Cortical Bone: Composition, Growth, and Strength

Bones provide structural support, protect vital organs, and serve as reservoirs for essential minerals. Among the two primary types of bone tissue—cortical and trabecular—cortical bone is denser and forms the outer layer of most bones, contributing significantly to their strength and durability.

Understanding cortical bone is crucial for orthopedics, sports medicine, and aging research due to its role in fracture resistance and skeletal integrity. Various biological factors influence its composition, growth, and mechanical properties throughout life.

Structural Features

Cortical bone, also known as compact bone, forms the dense outer shell of skeletal structures, providing rigidity and resistance to external forces. It consists of tightly packed cylindrical units called osteons, or Haversian systems, which are aligned parallel to the bone’s longitudinal axis. Each osteon contains a central Haversian canal housing blood vessels and nerves, surrounded by concentric lamellae composed of mineralized collagen fibers. This arrangement optimizes load distribution, allowing bones to withstand compressive and tensile stresses during movement and weight-bearing activities.

Osteon orientation varies based on mechanical demands. In long bones such as the femur, osteons align along the shaft to resist bending and torsional forces. In contrast, bones subjected to multidirectional stresses, such as the mandible or vertebrae, exhibit more varied osteon orientation. Interstitial lamellae, remnants of older osteons, fill spaces between newer ones, enhancing bone density and stability.

The periosteum and endosteum are essential for maintaining cortical bone integrity. The periosteum, a fibrous membrane covering the outer surface, contains osteogenic cells that aid in bone repair and adaptation. Sharpey’s fibers anchor tendons and ligaments to the bone, ensuring efficient force transmission. The endosteum lines the medullary cavity and houses osteoclasts and osteoblasts, facilitating continuous structural maintenance.

Main Components

Cortical bone consists of organic and inorganic elements that provide strength, resilience, and metabolic functionality. The inorganic phase, about 65-70% of the bone’s dry weight, is dominated by hydroxyapatite, a crystalline form of calcium phosphate responsible for hardness and resistance to compressive forces. Trace elements such as magnesium, fluoride, and carbonate influence mineralization quality and mechanical properties. Variations in these elements have been linked to differences in bone toughness and fracture risk.

The organic matrix, comprising 30-35% of cortical bone, is primarily type I collagen, which imparts tensile strength and flexibility. The triple-helical structure of collagen fibrils provides a scaffold for hydroxyapatite deposition, ensuring a balance between rigidity and elasticity. Cross-linking between collagen molecules enhances resistance to mechanical stress. Disruptions in collagen cross-linking, as seen in conditions like osteogenesis imperfecta or diabetes-induced bone fragility, can compromise bone integrity.

Non-collagenous proteins also contribute to cortical bone structure. Osteocalcin, a vitamin K-dependent protein, plays a role in hydroxyapatite binding and mineralization. Elevated levels of undercarboxylated osteocalcin are associated with impaired bone quality, particularly in individuals with vitamin K deficiency. Osteopontin facilitates cell adhesion and regulates bone remodeling, while proteoglycans and glycoproteins influence mineral deposition and mechanical behavior.

Microarchitecture

Cortical bone’s microarchitecture optimizes mechanical performance and biological function. Osteons, the fundamental structural units, contain an intricate network of canaliculi—narrow channels that interconnect osteocytes embedded within the bone matrix. These facilitate nutrient exchange and cellular signaling, ensuring metabolic activity.

Within each osteon, concentric lamellae feature alternating collagen fiber orientations, enhancing resistance to crack propagation. This arrangement distributes mechanical stress and prevents fractures from spreading. Regions subjected to higher torsional stress exhibit more pronounced lamellar interlocking, a key adaptation in load-bearing bones.

Cortical bone is not entirely solid; it contains vascular channels, including Haversian and Volkmann’s canals, which accommodate blood vessels and facilitate metabolic exchange. The size and distribution of these pores influence mechanical strength, with excessive porosity linked to reduced stiffness and fracture resistance. Aging and metabolic disorders can increase cortical porosity, diminishing the bone’s ability to withstand mechanical loads.

Mechanical Strength

Cortical bone’s ability to withstand external forces depends on its material composition and hierarchical structure. Its high mineral content provides stiffness, allowing it to bear weight efficiently, while the organic matrix introduces flexibility to prevent fractures. This balance ensures bones can absorb energy without breaking, particularly in load-bearing regions such as the femur and tibia.

The orientation of collagen fibers within the lamellae disperses stress across multiple directions. In long bones, osteons align along the longitudinal axis to optimize resistance against axial loads. The staggered arrangement of collagen fibrils at the nanoscale level helps dissipate strain and slow crack propagation. Interstitial lamellae between osteons further contribute to mechanical stability by preventing stress concentrations that could lead to fractures.

Growth And Remodeling

Cortical bone undergoes continuous growth and remodeling to adapt to mechanical demands, repair microdamage, and regulate mineral homeostasis. During development, endochondral ossification forms long bones, with cartilage templates gradually replaced by mineralized bone tissue. As bones mature, appositional growth thickens cortical bone by depositing new layers on the periosteal surface while resorption occurs along the endosteal side, balancing strength and weight. This adaptation is evident in athletes, whose dominant limbs often exhibit increased cortical thickness due to repetitive stress.

Bone remodeling persists throughout adulthood, driven by the coordinated activity of osteoclasts and osteoblasts. Osteoclasts resorb aged or damaged bone, creating cavities that osteoblasts subsequently fill with new matrix. This cycle, regulated by the RANK/RANKL/OPG system, ensures structural integrity. An imbalance in remodeling can lead to conditions like osteoporosis, where excessive resorption weakens cortical bone. Conversely, mechanical loading stimulates osteoblast activity, reinforcing bone structure through increased mineral deposition, a principle utilized in weight-bearing exercise regimens to enhance skeletal strength.

Age-Related Variation

Cortical bone undergoes significant changes in density, composition, and mechanical properties throughout life. During childhood and adolescence, rapid bone accretion occurs, with peak bone mass typically reached in the third decade of life. The rate of cortical thickening is influenced by genetics, physical activity, and nutrition, particularly calcium and vitamin D intake. Studies show individuals who engage in high-impact activities during adolescence achieve greater cortical bone strength, potentially reducing fracture risk later in life.

After peak bone mass is attained, a gradual decline in cortical bone integrity begins. Cortical porosity increases due to an imbalance in remodeling, where resorption outpaces formation, reducing stiffness and increasing fracture risk. This effect is particularly pronounced in postmenopausal women, where declining estrogen levels accelerate bone loss. Aging also alters collagen cross-linking, reducing toughness and increasing brittleness, contributing to higher fracture rates in older adults, particularly in weight-bearing bones like the femur and radius.

Nutritional And Hormonal Factors

Cortical bone integrity is heavily influenced by diet and endocrine regulation. Calcium and phosphorus are essential for hydroxyapatite formation, with deficiencies leading to impaired mineralization and reduced bone stiffness. Vitamin D facilitates calcium absorption, and insufficient levels have been linked to increased cortical porosity and decreased strength. Long-term studies show a direct correlation between adolescent calcium intake and peak cortical bone mass, emphasizing the importance of early-life nutrition in preventing fractures.

Hormones also regulate bone metabolism. Parathyroid hormone (PTH) and calcitonin modulate calcium homeostasis, with PTH stimulating osteoclast activity and calcitonin inhibiting bone resorption. Estrogen and testosterone suppress excessive resorption, and declines in these hormones with age contribute to bone loss. Estrogen deficiency, particularly in postmenopausal women, leads to increased cortical porosity and thinning, elevating fracture risk. Endocrine disorders such as hyperparathyroidism or glucocorticoid excess further disrupt bone remodeling, leading to pathological bone fragility.