Cortical Bone
Compact bone tissue forming the outer shell of every bone and the entire diaphysis (shaft) of long bones. ~80% of total adult bone mass (~2 kg in a 70 kg adult). Porosity ~4–10%, enabling high stiffness (Young's modulus 17–25 GPa) and high compressive strength (~170–190 MPa). Hierarchical composite: hydroxyapatite platelets (Ca₁₀(PO₄)₆(OH)₂, 70% wet weight) templated on type I collagen fibrils (22% wet weight). Osteon (Haversian system) is the primary structural unit — concentric lamellae with alternating fibril orientations surrounding a central vascular Haversian canal. Osteocyte lacunocanalicular network (LCN) provides mechanosensing, remodelling control, and endocrine functions (SOST, FGF23).
Overview
Cortical bone (compact bone) is the dense, solid bone tissue forming the outer shell of every bone in the human skeleton and constituting the entire diaphysis of long bones. It accounts for approximately 80% of total adult bone mass (~2 kg in a 70 kg adult). Compared with cancellous/trabecular bone (spongy, 20% of bone mass, predominating in vertebrae and flat bones), cortical bone has low porosity (~4–10%), high stiffness, and high compressive and tensile strength — making it the principal load-bearing material of the skeleton.
Beyond its mechanical role, cortical bone is the body's largest mineral reservoir, storing 99% of total body calcium (~1 kg) and 85% of phosphate as hydroxyapatite crystals. It participates in mineral homeostasis through osteoclastic resorption (releasing Ca²⁺ and Pi under PTH stimulation) and osteoblastic deposition (under calcitriol, oestrogen, and mechanical stimuli). Osteocytes embedded throughout the matrix serve as mechanosensors and endocrine cells, secreting sclerostin (Wnt inhibitor) and FGF23 (phosphate regulator) to couple mechanical loading, bone mass, and mineral metabolism.
Anatomy — Hierarchical Architecture
| Level | Structure | Dimensions | Key features |
|---|---|---|---|
| Macro | Cortical shell (diaphysis) | 1–10 mm thick | Encloses medullary canal; periosteum (outer) + endosteum (inner) cellular surfaces |
| Tissue | Osteon (Haversian system) | 100–300 µm diameter, mm long | 5–20 concentric lamellae surrounding Haversian canal; runs parallel to long axis; primary structural unit |
| Lamellar | Individual lamella | 3–8 µm thick | Collagen fibrils alternating ~30° helical orientation between adjacent lamellae — analogous to plywood cross-lamination; resists multidirectional loads |
| Canal | Haversian canal | 40–50 µm diameter | Arterioles, venules, unmyelinated nerve fibres, lymphatics; supplies nutrients/removes waste |
| Canal | Volkmann's canal | Transverse / oblique | Interconnects Haversian canals + periosteal/endosteal surfaces; nutrient highway across cortical thickness |
| Cellular | Osteocyte lacunocanalicular network (LCN) | ~25,000 lacunae/mm³; 40–60 canaliculi/osteocyte | ~42 billion osteocytes; Cx43 gap junctions; interstitial fluid shear → mechanosensing; SOST + FGF23 endocrine |
| Nano | Collagen-mineral composite | HA platelets: 60–70 nm × 2–4 nm | HA c-axis aligned along collagen fibril axis; 67 nm D-period banding; plywood architecture at lamellar scale |
Periosteum: Bi-layered outer membrane. Fibrous outer layer (type I collagen, Sharpey's fibres) + inner cambial layer (osteoprogenitor cells, fibroblasts, capillaries). Primary source of cortical appositional growth and fracture callus formation. Densely innervated — periosteal stretch is the dominant pain signal in fractures and bone metastases.
Endosteum: Thin cellular layer lining the marrow canal and Haversian canal walls; contains bone-lining cells (quiescent osteoblasts), osteoclasts, and osteoprogenitors; site of cortical remodelling and the osteoblastic HSC niche.
Function
Mechanical support. Cortical bone is anisotropic: ultimate compressive strength ~170–190 MPa (longitudinal axis), ultimate tensile strength ~100–130 MPa, fracture toughness 2–5 MPa·m^0.5. Hydroxyapatite provides stiffness (resists deformation); collagen fibril networks absorb crack energy (toughness). The femoral shaft sustains >3× body weight in running — this load-bearing orientation reflects habitual loading direction. Ageing reduces toughness: non-enzymatic collagen crosslinking by advanced glycation end-products (AGEs) → more brittle matrix; reduced water content also decreases fracture resistance.
Calcium and phosphate homeostasis. Osteoclastic cortical resorption releases Ca²⁺ and Pi; regulated primarily by PTH (↑osteoclast recruitment via RANKL on osteoblasts/osteocytes → ↑serum Ca²⁺ + ↑calcitriol synthesis → ↑intestinal Ca²⁺ absorption), calcitriol (1,25-dihydroxyvitamin D₃: ↑intestinal Ca²⁺/Pi absorption, ↑osteoclastogenesis for mineral mobilisation), and calcitonin (thyroid C-cells: ↓osteoclast activity → ↓serum Ca²⁺).
Mechanosensing and adaptive remodelling. Mechanical loading during locomotion drives interstitial fluid shear through canalicular channels (~2,000–4,000 microstrain) → osteocyte primary cilia and integrin mechanosensors activated → prostaglandin E₂, NO, ATP release → ↓sclerostin secretion → ↑Wnt/β-catenin in osteoblasts → ↑bone formation. Disuse (bed rest, paralysis, space flight) → ↑sclerostin → cortical thinning at ~1–2% per month in complete unloading.
Endocrine function. Osteocalcin (secreted by osteoblasts/osteocytes, carboxylated by vitamin K → Gla residues bind HA in matrix) is released in undercarboxylated form (ucOC) during bone resorption → circulates → binds GPRC6A on pancreatic β-cells (↑insulin secretion), skeletal muscle (↑glucose uptake during exercise), and Leydig cells (↑testosterone synthesis). FGF23 from osteocytes suppresses renal phosphate reabsorption (↓NaPi2a/2c) and ↓calcitriol synthesis — preventing hyperphosphataemia from excessive resorption.
Pathology
Osteoporosis (Cortical Component)
Cortical porosity increases from ~4% at age 40 to ~15% by age 80 as Haversian canals enlarge from accelerated remodelling. Loss of oestrogen at menopause → ↑RANKL, ↓OPG → accelerated cortical thinning → hip and distal radius fracture risk (cortical bone loss predicts these sites more strongly than trabecular loss). Treatments: bisphosphonates, denosumab (↓resorption), teriparatide/romosozumab (↑formation).
Stress Fractures
Fatigue failure when repetitive submaximal loading accumulates microcracks faster than osteocyte-directed remodelling can repair them. Common sites: metatarsal shafts (march fracture), tibial diaphysis, femoral neck (high-risk — complete fracture risk), navicular, sacrum. Risk factors: abrupt training intensity increase, low BMD, relative energy deficiency in sport (RED-S), vitamin D deficiency. High-risk fractures (femoral neck, anterior tibia) may require internal fixation.
Osteonecrosis (Avascular Necrosis, AVN)
Interruption of cortical/subchondral blood supply → osteocyte death within 12–48 h → structural failure → articular collapse. Most common site: femoral head (lateral femoral circumflex artery — vulnerable to intracapsular fracture or dislocation). Risk factors: corticosteroids (most common non-traumatic cause → ↓osteoblast proliferation, fat emboli to subchondral vessels), alcohol, sickle cell disease, decompression illness. Bisphosphonate-related osteonecrosis of the jaw (BRONJ): exposed, devitalised jaw cortex after dental extraction in patients on bisphosphonate or denosumab.
Osteosarcoma
Primary malignant bone tumour arising from osteoblastic progenitors in cortical bone; distal femur, proximal tibia, proximal humerus (adolescents); second peak in elderly (Paget's-associated). Radiographic features: Codman's triangle (elevated periosteum), sunburst pattern (mineralised tumour matrix), mixed lytic/sclerotic cortical lesion. Neoadjuvant chemotherapy (cisplatin, doxorubicin, methotrexate) + limb-salvage surgery; 5-year survival ~60–70% for localised disease.
Cross-Atlas Connections
References
- Hall JE, Hall ME. Guyton and Hall Textbook of Medical Physiology. 14th ed. Elsevier; 2021. elsevier.com
- Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 7th ed. W.W. Norton; 2022. ncbi.nlm.nih.gov/books/NBK26880
- Karsenty G, Ferron M. The contribution of bone to whole-organism physiology. Nature. 2012;481:314–20. doi:10.1038/nature10763
- Weiner S, Wagner HD. The material bone: structure-mechanical function relations. Annu Rev Mater Sci. 1998;28:271–98. doi:10.1146/annurev.matsci.28.1.271