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Long bone

A long bone is a type of bone in the human skeleton that is longer than it is wide, characterized by a central shaft called the diaphysis and two enlarged ends known as epiphyses.^[1] These bones primarily consist of a dense outer layer of compact bone surrounding a central medullary cavity filled with bone marrow, while the epiphyses contain spongy bone covered by a thin layer of compact bone.^[2] Long bones provide structural support, enable movement through leverage and articulation at joints, and serve as sites for hematopoiesis in the red marrow of their epiphyses.^[3] Examples include the femur in the thigh, humerus in the upper arm, and tibia in the lower leg, which are essential for weight-bearing and locomotion.^[4] The structure of a long bone facilitates both growth and repair throughout life. During development, the metaphysis—a region between the diaphysis and epiphysis—contains the epiphyseal plate (growth plate) composed of hyaline cartilage that allows longitudinal bone elongation until skeletal maturity, after which it ossifies into the epiphyseal line.^[5] Surrounding the bone are the periosteum, a fibrous membrane on the external surface that aids in nutrient delivery and muscle attachment, and the endosteum lining the medullary cavity, which supports osteoblast and osteoclast activity for bone remodeling.^[3] This remodeling process, governed by Wolff's law, enables long bones to adapt their shape and density in response to mechanical stresses, maintaining strength and integrity.^[6] Functionally, long bones contribute to the skeletal system's role in protecting vital organs, storing minerals like calcium and phosphorus, and producing blood cells via erythropoiesis in their marrow.^[3] In adults, the medullary cavity of the diaphysis typically contains yellow marrow for fat storage, while red marrow persists in the epiphyses for blood cell formation.^[7] Pathologies such as fractures, osteoporosis, or osteomyelitis often affect long bones due to their prominence in load-bearing activities, highlighting their critical biomechanical importance.^[3]

Definition and Classification

Definition

Long bones are defined as a category of bones in the vertebrate skeleton that are longer than they are wide, distinguished from short, flat, irregular, and sesamoid bones primarily by their elongated shape and proportions.^[2]^[3] These bones are characterized by a central shaft, known as the diaphysis, and two expanded ends called epiphyses, which provide structural support and articulation points for movement.^[1]^[8] The elongated shape of long bones allows for mechanical leverage that facilitates efficient motion and load distribution across the skeleton.^[2]^[3] This cylindrical or tubular form enhances their role in supporting body weight while enabling dynamic activities such as walking or running. In evolutionary terms, long bones represent an adaptation in vertebrates for weight-bearing and locomotion. Examples of long bones include the femur in the thigh and the humerus in the arm, with further classification provided elsewhere.^[3]

Classification and Examples

Long bones are classified as a distinct category within the skeletal system, characterized primarily by their elongated, cylindrical shape that exceeds their width, setting them apart from short, flat, or irregular bones. They belong to the appendicular skeleton, forming the structural framework of the limbs. This subdivision emphasizes their role in locomotion and support, with long bones enabling movement and load-bearing. Common examples of long bones are found in the upper and lower limbs. In the upper limb, these include the humerus (extending from the shoulder to the elbow), radius and ulna (forming the forearm), metacarpals (in the hand), and phalanges (fingers), which facilitate fine motor skills and arm extension. In the lower limb, key long bones are the femur (thigh bone, the longest and strongest in the human body, adapted for weight-bearing during bipedal gait), tibia and fibula (lower leg), metatarsals (foot), and phalanges (toes), supporting upright posture and propulsion. For instance, the femur's length and robust diaphysis provide critical leverage for vertical load transmission, underscoring location-specific adaptations. Across species, long bone morphology varies to suit locomotor demands; in quadrupeds like horses, they are proportionally longer relative to body size for enhanced stride stability and speed, whereas in humans, adaptations such as a straighter femur and angled tibia optimize bipedal efficiency and balance. These interspecies differences highlight evolutionary pressures on elongation for terrestrial locomotion.

Anatomy

Macroscopic Anatomy

Long bones are characterized by their elongated, cylindrical shape, consisting of three primary macroscopic regions: the diaphysis, metaphysis, and epiphyses. The diaphysis, or shaft, forms the central, tubular portion of the bone and encloses a medullary cavity that contains bone marrow.^[3] This region provides structural support and is composed of dense compact bone surrounding the hollow interior.^[9] The metaphysis represents the flared transitional zone between the diaphysis and each epiphysis, where the bone widens to connect the shaft to the expanded ends; it is particularly prominent in growing bones and serves as a site for metaphyseal growth.^[10] The epiphyses are the rounded, expanded extremities of the long bone, adapted for articulation with adjacent bones at synovial joints.^[11] At the epiphyses, the articular surfaces are covered by a layer of hyaline cartilage, which facilitates smooth, low-friction movement during joint function and helps distribute mechanical loads.^[12] Surrounding the external surface of the long bone is the periosteum, a tough, fibrous connective tissue membrane that provides attachment points for muscles, tendons, and ligaments while also contributing to nutrient supply and bone growth.^[5] Internally, the endosteum lines the medullary cavity and the inner surfaces of the trabecular bone in the epiphyses, supporting osteoblast and osteoclast activity for bone maintenance.^[13] Nutrient foramina, small openings in the diaphysis, allow the passage of blood vessels and nerves into the bone, ensuring vascular supply to the marrow and osseous tissue.^[9] Macroscopic variations exist among long bones based on their functional roles; for instance, weight-bearing lower limb bones like the femur exhibit a thicker, more robust diaphysis to withstand compressive forces during locomotion, whereas upper limb bones such as the humerus have a relatively slender shaft suited to lighter loads and greater mobility.^[10] These structural differences enhance biomechanical efficiency.

Microscopic Anatomy

The microscopic anatomy of long bones reveals a complex organization of tissues and cells that provide structural integrity and metabolic support. Long bones consist primarily of two types of bone tissue: compact (cortical) bone and spongy (trabecular) bone. Compact bone forms the dense outer layer, particularly in the diaphysis, and is characterized by its organized structure of osteons (Haversian systems), which consist of concentric lamellae surrounding central Haversian canals containing blood vessels and nerves, conferring high mechanical strength.^[14] In contrast, spongy bone predominates in the epiphyses and is composed of a porous, lattice-like network of trabeculae that enclose marrow spaces, facilitating shock absorption and reducing weight.^[7] These tissue arrangements are adapted to the functional demands of different regions within the long bone.^[15] At the cellular level, long bones contain specialized cells embedded within the bone matrix. Osteoblasts are cuboidal cells responsible for bone formation, synthesizing and secreting the organic matrix components such as type I collagen.^[16] Osteoclasts, multinucleated cells derived from monocyte-macrophage lineage, function in bone resorption by secreting acids and enzymes to dissolve the mineralized matrix.^[17] Osteocytes, the most abundant cell type, originate from osteoblasts and become entrapped in the matrix, where they maintain bone tissue through mechanosensory functions and communication via cell processes.^[18] These cells are situated within lacunae, interconnected by canaliculi that allow nutrient and waste exchange.^[19] Vascular and neural elements are integral to the microscopic structure, ensuring nutrient supply and innervation. Haversian canals run longitudinally through osteons, housing arterioles, venules, capillaries, and nerve fibers, while transverse Volkmann's canals interconnect adjacent osteons and link to the periosteum, forming a comprehensive vascular network.^[20] Canaliculi, fine channels extending from lacunae to these canals, enable the diffusion of nutrients and oxygen to osteocytes embedded deep within the avascular matrix.^[7] This system supports the metabolic demands of bone cells without direct blood access to the matrix.^[3] The bone matrix itself is a composite material, approximately 70% mineral by weight, primarily hydroxyapatite [Ca₁₀(PO₄)₆(OH)₂], which provides rigidity and compressive strength, and 30% organic components, mainly type I collagen fibers that offer tensile strength and flexibility.^[21] This mineral-organic balance is crucial for the overall durability of long bones.^[22]

Development and Growth

Embryonic Development

Long bones originate from mesenchymal cells within the embryonic limb buds, which condense and differentiate into chondroblasts to form hyaline cartilage models known as anlagen, beginning around the sixth week of gestation.^[23] These cartilage templates outline the future bone structure, including the diaphysis and epiphyses, and serve as scaffolds for subsequent ossification.^[24] By the seventh week, the full cartilage model is established, with chondrocytes proliferating to shape the developing skeleton.^[25] The transformation of these cartilage models into bone occurs through endochondral ossification, a multistage process that commences in the embryonic period. Chondrocytes in the central diaphysis hypertrophy, enlarging significantly and secreting alkaline phosphatase to initiate calcification of the surrounding cartilage matrix.^[26] This calcification leads to reduced nutrient diffusion, prompting chondrocyte apoptosis and creating channels for vascular invasion from the periosteum. Osteoprogenitor cells, carried by these vascular buds, invade the calcified matrix, differentiate into osteoblasts, and deposit bone tissue, establishing the primary ossification center in the diaphysis by the eighth week.^[23] Secondary ossification centers form later in the epiphyses during fetal development, remaining separated by cartilaginous growth plates until postnatal elongation.^[24] Key signaling pathways orchestrate chondrocyte differentiation and the progression of endochondral ossification. Indian hedgehog (Ihh), expressed by prehypertrophic and hypertrophic chondrocytes, promotes proliferation of immature chondrocytes while inhibiting premature differentiation, thereby coordinating growth and ossification timing.^[27] Bone morphogenetic proteins (BMPs) stimulate chondrocyte maturation and enhance Ihh expression independently of hypertrophy, supporting matrix mineralization.^[28] Fibroblast growth factors (FGFs), particularly via FGF receptor 3, interact with Ihh and parathyroid hormone-related protein (PTHrP) to fine-tune the balance between proliferation and differentiation in the chondrogenic zones.^[29] These pathways integrate to ensure orderly progression, with disruptions leading to skeletal abnormalities.^[30] By birth, the diaphysis of long bones is largely ossified, while epiphyses remain cartilaginous to allow for continued growth, marking the transition from embryonic patterning to fetal and postnatal remodeling.^[25]

Postnatal Growth and Remodeling

After birth, long bones primarily elongate through endochondral ossification at the epiphyseal plates, also known as growth plates, which are layers of hyaline cartilage located between the epiphysis and metaphysis.^[31] These plates consist of zones of chondrocytes that undergo proliferation in the resting and proliferative zones, followed by hypertrophy in the maturation zone, where cells enlarge and secrete extracellular matrix, enabling longitudinal expansion.^[31] The hypertrophic chondrocytes then undergo apoptosis, and the cartilage is invaded by blood vessels and osteoprogenitor cells, leading to primary ossification by osteoblasts that deposit bone matrix on the calcified cartilage scaffold.^[31] This process continues until the growth plates close, typically between ages 18 and 25, when the cartilage is fully replaced by bone, halting further elongation.^[31] In addition to lengthening, long bones increase in diameter through appositional growth, where new bone is added to the outer surface beneath the periosteum.^[25] Osteoblasts in the periosteal layer synthesize and mineralize new osteoid tissue, forming concentric lamellae of compact bone that expand the bone's circumference.^[25] Simultaneously, osteoclasts on the endosteal surface resorb bone from the inner medullary cavity, maintaining a balanced hollow structure to prevent excessive weight gain while supporting strength.^[25] This coordinated activity of osteoblasts and osteoclasts ensures proportional growth in width throughout postnatal life.^[25] Bone remodeling in long bones involves continuous turnover to adapt to mechanical and physiological demands, governed by Wolff's law, which posits that bone architecture modifies to withstand applied stresses by increasing density and thickness in loaded regions.^[32] This adaptation occurs through basic multicellular units, where osteoclasts resorb old bone and osteoblasts deposit new bone in response to mechanical loading, such as from weight-bearing or muscle pull.^[32] Hormonal regulation plays a critical role; growth hormone stimulates chondrocyte proliferation and overall longitudinal growth via insulin-like growth factor-1, while estrogen and testosterone promote epiphyseal closure by accelerating ossification and reducing proliferative activity in the growth plate.^[33] With aging, long bones reach peak mass around age 30, after which remodeling shifts toward net resorption, leading to gradual bone loss.^[34] This decline involves cortical thinning due to endosteal resorption outpacing periosteal apposition, increased porosity, and reduced trabecular connectivity, compromising mechanical integrity.^[34] Although men experience slower loss than women post-menopause, both sexes face accelerated resorption after age 40, contributing to age-related fragility.^[34]

Functions

Mechanical Roles

Long bones serve as critical biomechanical structures in the skeletal system, primarily facilitating support, locomotion, and force transmission throughout the body. They act as rigid levers that amplify the force generated by skeletal muscles, enabling efficient movement such as walking, running, and manipulating objects. This lever action is essential for the appendicular skeleton, where long bones like the femur and humerus bear the majority of dynamic loads during daily activities.^[35]^[36] In terms of leverage and movement, long bones function as third-class levers, with muscles attaching via tendons to the periosteum—the dense fibrous outer layer of the bone—allowing for precise control over joint actions. For instance, the femur serves as a lever in the hip and knee joints, where contractions of the quadriceps and hamstrings produce flexion and extension, propelling the body forward during gait. This arrangement optimizes mechanical advantage, reducing the energy required for motion while distributing forces across joints.^[37]^[10] Long bones excel in load-bearing due to their composite structure, comprising cortical bone on the exterior for high compressive strength—reaching up to 170 MPa in longitudinal loading—and trabecular bone internally, where collagen fibers provide tensile resistance. The alignment of trabeculae follows principal stress trajectories, which efficiently distributes compressive and shear stresses, minimizing material waste and preventing localized failure under body weight or impact. This optimization is evident in the femur, which supports up to several times the body's mass during activities like jumping.^[38]^[39]^[40] Additionally, long bones provide structural protection by encasing the marrow cavity within a robust cortical shell that resists torsion and bending moments encountered during twisting motions or uneven terrain navigation. The tubular diaphyseal shape enhances torsional rigidity, with polar moment of inertia scaling favorably to withstand rotational forces up to 140 Nm before deformation. This protective role ensures the integrity of internal tissues while maintaining overall skeletal stability.^[41]^[42] The biomechanical properties of long bones, particularly cortical bone, exhibit anisotropy, with Young's modulus approximately 20 GPa in the longitudinal direction due to the oriented arrangement of osteons and collagen fibrils, compared to lower values transversely. This directional variation, influenced by microscopic tissue organization, allows long bones to adapt to predominant loading patterns in vivo, such as axial compression in the lower limbs.^[43]^[44]^[45]

Hematopoietic Role

Long bones play a crucial role in hematopoiesis, the process of blood cell formation, primarily through their bone marrow cavities, which house hematopoietic tissue.^[46] In these bones, the marrow is divided into red marrow, which is actively hematopoietic and produces red blood cells (erythrocytes), white blood cells (leukocytes), and platelets, and yellow marrow, which is largely fatty and serves as an energy reserve.^[47] In children and adolescents, red marrow predominates in the epiphyses and metaphyses of long bones such as the femur and humerus, supporting robust blood cell production during growth.^[48] By adulthood, the diaphysis of long bones converts to yellow marrow, while red marrow persists mainly in the proximal epiphyses and metaphyses, though it becomes less extensive overall as hematopoiesis shifts toward the axial skeleton.^[49] Hematopoiesis occurs within the red marrow of long bones, where hematopoietic stem cells (HSCs) differentiate into mature blood cells under the influence of the marrow's stromal microenvironment.^[50] Stromal cells, including mesenchymal cells and endothelial cells, provide structural support and secrete cytokines and growth factors that regulate this process; for instance, erythropoietin, primarily produced by the kidneys, stimulates erythroid progenitor cells to produce red blood cells in response to hypoxia.^[51] Other cytokines, such as thrombopoietin and various interleukins, guide the formation of platelets and leukocytes, respectively, ensuring balanced output to meet physiological demands.^[52] During fetal development, hematopoiesis initially occurs in the yolk sac, liver, and spleen before shifting postnatally to the bone marrow of long bones and other sites, where it becomes the primary location by early infancy.^[53] In a typical adult weighing around 65 kg, the total bone marrow mass is approximately 2.6 kg, with about half being active red marrow capable of hematopoiesis.^[54] While the majority of red marrow in adults is distributed in the axial skeleton—such as the pelvis, vertebrae, ribs, and sternum—long bones like the femur and humerus contribute a significant portion, particularly in their proximal regions, accounting for up to 20-30% of total hematopoietic activity depending on age and health status.^[55] This distribution allows long bones to serve as a substantial reservoir for blood cell production, with the red marrow in these sites producing roughly 500 billion blood cells daily under normal conditions.^[46] The hematopoietic capacity of long bone marrow is dynamically regulated to adapt to bodily needs; in cases of hypoxia, anemia, or blood loss, yellow marrow in the diaphysis can reconvert to red marrow through a process driven by increased cytokine signaling and HSC mobilization, thereby expanding sites of active hematopoiesis.^[56] This reconversion prioritizes peripheral long bones when demand is high, ensuring rapid restoration of blood cell populations without compromising the primary axial reserves.^[57]

Clinical Significance

Injuries and Fractures

Long bones, such as the femur, tibia, humerus, and radius, are susceptible to traumatic injuries, particularly fractures, due to their elongated structure and mechanical loading during daily activities and trauma. These fractures occur when applied forces exceed the bone's strength, often from high-energy impacts like motor vehicle accidents or low-energy falls in vulnerable populations. The immediate implications include pain, swelling, deformity, and potential neurovascular compromise, necessitating prompt diagnosis via imaging and stabilization to prevent complications like infection or malunion.^[58] Fractures in long bones are classified by pattern and exposure. Transverse fractures feature a horizontal line perpendicular to the bone's axis, typically resulting from direct high-impact forces that bend the bone across its width. Spiral fractures arise from twisting or rotational mechanisms, producing a helical break along the diaphysis, often seen in sports injuries or assaults. Comminuted fractures involve the bone shattering into three or more fragments, commonly from high-velocity trauma such as falls from height or collisions, which disperses energy across multiple sites. Additionally, fractures are categorized as closed if the skin remains intact or open (compound) if the bone pierces the skin or a wound exposes the fracture site, increasing infection risk due to external contamination.^[58]^[59]^[60]^[61] Common fracture sites in long bones reflect biomechanical vulnerabilities and demographics. The distal radius is a frequent location, particularly for Colles' fractures, which involve dorsal displacement of the distal fragment and occur commonly from falls on an outstretched hand, accounting for a significant portion of upper extremity injuries. In the elderly, femoral neck fractures predominate, often resulting from minor falls due to reduced bone quality, and represent a leading cause of hip fractures with high morbidity.^[62]^[63] The healing of long bone fractures follows a sequential biological process involving inflammation, repair, and remodeling. Initially, hematoma formation occurs at the fracture site within hours, providing a scaffold for inflammatory cells and growth factors. This progresses to soft callus formation, where fibrocartilage bridges the gap over 2-3 weeks, followed by hard callus development as woven bone replaces the cartilage around 3-4 weeks. Remodeling then reshapes the callus into organized lamellar bone, restoring original strength over months to years. For simple fractures, clinical union typically achieves stability in 6-8 weeks, though full recovery varies by site and patient factors.^[64]^[65] Osteoporosis serves as a key risk factor for long bone fractures by diminishing bone mineral density and altering microstructure, thereby reducing load-bearing capacity and predisposing bones to failure under normal or minimal stresses. This condition accelerates fragility fractures, particularly at sites like the femoral neck and distal radius, where trabecular bone loss is pronounced.^[66]^[67]

Diseases and Disorders

Long bones are susceptible to various pathological conditions that compromise their structural integrity and function. These diseases and disorders can arise from metabolic imbalances, infections, neoplastic processes, or congenital anomalies, leading to altered bone density, growth disturbances, or tissue destruction. Metabolic disorders, such as osteoporosis and osteomalacia, primarily affect bone mineralization and strength, while infectious conditions like osteomyelitis involve inflammatory responses to microbial invasion. Neoplastic diseases, including osteosarcoma and Ewing's sarcoma, represent malignant transformations within bone tissue, often requiring aggressive therapeutic interventions. Congenital disorders, exemplified by achondroplasia, impair longitudinal growth through genetic mechanisms. Osteoporosis is characterized by reduced bone mineral density and altered bone microstructure, resulting in increased fragility and susceptibility to low-impact fractures, particularly in the long bones of the hip, spine, and wrist.^[66] This condition disproportionately affects postmenopausal women due to estrogen deficiency, which accelerates bone resorption and leads to rapid bone loss in the early postmenopausal period.^[68] The weakened cortical and trabecular bone in long bones heightens the risk of fragility fractures, contributing to significant morbidity in affected individuals.^[69] In contrast, osteomalacia involves the softening of bones in adults, primarily due to prolonged vitamin D deficiency, which impairs calcium absorption and leads to defective mineralization of the osteoid matrix in long bones.^[70] This results in bone pain, muscle weakness, and an increased propensity for deformities or fractures, as the undermineralized bone lacks sufficient rigidity to withstand mechanical loads.^[71] Unlike osteoporosis, which features brittle bones from imbalanced resorption and formation, osteomalacia specifically arises from impaired matrix mineralization, often reversible with vitamin D supplementation.^[72] Osteomyelitis represents a serious bacterial infection of the bone, commonly affecting the marrow and cortical structures of long bones, and can manifest as acute or chronic inflammation leading to bone necrosis.^[73] Staphylococcus aureus is the predominant causative pathogen, responsible for the majority of cases, where it invades the bone via hematogenous spread or direct inoculation, forming abscesses within the marrow cavity that exacerbate tissue destruction.^[74] These abscesses, often surrounded by necrotic bone and inflammatory cells, contribute to persistent infection and potential sequestration if untreated, highlighting the need for prolonged antibiotic therapy and possible surgical debridement.^[75] Among neoplastic disorders, osteosarcoma is the most common primary malignant bone tumor, typically arising in adolescents during periods of rapid growth and predominantly located in the metaphysis of long bones such as the femur and tibia.^[76] This aggressive tumor produces osteoid matrix directly from malignant cells, leading to rapid proliferation and a high risk of metastasis, most often to the lungs, with about 10-20% of cases presenting with pulmonary involvement at diagnosis.^[77] Its metaphyseal origin correlates with the active growth plate regions in adolescents, where disrupted endochondral ossification facilitates tumor initiation.^[78] Ewing's sarcoma, another malignant bone tumor, frequently originates in the diaphysis of long bones, particularly in children and young adults, and is characterized by small round blue cells infiltrating the medullary cavity.^[79] Unlike osteosarcoma, it shows a predilection for the shaft of bones like the femur and humerus, often extending to surrounding soft tissues and presenting with systemic symptoms such as fever and pain due to its aggressive nature.^[80] This tumor's diaphyseal location distinguishes it from metaphyseal-predominant sarcomas and underscores its association with primitive neuroectodermal origins.^[81] Congenital disorders affecting long bones include achondroplasia, the most common form of dwarfism, caused by a gain-of-function mutation in the fibroblast growth factor receptor 3 (FGFR3) gene, which inhibits chondrocyte proliferation and differentiation in the growth plate.^[82] This autosomal dominant mutation, often arising de novo, results in shortened long bones with rhizomelic shortening (proximal segments most affected), leading to disproportionate stature and potential complications like spinal stenosis.^[83] The FGFR3 mutation constitutively activates signaling pathways that suppress longitudinal bone growth, thereby restricting endochondral ossification without impacting membranous bone formation.^[84]

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Aug 30, 2022 · The Young's modulus of large tensile cortical specimens has been shown to be in the 14–20 GPa range. Choi et al. measured the elastic moduli of ...
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Mechanical properties of bone - DoITPoMS
The actual values for the Young's modulus of bone, compared to collagen and hydroxyapatite, are shown in the table below. The measured value of Young's Modulus ...
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Biomechanical Basis of Bone Fracture and Fracture Osteosynthesis ...
Long bones are stronger in longitudinal orientation than in tangential or radial orientation, since osteons have a longitudinal orientation in cortical bone.
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Fractures (Broken Bones) - OrthoInfo - AAOS
Transverse fracture. This type of fracture has a horizontal fracture line. Oblique fracture. This type of fracture has an angled pattern. Comminuted fracture.Missing: spiral | Show results with:spiral
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Orthopaedic traumatology: fundamental principles and current ... - NIH
Jan 8, 2018 · A transverse fracture is perpendicular to the bone's line of axis. Spiral and oblique are often confused. Both can be the result of a rotational ...
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Basic concepts regarding fracture healing and the current options ...
Comminuted fracture is characterised by breaking a bone into several small pieces and is the result of high‐velocity injuries, such as car accidents or falls ...
[51]
Open Fracture Management - StatPearls - NCBI Bookshelf - NIH
An open fracture is an injury where the fractured bone and/or fracture hematoma are exposed to the external environment via a traumatic violation of the soft ...
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Distal Radius Fractures (Broken Wrist) - OrthoInfo - AAOS
One of the most common distal radius fractures is a Colles fracture, in which the broken fragment of the radius tilts upward. This fracture was first described ...
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Femoral Neck Fracture: Background, Etiology, Epidemiology
May 2, 2024 · Femoral neck fractures in elderly patients occur most commonly after minor falls or twisting injuries, and they are more common in women. In ...
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Fracture Healing Overview - StatPearls - NCBI Bookshelf
Apr 8, 2023 · Fracture healing is complex, and it involves the following stages: hematoma formation, granulation tissue formation, callus formation, and bone remodeling.
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Impact of osteoporosis and osteoporosis medications on fracture ...
Apr 8, 2024 · Most metaphyseal long bone fractures heal in 6–8 weeks and vertebral fractures in 8–10 weeks, whereas diaphyseal fracture of long bones may ...
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Osteoporosis - StatPearls - NCBI Bookshelf - NIH
Osteoporosis is defined as low bone mineral density caused by altered bone microstructure, ultimately predisposing patients to low-impact, fragility fractures.
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Osteoporosis - Symptoms and causes - Mayo Clinic
Sep 20, 2025 · Low calcium intake contributes to lower bone density, early bone loss and an increased risk of fractures.
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Osteoporosis in Females - StatPearls - NCBI Bookshelf
Jun 29, 2025 · Osteoporosis is a silent, progressive disease that disproportionately affects postmenopausal women and predisposes them to fracture.
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A Comprehensive Review on Postmenopausal Osteoporosis in ...
Nov 9, 2023 · Issues related to aging in women are an increased risk of broken bones, a decrease in cortical and cancellous bone thickness, and a decrease in ...
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Osteomalacia - StatPearls - NCBI Bookshelf - NIH
Osteomalacia describes a disorder of "bone softening" in adults that is usually due to prolonged vitamin D deficiency that can result in abnormal osteoid ...Continuing Education Activity · Introduction · Etiology · Evaluation
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Osteomalacia: MedlinePlus Medical Encyclopedia
May 20, 2024 · Osteomalacia is softening of the bones. It most often occurs because of a problem that leads to vitamin D deficiency, which helps your body absorb calcium.
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Osteomalacia and Vitamin D Status: A Clinical Update 2020 - PMC
Dec 21, 2020 · Osteomalacia related to vitamin D deficiency evolves in three stages. The initial stage is characterized by normal serum levels of calcium and phosphate.Missing: softening | Show results with:softening
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Osteomyelitis - StatPearls - NCBI Bookshelf - NIH
May 31, 2023 · Osteomyelitis is a serious infection of the bone that can be either acute or chronic. It is an inflammatory process involving the bone and its structures.
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Staphylococcus aureus Osteomyelitis: Bone, Bugs, and Surgery - PMC
Osteomyelitis, or inflammation of bone, is most commonly caused by invasion of bacterial pathogens into the skeleton.
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Mechanisms of Antibiotic Failure During Staphylococcus aureus ...
Feb 12, 2021 · During osteomyelitis, abscesses commonly form within the bone marrow space as well as in the surrounding soft tissues (15, 17, 18). Abscess ...
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Osteosarcoma (Osteogenic Sarcoma) - StatPearls - NCBI Bookshelf
Osteosarcoma demonstrates a bimodal age distribution and most commonly occurs in the extremities.
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The epidemiology of osteosarcoma - PubMed
Osteosarcoma commonly occurs in the long bones of the extremities near the metaphyseal growth plates. The most common sites are the femur (42%, with 75% of ...
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Diagnosis and staging of malignant bone tumours in children - NIH
Aug 20, 2021 · Osteosarcoma metastasizes mainly to the lung and bone. About 10% to 20% of patients already have pulmonary metastases at initial presentation.
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Ewing Sarcoma - StatPearls - NCBI Bookshelf
Ewing sarcoma is commonly found in the diaphysis of long bones but can occur in different locations with varying presentations. Bone or metastatic lesions ...
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Educational Case: Ewing Sarcoma of Bone - PMC - PubMed Central
Aug 31, 2021 · The tumor typically arises in the medullary cavity of long bones. It invades the cortex, periosteum, and surrounding soft tissue. Ewing sarcoma ...
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Ewing's sarcoma - PubMed
The lower extremity long bones are predominantly affected and most lesions are diaphyseal or metadiaphyseal. CT and particularly MR imaging are invaluable ...
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Achondroplasia - StatPearls - NCBI Bookshelf - NIH
Achondroplasia results from a point mutation in the gene coding for the transmembrane portion of fibroblast growth factor receptor 3 (FGFR3), which resides on ...Introduction · Pathophysiology · Evaluation · Differential Diagnosis
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Achondroplasia: MedlinePlus Medical Encyclopedia
Nov 6, 2023 · Achondroplasia is caused by a change (mutation) in the fibroblast growth factor receptor 3 (FGFR3) gene. This prevents bone growth and mainly ...
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Achondroplasia: Development, Pathogenesis, and Therapy - PMC
FGFR3 is expressed in chondrocytes and mature osteoblasts where it functions to regulate bone growth. Analysis of the mutations in FGFR3 revealed increased ...