Overview — Definitions & Biology of Fracture Healing
Fracture healing is a complex regenerative process involving four overlapping phases: inflammation (days 1–7), soft callus formation (weeks 1–3), hard callus formation (weeks 3–12), and remodelling (months to years). Normal secondary bone healing proceeds through enchondral ossification of the fracture callus; primary cortical healing occurs only under conditions of absolute stability and compression (as with compression plating). Malunion and nonunion represent the two most important failures of this process — the former representing misdirected healing, the latter representing arrested healing — and both require an understanding of the biology of fracture healing to manage effectively.
- Malunion: a fracture that has healed in an abnormal position — with angular deformity, rotational deformity, shortening, or a combination; it is healed (united) but with poor alignment; the clinical significance depends on the degree of deformity, the bone involved, and the adjacent joint mechanics; malunion of a lower limb fracture causes altered gait biomechanics, joint overload, and early osteoarthritis; malunion of a forearm fracture causes restriction of pronation/supination; malunion of the distal radius is the most common malunion in clinical practice
- Nonunion: failure of a fracture to unite; the US FDA definition is fracture not healed by 9 months with no radiological progression over 3 consecutive months; in clinical practice, the threshold is adapted to the individual fracture and patient context; nonunion implies that the healing process has ceased — distinguished from delayed union (healing is occurring but slower than expected)
- The diamond concept (Giannoudis 2007): four elements are required for fracture healing — (1) osteogenic cells (mesenchymal stem cells from the periosteum, endosteum, and marrow); (2) osteoinductive growth factors (BMPs — bone morphogenetic proteins, TGF-β, FGF, PDGF, IGF); (3) osteoconductive scaffold (extracellular matrix, fibrin clot, bone graft); (4) mechanical stability (fixation, immobilisation); deficiency in ANY of these elements leads to impaired healing and potentially nonunion; treatment must identify and correct the deficient element(s)
Malunion — Assessment & Management
| Parameter | Assessment Method | Clinical Significance |
|---|---|---|
| Angular deformity | Long-leg standing AP radiograph (hip-to-ankle film) for lower limb; mechanical axis (from centre of femoral head to centre of ankle joint) deviates medially (varus) or laterally (valgus) of the centre of the knee; CORA (Centre of Rotation of Angulation) is identified at the apex of the deformity — the level at which correction must be applied | Each 1° of varus or valgus deformity in the lower limb shifts the mechanical axis by approximately 6–7 mm; >5° varus malunion at the tibial shaft causes medial compartment overload — significantly increases medial knee OA risk; >10° valgus causes lateral compartment overload; lower limb angular malunion is the most common cause of early post-traumatic OA |
| Rotational deformity | Clinical assessment (gait observation; foot progression angle — normal 5–10° external rotation; thigh-foot angle; Craig test for femoral version); CT scanogram for precise measurement (CT of the femoral neck angle + CT of the knee epicondyles for femoral malrotation; tibial torsion measured from tibial plateau to ankle joint level) | Rotational malunion of the femur or tibia is frequently missed; clinical: internal rotation malunion = `in-toeing` gait, hip impingement; external rotation = abnormal foot progression angle; >10° rotational deformity in the tibia or femur is generally symptomatic; CT scanogram is the gold standard for measuring rotational deformity |
| Shortening | Clinical (blocks test — measure leg length discrepancy on standing with blocks under the short side until pelvis levels); X-ray (standing long-leg; scanogram); CT scanogram (most accurate — measures each bone segment independently) | <1 cm shortening — usually asymptomatic; 1–2 cm — minor functional impairment; >2 cm — significant gait disturbance, low back pain, pelvic obliquity; >4 cm — severe disability, requires surgical correction; in children: reactive overgrowth of 0.5–2 cm is expected after femoral shaft fractures (under 10 years) — accept some shortening acutely |
- Corrective osteotomy principles: the osteotomy must be planned at the CORA (Centre of Rotation of Angulation) to achieve true mechanical axis correction without translation; the Paley/Herzenberg method: identify the mechanical axis deviation (MAD), the CORA, and the magnitude of correction needed; opening wedge vs closing wedge vs neutral wedge osteotomy; opening wedge (adds length, creates bone defect requiring graft or substitute); closing wedge (shortens, removes bone, but no graft needed — simpler healing); dome osteotomy (at the CORA — allows rotation without translation); the Taylor Spatial Frame (TSF — computer-aided hexapod Ilizarov ring fixator) allows gradual, multi-planar, simultaneous correction of angular, rotational, and translational deformity with high precision
Nonunion — Weber & Cech Classification Revisited
| Type | Biology | X-Ray | Treatment Principle |
|---|---|---|---|
| Hypertrophic (elephant foot) | Excellent biology (vascularity, osteogenic activity); problem = mechanical instability | Exuberant callus at both ends; fracture line still visible | Stabilisation ONLY (exchange nail, compression plate); no graft needed; biology excellent — just add stability |
| Oligotrophic | Some vascularity; minimal callus; fragments not in contact (distracted) | Minimal callus; gap; fracture ends present but not reactive | Stabilisation + reduce gap (bring into contact) + bone graft to stimulate biology |
| Atrophic | Avascular bone ends; no callus; both stability AND biology are deficient | Pencil-point tapering; no callus; gap; sclerotic ends | Stabilisation + debride atrophic ends to bleeding bone + aggressive bone grafting (iliac crest autograft, RIA, Masquelet technique for large defects) |
Biology of Bone Graft — The Three Properties
- Osteogenesis: the capacity of the graft to directly form new bone via transplanted viable osteogenic cells (osteoblasts and mesenchymal stem cells); only autologous fresh cancellous bone graft has significant osteogenic potential (living cells transplanted with the graft); allograft has minimal osteogenic activity (cells are killed by processing/sterilisation)
- Osteoinduction: the ability of the graft to stimulate the host`s own cells to differentiate into bone-forming cells; mediated by bone morphogenetic proteins (BMPs — BMP-2, BMP-7) and other growth factors present in the bone matrix; autograft has the highest osteoinductive potential; demineralised bone matrix (DBM) retains osteoinductive properties after processing; synthetic BMP-2 (Infuse) and BMP-7 (Osigraft) are recombinant osteoinductive agents
- Osteoconduction: the ability of the graft to provide a physical scaffold (3-dimensional lattice) for vascular ingrowth and new bone deposition by the host`s cells; the graft acts as a `scaffold` rather than generating or inducing bone formation; all graft types (autograft, allograft, synthetic calcium phosphate/calcium sulphate, bioactive glass) have osteoconductive properties; autograft has all three properties (osteogenesis + osteoinduction + osteoconduction) — the gold standard; synthetic substitutes have osteoconduction only unless combined with growth factors
- Iliac crest autograft: gold standard for bone grafting; cancellous autograft from the anterior iliac crest provides all three properties; donor site morbidity (10–30% chronic pain, seroma, haematoma, LFC nerve injury); the posterior iliac crest provides a larger volume; Reamer-Irrigator-Aspirator (RIA) graft from the femoral or tibial canal provides large volumes (30–90 mL) of autologous graft with lower donor site morbidity than iliac crest
Exam Pearls
- Diamond concept: 4 requirements for fracture healing — osteogenic cells + osteoinductive factors + osteoconductive scaffold + mechanical stability; nonunion = failure of one or more; treatment = identify and restore the deficient element(s)
- CORA (Centre of Rotation of Angulation): the apex of the deformity; the level at which corrective osteotomy must be applied; if osteotomy is not at the CORA, angular correction creates translation — a new secondary deformity; CORA identification is the first step in osteotomy planning
- MAD (Mechanical Axis Deviation): normal = mechanical axis passes through centre of knee (Mikulicz point); varus malunion = MAD medial to knee centre = medial compartment overload = early medial OA; valgus = MAD lateral = lateral compartment overload; measured on long-leg standing film
- Malunion in children: accept more deformity than adults due to remodelling potential; tibial shaft — up to 15° sagittal angulation, 10° coronal; rotational deformity does NOT remodel (must correct);
- Three bone graft properties: osteogenesis (cells that form bone — only autograft); osteoinduction (stimulate host cells — autograft + BMPs + DBM); osteoconduction (scaffold for vascular ingrowth — all grafts); autograft = gold standard (all three); synthetic substitutes = osteoconductive only
- Exchange nailing: for hypertrophic/oligotrophic tibial nonunion after prior IMN; remove old nail, ream to larger diameter (stimulates biology + larger stiffer nail); union rate 70–90%; most effective single treatment for tibial shaft nonunion
- Masquelet technique: cement spacer induces membrane rich in growth factors (VEGF, BMP-2, TGF-β) over 6–8 weeks; Stage 2 = remove spacer + pack autograft into membrane envelope; for defects 2–10 cm; avoids prolonged Ilizarov bone transport
- Modifiable risk factors for nonunion: smoking (most important — must stop before elective nonunion surgery); NSAIDs (inhibit COX-2 = impaired prostaglandin-driven osteoblast recruitment — stop perioperatively); diabetes (optimise HbA1c); hypothyroidism; malnutrition; infection