Functions of bone
Bone provides:
- structural support
- protection of organs
- a lever system for movement
- mineral storage, particularly calcium and phosphate
- a marrow environment for haematopoiesis
Composition
Bone contains an organic matrix and a mineral phase.
Organic component
- predominantly type I collagen
- non-collagenous proteins regulate mineralisation and cell behaviour
Mineral component
- principally hydroxyapatite crystals
- gives stiffness and compressive strength
Collagen contributes toughness and tensile strength; mineral contributes stiffness. Normal bone requires both.
Woven and lamellar bone
Woven bone
- rapidly formed
- collagen is irregularly arranged
- relatively cellular
- mechanically weaker
- seen in early fracture callus and some pathological states
Lamellar bone
- organised collagen architecture
- deposited more slowly
- stronger and more mechanically efficient
- forms mature cortical and trabecular bone
Cortical and trabecular bone
Cortical bone
- dense outer shell
- organised into osteons in mature long-bone cortex
- adapted to bending and torsion
Trabecular bone
- lattice-like internal structure
- greater surface area
- remodels more rapidly
- architecture adapts to habitual loading
Bone cells
Osteoblast
Derived from mesenchymal lineage. Produces osteoid and regulates mineralisation. Some osteoblasts become osteocytes or surface lining cells.
Osteocyte
Mature bone cell within lacunae. Forms a mechanosensory network through canaliculi and contributes to regulation of remodelling.
Osteoclast
Large multinucleated cell derived from the monocyte-macrophage lineage. Resorbs bone through an acidified sealed zone and proteolytic enzymes.
Osteoblasts arise from mesenchymal lineage cells. They synthesise osteoid and participate in mineralisation. Some become osteocytes, some become lining cells and others undergo apoptosis.
Osteocytes are embedded within mineralised matrix and communicate through canaliculi. They function as important mechanosensors. Altered strain and microdamage influence osteocyte signalling, which helps target remodelling to areas that need repair.
Osteoclasts are multinucleated cells derived from the monocyte-macrophage lineage. They attach to bone, create a sealed resorption compartment and acidify it to dissolve mineral before proteolytic enzymes degrade the organic matrix.
RANK-RANKL-OPG system
- RANK is expressed on osteoclast precursors
- RANKL promotes osteoclast differentiation and activation
- osteoprotegerin acts as a decoy receptor and reduces RANKL signalling
This pathway links osteoblast-lineage cells with osteoclast activity.
Bone remodelling
Remodelling replaces old or damaged bone while maintaining mineral homeostasis.
A useful sequence is:
- activation
- osteoclastic resorption
- reversal
- osteoblastic formation
- mineralisation
Remodelling is influenced by:
- mechanical loading
- hormones
- local cytokines
- age
- systemic disease
- drugs
Modelling versus remodelling
Modelling changes bone size or shape by formation and resorption on different surfaces. It is prominent during growth.
Remodelling couples resorption and formation at the same site and is the dominant renewal process in adult bone.
Mechanical adaptation
Bone changes its architecture in response to mechanical demand. Increased habitual loading tends to increase bone mass or alter trabecular orientation; unloading promotes loss of bone.
Bone responds to its mechanical environment. The clinically useful concept is that strain influences whether bone is maintained, formed or resorbed. Prolonged unloading can produce loss of bone mass, while appropriate loading favours maintenance or gain. Abnormal stress concentration can also cause microdamage and fatigue failure.
Stress shielding around a rigid implant illustrates load-dependent adaptation: if an implant carries a greater share of load, the adjacent bone may experience reduced stimulus and remodel to a lower mass.
Clinical links
- osteoporosis: resorption exceeds formation over time
- Paget disease: disordered high-turnover remodelling
- stress fracture: repetitive loading exceeds the rate at which microdamage can be repaired
- immobilisation: reduced mechanical stimulus causes bone loss
Viva framework
Start with composition, then describe cortical versus trabecular bone, woven versus lamellar bone, the three principal cell types and the remodelling cycle.
Hierarchical structure
Bone is a composite material in which the mineral phase provides stiffness and resistance to compression while the collagen-rich organic phase contributes toughness and tensile behaviour. The combination explains why bone is much less brittle than mineral alone.
Cortical bone is dense and organised around osteons. Each osteon contains concentric lamellae surrounding a Haversian canal, with Volkmann canals linking vascular channels. Trabecular bone is arranged as a lattice of plates and rods whose orientation reflects the habitual mechanical environment. It has a much larger surface area relative to volume and therefore a high remodelling activity.
Woven bone is produced rapidly, with disorganised collagen. It appears in fracture callus and some pathological states. Lamellar bone is laid down more slowly and has an organised collagen architecture. During fracture healing, woven bone is progressively remodelled into lamellar bone.
Coupled remodelling
Bone remodelling is organised into basic multicellular units. A simplified sequence is:
- activation
- osteoclastic resorption
- reversal
- osteoblastic formation
- mineralisation
RANKL promotes osteoclast differentiation and activity through RANK. Osteoprotegerin acts as a decoy receptor and limits RANKL signalling. This pathway links endocrine, inflammatory and mechanical influences to bone resorption.
Remodelling differs from modelling. Remodelling replaces existing bone without necessarily changing gross shape. Modelling allows formation and resorption on different surfaces and changes bone geometry, particularly during growth and adaptation.
Mineralisation
Osteoblasts deposit osteoid, mainly type I collagen with non-collagenous proteins. Mineralisation then introduces hydroxyapatite crystals into this matrix. Primary mineralisation is relatively rapid; secondary mineralisation continues more slowly.
Bone stiffness therefore reflects both the amount of bone and the quality of its material and microarchitecture. Bone mineral density alone does not capture every determinant of fracture strength.
Cortical versus cancellous healing relevance
Cancellous bone has a rich blood supply and large internal surface area and can heal rapidly when mechanically favourable. Cortical bone, especially where directly reduced and rigidly compressed, may heal by direct remodelling with little visible callus. This is biologically different from secondary healing with external callus.
FRCS synthesis
A good viva answer should connect:
- composition → stiffness and toughness
- microstructure → mechanical function
- osteocyte sensing → targeted adaptation
- RANK/RANKL/OPG → osteoclast regulation
- modelling/remodelling → growth, repair and implant-related change
- bone quantity plus bone quality → fracture resistance