STRUCTURE AND FUNCTION

Bone is an intense metabolically active tissue. Bone has unique mechanical characteristics that are determined primarily by the structural components of bone tissue. Chemically complex, bone tissue is approximately 65% mineral and 35% organic matrix. The major organic constituent of bone is type I collagen, representing about 90% of the dry weight of bone.³⁵ The remaining 10% is composed of noncollagenous matrix proteins, lipids, phospholipids, proteoglycans, and phosphoproteins. The principal inorganic component of bone is a crystalline calcium phosphate hydroxyapatite.³⁵ This compound is generally brittle, tolerating only small amounts of deformation before fracture. The remaining tissue volume includes fluid-filled vascular channels and cellular spaces.¹²

Types of Bone

The microscopic organization and classification of bone tissue involves two distinct forms that change or adapt as we age: (1) normal, mature lamellar bone; and (2) weak, fragile, immature woven bone (Fig. 9-1).

Woven bone is structurally immature, embryologically (primary) fragile, and weak with a random disorganized collagen arrangement.³ This random arrangement of collagen fibers allows strength in all directions, while preferring strength in none specifically. Therefore this form of bone is not nearly as strong as mature bone. This specific type of bone is more commonly seen in embryos and newborns, but can also be seen in the adult during fracture repair callus, bone tumors, and various bone pathologies.³⁵

One of the unique features of woven bone is that it can be deposited without any previous part of a cartilaginous model existing.²³ Woven bone’s primary function is to provide temporary, quick acting mechanical support for injured skeletal tissue.

Very early after birth (approximately 2 months to 4 years), woven bone slowly remodels into organized, structurally mature lamellar bone. A clinically relevant feature of woven bone is that its specific mechanical behavior is termed isotropic; that is, woven bone does not conform to Wolff’s law, so its biomechanical reactions to applied forces and stress is similar in all planes.³ The disorganized arrangement of collagen fibers in woven bone strongly contributes to this unique characteristic (Fig. 9-2).³

Lamellar bone refers to mature remodeled woven bone. Mature bone begins formation at about 1 month after birth¹¹ and comprises most of the skeleton by age 4 years.² The collagen arrangement in lamellar bone is highly structured and organized. This gives normal mature lamellar bone anisotropic mechanical properties that are stress oriented, which characteristically respond to Wolff’s law.³

Bones are not only classified into various types, but also by their shape. Long bones are considered to have greater length than width. Examples of long bones are the femur and the humerus. These bones are tube shaped with widening at each end. Long bones have a diaphysis, which is the tubular shaped midportion that houses cancellous bone and the intermedullary canal where blood cells are formed (Fig. 9-3). The proximal and distal ends of the long bone widen to form a metaphysis, which continues to widen even more into the epiphysis or the end of the bone. In growing children, before skeletal maturity, the metaphysis and the epiphysis are separated by an epiphyseal growth plate. This can be a common area of fracture before skeletal maturity, at which time the two ends fuse and demarcation is not detectable.

Short bones are described as such because they are typically equal length in their main dimensions. These bones occur in the hands and feet. Short bones are composed of spongy inner bones that are enclosed by a thick layer of compact bone. Sesamoid and accessory bones are other forms of short bones.

Flat bones are typically larger and appear to serve a purpose in protection of organs. These bones consist of two layers of compact bone with a portion of spongy bone between. Bones like the ribs, sternum, scapula, and skull bones form the majority of flat bones. Many of these flat bones are actually curved and also serve as attachment sites for multiple muscles.

Irregular bones are those that do not seem to fit in the other categories. These include skull, vertebrae, and hip bones. These bones have a thin cortical exterior with a larger spongy interior.

Vascular Supply to Bone

The adult skeletal system receives between 5% and 10% of the body’s total cardiac output.³⁵ Bone receives blood supply from three distinct but interconnected systems: (1) the nutrient artery, (2) metaphyseal–epiphyseal system, and (3) periosteal systems (Fig. 9-4).

The arterial vascular system provides the origin of the nutrient system via a nutrient foramen in the diaphysis of long bones. The total number of nutrient vessels and foramen varies with each bone.³ The nutrient arteries enter the medullary space, then ascend and descend into the arterioles within the endosteal surface supplying the diaphyseal area of long bones.³ The metaphyseal–epiphyseal system is supplied by a periarticular complex system of the genicular arteries that penetrates the thin cortices of the metaphysis of long bones.³ Muscular attachment to the periosteal cortical sites of bone provides nutrition through the periosteal capillary system.³

Fractures, internal fixation devices, external fixation, and prosthetic joint implants devitalize the microcirculation of the cortical–periosteal and endosteal portion of the bone. The resultant ischemia of bone can lead to nonunion and bone infections.³ These important clinical ramifications of bone circulation disruption are evident when initiating therapeutic interventions of early weight bearing and closed kinetic chain (CKC) resistance exercise after fractures or joint replacement.

OSTEOPOROSIS

Osteoporosis is an age-related heterogeneous bone disease characterized by decreased bone tissue. Osteoporosis occurs when osteoblast (bone formation) activity is surpassed by osteoclast (bone resorption) activity (Fig. 9-5).²¹ This creates weaker bones that are subjected to greater rates of fracture. More than 1 million fractures a year can be attributed to osteoporosis²⁷; vertebral body compression fractures are the most common.

Causes of osteoporosis may be multifactorial, including hormonal alterations following menopause, prolonged immobilization, diseases, and prolonged steroid administration. Women are at greater risk for developing osteoporosis for several reasons. Age-related cortical bone loss generally begins at about age 40 years,²¹ with the rate thereafter being approximately 0.5% annually for both men and women. However, because of lowered estrogen during menopause,²¹ women lose bone at a rate of 2% to 8% annually, resulting in a much greater total loss.

Poor absorption of calcium that leads to decreased bone mineralization is called osteomalacia.²⁷ Causes include calcium-deficient diet, accelerated calcium loss, and malabsorption of calcium.²¹ Femoral neck fractures are common in patients with osteomalacia.²⁷

To appreciate the fragile nature of fractures that occur as a result of osteoporosis or osteomalacia, the following case should be considered:

CLASSIFICATIONS OF FRACTURES

By definition a fracture is any abnormal disruption in the normal anatomic continuity of bone. Therefore the classification of fractures takes into account the following criteria32,33:

 Site of injury: The area of insult on the bone itself. An epiphyseal fracture describes the site, as does an intraarticular fracture or diaphyseal (shaft) fracture. Generally the site is described as the proximal, middle, or distal portion of a bone (Fig. 9-6).

 Extent of injury: Complete or incomplete (Fig. 9-7). As the name implies, a complete fracture traverses the bone entirely. Incomplete fractures are commonly described as hairline cracks or greenstick fractures.

 Configuration or direction of abnormality: The direction of the fracture. In a transverse fracture, the fracture line goes straight across (horizontally) through the bone; an oblique fracture crosses the bone diagonally. A spiral fracture describes a torsion or rotational injury where the fracture line literally spirals through the bone. An impacted fracture is a long-axis compression injury where the fracture fragments are forced together. The fracture is classified as comminuted when more than two fragments are present.

 Relationship of fracture fragments to each other: Can be displaced, nondisplaced, angulated, twisted, rotated, or overriding. An example is an avulsion fracture where a portion of bone is pulled away as part of a musculotendinous attachment or ligament–bone attachment.

 Relationship of fracture fragments to the environment: Whether the injury is open (compound fracture) or closed (simple).

 Complications: Resulting in delayed union, nonunion, or malunion of the fracture fragments. An uncomplicated course of healing is called uneventful.

Pediatric fractures have a special classification of injuries involving the epiphysis. Depending on the type of epiphyseal fracture, the eventual growth of the bone can be profoundly affected.

Salter’s fracture classification is outlined in Figure 9-8. Type I Salter-Harris fractures, modified by Rang,^27,31–33 are transverse fractures through the physis. Type II fractures are the same as type I, but also have a metaphyseal fragment. Type III fractures involve both the physis and epiphysis. Typically these are intraarticular fractures. Type IV fractures are the same as type III but include the metaphysis. These are significant injuries that can lead to a reduction in bone growth. Type V fractures are severe injuries classified as crush injuries to the physis. This type of fracture also can lead to the arrest of growth. The PTA should also be aware of the Arbeitsgemeinschaft für Osteosynthesefragen (AO) classification system, which is universally applied to both fracture patterns and the devices used for internal fixation. This system will be discussed later in this chapter.²⁶

Other fractures that are commonly seen in children are incomplete fractures. This is typically because a child’s bones are more flexible than an adult’s. A buckle fracture is one in which a deformation or “bending” of the cortex occurs on one side of the bone. A greenstick fracture is one that involves a linear fracture through one cortical surface and a flexing deformation of the opposite surface. A bowing fracture is one that may be caused by multiple microfractures along the length of a long bone so that the entire bone is bent or curved.

Pathologic fractures are caused by tumors²⁷ (malignant or primary bone disease), osteoporosis (most common), microtrauma from repetitive overload (stress fractures), or metastatic bone disease (second most common). These usually occur in the elderly person secondary to osteoporosis and can happen spontaneously or with very minor trauma.²⁷

COMPONENTS OF BONE HEALING

Most of the adult skeleton (80%) is composed of compact, cortical bone. Approximately 20% of the skeleton is cancellous or spongy bone. Compact bone is extremely dense and unyielding to bending, whereas cancellous bone is more elastic and less dense than cortical bone.²⁷

Three types of cells take part in the highly dynamic, reparative process in bone. Osteoblasts help form and synthesize bone. Osteocytes are mature bone cells that account for approximately 90% of all bone tissue. Osteoclasts are active in bone resorption.

The normal dynamic process of bone synthesis and resorption is termed remodeling. Remodeling and stress occur together, which profoundly influences bone shape, density, internal architecture, and external configuration.1,18,22,27 With normal bone remodeling, weight-bearing forces and muscular contractions provide the stress needed for bone formation and adaptation. The absence of physiologic loading, or stress, is detrimental to bone, ligament, cartilage, muscle, and tendons, as well as the cardiorespiratory system. Wolff’s law¹ states that intermittently applied stress, as well as changes in function of bone, causes definite changes.^4,22 After a fracture, treatment may involve rigid cast immobilization and non–weight bearing over a period of weeks. This decreased stress on the bone causes rapid osteoclast activity (bone resorption) and decreased osteoblast activity.²⁸ Therefore although the removal of stress is paramount for healing, the decrease in external force also causes significant bone loss.²⁷ Bone loss caused by immobilization is reversible after progressive weight bearing, active motion, resistive exercise, and vertical loading (CKC exercise).²⁷ It is recommended that strict, long-term, rigid cast immobilization be minimized whenever possible.

Although normal stresses promote bone development, excessive stress also can lead to gradual bone resorption.²² Stress that is unrelenting and does not allow for osteoblastic repair of bone can lead to pathologic accelerated bone resorption and eventual stress fracture.^1,18,22

Bone remodeling is also influenced by electrical charges when forces are applied to bone. The piezoelectric effect describes a negative electric charge toward the concave, or compression, side of a force applied to a bone. An electropositive charge is seen on the tension, or convex, side of the bone. The negative-charge side responds by stimulating osteoblasts, whereas the positive-charge side (tension side) responds by increasing osteoclast activity.²⁷

BONE INJURY AND REPAIR

Injury repair and eventual regeneration of osseous tissue is a complex process that involves the bone marrow, bone cortex, periosteum, and external soft tissues.

Trauma to the bone disrupts the biological, mechanical, structural, architectural, and histochemical environment of bone. Classic descriptions of fracture healing are divided into primary (direct) cortical healing and secondary (indirect) fracture healing.

The spontaneous natural course of fracture repair can be described as interfragmentary stabilization by periosteal and endosteal callus formation and by interfragmentary fibrocartilage differentiation, restoration of continuity and bone union by intramembranous and endochondral ossification, substitution of avascular and necrotic areas by haversian remodeling, modeling of the fracture site, and functional adaptation.1,3,4,8,10,20

Fracture healing responses differ according to the nature of stabilization provided (direct, internal, compression–appositional, alignment fixation, versus cast immobilization). That is, rigid internal fixation results in primary–direct cortical healing, which is an attempt by the cortex of bone to reestablish mechanical and anatomic continuity. In primary fracture healing the new bone grows directly across the bone ends to unite the fracture site. This form of bone healing is very slow and cannot bridge a fracture gap, thus the two fractured ends are not able to appose each other. This requires rigid fixation with direct contact of cortical bone and an intact intramedullary vasculature. This type of fracture healing response usually is devoid of periosteal soft callus formation. Secondary or indirect fracture repair is noted for external periosteal soft-tissue callus bridging between fracture fragments. In secondary healing, a cartilage matrix is initially formed, which gradually takes on a callus appearance. This method of healing involves adding stability by creating a callus that is actually larger (wider) than the two opposing bones.

Complications

Occasionally the process of bone healing leads to three distinct complications:

1. Delayed union

2. Nonunion

3. Malunion

In delayed union, the dynamic biological repair processes of bone healing occur at a slower rate than anticipated. Brashear and Raney⁴ describe delayed union as clinically detectable when firm callus is not present at 20 weeks (for fractures of the tibia and femur) and at 10 weeks (for fractures of the humerus). An important cause of delayed union is “inadequate or interrupted immobilization.”⁴ Rehabilitation can significantly affect the healing process either positively or negatively. If therapeutic interventions are begun too soon or too vigorously, delayed union may occur because of excessive motion occurring at the fracture site. Unfortunately, the trade-off when caring for delayed bone union cases is the need to provide extended periods of immobilization for healing. However, cast braces and walking casts can be used to provide the weight bearing (Wolff’s law) necessary to enhance healing. In nonunion, the healing processes have stopped. Nonunion occurs when there is a significant and severe associated soft-tissue trauma, poor blood supply, and infections.

In malunion, healing results in a nonanatomic position (Fig. 9-9). Malunion is caused by ineffective immobilization and failure to maintain immobilization for an adequate period of time. For appropriate bone healing to occur, anatomic alignment (apposition) of fragments, adequate fixation (external or internal), and length of time of immobilization must occur in concert. If these factors are not balanced, the chance of complications is increased. Regardless of the type of complication, fracture healing fails or is delayed 5% to 10% of the time.^6,9

External Fixation and Fracture Repair

External fixators are used for a wide variety of clinical situations and allow for modification of stiffness and rigidity of fixation during fracture healing.4,30

The geometric composite construct of these elaborate frame configurations usually can be altered by several orders of magnitude. Several factors significantly contribute to the stability, rigidity, stiffness, and compression of the fracture site, as well as the mechanical properties of the frame.³⁰ The number of pins used; the length, diameter, and type of pin material; the number of side bars set in the spacing between pins; the spacing between side bars and bone surface; pin–bone contact; and proximal–distal pin spacing all contribute to the material characteristics: stability, stiffness, and compression of the fracture site.^8,30

Fracture healing characteristics using external fixators depend on the rigidity obtained by the device. Overall, the more rigid the fixation, the earlier the radiographic confirmation of bone union. Less rigid fixators create greater periosteal callus formation, whereas rigid fixators characteristically stimulate direct primary cortical fracture healing.8,30

As stated, a unique advantage of external fixation is the ability to alter or modify rigidity during various stages of fracture healing. Several models demonstrate the effect of dynamization (mechanisms used to decrease stiffness of the fixation or mechanisms that allow for controlled micromotion between fracture fragments) on blood flow and bone callus formation.8,20,25,30,35 A 25% increase in fracture site micromotion resulted in a 400% increase in regional blood flow and substantially more callus formation with animals receiving semirigid external fixators compared with rigid external fixation.³⁰

Bone Fixation Devices

When caring for patients who have had fractures, the PTA must be aware of various methods used to immobilize or stabilize the fracture so a clear understanding of the extent of trauma can be appreciated. This also allows the PTA to understand the degree of tissue healing necessary before vigorous rehabilitation exercises can be undertaken.

The remarkable sensitivity of bone to normal biological stress is well-known.1,22,27,33 After fractures, an attempt is made to stabilize the fracture, bring the fragments together by apposition (approximation) and alignment, and remove or minimize forces that may slow the normal healing process. Two general methods of immobilization are used in the treatment of fractures. In one method, the area is immobilized by external fixation devices. This method involves the use of casts, traction, splints, and braces and the external fixation devices employed with significant open (compound comminuted) fractures where the risk of infection is present (Fig. 9-10). These ominous-looking devices help fix the fracture site while allowing care of the open wounds with skin grafts, tissue flaps, or débridement. These are classified as external fixation devices because the pins used to immobilize the fracture do not contact the fragments directly, but are used to hold the bone segments in rigid alignment and anatomic apposition. With closed (simple) fractures, various rigid lightweight fiberglass casts, plaster casts, hinged-plaster casts, and adjustable-range hinged braces are used for immobilization.

The second method of immobilization uses internal fixation devices and is best for displaced fractures where external fixation does not provide the degree of immobilization necessary to effect healing. (See Box 9-1 for the background on the AO classification system, designed by the Association for the Study of Internal Fixation [ASIF or AO].) Internal fixation is called open reduction with internal fixation (ORIF) and involves surgically exposing the fracture site to reduce, approximate, and align the bone fragments. The materials used for ORIF procedures include metals (stainless steel and metal alloys of cobalt–chromium–molybdenum and titanium) and nonmetals (high-density polyethylene, polymethylmethacrylate, silicones, and ceramics). Metal internal fixation devices frequently are combinations of screws, staples, pins, nails, tension-band wires, and various plates. The placement of these materials can affect the delivery of certain therapeutic agents, such as ultrasound. Also, a hole or tunnel defect in a bone, with or without a screw in it, effectively reduces the overall strength of the bone up to 50%.²⁷ Even after screw removal, the bone will not regain normal strength for up to 1 year.²⁷

Metal internal fixation devices occasionally loosen and can “back out,” as is the case with screws. If the PTA notes signs of hardware loosening (pain, swelling, or crepitus), he or she must immediately consult with the supervising physical therapist (PT) and physician. Many metal fixation devices are designed to be left in place, as with most plates, but these devices should be removed if metal allergy reactions occur. Table 9-2 depicts the various internal fixation devices.

Factors Influencing Bone Healing

Several key factors are implicated in delayed biologic fracture repair. Tobacco smoke, malnutrition, inadequate reduction of the fragments, excessive motion from inadequate immobilization, poor vascular supply, soft-tissue interposition between fracture fragments, and infection significantly limit spontaneous fracture repair.3,8

Cigarette smoke is a vasoconstrictor that may reduce blood supply to the injury site. In addition, smoking directly interferes with osteoblast formation.³⁶ Protein, malnutrition, and calorie deprivation reduce skeletal muscle mass and may contribute to reduced periosteal and cortical bone formation.⁸ Poor reduction of the fracture fragments and inadequate immobilization create excessive motion and reduced vascular supply to the bone (Box 9-2).³⁶ Occasionally a sleeve of soft tissue becomes interposed within the fracture site, significantly reducing both primary, cortical, and secondary–periosteal bridging callus, and rendering the fragments devitalized.

Stimulation of Fracture Repair

There are several methods available to augment, stimulate, or enhance fracture repair. Bone grafts are used to fill osseous defects and stabilize fractures. Bone autografts are taken from the same individual. Allograft bone tissue is used from the same species. An example of a fresh autograft is harvesting bone from the iliac crest to transpose (heterotopic transportation) to the lumbar spine for fusion.

Conversely, cadaveric bone allografts must be sterilized chemically. This process renders all cells nonviable. In both autografts and allografts, the implanted graft acts as a scaffold to support the growth of host bone tissue. This process is known as passive osteoconduction.⁸ Gradually the implant bone tissue becomes revascularized with stimulation and transportation of osteoblasts into the new graft. This process is referred to as osteoinduction.⁸ Although the sequence of events is similar (passive osteoconduction, gradual revascularization, and osteoinduction) with both graft materials, allogenic bone requires a longer time for creeping substitution to take place. Additional materials used for osteoconduction that support vascular ingrowth, growth, attachment, division, and remodeling of bone include ceramics, bioactive glass, and synthetic polymers.⁸

Ceramic bone graft substitutes include hydroxyapatite and tricalcium phosphate. Some of these graft substitutes are formed from marine coral and crystalline hydroxyapatite. These bone substitutes generally have been shown to be as effective as autograft bone.⁸

Two clinically relevant methods of fracture healing augmentation are electromagnetic field application and low-intensity ultrasound. The use of exogenously applied pulsed electromagnetic fields over nonunion fractures is based on the piezoelectric effect in response to load deformation of crystalline–collagen component’s of Wolff’s law.⁸ The use of specific electrical stimulation waveforms to induce bone formations is supported by scientific investigation and clinical observation that electric stimulation affects enchondral bone formation and connective tissue repair.

Basic science research suggests that the use of nonthermal, low-intensity ultrasound (30 mW/cm²) has very strong biological value to bone healing due to signal transduction and gene expression; stimulation of chondroblasts and osteoblasts and increasing blood flow; and enhancement of greater mechanical and histologic influence on enchondral and periosteal bone healing.¹⁶ Various studies have demonstrated that use of brief low-intensity ultrasound on the order of 20 minutes per day can reduce the time to fracture union.^{8,14,19,24,29}

However, a recent systematic review⁷ of the use of low-intensity pulsed ultrasound for fractures that assessed randomized controlled trials determined that many of the studies had only moderate to low quality evidence for its use. Studies rarely included functional endpoints, and two of the highest quality studies showed no difference in functional outcome with the use of ultrasound.

Clinical Application of Rehabilitation Techniques During Bone Healing

Immobilization after bone injury may not be total. Nonimmobilized structures should be exercised throughout the period of immobilization. For example, a program of lower extremity strengthening and endurance activities (stationary cycle, treadmill, and leg extension) should be instituted for patients with upper extremity fractures. The same principle applies for patients with lower extremity fractures. Endurance activities can be either single-leg stationary cycling or upper body ergometer (UBE) exercises in these cases.

Specific exercises for the injured area frequently involve isometric muscle contractions. Therapeutic exercise programs during bone healing are designed to minimize muscle atrophy while maintaining or improving muscular strength. Muscle contractions provide forces acting to approximate fragments, improve circulation, promote motion to nonimmobilized body parts, and stimulate the piezoelectric effect.

The cast or brace serves as resistance in the initial phases of active range of motion (AROM) exercises involving the affected limb. Ankle weights can be applied to the cast or brace for added resistance in later stages. It is best to apply the external resistance superior to the injury site at first, such as in ligament injuries. A more distal application of external force may produce excessive, unwanted shearing, or torque through the fracture site.

Occasionally, electrical muscle stimulation (EMS) is used during cast immobilization to help retard atrophy and maintain strength. A small “window” is cut in the cast to allow the application of the electrodes. The patient is instructed to isometrically contract simultaneously with the electrically evoked muscle contraction. The benefits of electrical stimulation on muscle tissue during immobilization are controversial. The piezoelectric effect is enhanced by applying a negatively charged electrode to stimulate osteoblast activity, which is called direct current (any current in which electrons flow in one direction). An externally applied electrode with an external power source is called inductive coupling.²⁷

Continuous passive motion (CPM) devices are used in some cases of intraarticular or extraarticular fractures of the tibia and femur.¹³ Although this appears to conflict with the notion of secure immobilization leading to bone healing, Salter and colleagues³⁴ found positive effects of CPM on the development of chondrocytes and the reduction of intraarticular synovial adhesions when judiciously applied to healing intraarticular fractures.

The goals of rehabilitation programs during immobilization of healing fractures are as follows:

After immobilization, progressive exercise must be directed cautiously. Motion and circulation can be promoted by using various thermal agents. Strengthening exercises should systematically progress through isometrics, concentric and eccentric resistance, isokinetics, and CKC resistance exercises. Balance, coordination, and proprioceptive exercises are also included during the postimmobilization phases of rehabilitation. Stationary cycle ergometers, UBEs, stair climbers, and treadmills are tools that can enhance cardiorespiratory fitness both during and after immobilization.