A fracture occurs when the bone tissue is subjected to tensile, compressive, or shear forces in excess of its strength. Both the strength of the bone tissue and the nature of the forces acting on bone change from infancy to old age, both normally and as a result of disease. Therefore, the incidence and type of fractures change with age.

The bone tissue in young adults has high resistance to mechanical deformation. Fractures of cortical bone in adults require tremendous forces, such as those encountered in motor accidents, and are therefore often associated with severe skin injuries and other lesions of soft tissue. Bones in children are springy and resilient, and the membrane enclosing the bones—the periosteum—is thick. Angular deformation of long bones in children therefore often results in incomplete, or “greenstick,” fractures. In the elderly the bone tissue becomes more brittle, especially the cancellous bone in vertebrae and in shoulder, wrist, hip, and knee joints.

The forces acting on the skeleton of a child normally are defined by body size and weight. Fractures in children are therefore rarely severely displaced or associated with severe soft tissue injury. In adults age 20 to 50, fractures are often caused by direct high-energy forces that have an explosive effect on bone and soft tissues and may cause severely displaced open fractures. In the elderly, fracture is usually caused by mild forces acting on brittle bone. Such fractures are rarely associated with soft tissue injury and often involve cancellous rather than cortical bone.

Many diseases decrease the strength of the bone tissue, and some expose the body to increased mechanical forces. Osteoporosis, which is prevalent in postmenopausal women, is the major cause of fractures in old age. Less-common causes of decreased bone strength are osteogenesis imperfecta, long-term treatment with corticosteroid medications, and osteomalacia. Common causes of locally decreased bone strength are injury of peripheral nerves and tumours.

The existence of a fracture is often deduced from a history of injury and observation of swelling, tenderness, faulty alignment, the sound that the broken ends make, loss of function, and associated injuries. Precise diagnosis is made by X-ray examination.

Most fractures occur without skin injury (closed fractures). The skin wound in open fractures is caused either by severe direct trauma or by a sharp bone fragment that pierces the skin from within.

Fracture sometimes develops slowly rather than suddenly. Fatigue, or stress, fractures occur because the bone tissue is exposed to forces that overwhelm its capacity for structural adaptation. Examples include fracture of the thighbone and fracture of the bones of the foot (march fracture) in soldiers during their initial months of physical training. Stress fractures usually produce pain even before bone abnormality can be seen by X-ray. Fractures that occur because of preexisting disease are called pathologic fractures. Bone diseases associated with pathologic fracture are osteomalacia, Paget disease, and radiation injury to bone.

Except when forces act with explosive suddenness, vessels and nerves usually escape injury because of their elasticity and resilience. For anatomic reasons, nerve injury may occur in fracture-dislocation of the hip and in fracture of the long bone of the upper arm (humerus) through the diaphysis in adults and just above the elbow in children; the latter fracture is associated with compression of the accompanying artery. Fracture and dislocation of the vertebrae caused by severe forces may be associated with spinal cord injury. Certain fractures injure the nutrient blood vessels of the bone tissue, with osteonecrosis as a result.

The bone blood vessels rupture when there is fracture. The resultant bleeding causes swelling at the site of fracture (fracture hematoma) and later discoloration of the skin. Occasionally the bleeding is so severe that the circulating blood volume is significantly diminished and shock ensues. The nerve endings of the periosteum are distended by the bleeding caused by fracture, and motion or pressure at the fracture site is painful.

A fracture starts to heal at the very moment that it occurs. The fracture hematoma is invaded by cellular elements, and eventually bone (callus) formation occurs that bridges the fracture. Formation of callus is faster in children than in adults and in cancellous bone than in cortical bone. Fracture of the thigh, which may heal in four to six weeks in a toddler, may require as many months in an adult. Similarly, fracture of the cancellous bone of the upper end of the humerus usually requires one-third or less of the time required for healing of a fracture of the cortical shaft of the same bone. Bridging of the fracture is hindered by separation and motion of the bone fragments, poor blood supply, and infection. After the fracture has healed, the region is remodeled by resorption and formation of bone so as to accommodate the microstructure of the bone tissue to precise mechanical demands. This remodeling is most effective in children; in adults, gross deformity may exceed the remodeling capacity.

The most severe and most common cause of deficient healing is osteomyelitis (bone infection) associated with open fractures, which permit direct access for disease-causing organisms. This condition is prevented by treatment of open fractures with antibiotics and closure of the skin. A fracture may also unite slowly or not at all because of deficient blood supply to one or more of the bone fragments, separation of the fragments by distention or interposition of a tendon, ligament, or fat, or excessive motion at the fracture site.

The guiding principle in treatment of fractures is restoration of normal length and alignment when necessary and avoidance of motion between the fracture fragments. Some fractures, notably compression fractures of cancellous bone, are inherently stable (remain in normal alignment) and require temporary immobilization by bed rest or a sling only because of pain. Most fractures are stable in acceptable position only after reduction of dislocation and immobilization by fixation, either externally by traction or plaster or internally by introduction of metallic screws, plates, nails, or wire.

Nonunion results in a false joint—pseudarthrosis—characterized by pain and motion at the fracture site. Healing may be achieved by immobilization with or without internal fixation and by transplantation of bone to bridge the defect.

Fracture may cause permanent deformity by residual angulation or by shortening due to overlap of cortical bone fragments, compression of cancellous bone, or, in children, arrest of metaphyseal cartilage growth. Osteoarthritis is a late complication of fracture at a joint when the joint cartilage surfaces are disturbed and the joint is unstable.

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Developmental abnormalities and hereditary conditions

Congenital bone diseases

Many diseases of the skeletal system are congenital in the sense that they become evident at or soon after birth. This does not imply that they all are genetically determined. Most are caused by factors operating during pregnancy, delivery, or early infancy.

Intrauterine injuries of the skeletal system were dramatically seen in children born of some women who received thalidomide, a drug previously used to treat morning sickness, during the initial three months of pregnancy. These children suffered severe extremity defects such as shortened or malformed limbs (phocomelia). Most intrauterine injuries are probably not caused by drugs, however, but perhaps by viral, hormonal, or mechanical factors. Intrauterine amputations, clubfoot, and congenital dislocation of the hip probably belong to this group. Birth injuries with fracture of the collarbone or humerus may occur because of mechanical difficulties during delivery; these fractures heal extremely fast.

Developmental abnormalities may affect isolated or multiple regions of the skeleton, or they may involve a specific tissue system; the latter are often hereditary. Examples of isolated abnormalities are partial or total absence of the collarbone, the radius (the long bone on the thumb side of the forearm), and the thighbone; congenital false joint in the shinbone (tibia); and absence of a middle segment of a limb (phocomelia). Treatment of these conditions is difficult, often requiring advanced transplantation or orthopedic devices and sometimes necessitating amputation in childhood. Multiple abnormalities occur in polyostotic fibrous dysplasia, in which affected bone is replaced by fibrous connective-tissue matrix. The condition may cause multiple deformities that require surgical correction.

Inherited disorders

Hereditary disorders of the skeleton include osteogenesis imperfecta, Hurler and Marfan syndromes, and several disorders of epiphyseal and metaphyseal growth centres. (For detailed treatment of these disorders, see connective tissue disease.)

Hereditary metaphyseal dysplasias, causing bone deformities near the joints, exist in several forms. The primary defect lies in the growth zone of the long bones. One of these conditions, hypophosphatasia, results from a deficiency of the enzyme alkaline phosphatase. Multiple defects in the growth zones of the skeleton are distinct from familial hypophosphatemia, a condition characterized by low phosphate levels in the blood; it affects the kidney primarily and the skeleton only secondarily. Hemophilia, finally, is a generalized hereditary condition that affects the skeletal system only secondarily by bleeding in the bones and joints.