The fracture of a bone has a profound impact on any member of the aging population, as the consequences may negatively impact independence and can even lead to death (Leslie et al., 2013). Fractures in aging individuals are usually associated with low bone mineral density (BMD) and osteoporosis (see Chapter 18), as defined by the World Health Organization in Box 60.1. It is estimated that there are nearly 9 million osteoporotic-related fractures a year worldwide. One in five females over the age of 50 in developed countries is likely to sustain a hip fracture with associated high morbidity and mortality (WHO, 2007). The proportion of all fractures from osteoporotic bone reported from international community-based populations is 0.716–0.924. These data include males and females aged 50 years and older (Morrison et al., 2013).

In a population study of all persons over age 49 from Manitoba, 5-year survival after hip fracture was 51% females and 36% males. The average first year costs were 23 361 Canadian dollars for hip fractures and total healthcare costs for all incident fractures were $194 million (Leslie et al., 2013). In the US there were about 2 million osteoporotic fractures in 2010 with costs projected to exceed $18 billion (Levis & Theodore, 2012).

A bone fractures when a force or stress is placed upon it that is greater than the bone can withstand. Bone has a tensile strength of approximately 140 MPa (megapascals; one MPa equals 145 pounds per square inch) in the second decade of life, and it decreases to approximately 120 MPa by the eighth decade of life. The fracture threshold for the vertebrae and the epiphyseal areas of the femur is a bone density of less than 1 g/cm³ (Gerhart, 1995). Even though the stiffness and strength of trabecular bone depends on bone density and the direction of loading, trabecular bone appears to be more susceptible to failure from shear rather than compressive loads (Sanyal et al., 2012). The major physical difference between trabecular bone and cortical bone is the increased porosity exhibited by trabecular bone. This porosity is reflected by measurements of the apparent density (i.e. the mass of bone tissue divided by the bulk volume of the test specimen, including mineralized bone and marrow spaces). In the human skeleton, the apparent density of cortical bone is about 1.8 g/cm³, whereas the apparent density of trabecular bone ranges from approximately 0.1 to 1.0 g/cm³

Fragility fractures are usually related to lower BMD; however, urinary markers of bone resorption including collagen cross-linked N, C-telopeptide and free deoxypyridinoline may be predictive of hip fracture independent of bone mass (Garnero et al., 2009). Additionally, the large majority of fractures result from falls and physical interventions are successful but probably not utilized as widely as they should be (see Chapters 15, 16, 58, 59).

Normal fracture healing can be divided into three overlapping phases. First, there is an immediate inflammatory phase in which there is bleeding resulting from the injury to the bone and surrounding soft tissue, and a hematoma forms (Fig. 60.1A). The bone cells at the fracture line die. The reparative, or proliferative, phase starts shortly after the injury, usually 24–48 hours if a good local blood supply to the fracture exists (Fig. 60.1B). Good reduction and immobilization of the fracture also help the bone during the reparative phase. Osteogenic cell proliferation lifts the fibrous layer of the periosteum from the bone and, somewhat more slowly, the osteogenic cells of the bone marrow cavity also proliferate (Fig. 60.1C). This proliferation gradually forms a collar, or callus, around the fracture line, which usually takes place in 2–4 weeks, but radiographic evidence of external callus formation may not appear until 3–6 weeks. A bone scan usually reveals increased metabolic activity shortly after the fracture and before the callus can be seen on a radiograph (McRae, 2008).

The remodeling phase starts during proliferation as the osteogenic cells begin to differentiate into osteoblasts, which start to form bony trabeculae that bridge the living and dead bone across the fracture line (Fig. 60.1D). Some of the osteogenic cells differentiate into chrondrocytes and form cartilage in the fracture callus, which eventually calcifies, becoming bone. Osteoclasts gradually remove the necrotic bone at the fracture site. The callus, consisting mostly of cancellous bone that has now formed across the fracture site, is fusiform. The cancellous bone is slowly remodeled into compact bone and, finally, the original fracture line is no longer discernible.

The rate of fracture repair in the aging patient should always be considered to be similar to that of a younger person with early callus formation in 2–4 weeks and bony bridging over the fracture in 6 weeks, as shown on radiographs. However, a host of factors such as degranulating platelets, cytokines, transforming factor-beta, interleukins 1 and 6, prostaglandin E₂ and tumor necrosis factor alpha (Borelli et al., 2012), are crucial to this normal progression. Osteoporotic bone may not heal as well as bone with normal tissue density. The inflammatory response to the injury and the blood supply may be inadequate, and failure to immobilize the fracture site also delays the healing process. Morphogenetic proteins and growth factors in fracture healing and adequate nutrition are crucial. Diabetes and hypovitaminosis, especially vitamins D and C, have deleterious effects on bone repair. Polytrauma, chronic inflammation (Borelli et al., 2012), overall health or frailty as well as impaired cognition can also delay the healing process (see Chapter 18).

In the case of open reduction and internal fixation of a fracture, there is greater risk of further bone injury, called a stress riser, due to the orthopedic hardware. The use of screws and plates may weaken or pull out from bone that is already osteopenic.

Not all fractures in the elderly are considered to be complete fractures. Stress fractures, also referred to as insufficiency fractures, occur in areas of repeated trauma when bone remodeling is insufficient to repair the stresses of repetitive loading. Clinically, this is a particular concern when treating a patient who is at risk for increased bone fragility. Orthopedic internal fixation devices can become stress risers and cause increased loosening at the bone–appliance interface (Kim et al., 2011). People with spinal cord injury who have been fitted with a new orthotic device may develop stress fractures due to new movement abilities. The sedentary and overweight elderly, especially with low vitamin D (Breer et al., 2012), are at risk when they start new, strenuous physical activities. Physically, these patients will present with pain, swelling and warmth. Stress fractures or pseudofractures may arise in bone that has faulty mineralization, which is associated with inadequate repair of microtraumas.

Microfractures of the bony trabeculae have been demonstrated. The proclivity of these microfractures to cause pain is unclear. However, they may progress and lead to the silent fractures that are recognized on radiograph but may be old fractures. Despite the radiograph evidence of fracture, a patient can be unaware of having experienced any frank trauma – hence the term ‘silent fracture’. This may be one of the causes of the lumbar kyphosis that is seen in some individuals who spend excessive amounts of time sitting.

Occult fractures, also referred to as insufficiency fractures, are best diagnosed with bone scan or magnetic resonance imaging (MRI). This type of fracture is usually intramedullary and undisplaced, and frequently occurs as a result of some minor or major trauma, but radiograph examination is negative. Typically, occult fractures occur in the proximal femur or humerus after a fall, but they have also been reported in the sacrum, acetabulum, calcaneus, tibia and spine. Quickly these patients present with moderate to severe pain and tenderness. There is a concomitant reduction in range of motion and strength and, if in the femur, there is a marked antalgic gait. In nursing and rehabilitation this type of fracture should be treated seriously even if it has not been confirmed on initial radiograph. If pushed too aggressively, complete disruption of bone may occur. Protected ambulation with a walker is requisite while the femoral or pelvic occult fracture heals.

A pathological fracture results from primary or metastatic malignant tumors in bone. These types of fractures usually present as pain without any reported history of trauma; however, at times, metastatic bone disease is found in a patient who is being radiographed because of trauma. Significantly, these patients complain of increased pain at night and of being awakened by the pain. The pain frequently increases with bedrest and the severity increases with time. Those presenting with primary tumors of the breast, prostate, thyroid, kidney, or other organs should be suspected of having metastatic disease if pain complaints fit these descriptions. Standard radiographs are helpful for specific bony sites; however, for diffuse bone metastasis, a nuclear medicine bone scan may be important for a total skeletal evaluation (see Chapter 14).

As stated above, natural fracture repair in the elderly may not proceed in precisely the same pattern as repair proceeds in younger individuals. However, several medical and physical methods for enhancing bone repair are being investigated. A number of factors have been found that influence fracture repair, including fibroblast growth factor, platelet-derived growth factor, transforming growth factor 13 and bone morphogenic protein. Insulin-like growth factor may stimulate fibroblast proliferation (Glass et al., 2011; Borelli et al., 2012).

Ceramic composites of calcium phosphate have been used for bone grafts. Electrical stimulation and ultrasound at specific parameters are two physical modalities that are currently being used to promote fracture healing. Fracture treatment in the future is likely to involve active intervention to promote healing and thereby reduce morbidity.