Core Content - Core Orthopaedic Concepts - Bone Structure, Metabolism and Healing

Bone Structure


Anatomic Structure:
Long bones, such as the femur, tibia and humerus, have the following anatomical regions:

Anatomic regions of long bones
Physis - Red, Diaphysis - White, Metaphysis - Light Grey, Epiphysis - Dark Grey

  • Diaphysis          
    • 'Dia-' from latin for 'between' = 'between physes'
    • Thick cortex around central concellous bone
  • Metaphysis
    • 'Meta-' from latin for 'change' = change from diaphysis to epiphysis
    • Thin cortex around trabecular bone
  • Epiphysis
    • 'Epi-' from latin for 'nearby' = near/next to the physis 
    • Articular surface, subchondral region, physis



Macroscopic Structure:

  • Cortical (80% of skeleton) 
    • Osteon - This is the primary unit of cortical bone. It consists of osteoblasts and –clasts around a Haversian canal
    • Vascular canals - A canal in which contains arterioles, venules, capillaries and nerves. If oriented with long axis of the bone, it is called a Haversian canal. If it connects transversely between Haversian canals, then it is called a Volkmann’s canal
    • Lamellae - The solid layer between osteons
  • Cancellous (20% of skeleton)
    • Irregular network of bone struts
    • Mostly porous, containing bone marrow and haematopoietic stem cells (produce platelets and red/white blood cells)
  • Periosteum 
    • Fibrous membrane that covers the outside surface of a bone
    • Provides the periosteal blood supply to bone
    • Osteogenic – contains progenitor cells that differentiate into osteoblasts/chondroblasts for bone growth and fracture healing.

Osteons, vascular canals and periosteum
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Osteons and Haversian canals
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Blood Supply:

  • Bones account for around 5-10% of cardiac output
  • Periosteum supplies 1/3
  • Nutient artery system 2/3
    • Branches of major arteries enter bone through nutrient foramen and branch repeatedly. Travel intracortically through Haversian and Volkmann canals

Microscopic Structure:

  • Woven Bone 
    • Randomly orientated collagen fibres
    • Mechanically weak
    • High number of osteocytes
    • Present in immature (including post-fracture) or pathological bone
  • Lamellar Bone
    • Mature bone from remodelled woven bone
    • Organised structure orientated to lines of stress 
    • Mechanically strong

Cell Types: 

  • Osteoblasts
    • Form bone by synthesising non-mineralised matrix
    • Activated through several pathways (see bone metabolism)
    • Regulate osteoclast function
  • Osteoclasts
    • Reabsorb bone
    • Activated by osteoblast signalling
  • Osteocytes
    • 90% of cells in adult skeleton
    • Osteoblasts trapped in bone matrix
    • Maintain bone and cellular matrix
    • Important in calcium and phosphorus homeostasis

Cell types in bone
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Bone Matrix:

  • Organic component (40% of dry weight of bone)
    • Collagen – 90% of organic component. Provides tensile strength
    • Proteoglycans
    • Matrix proteins
    • Cytokines and growth factors
  • Inorganic component (60% of dry weight of bone)
    • Calcium hydroxyapatite – Provides compressive strength
    • Other calcium/phosphate salts

Bone Metabolism


Metabolic function of bone is mainly the homeostasis of calcium and phosphate.


  • 99% located in bones as hydroxyapatite     


  • 86% located in bones as hydroxyapatite, 14% intracellular           


Hormones (main regulators):

  • Parathyroid hormone
    • Increase serum calcium, decrease serum phosphate
    • Bone:
      • Stimulates osteoblasts to secrete factors which activate and increase the number of osteoclasts
      • Does not act directly on osteoclasts (no receptors)
    • Kidneys:
      • Stimulates conversion of calcidiol into calcitriol (see below)
  • Thyroid hormones
    • Increase bone resorption
  • Calcitonin
    • Decreases number and inhibits activity of osteoclasts
  • Sex hormones
    • Oestrogen decreases frequency of bone resorption and remodeling
  • Growth hormones
    • Increase serum calcium by increasing absorption in intestine and decrease secretion in kidneys


Steroids (lesser regulators):

  • Vitamin D
    • Activates osteoclasts to increase bone resorption
    • Increases intestinal absorption of calcium
    • Dual hydroxylation
    • Vit D converted into pre-hormone calcidiol (25-Hydroxyvitamin D) in liver Converted into active form calcitriol (1,25-dihydroxyvitamin D3) in kidneys
  • Glucocorticosteroids
    • Increase bone loss by decreasing calcium absorption in intestine
    • Decrease bone formation by inhibiting osteoblast activity


Bone Healing


2 modes of bone healing, depending on the stability of the fracture during the healing period

If too much movement then a non-union will occur


Primary (direct) Healing

  • Very rigid construct with absolute stability (minimal/no movement at fracture site)
    • Compression plate
  • No callus formation
  • Haversian/osteonal remodelling with ‘cutting cones’
    • Osteoclasts ‘drill’ holes through bone/across fracture
    • Osteoblasts migrate behind and deposit new bone
    • New osteons constructed with capillaries in Haversian canal
    • The new bone is lamellar bone (mature, organised bone)

Secondary (indirect) Healing

  • Occurs with non-rigid constructs (small amount of movement at fracture site)
    • Brace
    • Plaster cast
    • External fixator
    • IM Nail
  • Bone ends are close but not anatomically reduced


3 Stages occur as a continuum

  • Inflamation
    • Haematoma forms
    • Influx of inflammatory cells and progenitor cells
    • Osteoblasts and fibroblasts proliferate
    • Granulation tissue forms around fracture ends
  • Repair
    • Primary (soft) callus forms within 2 weeks
    • Secondary (hard) callus forms by conversion of primary callus into woven bone
  • Remodelling
    • Once fracture solidly united with woven bone, remodelling begins
    • Woven bone replaced with lamellar bone through Haversian/osteonal remodelling
    • This can take several years

Disturbed Facture Healing:

Delayed union – Fracture heals but at a much slower rate (>2x slower)

Malunion – Fracture heals but with significant deformity. Remodelling can compensate partially with greatest potential in children

Non-union – No fracture healing occurs within 6-9 months. Can be aseptic or septic. Often treated with bone grafting or revision of fixation.


Factors affecting fracture healing

  • Mechanical stability
  • Poor blood supply – Due to anatomy (eg scaphoid) or systemic (eg diabetes)
  • Soft tissue injury – either from the injury itself or from ‘stripping’ during operative fixation
  • Infection
  • Nutrition
  • Smoking – inhibits blood supply to the healing bone
  • Malignancy
  • Medications – Bisphosphonates, Corticosteroids, NSAIDS, Quinolones