Blood supply of a long bone
A mature long bone receives blood from several sources:
- nutrient artery
- periosteal vessels
- metaphyseal vessels
- epiphyseal vessels
The nutrient artery enters through the nutrient foramen, divides within the medullary canal and supplies much of the inner cortex through endosteal branches. Periosteal vessels supply the outer cortex. At a fracture, the relative contribution of these systems changes as new vessels grow into the repair tissue.
Why vascularity matters
Bone formation requires:
- viable cells
- oxygen and nutrients
- an appropriate mechanical environment
Severe soft-tissue stripping, periosteal damage and disruption of local blood supply can impair union even when fixation appears mechanically adequate.
Secondary fracture healing
Secondary healing occurs when there is controlled interfragmentary movement and usually produces callus.
Inflammatory phase
- haematoma forms
- inflammatory mediators recruit repair cells
- necrotic tissue is removed
- angiogenesis begins
Reparative phase
- granulation tissue develops
- fibrocartilaginous callus bridges the fracture
- endochondral and intramembranous ossification convert the callus to woven bone
Remodelling phase
- woven bone is replaced by lamellar bone
- medullary architecture and cortical shape progressively adapt to loading
Primary fracture healing
Primary or direct healing requires very high stability and minimal fracture gap. It occurs by direct osteonal remodelling across the fracture rather than through visible external callus.
It is associated with:
- anatomical or near-anatomical reduction
- absolute stability
- interfragmentary compression where appropriate
Strain and tissue differentiation
Interfragmentary strain is the change in fracture gap divided by the original gap. Different tissues tolerate different levels of strain:
- bone tolerates relatively little deformation
- cartilage tolerates more
- fibrous tissue tolerates still more
As callus enlarges, the effective strain at the fracture decreases, allowing progression from fibrous tissue to cartilage and then bone.
Factors that impair healing
Local:
- devascularisation
- infection
- excessive instability
- excessive gap
- severe soft-tissue injury
- interposed tissue
Systemic:
- smoking
- poor nutrition
- metabolic disease
- some medications
- advanced age and major comorbidity
Delayed union and nonunion
Assessment should consider both biology and mechanics.
A practical framework:
- biology: blood supply, soft tissues, infection, host factors
- mechanics: stability, alignment, gap, implant construct
Hypertrophic nonunion generally indicates preserved biological activity with inadequate mechanical stability. Atrophic patterns raise greater concern about biological compromise, although real cases may contain both problems.
Clinical principle
Successful fracture treatment balances mechanical stability with preservation of biology. More fixation is not automatically better if it requires extensive disruption of vascular soft tissues.
Blood supply of bone
Long bones receive blood from several interconnected systems:
- nutrient arteries supplying the medullary circulation and inner cortex
- periosteal vessels supplying the outer cortex
- metaphyseal and epiphyseal vessels
- muscular and soft-tissue attachments that contribute regional blood supply
The relative importance of these sources changes after injury. Periosteal stripping, devascularising exposure, repeated dissection and excessive thermal injury can all reduce biological potential even when fixation looks mechanically satisfactory.
In children, the physis influences vascular anatomy. The relationship between metaphyseal and epiphyseal vessels changes with skeletal maturity and is relevant to infection patterns and growth-plate injury.
Early fracture response
Immediately after fracture there is disruption of vessels, haematoma formation and local hypoxia. The haematoma is biologically active and contains inflammatory cells, platelets, cytokines and signalling molecules. The early inflammatory phase recruits progenitor cells and establishes the environment for repair.
Angiogenesis is central. Fracture healing is not simply deposition of callus; it requires restoration of a functional vascular network.
Secondary bone healing
Secondary healing occurs when there is some interfragmentary strain and usually includes visible callus.
The broad sequence is:
- inflammatory phase and haematoma
- granulation tissue and early repair
- soft callus formation
- mineralisation and hard callus
- remodelling toward lamellar bone and restoration of structure
The type of tissue that can survive within the fracture gap depends strongly on the local mechanical environment. High strain favours fibrous tissue; lower strain permits cartilage and then bone formation. As callus enlarges and stiffens, strain falls and progressive ossification becomes possible.
Primary bone healing
Primary or direct healing requires very small fracture gaps and high stability. With absolute stability, cutting cones can cross the fracture line and remodel bone directly. There is little or no external callus.
This is the biological basis for interfragmentary compression in suitable simple articular or diaphyseal fracture patterns. It should not be confused with “better” healing in all situations. Comminuted fractures generally need preservation of biology and relative stability rather than extensive dissection to obtain exact reduction.
Mechanical environment
Fracture healing is governed by both biology and mechanics. Important mechanical variables include:
- interfragmentary motion
- construct stiffness
- working length
- fracture gap
- load sharing versus load bearing
- pattern of loading
- contact between fragments
A construct can fail because it is too flexible for the biological situation, but excessive stiffness can also reduce useful strain and callus stimulus in some bridging constructs. The goal is an appropriate environment for the chosen healing strategy.
Delayed union and non-union
Think in terms of:
- host factors
- biology
- stability
- infection
- defect or bone loss
Hypertrophic non-union indicates biological activity with inadequate mechanical stability. Atrophic or oligotrophic patterns raise concern about impaired biology, instability, infection or combinations of these factors. Radiographic appearance alone does not exclude infection.
Important modifiable influences include smoking, poor nutrition, uncontrolled diabetes, severe vascular disease and certain medications or systemic illnesses. Local factors include open injury, soft-tissue damage, segmental bone loss and previous surgery.
Clinical application
When planning revision of a non-union, the question is not simply “plate or nail?” First define:
- Is infection present?
- Is alignment acceptable?
- Is there a defect?
- Is fixation mechanically adequate?
- Is the local biology viable?
- Does the host need optimisation?
Treatment then addresses the deficient elements: debridement when indicated, stable fixation, restoration of alignment, bone graft or biological augmentation when required, and soft-tissue reconstruction where necessary.
FRCS synthesis
A strong answer links vascularity and mechanical strain. The memorable principle is: healing requires viable biology plus an appropriate mechanical environment. The fixation strategy should be selected to create the type of healing intended without sacrificing the blood supply needed to achieve it.