Phases of Fracture Healing: Inflammation, Callus Formation and Remodelling

Fracture healing occurs in overlapping phases rather than a single event. The fracture haematoma establishes the inflammatory niche; granulation tissue and a soft callus stabilise the gap; hard callus bridges it with woven bone; and remodelling converts that temporary scaffold into organised lamellar bone. Knowing what should happen in each phase helps emergency clinicians recognise normal recovery, detect infection or non-union early and avoid interventions that disrupt biology.

Learning outcomes

After this lesson, the learner should be able to describe the cellular and vascular events of each phase, connect them with clinical and radiographic findings, explain direct versus callus-mediated healing, identify factors that interrupt a phase, and use phase-based reasoning in open fractures, delayed union and non-union.

1. Why phases overlap

Inflammatory mediators remain active while soft callus forms; angiogenesis continues as cartilage is converted to bone; and remodelling begins before a fracture has regained full strength. The phase model is therefore a map of dominant activity, not a set of watertight compartments. Severe infection, instability or ischaemia can return a wound to a prolonged inflammatory state and prevent progression.

2. Phase 1—Fracture haematoma and inflammation

2.1 The first minutes and hours

Fracture tears periosteal, endosteal and soft-tissue vessels. Blood collects between and around the fragments, forming a fibrin-rich haematoma. Platelets degranulate and create a provisional matrix containing platelet-derived growth factor, transforming growth factor-beta and other signals. The clot provides a temporary scaffold for incoming cells; removing it unnecessarily or stripping the surrounding soft tissue can impair repair.

2.2 Innate immune response

• Neutrophils arrive early and clear bacteria and debris.
• Monocytes differentiate into macrophages that remove necrotic tissue and coordinate the transition from inflammation to repair.
• Cytokines such as interleukin-1, interleukin-6 and tumour necrosis factor-alpha recruit progenitor cells and induce angiogenic and osteogenic pathways.
• Controlled inflammation is essential. Excessive or prolonged inflammation—especially from infection, retained foreign material or repeated tissue trauma—causes osteolysis and inhibits osteoblast function.

2.3 Vascular events

Hypoxia around the fracture activates hypoxia-inducible pathways and vascular endothelial growth factor. New vessels begin to grow from periosteum and surrounding muscle. A small degree of hypoxia favours cartilage formation in the flexible central callus, while later revascularisation is necessary for mineralisation. Complete loss of perfusion, however, produces necrotic fragments and a biologically inactive gap.

2.4 What the clinician sees

• Pain, local tenderness, bruising, swelling and guarding are expected.
• Distal pulses and neurological function should be documented; they are not explained away as “part of healing.”
• Increasing pain out of proportion, pain with passive stretch, tense compartments, fever, crepitus or rapidly spreading erythema are red flags.
• Plain radiographs show the fracture but usually cannot show the haematoma. CT or MRI is used selectively for complex anatomy, occult fracture or soft-tissue questions.

2.5 How this phase is protected

Control haemorrhage, cover open wounds, provide analgesia, align and splint the limb, preserve soft tissue and avoid repeated unnecessary manipulation. In open fractures, early antibiotics and operative debridement according to local protocol reduce the microbial burden before it can convert the inflammatory niche into destructive infection.

3. Phase 2—Granulation tissue and soft callus

3.1 Cellular composition

Mesenchymal progenitor cells migrate into the haematoma. Fibroblasts lay down collagen; endothelial cells create capillary loops; and chondrocytes form cartilage where oxygen tension and mechanical stability favour a cartilaginous matrix. This mixture is granulation tissue and soft callus. It bridges the fragments but is not yet strong enough for unrestricted loading.

3.2 Endochondral and intramembranous pathways begin

• Endochondral ossification: cartilage is produced in relatively hypoxic, more mobile areas and will later be replaced by bone.
• Intramembranous ossification: osteoblasts form woven bone directly in well-vascularised periosteal regions.
• These pathways occur side by side. The balance reflects strain, oxygen, blood supply and the fixation construct.

3.3 Mechanical meaning

Soft callus reduces gross motion and strain at the fracture. Controlled relative movement can stimulate callus, but excessive shear prevents maturation and leaves fibrocartilage or fibrous tissue between the fragments. A new increase in pain or deformity during this phase suggests loss of fixation, cast failure, premature loading or infection.

3.4 Clinical and radiographic findings

Finding	Expected progression	Concerning pattern
Pain	Less at rest and with gentle movement	Increasing pain, night pain or pain after a period of improvement
Swelling	Gradually decreases	New tense swelling, erythema, fever or drainage
Stability	Less abnormal motion on protected examination	Persistent gross mobility or new angulation
Radiograph	Early periosteal reaction or faint callus may appear	Widening gap, implant migration or no serial progression

4. Phase 3—Hard callus and woven bone

4.1 Cartilage maturation

Chondrocytes enlarge and the cartilaginous matrix becomes mineralised. The cells undergo apoptosis, leaving a scaffold invaded by capillaries, osteoclasts and osteoblast precursors. This transition is vulnerable to persistent hypoxia, infection and instability.

4.2 Woven bone formation

Osteoblasts deposit osteoid on the mineralised cartilage scaffold and directly along vascularised periosteal surfaces. Woven bone has randomly arranged collagen and is less strong than mature lamellar bone, but it rapidly bridges the fracture. As the external and internal callus connect, abnormal movement and tenderness decline.

4.3 Clinical and imaging progression

• Weight-bearing or functional use becomes more comfortable within the limits of the prescribed plan.
• Callus becomes visible and increasingly mineralised on serial radiographs; the fracture line gradually fades.
• Bridging should be judged across multiple cortices and views, not from a single projection.
• Apparent radiographic callus with persistent pain or motion warrants assessment for infection, a hypertrophic non-union or an unstable construct.

4.4 Direct healing can bypass a large callus

With anatomic reduction and very rigid fixation, osteoclast cutting cones cross the tiny fracture gap and osteoblasts rebuild osteons. This primary/direct process can produce little external callus. Absence of a large callus does not automatically mean failure if alignment, fixation and clinical progress support direct healing.

5. Phase 4—Remodelling

5.1 Woven to lamellar bone

Remodelling replaces disorganised woven bone with stronger lamellar bone. Osteoclasts resorb excess or poorly oriented tissue, while osteoblasts refill the tunnels and align new trabeculae with habitual loads. The medullary canal may reopen and the cortex becomes more uniform.

5.2 Functional adaptation

Mechanical loading influences trabecular orientation and cortical thickness. Rehabilitation therefore aims for graded, safe loading rather than either prolonged complete inactivity or unprotected stress. The exact plan depends on fracture stability and specialist instructions.

5.3 Age and bone differences

• Children generally have thicker periosteum, stronger blood supply and faster callus formation. They remodel some angular deformities, especially near an active growth plate.
• Rotational deformity, major shortening and articular incongruity remodel poorly and can cause lasting dysfunction.
• Adults and older patients may require longer protection, particularly with poor vascularity, osteoporosis, diabetes or smoking.

6. Phase-specific causes of failure

Phase interrupted	Typical causes	Possible outcome
Haematoma/inflammation	Severe devascularisation, repeated stripping, uncontrolled bleeding, infection or systemic shock	Necrotic fragments, poor recruitment, atrophic non-union
Soft callus	Excessive motion, large gap, interposed tissue, inadequate nutrition or smoking	Persistent fibrous tissue, pain and delayed union
Hard callus	Persistent hypoxia, infection, implant instability or premature high loading	Callus fails to bridge or breaks down
Remodelling	Malalignment, rotation, severe displacement or prolonged unloading	Malunion, stiffness or reduced final strength

7. Primary versus secondary healing by phase

Feature	Secondary/callus-mediated	Primary/direct
Stability	Relative stability with controlled strain	Very rigid, near-anatomic fixation
Early tissue	Haematoma, fibrous tissue and cartilage	Minimal external callus; osteonal continuity
Radiograph	Periosteal and bridging callus expected	Callus may be subtle or absent
Typical fixation	Cast, splint, intramedullary nail or bridge construct	Compression plate or other construct that eliminates motion

8. How emergency care supports every phase

9. Fracture healing in special situations

Open fractures

Contamination, tissue loss and vascular disruption can prolong inflammation and prevent callus. Source control, soft-tissue coverage and appropriate stabilisation are central; a small skin wound can hide severe deep injury.

Intra-articular fractures

Articular cartilage has limited regenerative capacity. Restoring joint congruity and early safe motion are important to reduce post-traumatic arthritis and stiffness, while the metaphyseal component heals through the usual bone phases.

Pathological fractures

Tumour, infection or metabolic bone disease changes both the mechanical environment and biological response. A fracture through abnormal bone needs imaging and specialist investigation rather than being treated as an ordinary injury.

Stress fractures

Repeated submaximal loading produces microdamage faster than remodelling can repair it. Early rest and correction of training, nutritional or endocrine factors may allow healing; continued loading can convert a stress injury to a complete fracture.

10. Recognising delayed union, non-union and malunion

• Delayed union: slower than expected but with serial clinical or radiographic progress.
• Non-union: failure of progressive repair, often with persistent pain or motion and stagnant serial films. Investigate infection, blood supply, stability, gap, smoking and systemic disease.
• Hypertrophic non-union: abundant callus but inadequate mechanical stability.
• Atrophic non-union: little callus and poor biology, often with devascularisation or infection.
• Malunion: union in an unacceptable angulation, translation, shortening or rotation.

11. Case-based phase reasoning

Case 1: Normal progression

Two weeks after a stable forearm fracture, swelling and pain are declining and a faint periosteal reaction is present. This fits the transition from inflammation to soft callus; the absence of a large hard callus at this time is not, by itself, failure.

Case 2: Failure to progress

At serial reviews a patient has persistent focal pain, a mobile fracture and no bridging callus. Assess cast or implant stability, infection, smoking, nutrition and vascularity. A “wait longer” approach without finding the cause may allow a reversible delayed union to become established non-union.

Case 3: Red flag during early healing

A patient with a tibial fracture develops escalating pain, pain on passive toe stretch and a tense leg. This is a compartment-syndrome emergency, not normal inflammation. Remove constrictive dressings, keep the limb at heart level and obtain urgent surgical assessment according to local protocol.

12. Exam pearls

• The four dominant phases are haematoma/inflammation → soft callus → hard callus → remodelling.
• Soft callus is mainly fibrous and cartilaginous; hard callus is mineralised woven bone.
• Angiogenesis is required for progression from cartilage to bone.
• Healing needs both biology and mechanics: vascular, viable tissue plus appropriate stability.
• A large callus is expected in secondary healing but may be absent in primary/direct healing.
• Children remodel some angular deformity, but rotation and articular incongruity remain important.

References and further reading

• NCBI Bookshelf: Fracture Healing.
• NCBI Bookshelf: Open Fracture Management.
• NCBI Bookshelf: Compartment Syndrome.
• Use local orthopaedic, trauma, antimicrobial and rehabilitation protocols for treatment timing and follow-up.