cortical bone
Summary
Cortical (compact) bone is the dense, outer shell of bone making up ~80% of skeletal mass. It provides mechanical strength and protection, and is organized into osteons (Haversian systems) with lamellar bone. It has a slower turnover than trabecular bone (~15-25% of annual remodeling vs. higher in trabecular), and is predominantly affected in hyperparathyroidism.
Detail
STRUCTURE: Cortical bone is dense, compact bone forming the diaphysis (shaft) of long bones and the outer shell (cortex) of all bones. Its functional unit is the osteon (Haversian system): concentric lamellae surrounding a central Haversian canal (contains blood vessels, nerves). Volkmann canals run perpendicular and connect adjacent Haversian canals. Interstitial lamellae are remnants of old osteons; circumferential lamellae lie at the inner and outer surfaces. Periosteum covers the outer surface (Sharpey fibers anchor it; rich in nerves, hence painful) and endosteum lines the inner surface. Osteocytes reside in lacunae and communicate via canaliculi.
COMPOSITION: ~80-90% calcified (hydroxyapatite mineral plus type I collagen). Low surface area-to-volume ratio (~80% of skeletal mass but only ~20% of bone surface area). Mature cortical bone is lamellar; woven bone is the immature, disorganized form (seen in fracture callus, Paget disease, osteosarcoma, fetal bone).
FUNCTION: Mechanical support, protection, and resistance to bending/torsion. Trabecular (cancellous/spongy) bone, by contrast, makes up ~20% of mass but ~80% of surface area, is found in vertebral bodies, pelvis, and metaphyses/epiphyses of long bones, has a higher metabolic turnover, and houses marrow.
CLINICAL CORRELATIONS: - Primary hyperparathyroidism: PTH preferentially causes cortical bone loss (e.g., distal 1/3 radius), classically with subperiosteal resorption (radial aspect of middle phalanges), "salt-and-pepper" skull, and osteitis fibrosa cystica (brown tumors). - Postmenopausal osteoporosis (type I): predominantly trabecular loss, causing vertebral compression and distal radius (Colles) fractures. Senile osteoporosis (type II) involves both cortical and trabecular bone (hip fractures). - Osteomyelitis: infection can cause cortical destruction; involucrum is new periosteal bone formed around necrotic bone (sequestrum). Cloaca is the opening through the cortex permitting pus drainage. - Osteosarcoma: periosteal reaction with Codman triangle and "sunburst" pattern as the tumor breaks through the cortex. Ewing sarcoma: "onion skin" periosteal reaction (diaphysis). - Osteoid osteoma: small cortical lesion (<2 cm) with a nidus, night pain relieved by NSAIDs (COX-mediated prostaglandins). - Paget disease: cortical thickening, with increased alkaline phosphatase and normal calcium/phosphate. - Osteopetrosis: defective osteoclasts (carbonic anhydrase II deficiency) with dense but brittle bone, "Erlenmeyer flask" deformity, and marrow crowding (pancytopenia). - Fracture healing: hematoma, soft callus (type II collagen/cartilage), hard callus (woven bone), then remodeling to lamellar bone (Wolff's law). - Imaging: DEXA assesses mostly trabecular-rich sites (spine) and cortical sites (femoral neck, radius). Cortical thinning on imaging suggests metabolic bone disease. Cortical bone remodeling is driven by osteoclasts (RANKL/OPG regulation) and osteoblasts. - Vitamin D deficiency: rickets (children; defective mineralization of growth plate/osteoid) and osteomalacia (adults; Looser zones/pseudofractures through cortex).
BLOOD SUPPLY (long bones): nutrient artery (supplies medullary cavity and inner two-thirds of cortex), periosteal arteries (outer third of cortex), and metaphyseal/epiphyseal arteries. Disruption (e.g., femoral neck fractures damaging the medial circumflex femoral artery) causes avascular necrosis.
HIGH-YIELD PEARL: Cortical = compact, Haversian systems, slow turnover, affected early in hyperparathyroidism. Trabecular = spongy, high turnover, affected early in estrogen deficiency and glucocorticoid excess.
Sources
- First Aid for the USMLE Step 1 (Musculoskeletal: Bone Physiology and Pathology)
- Robbins & Cotran Pathologic Basis of Disease (Bones, Joints, and Soft Tissue Tumors)
- Junqueira's Basic Histology (Bone chapter)
- Pathoma (Fundamentals of Pathology), Bone Pathology chapter
- Gray's Anatomy for Students
Reviewed by Medusa editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.