Bone is comprised of three main components: an organic matrix, an inorganic mineral content, and water. Accounting for approximately 25% of bone weight is an organic matrix (called osteoid) that is composed mostly of collagen fibers (about 94% of matrix). These collagen fibers, extending along lines of tension, give bone its tensile strength and some flexibility. Also part of the organic matrix is a homogeneous ground substance composed of protein polysaccharides, particularly proteoglycan, which binds between collagen fibers. These proteins may serve to transfer mechanical information within the matrix to bone cells.1

The cellular component of the organic matrix includes predominantly osteoblasts, osteocytes, and osteoclasts. Osteoblasts, formed from osteoprogenitor cells that line bone surfaces, produce the organic matrix (osteoid), which is subsequently mineralized to form new bone. Osteoblasts communicate with each other in a network of cell extensions to exchange minerals, nutrients, and stimulatory signals. When an osteoblast becomes engulfed in its own calcified matrix, it becomes a mature osteocyte within the bone but is still connected with other cells via its extended cell processes. Osteoclasts migrate to the bone surfaces in response to certain stimuli and are responsible for bone resorption and mobilization of minerals.

The second and largest component of bone is the inorganic material (mineral salts such as calcium and phosphate), which accounts for approximately 70% of bone weight. This mineral content, bound and embedded within the matrix mostly in crystals of calcium hydroxyapatite, gives bone its hard, rigid structural strength while also serving as the body’s main reservoir for calcium and phosphorus.¹

Approximately 5% of bone weight is from water located within the organic matrix surrounding collagen fibers and ground substance and within the canals that carry nutrition to bone tissues.

Microscopically, the basic unit of bone is the osteon or the haversian system (Figure 50-1). The haversian canal lies at the center of each osteon and contains blood vessels and nerve fibers. A concentric series of lamellae of mineralized matrix surrounds the central canal. Bordering the lamellae are small cavities (lacunae) that contain a bone cell, the osteocyte. Many small channels, the canaliculi, connect adjacent lamellae with each other and eventually with the main haversian canal. This canal system allows nutrients from blood vessels in the haversian canal to reach osteocytes. Collagen fibers connect one lamella to another within the osteon and increase the mechanical strength of bone.²

At the tissue level, bones are classified as two types: cancellous or trabecular bone and compact or cortical bone (Figure 50-2). Cancellous bone is formed in thin plates called trabeculae found within the center of long bones, vertebral bodies, and flat bones such as the pelvis. Trabeculae are laid down in response to stress and are shaped to accommodate loads placed on the bone. Cancellous bone is covered by compact bone. Compact bone is quite resistant to compression and is dense in structure. Compact bone is laid down in concentric layers. A tough fibrous membrane called the periosteum covers all bones. The periosteum is highly vascularized and provides nutrition for bone via Volkmann canals (see Figure 50-1). An inner layer of the periosteum contains osteoblasts, which are responsible for bone growth and repair. The periosteum covers the entire bone except for the ends, which are covered by hyaline cartilage.

In longer bones, a central cavity (medullary cavity) is present (see Figure 50-2). A thin membrane called the endosteum covers this cavity. The central cavity is filled with fatty marrow. Osteogenic cells are located in the endosteum.

Blood vessels are distributed through the haversian canals. Living cells in bone communicate with each other and the haversian system via threadlike processes.

The ability of bone to remodel after injury is important. Although remodeling of bone continues throughout life, death of the osteon or removal of calcium from bone requires that new bone be deposited to retain strength and function. Physical stresses lead to the realignment of bone trabecular systems and the deposition of additional bone at the site of increased stress. The response of bone to stress is summarized by Wolff’s law, which states that bone is laid down where it is needed and resorbed where it is not needed.5 If bone is immobilized or not subjected to mechanical stress, as occurs with prolonged bed rest, the activity of bone-resorbing cells increases.⁶ Without external forces (or loads), osteoclast activity is greater than osteoblast activity and bone mass decreases. It is probable that during bed rest, age-related bone loss might be temporarily accelerated and may result in a greater decline in bone mass over time. Patients becoming mobile after prolonged bed rest are at risk for fractures because of a combined loss of muscle and bone strength. With loss of muscle, gait becomes unsteady and patients are more prone to falls.

Internal fixation of a fracture may also cause decreased bone strength. With metal implants, mechanical stress is dispersed from bone and carried by the implant. Bone under the plate is resorbed, and “stress relief” osteoporosis may occur. Care must be taken once implants are removed, and the bone must be protected until strength returns. Some implants are designed to compress fracture fragments to aid healing.

GERIATRIC CONSIDERATIONS

Changes in the Skeletal System

With aging, bone absorption exceeds bone formation. There is a net loss of bone mass and bone protein matrix. The interior of the long and the flat bones is absorbed faster than that of other bones. Trabecular bone destruction is greater than cortical bone loss. Compared to aging men, aging women have a greater amount of bone loss. The bone marrow space is decreased, with fat replacing marrow cells.

Although interior bone is lost, the circumference of the bones increases because osteoblasts on the exterior bone beneath the periosteum continue bone formation. The long bones, metacarpals, and ribs become bigger in circumference, whereas the pelvis becomes wider and the skull thicker.

The intervertebral disks become dehydrated, with narrowing of the disk space leading to a decrease in height of 3 to 5 cm. An increase in the thoracic curve occurs, resulting in kyphosis and anterior scapular displacement. This change leads to an increase in the anteroposterior diameter of the chest. A decrease in the lordotic curve results in lumbar flattening and a decrease in lumbar flexibility. Greater flexion of the knees and hips is noted. The relationship between the pelvis and the femoral head and neck also changes.

Fissuring, erosion, and thinning of cartilage occur. With the loss of cartilage, the greater pressure that subchondral bone must withstand results in increased density and the formation of joint margin osteophytes. The synovial membrane undergoes fibrosis and the synovial fluid thickens.

Bone mass decreases with age. Studies have shown that elderly individuals express higher levels of certain markers associated with bone resorption, whereas bone formation markers are much more variable. One common cause of increased bone resorption is calcium and vitamin D deficiency, which causes more rapid mobilization of calcium from bone. A secondary hyperparathyroidism can also result. Decreased levels of estrogen in elderly women and men can contribute to age-related bone loss because osteoblasts have estrogen receptors and their ability to increase bone formation may be affected by the estrogen deficiency. An increase in the local production of cytokines that influence bone resorption may also occur with decreased estrogen levels. The end result is an imbalance between osteoblast and osteoclast function and progressive decline in bone mass4 (see Geriatric Considerations: Changes in the Skeletal System).

Bone mass can also decrease with certain disease processes. For example, osteoporosis is a metabolic bone disease characterized by a severe general reduction in skeletal bone mass and thus a susceptibility to fractures. In short, bone resorption is more rapid than bone formation.

Fracture Healing

Bone may heal in one of two ways after a fracture. A periosteal or external callus forms in fractures managed by closed methods. The blood supply to surrounding soft tissue and motion at the fracture site contribute to healing. Medullary callous formation takes place with rigid immobilization at the fracture site. The process of bone turnover contributes to healing.

The five stages of fracture healing are: (1) hematoma formation, 1 to 3 days; (2) fibrocartilage formation, 3 days to 2 weeks; (3) callous formation, 2 to 6 weeks; (4) ossification, 3 weeks to 6 months; and (5) consolidation/remodeling, 6 weeks to 1 year (Figure 50-6). These five stages can be grouped into three phases: (1) inflammatory phase, (2) reparative phase (stages 2 to 4), and (3) remodeling phase.

Stage 1 begins when a hematoma forms at the fracture site. The size of the hematoma depends on the amount of damage at the fracture site. The hematoma offers some stability to fractured ends. Aseptic inflammation occurs at the fracture site.

Healing continues during stage 2 with the formation of granular tissue containing blood vessels, fibroblasts, and osteoblasts. The hematoma provides the foundation for reparative tissue and bone healing. Vascular and mechanical factors such as motion and distraction of fragments influence stage 2.

Callous formation occurs during stage 3 after the granulation tissue matures. If this stage is delayed or interrupted, the final stages cannot occur.

Stage 4, or ossification, occurs as the space in the bone is bridged and the fractured ends are united. The callus is slowly replaced by trabecular bone along the lines of stress, and unnecessary callus is reabsorbed.

During stage 5, consolidation and remodeling occur as the medullary canal is reestablished. Bone is resorbed and deposited along stress lines as bone reshapes to meet its mechanical requirements.

Fractures are usually considered healed when clinical healing is achieved. Clinical healing occurs when the fracture is stable and strong enough to resume its function, the fracture site is free of pain, no gross movement is seen across the fracture site, and radiographs show bone crossing the fracture site.

KEY POINTS

• Bone is capable of altering its shape and density in response to mechanical demands.

• The osteon is the basic unit of bone.

• Bone tissue may be dense and compact (cortical) or lighter and trabecular (cancellous).

• In long bones, the epiphyseal plate is the site of linear growth. Fracture through this plate may lead to limb length discrepancy after fracture healing in children. Increases in bone width are mediated by osteocytes in the periosteum.

• Bone cells responsible for deposition are called osteoblasts; osteoclasts mediate bone resorption. The balanced coupling of bone resorption and new bone formation is called remodeling.

• Absence of bone stress because of immobility or altered weight bearing leads to demineralization.