomes infected. Flap cover brings back a blood supply.

7.6.1 Classification of open fractures (Gustilo and Anderson)

Gustilo and Anderson 1976; Gustilo, Mendoza and Williams 1984. The type is decided after debridement, not at first inspection.

Principles of management of a Gustilo IIIB fracture (orthoplastic approach): early antibiotics; debridement by senior orthopedic and plastic surgeons together; skeletal stabilization; temporary dressing (negative pressure); definitive soft tissue cover as early as possible, within 72 hours where the patient and wound allow (British BOAST standard); bone reconstruction later if there is a defect.

Choice of flap by level in the leg: proximal third: gastrocnemius muscle flap; middle third: soleus flap or local fasciocutaneous flap; distal third: free flap (or propeller or reverse sural flap in selected cases).

Godina studied 532 patients with limb trauma treated by free flap. He compared early and late flap cover:

Early cover gave less infection and faster bone union. Later studies have questioned the exact 72-hour limit, but the principle of early cover remains. In the "fix and flap" series from Leeds (84 severe open tibial fractures treated by orthopedic and plastic surgeons together), limb salvage was 95% (Gopal 2000).

Local data (USM). Yusof and Halim (2012) reported 11 infected Gustilo IIIB open tibial fractures treated in stages: repeated debridement, flap cover, then bone reconstruction. Infection resolved in all 11. Nine united, at a mean of 15 months. Compare this with 6.8 months in Godina's early group: delay and infection make union much slower.

7.7 Fixation of the facial skeleton

Plastic surgeons fix bone most often in the face and the hand.

7.7.1 Mandible

When the mandible is loaded during biting, the upper border (near the teeth) is pulled apart. This is the tension zone. The lower border is pushed together. This is the compression zone.

Champy showed that a small plate placed along the tension zone is enough to hold a simple fracture, because the bone itself carries the compression at the lower border. These positions are called Champy's lines of osteosynthesis: one plate at the angle (on the external oblique ridge), one plate in the body (below the roots), and two plates at the symphysis (because of torsion).

(Michelet 1973; Champy 1978; Ellis 1999)

This gives two types of fixation:

7.7.2 Midface

The midface is made of thick vertical pillars of bone called buttresses, with thin bone between them. The buttresses carry the chewing force up to the skull base. There are three on each side: nasomaxillary, zygomaticomaxillary and pterygomaxillary (Manson 1980).

• In midface fractures, we plate the buttresses. This restores the height and projection of the face.
• If part of a buttress is missing, it is replaced with a bone graft at the same operation (Gruss and Mackinnon 1986).
• The thin walls (orbital floor, sinus wall) do not carry load. They only need a thin sheet to restore their shape: bone graft, titanium mesh or a polymer sheet.

7.7.3 The skull in young children

The dura of an infant can form new bone. Small defects of the skull in infants can close by themselves. This ability is lost early. In 81 children after fronto-orbital advancement, bone gaps closed if surgery was before about 9 to 11 months of age, and stayed open if surgery was later (Paige 2006). After this age, skull defects need a bone graft.

7.8 Fixation in the hand

In the hand the main problem after a fracture is usually stiffness, not nonunion. The flexor and extensor tendons lie directly on the periosteum of the phalanges. Callus, plates and surgical dissection all cause the tendons to stick to the bone.

Page and Stern (1998) reviewed 105 metacarpal and phalangeal fractures fixed with plates:

• 36% had a major complication (stiffness, nonunion, plate prominence, infection, tendon rupture).
• Only 11% of plated phalangeal fractures regained good movement (total active motion over 220°).

So in the hand we choose the smallest fixation that still allows early movement: K-wires or lag screws where possible, plates only when needed.

Replantation. In replantation the bone is shortened by a few millimeters before fixation. This is done on purpose. It allows the vessels, nerves and skin to be repaired without tension and often without vein grafts.

7.9 Factors that delay bone healing

So far we have covered what bone needs to heal. This section lists what interferes with it. It is useful to separate patient factors from surgical factors, because the surgical factors are under our control.

Irradiated bone

Radiotherapy damages bone permanently. Marx (1983) described irradiated tissue with "three H's":

• Hypovascular: small vessels are narrowed and reduced.
• Hypocellular: osteoblasts and their stem cells are reduced.
• Hypoxic: oxygen level in the tissue is low.

Irradiated bone cannot repair itself after injury, such as a tooth extraction or an osteotomy. This leads to osteoradionecrosis. A non-vascularized bone graft will not survive in an irradiated bed, because there are no vessels to grow into it. Bone placed here must bring its own blood supply: a vascularized bone flap.

Two theories of osteoradionecrosis (ORN):

Risk rises with dose (especially above 60 Gy), mandible more than maxilla, and dental extraction after radiotherapy.

7.10 Delayed union and nonunion

Healing may be slow, or it may fail.

• Delayed union: the fracture is healing, but more slowly than expected.
• Nonunion: healing has stopped, and the fracture will not unite without further treatment.

Working definition (FDA): nonunion is a fracture at least 9 months old that has shown no progression of healing for 3 consecutive months. The time varies with the bone: a mandible or a metacarpal is expected to unite much sooner than a tibia.

7.10.1 Classification (Weber and Cech)

Infected nonunion is considered separately, because infection must be treated first.

7.10.2 Assessment

• History: injury, previous surgery, infection, smoking, diabetes, drugs, radiotherapy.
• Examination: pain, abnormal movement, soft tissue, sinus, neurovascular status.
• Blood tests: white cell count, ESR, CRP; vitamin D, calcium, glucose, albumin.
• Imaging: X-rays; CT to confirm bridging. The RUST score (Radiographic Union Score for Tibial fractures) grades each of 4 cortices from 1 to 3; total 4 (not healed) to 12 (healed) (Whelan 2010).
• At surgery: multiple deep tissue samples for culture.

The X-ray appearance shows what was missing, and so what treatment is needed:

Figure 7.11. Hypertrophic and atrophic nonunion.

The diamond concept

Giannoudis (2007) summarized the requirements for bone healing as four items, called the diamond concept:

1. Mechanical stability (this chapter)
2. Osteogenic cells
3. Growth factors (osteoinductive signals)
4. Scaffold (osteoconductive matrix)

All of these must be in a well-vascularized bed. Items 2 to 4 are what a bone graft provides.

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