Soft tissues

Soft tissue abnormalities frequently accompany and often precede active bone disease. Recognizing the presence or absence of soft tissue swelling is extremely useful when trying to decide whether the appearance of a bony structure represents a normal anatomic variation, an inactive lesion, or an active disease process. In some cases, the cause of pain or lameness is limited to the soft tissues, such as sprains (ligament injuries), strains (muscle injuries), bruises, inflammation, and others. Conditions that can mimic a soft tissue abnormality include bunching of the skin, superimposed skin folds, and dirt, debris, or fluid on the skin or in the hair coat.

Soft tissue swelling may be localized or diffuse. Localized swelling can be caused by a mass. Diffuse swelling often is caused by fluid (e.g., edema, hemorrhage, inflammation, others). Swelling may be identified by the displacement or effacement of the nearby fascial planes.

A soft tissue mass is a localized area of swelling with a defined margin. The margin may or may not be visible in radiographs, depending on the opacity interface with the adjacent tissues. A soft tissue mass in muscle or surrounded by fluid, for example, is not distinguished because the opacities are the same. A soft tissue mass must be large enough to distort the border of the muscle or displace a fascial plane to be identified. Types of soft tissue masses include tumor, hematoma, cyst, abscess, granuloma, and lymphadenomegaly, the latter occurring at a known location for a lymph node.

Lipomas are fat opacity masses, they often can be distinguished from soft tissue in survey radiographs (Figure 5.1). Many lipomas develop in fascial planes. Mixed opacity lipomas may result from fluid mixing with fat or due to a more aggressive type of lipoma such as dissecting lipoma or liposarcoma. The margins of liposarcomas tend to be indistinct.

An arteriovenous fistula is an abnormal communication between an artery and a vein, which can appear as a soft tissue opacity mass. They occur more often in a limb and may be accompanied by a periosteal response or pressure remodeling in the adjacent bone.

Lymphedema is an abnormal accumulation of lymphatic fluid in one or more limbs. Swelling typically is more severe in the distal part of the limb due to the effects of gravity. Unless the edema is due to trauma, the skeletal structures usually are normal.

A loss or reduction of soft tissue may be due atrophy or the physical absence of tissue. Atrophy generally results from disuse, which may be due to pain, immobilization, or paralysis. A physical deficit may be caused by severe trauma or surgical removal.

Gas in the soft tissues can result from a penetrating wound, migration of gas from a nearby damaged structure (e.g., ruptured trachea), or a gas‐producing bacterial infection. The gas may be localized or diffuse and usually produces a heterogeneous pattern due to multiple bubbles. Soft tissue emphysema can occur in the subcutaneous, intramuscular, or interfascial tissues. The volume of subcutaneous gas sometimes is quite large and widespread, displacing the skin away from the body and making the patient appear bloated. Conditions that may be mistaken for soft tissue emphysema include fat opacity in the soft tissues (e.g., fascial plane, lipoma) and superimposition of skin folds.

Mineralization in the soft tissues may be dystrophic, metastatic, neoplastic, or due to foreign material. There are several different mechanisms by which soft tissue structures can mineralize, but they are difficult to differentiate in radiographs. The location of the mineralization and results of laboratory testing sometimes provide clues to the etiology. Soft tissue mineralization ranges from disorganized to highly organized. Clinical signs usually are absent unless a secondary complication develops, such as interference with mobility, ulceration, or infection. Dystrophic mineralization occurs locally in damaged, degenerating, or dead tissue. Serum calcium and phosphorous usually are normal. Metastatic mineralization occurs in normal tissues away from the site of disease. It frequently is associated with abnormal serum calcium and phosphorous, but blood work sometimes is normal.

Calcinosis cutis is mineralization in the skin. It most often is associated with hypercortisolism, but it can result from trauma, chronic inflammation, and others. In radiographs, calcinosis cutis typically appears as thin, linear mineralization near the skin surface. It may be focal or multifocal.

Calcinosis circumscripta is mineralization in the subcutaneous tissues. The etiology is unknown. It is uncommon in dogs and rare in cats, most often reported in young, large breed dogs. Calcinosis circumscripta tends to occur at bony prominences and under footpads. In radiographs, it appears as well‐defined, rounded clusters of heterogeneous mineralization (Figures 5.2 and 5.3), sometimes called tumoral calcinosis. It often develops near a skeletal structure and may be mistaken for bone disease, but there is no periosteal response nor evidence of osteolysis.

Vascular mineralization occurs in the walls of blood vessels, usually arteries. In dogs, it most often is seen along the abdominal aorta and its major branches. In cats, particularly older animals, it more often occurs in the thoracic aorta. Vascular mineralization frequently is idiopathic, but it may be associated with a systemic or endocrine disease.

Mineral and metal opacity foreign materials usually are readily identified in radiographs, but they must be confirmed in orthogonal views to avoid misdiagnosing a superimposition artifact. Soft tissue opacity foreign materials seldom are distinguished unless adjacent to fat or gas (e.g., glass, wood, plastic, plant materials). A fistulogram may help locate a foreign object if a draining tract or site of entry is found.

Orthopedic anatomic considerations

Bone is approximately one‐third organic material (osteoid) and two‐thirds inorganic material (mineral). Osteoid is soft tissue opacity and not differentiated from the adjacent soft tissues. In most cases, only the mineral portion of bone is visible in radiographs.

The average number of bones in a dog is about 320 and the average number in a cat is about 240. A typical dog skeleton includes:

• 50 vertebrae
  
• 26 ribs
  
• 8 sternebrae
  
• 41 skull bones
  
• 9 hyoid bones
  
• 45 bones in each pectoral limb
  
• 48 bones in each pelvic limb
  
• 1 os penis in males (an extra‐skeletal bone, not attached to the skeleton).

Types of bone

There are two general types of bone: cortical and cancellous. Cortical bone forms the outer layer or cortex of most bones, including all long bones. Cortical bone is also called compact bone and makes up about 80% of the total bone mass in the body. In radiographs, it is relatively uniform in appearance and homogeneous in opacity (Figure 5.4).

Cancellous bone consists of a network of thin bony plates called trabeculae with many open spaces, or “pores”, in between. Cancellous bone is also called trabecular bone and makes up about 20% of the skeletal mass. Because of the trabeculae, the surface area of cancellous bone is nearly 10 times that of cortical bone. Trabecular bone is found at the ends of long bones, in the vertebrae, and in flat bones. In radiographs, it is more porous and heterogeneous in opacity than cortical bone (Figure 5.4), sometimes described as sponge‐like in appearance.

Bone development

Most bones form via endochondral ossification, which means they develop in a cartilaginous frame. Some bones form via intramembranous ossification, which means they grow in connective tissue without an intervening cartilage model. Many of the bones in the skull form via intramembranous ossification.

During endochondral ossification, growing cartilage is systematically replaced by bone. The points in the cartilage frame where bone initially forms are called ossification centers.

Primary ossification centers develop in the shafts of long bones and in the bodies of short bones, irregular bones, and sesamoid bones. Secondary ossification centers develop at the ends of long bones and form bony prominences, which serve as attachment sites for ligaments, tendons, and other structures. There may be multiple secondary ossification centers in one bone. Secondary centers sometimes fail to fuse to the parent bone and instead develop into separate small, round or oval‐shaped mineral opacity structures. These are called accessory ossification centers or accessory ossicles. The locations of many accessory ossicles are known (often they occur near a joint) and they are described and illustrated in this chapter. Knowledge of accessory ossification centers is important because they may be mistaken for pathology, such as avulsion fractures.

Long bones form in a cartilage frame. Longitudinal growth occurs at growth plates called physes, which are located near one or both ends of the bone. A physis appears in radiographs as soft tissue opacity band. The different parts of a long bone are named in relation to the physis (Figure 5.5).

The diaphysis is located “between the physes.” It is the shaft of the long bone, the diaphysis appears in radiographs as homogenous cortical bone on either side of a less opaque medullary cavity. Although cortical bone completely encircles the medullary cavity, the bony cortex appears as two distinct divisions due to the summation of bone (Figure 5.6).

The metaphysis is located “next to the physis.” It is the wider end of the shaft of a long bone and consists of mostly cancellous bone. Metaphysis also means “change next to the physis” because this is where the wider bone is actively remodeled to become the narrower shaft. This area of bone remodeling is called the cut‐back zone and appears in radiographs as a part of the cortex with a less distinct margin. The cut‐back zone sometimes is mistaken for pathology; however, there is no soft tissue swelling or pain with normal bone growth.

The epiphysis is located “upon the physis.” It is the rounded end of a long bone that supports the articular cartilage. The epiphysis is mostly cancellous bone with a thin layer of dense subchondral bone. The subchondral bone appears in radiographs as a thin line of increased opacity at the articular border.

An apophysis is a non‐articular epiphysis. It forms a bony prominence that serves as an attachment site for a tendon, ligament, or joint capsule. Examples include the greater trochanter, greater tubercle, and tibial tuberosity. An apophysis sometimes is called a traction epiphysis because the structures that attach here exert a pulling force, whereas the structures at an epiphysis exert compressive forces due to weight bearing.

The parts of growing bones are not visible in radiographs until they ossify. Ossification centers become visible at predictable times in dogs and cats, and the secondary centers are expected to fuse with the parent bone within certain time intervals. These are listed in Table 5.1 and illustrated in Figures 5.7–5.13.

Bone growth ceases when cartilage growth stops. After the cartilage stops growing, the metaphyses and epiphyses gradually blend together and the physes become thinner and thinner until the physes “close.” A “closed” physis appears in radiographs as a thin sclerotic line which is called a physeal scar. The physeal scar slowly fades as the animal matures and eventually disappears.

Nearly all bone surfaces are covered with a thin membrane called the periosteum. The articular surfaces and most of the sesamoid bones are not covered with periosteum. The periosteum consists of two layers, a tough fibrous outer layer and an inner layer that produces bone. The outer layer provides protection and connection, the latter because it blends continuously with tendons and ligaments at their attachment sites. The inner layer of the periosteum, called the cambium layer, is attached to the bone cortex by Sharpey’s fibers. The periosteum contributes to the circumferential growth of long bones and aids in bone healing.

Bone response to disease or injury

Bone responds to disease with either an increase in mineral or a decrease in mineral, and often it is both. At least 30%–50% of the mineral content must change before a bone lesion can be seen in a radiograph. This amount of change typically requires at least one to two weeks to occur.

Bone production is a non‐specific periosteal response to bone damage. The formation of new bone is an attempt to heal, not a “reaction” to any particular disease. Whenever the periosteum is separated from the cortex and maintains its blood supply, it will produce mineral to fill the space between the lifted periosteum and the cortex of the bone. Mineral is produced by the cambium layer and deposited along the fibrous and vascular tissues that remain connected to the cortex. The formation of new bone, therefore, is perpendicular to the periosteum. The further the periosteum is separated from the cortex, the larger and more irregular the new bone production because there is more space to fill. The stages of a periosteal response are illustrated in Table 5.2.

Bone disease results in separation of the periosteum from the cortex.

The periosteum is elevated due to subperiosteal accumulation of fluid or cells. Soft tissue swelling is present.

The elevated periosteum is connected to the underlying cortex by Sharpy’s fibers and blood vessels, which extend perpendicular from the periosteum to the cortex.

The cambium layer produces mineral to fill the subperiosteal space. The mineral is laid down along the perpendicular fibers and vessels from the periosteum to the cortex.

Mineral deposits continue until the subperiosteal space is completely filled.

Mineral gradually matures into organized bone with a well‐defined margin. Over time, normal stresses remodel the new bone until it gradually returns to original shape.

When you see a periosteal response, the first thing to determine is whether it is active or inactive. If it is active, you must deal with the bone disease now. If it is inactive, you can observe the lesion to see whether it remains inactive (i.e., a benign process). It is important to make sure an apparently benign lesion remains inactive before abandoning diagnostics or treatment. To determine whether new bone production is active or inactive, look at its margin. The less distinct the margin, the more active the periosteal response. The simplest way to evaluate a bony margin is to trace it with an imaginary pencil or stylus. If it is easy to draw a line along the edge of the new bone, it is well‐defined and not very active. The more difficult it is to trace the margin, the more active the disease process.

Active disease processes continue to push the periosteum away from the cortex. The subperiosteal space may fill with blood, tumor cells, edema, or purulent material, any of which will prevent complete mineralization of the subperiosteal space. As long as the disease process is active, the edges of the new bone being produced will remain indistinct. A well‐defined margin can only be established once the disease process has stopped and there is time for mineral deposits to fill the space. The better defined the margin, the less active the process.

It is essential to realize that the definition or sharpness of the new bone margin has nothing to do with its size or shape. New bone with an “irregular” border does not mean the margin is ill‐defined, and new bone with a “smooth” border does not mean the margin is well‐defined. Some periosteal responses are quite extensive, producing large amounts of new bone with irregular or uneven borders, but this does not tell us whether the disease is active or inactive. It may give us some idea about the severity of the bone damage, but we must evaluate the margin to determine whether further diagnostics or treatment are immediately needed.

The aggressiveness of a bone lesion is reflected by the degree of osteolysis. Osteolysis is the pathologic destruction of bone. The less distinct the margin around an area of osteolysis, the more aggressive the disease process. In addition to tracing the margin to determine its sharpness, look at the zone of transition between the abnormal bone and bone that appears normal. The longer and less defined the zone between abnormal and normal, the more aggressive the disease process.

The aggressiveness of a bone lesion is also assessed by its rate of change in serial radiographs. The more rapid the change, the more aggressive the disease. Very aggressive bone diseases can produce visible osteolysis in 5–7 days. Bone production, however, usually takes at least 7 to 10 days to become visible in a radiograph, regardless of the cause of the periosteal response. Occasionally, periosteal new bone production is visible in less than 7 days in a young, rapidly growing animal. Note: a periosteal response does not tell us how aggressive the disease is, only how active.

The radiographic appearance of periosteal new bone also tells us something about its chronicity. New bone production initially is more opaque near the displaced periosteum because this is where it is being formed. As healing progresses and more mineral is deposited, the new bone increases in opacity and becomes more homogeneous. New bone gradually matures over the following weeks, becoming more organized and trabeculated. During the following months and years, normal stresses gradually remodel the bone until it eventually resembles the original size and shape. The change from unorganized mineral deposits to organized bone reveals the chronicity of the lesion. Knowing how long a lesion has been present is valuable for patient management and may provide clues to its etiology. With many bone diseases, it is a race between the pathologic process and the healing response. Serial radiographs help monitor the progression of disease and the patient’s response to therapy.

Patterns of bone remodeling

Patterns of bone production and bone destruction have been used over the years in an attempt to narrow the list of differential diagnoses. Most patterns, however, are not diagnostic of any specific disease. Patterns sometimes are helpful to describe radiographic findings, and some of the classic patterns are discussed on the following pages. However, any aggressive disease process, regardless of etiology (e.g., malignant tumor, bacterial infection, severe trauma) can produce radiographic signs of aggressive bone disease. Likewise, any benign disease process, regardless of etiology (e.g., bone bruise, bone cyst, tumor) can produce radiographic signs of benign bone disease.

The value of radiography is to help determine the activity, aggressiveness, chronicity, and extent of bone disease. Bone lesions may be solitary or multifocal, monostotic or polyostotic, and may arise in the diaphyseal, metaphyseal, or epiphyseal region of a bone. It is important to remember that radiographs are snapshots in time. They depict the appearance of a lesion only at the moment the images were made. Serial radiographs often are needed to determine the true nature of a disease process. In addition, some diseases may be obscured by a pre‐existing condition, such as degenerative joint disease masking a tumor.

Patterns of periosteal response

Patterns of bone production tend to emphasize the shape of the new bone rather than its margination. Remember, the shape is not the same as the margination. In all of the patterns discussed below, the margins of the new bone may be well‐defined or ill‐defined, depending on how active the disease process was at the time of radiography. Note: it is the bony margin at the edge of the periosteal response, away from the underlying cortex, that must be evaluated to determine lesion activity. Lesion aggressiveness (i.e., osteolysis) is determined by evaluating the cortex and underlying bone.

Smooth bordered new bone production generally occurs when the periosteum was not separated very far from the cortex. This may occur with a slow‐growing disease process or early in the course of a more aggressive disease. When the periosteum is only mildly elevated from the cortex, mineral can quickly fill the subperiosteal space to produce new bone with a smooth, even border. Again, the margin may be well‐defined or ill‐defined, depending on the activity of the disease process. Uneven or irregular‐shaped new bone production occurs when at some point, the periosteum was separated a considerable distance from the cortex (Figure 5.14).

Multilayered new bone production occurs with diseases that grow intermittently, each time elevating the periosteum. New bone is produced in layers between growth episodes of the disease. The radiographic appearance has been described as lamellar, laminated, or onion skin. The shape of the new bone tends to be even and smooth‐bordered (Figure 5.15). Again, the margin of the outer‐most layer may be well‐defined or ill‐defined, depending on the current activity of the disease.

Brush border new bone production occurs when the periosteum is elevated along a broad expanse of cortex. Mineralization is perpendicular to the periosteum, creating an appearance which has been described as resembling the bristles of brush or “hairs‐standing‐on‐end” (Figure 5.16). If the separation between the periosteum and the cortex is larger and more chronic, the new bone may be more organized and appear “columnar” or “palisading.”

The sunburst pattern of new bone production occurs when the periosteum is separated from the cortex in all directions. This typically is caused by a rapidly growing lesion that originates at a single site. Periosteal mineral is produced perpendicular to the elevated and rounded periosteum and extends toward the cortex. The mineralization is not perpendicular to the cortex, rather it appears to radiate from the center of the lesion as numerous bony spicules that resemble a “sunburst” (Figure 5.17). A sunburst periosteal response most often is attributed to neoplasia, but it can occur with severe osteomyelitis or trauma.

Amorphous new bone production occurs with very rapidly growing disease processes that actually break through the periosteum. In these cases, the elevated periosteum is ruptured and discontinuous. Parts of the periosteum that retain a blood supply produce perpendicular mineralization which appears in radiographs as multiple mineral opacity foci without any form or organization (Figure 5.22). Amorphous new bone tends to develop further away from the cortex than most other periosteal responses. It most often is seen with aggressive tumors or severe trauma.

Codman’s triangle is another finding that occurs with very rapidly growing disease processes and frequently is attributed to neoplasia. It is caused by continued growth of the disease that elevates the periosteum again, lifting the newly formed bone away from the cortex. Codman’s triangle appears as a small, well‐defined, wedge‐shaped area of mineralization at the periphery of the lesion (Figure 5.18). The triangular‐shaped mineralization may be separated from the cortex by soft tissue opacity material (e.g., fluid, cells) or the mineralization may extend to the cortex. Because the margin associated with Codman’s triangle is well‐defined, the disease process may be erroneously diagnosed as inactive. But the triangle occurs at the periphery of the actual lesion and does not represent the true character of the disease.

Patterns of osteolysis

Patterns of bone destruction generally emphasize the sizes of the contiguous osteolytic lesions. However, it is the sharpness of the margins that is the key to determine aggressiveness. There are three classic patterns of osteolysis. From least aggressive to most aggressive, they are: geographic, moth‐eaten, and permeative. In many bone lesions, there is more than one pattern present. The most aggressive pattern determines the true nature of the disease process.

A geographic pattern of osteolysis refers to a larger area of bone loss, over 10 mm in size (Figure 5.19). It often is caused by a benign condition but can result from aggressive disease. Benign is differentiated from aggressive by the sharpness of the margin and the zone of transition between abnormal and normal bone. A well‐defined osteolytic margin suggests a slow‐growing lesion (e.g., bone cyst, benign tumor, pressure remodeling). In these cases, the area of bone loss may be surrounded by osteosclerosis, indicating that the body actually is “reacting” to the disease. A slow‐growing lesion may cause thinning or outward expansion of the adjacent cortex, but rarely will the cortex be disrupted. Geographic osteolysis with an ill‐defined margin and a longer zone of transition generally results from the coalescence of moth‐eaten and permeative osteolysis.

A moth‐eaten pattern of osteolysis appears as multiple smaller areas of bone loss, each about 3–10 mm in size. The margins usually are indistinct with a longer zone of transition from abnormal bone to normal bone (Figure 5.20). A moth‐eaten pattern tends to occur with more aggressive disease processes (e.g., neoplasia, osteomyelitis). The adjacent cortex may be thin and irregular in shape, sometimes with a disrupted border.

A permeative pattern of osteolysis appears as numerous, tiny areas of bone loss, 1–2 mm in size, with no clear distinction between normal and abnormal bone (Figure 5.21). These pinpoint lesions are caused by a very aggressive disease process (e.g., malignant neoplasia, severe osteomyelitis). They may be difficult to detect until a larger area of osteolysis has developed. The adjacent cortex often is thin and less distinct, or it may not be visible at all due to severe disruption by the disease.

Mixed patterns of osteolysis are common, especially with aggressive diseases (Figure 5.22). In many cases, osteolysis is a continuum of patterns, with permeative progressing to moth‐eaten and then to geographic bone loss. In the race between pathology and healing, one pattern may change to another as the disease process waxes and wanes over time. As long as the disease remains unchecked, bone destruction will continue, and margins will remain ill‐defined with a longer zone of transition.

Bone production

The formation of new bone may be associated with growth, healing, or metabolic disease. In radiographs, new bone production appears as increased opacity. Bone growth and development have been discussed. Bone healing generally involves a periosteal response, which also has been discussed. It is worth mentioning that bone healing includes an endosteal response, which is similar to a periosteal response but occurs along the inner surface of the cortex. Endosteal bone production tends to be less evident in radiographs than periosteal bone production.

A frequently encountered type of bone production is an exostosis. An exostosis is any abnormal mineralized structure that extends outward from the surface of a bone. The term is not specific to any condition or disease; however, exostoses are important to recognize, and they must be differentiated from normal prominences. The most common exostoses are osteophytes and enthesophytes, which are discussed in greater detail with joint disease.

Osteosclerosis is new bone production within the bony matrix. It leads to thicker trabeculae and smaller spaces between them, both of which increase bone opacity (Figure 5.23). Osteosclerosis is caused by an increase in mineral deposit, a reduction in the resorption of mineral, or both. It may be a localized attempt to heal a lesion, as the body tries to wall‐off or repair the damaged part of the bone, or it may be diffuse due to abnormal bone metabolism (i.e., osteopetrosis). In radiographs, localized osteosclerosis may appear as a rim of increased opacity adjacent to a bone lesion. It sometimes is seen in subchondral bone near a damaged joint. The presence of osteosclerosis can help differentiate osteomyelitis from osseous neoplasia because the body is much more likely to wall off an infectious agent than a tumor. Histopathology, however, usually is necessary for definitive diagnosis.

Osteopetrosis is a form of osteosclerosis that affects the entire skeleton. It results from decreased resorption of bone due to abnormal osteoclastic activity. In radiographs, the bones are relatively normal in length and profile but increased in opacity. The appearance has been described as “ivory,” “marble,” or “chalky” bones (Figure 5.24). The cortices are thickened and the medullary cavities are narrowed. The corticomedullary contrast is less distinct. In cancellous bone, the trabeculae become thickened and the spaces obscured by the increased mineral. Osteopetrosis is a rare congenital disease in dogs and cats. It results in brittle bones that lead to pathologic fractures and it causes anemia due to reduced bone marrow function.

Lead poisoning in young animals can produce thin, transverse lines of osteosclerosis in the metaphyseal regions of long bones. The lines form parallel to the physes and most often are seen in the distal radius and ulna. They also have been reported in the vertebrae. Chronic lead poisoning (plumbism) can lead to osteopenia.

Growth arrest lines are thin, transverse lines of osteosclerosis in the diaphyseal regions of long bones (Figure 5.25). They are caused by changes in the rate of growth in an immature bone, which may result from a systemic illness, dietary change, or other stressor. The lines are sharply‐defined and seen most often in the femurs, usually bilaterally. There is no soft tissue swelling, periosteal response, or evidence of active bone remodeling. The importance of growth arrest lines is their potential to mimic pathology, such as a fracture, bone infarct, or panosteitis.

Bone infarcts appear in radiographs as distinct foci of osteosclerosis that are irregular in shape with well‐defined margins (Figure 5.26). They most often are seen in the medullary region of a long bone, generally distal to the elbow or stifle. Bone infarcts usually are multiple and may be monostotic or polyostotic. They result from a localized loss of blood supply, typically caused by embolic disease (e.g., neoplasia, trauma, vasculitis, recent orthopedic surgery). Most infarcts are asymptomatic.

Bone loss

The loss of mineral from bone may be due to increased resorption, reduced deposition, or active bone destruction. Sometimes it is a combination of these. The term osteopenia means “too little bone” and is used to describe diminished bone opacity. Osteopenia may result from osteolysis, osteoporosis, or osteomalacia.

Osteolysis was discussed earlier as it pertains to the aggressiveness of bone lesions. Specifically, it is the pathologic destruction of bone that results in loss of both mineral and matrix. Causes of osteolysis include neoplasia, infection, and pressure necrosis.

Osteoporosis means “porous bone” and refers to the loss of bone mineral due to an imbalance between bone formation and bone resorption. Osteoporosis that affects the entire skeleton and is caused by a systemic disease, such as hyperparathyroidism. Osteoporosis in a single limb is caused by disuse (e.g., immobilization, pain, paralysis). Generalized osteoporosis tends to initially be more evident in the vertebrae, followed by the mandible and then the long bones. Osteoporosis in a single limb initially is more severe in the distal bones (e.g., distal epiphyses, cuboidal bones). Osteoporosis sometimes is called “bone atrophy” and leads to thin, weak bones that are prone to pathologic fractures (Figure 5.23).

Osteomalacia means “soft bone” and refers to the loss of bone mineral due to faulty ossification. The most common cause is a dietary deficiency (e.g., Vitamin D, calcium, phosphorous). Osteomalacic bones are soft, but many affected dogs and cats do not exhibit orthopedic signs of disease. In immature animals, osteomalacia is called rickets.

Osteoporosis and osteomalacia rarely can be differentiated in radiographs. The term osteopenia applies to both. Osteopenic bones are less opaque and there is less contrast between bone and soft tissues (Figure 5.27). The cortices become thin and faint, sometimes developing a “double cortical line” due to intracortical resorption of bone. Cancellous bone becomes more porous in appearance due to the larger spaces and thinner trabeculae, commonly described as a “coarse trabecular pattern.” Corticomedullary contrast is diminished.

Fractures

A fracture is a break or a discontinuity in a bone. It is caused by a physical force that exceeds the bone’s structural capacity. Fractures are more likely in bone that has been weakened by disease. Soft tissue swelling usually accompanies a fracture, especially in the acute stages, which is helpful to distinguish pathology from normal anatomy or an imaging artifact. Knowledge of sesamoid bones, accessory ossification centers, nutrient foramina, growth plates, and the normal shapes of bones is essential to avoid a misdiagnosis. Non‐displaced fractures may not be evident in initial radiographs but may be detected in a follow‐up study when a periosteal response develops or when the fracture line widens during healing or as a result of displacement. The radiographic description of a fracture should include the type of fracture, the parts of the bones involved, the degree of displacement and rotation, whether the fracture is articular, and an assessment of the adjacent soft tissues (Box 5.1).

Most fracture lines are less opaque than the adjacent bone. The fracture sometimes is more opaque than adjacent bone due to summation of overlying fracture fragments (e.g., compression fracture, folding fracture).

Incomplete fractures are those in which the cortex is broken on only one side and the bone is not in complete discontinuity. When the cortex is broken on the convex side, it is called a greenstick or hairline fracture (Figure 5.28). If the cortex is broken on the concave side, it is a folding, torus, or buckling fracture (Figure 5.29). An incomplete fracture in a fracture fragment is called a fissure fracture (Figure 5.31), which is important to identify because a fissure can become a complete fracture during reduction and repair. Stress or fatigue fractures are caused by repetitive cycling injuries that damage the bone at a rate faster than it can heal. An incomplete fracture may not be visible in radiographs unless the x‐ray beam is aligned with the fracture line.

Complete fractures are those in which the fracture line extends through the entire bone. A simple complete fracture consists of one fracture line and two fragments (Figure 5.30). In a complex complete fracture, there are multiple, non‐continuous fracture lines and more than two fragments (Figure 5.31). The fracture is comminuted if all of the fracture lines communicate at a single point. Comminuted fractures consist of three or more fragments. More than five fragments is considered highly comminuted. Fragments that are wedge‐shaped commonly are called “butterfly” fragments. In a segmental fracture, the fracture lines do not communicate and the result is one or more isolated segments of bone (Figure 5.32).

Fractures in paired long bones sometimes are accompanied by a luxation in the adjacent joint. A Monteggia fracture, for example, is a fracture in the proximal 1/3 of the ulna with a concurrent luxation of the radial head. It is important to identify the luxation prior to treating the fracture.

Closed fractures are those in which the overlying skin and soft tissues are intact. Open fractures occur when the overlying tissues are perforated (also called compound fractures). Open fractures usually are accompanied by subcutaneous emphysema and are at increased risk for infection (Figure 5.33).

T or Y fractures describe fractures in which the bone splits both longitudinally and transversely (Figure 5.34).

Avulsion fractures occur at attachment sites for ligaments, tendons, or joint capsules. A piece of bone is pulled away from main bone (Figure 5.35). The origin or “bed” of an avulsed fragment may be visible as a similar‐sized defect in the main bone.

Compression fractures are those in which the ends of the bone fragments are jammed into each other resulting in a shortened or collapsed bone. The fracture line may or may not be visible in radiographs. When visible, the line may be less opaque or more opaque than the adjacent bone. Compression or impaction fractures most often are seen in the vertebral bodies (Figure 5.210) and in the short bones in the carpus or tarsus.

Chip fracture is a descriptive term that means “knocking off a corner.” A small fragment is displaced from the main bone. Chip fractures occur most often in a short bone in the carpus or tarsus. They usually are articular. The site of origin or bed for the fracture fragment may or may not be identified.

Slab fracture is a descriptive term that means “knocking off a chunk.” As with chip fractures, they occur most often in a short bone in a tarsus or carpus. Slab fractures involve the articular surfaces on both ends of the bone. If the fracture involves only one articular surface, it is a chip fracture.

Shearing fractures are caused by severe friction or a glancing trauma, such as an animal being dragged on pavement. Also called abrasion fractures, these are open fractures due to loss of overlying soft tissue.

Pathologic fractures are caused by normal stresses on abnormal bone. They occur in bone that has been weakened by an underlying disease or a developmental defect. Disease may be systemic (e.g., osteoporosis) or localized (e.g., tumor, cyst). In radiographs, the bone opacity at or near the fracture site usually is diminished and a periosteal response may be present, earlier than expected for normal fracture healing (Figure 5.42). Pathologic fractures tend to occur at the periphery of the abnormal part of the bone.

Physeal fractures occur in immature bones. They are classified based on the degree of physeal, metaphyseal, and epiphyseal involvement using the popular method proposed by Salter and Harris (Table 5.3). The Salter–Harris classification ranks physeal fractures according to the increasing probability (from less likely to more likely) of a growth deformity during fracture healing.

	Dorsopalmar view of a normal immature dog carpus for comparison.		Type I physeal fracture involves only the physis; commonly called a “slipped physis.”
	Type II physeal fracture involves the physis and the metaphysis.		Type III physeal fracture involves the physis and the epiphysis; the fracture is articular.
	Type IV physeal fracture involves the physis, metaphysis, and epiphysis; the fracture is articular.		Type V physeal fracture is a compression fracture involving the entire physis.
	Type VI physeal fracture is a compression fracture involving only part of the physis; growth on the damaged side may slow or stop, while the other side grows normally.		Bony bridging on one side of the physis (arrow) can restrict or stop growth on that side, similar to the Type VI physeal fracture described above.

Fracture healing

Fracture healing may be primary or secondary. Primary healing occurs when the fragments are in close apposition and the cortex is reestablished without the formation of a callus. This requires rigid stabilization and excellent anatomic alignment. Secondary fracture healing is more common and involves callus formation and subsequent remodeling (Table 5.4).

0–5 days	5–10 days	10–20 days	20–30 days	40 days (6 weeks)
0–5 days: initial fracture with hemorrhage and soft tissue swelling; a hematoma forms. 5–10 days: the hematoma organizes into a soft tissue callus; the fracture line widens; the fracture ends are less distinct; soft tissue swelling diminishes. 10–20 days: mineral deposits from the periosteum and endosteum begin to mineralize the callus; the fracture line begins to narrow, but it is still visible; boney callus does not yet bridge the fracture fragments. 20–30 days: the fracture line is gradually disappearing; boney callus is more homogeneous and bridges the fracture site; the callus is becoming smoother with more defined margins. 40 days (6 weeks): the fracture line is barely visible, if at all; the boney callus is smaller, better‐defined, and nearly the opacity of the parent bone. 90 days and more: (no image) the boney callus matures and develops trabeculation; the medullary cavity is gradually reestablished; the cortical margins become more distinct. Over time, the bone continues to remodel and eventually resembles its original shape.

After a fracture occurs, bleeding from ruptured blood vessels results in a hematoma at the fracture site. The hematoma provides a temporary framework for subsequent healing. Within the framework, granulation tissue develops and a fibrocartilaginous callus forms, bridging the fracture fragments. This callus is soft tissue opacity and not visible in radiographs. It gradually becomes visible as mineral deposits are added from the periosteum and endosteum. The ends of the fracture fragments often become less distinct during early fracture healing due to active bone remodeling. The fracture line initially widens as bone is resorbed and then begins to narrow as bone is produced. As the fracture fills with mineral, it gradually disappears over the next 3–4 weeks. During this time, the callus continues to mineralize, increasing in opacity and making it better defined. Over the next few months, the new bone matures and develops trabeculation. The cortical margins become more distinct and the medullary cavity gradually is reestablished. The bone eventually resembles its normal appearance. Soft tissue swelling and emphysema that were present at the time of injury or introduced during open reduction and stabilization usually resolve during the first 5–10 days, unless there is an infection.

A fracture may be considered radiographically healed when the fracture line is no longer visible, the cortex is continuous and uninterrupted, and an ossified callus completely bridges the fracture fragments. Removal of fixation devices may be considered when there is radiographic evidence of a bridging bony callus.

Fracture complications

Multiple factors affect fracture healing, including the blood supply, the alignment and stability of the fracture fragments, and the overall health of the patient.

An adequate blood supply is important to callus formation and periosteal/endosteal bone production. A loss of blood supply may be due to severe tissue damage or removal of the hematoma. Intramedullary implants can disrupt endosteal blood supply and delay healing. Prolonged disuse of a fractured limb can lead to reduced blood flow and delayed healing.

The apposition of the fracture fragments is important to healing. In general, at least 50% contact between bone fragments is needed for efficient healing. Spiral and oblique fractures tend to heal faster than transverse fractures due to the increased area of contact. The smaller the gap between fragments and the less movement at the fracture site, the quicker the bone will heal. Some bones naturally heal more slowly than others (e.g., distal radius, ulna, tibia).

Delayed union is fracture healing that takes longer than expected, but the bone eventually heals, both clinically and radiographically. Although no definite timetable exists, healing generally is considered delayed if bridging callus is not evident within 6–8 weeks (Figure 5.36).

Nonunion occurs when fracture healing stops before there is complete union. A fracture generally is considered a nonunion when there is no progression of callus formation after 6 months, and no further healing is expected unless intervention occurs. In radiographs, there is no evidence of active bone remodeling for several weeks; the fracture margins remain sharp and well‐defined (Figure 5.37).

A hypertrophic nonunion results from chronic instability at the fracture site that prevents callus from bridging the fragments. Organized but inactive new bone builds up at the ends of the fracture fragments. The new bone tends to flair out from the cortical ends. In some cases, the ends of the fragments appear to “fit together” because of motion (e.g., one end becomes convex and the other concave) but there is a gap separating the fragments.

An atrophic nonunion occurs when the fracture fragments are chronically separated. There is no callus formation. The ends of the fragments appear thin and tapered due to bone resorption. Atrophic nonunions occur more often in small breed dogs and usually are accompanied by disuse osteopenia in the affected limb.

A dystrophic nonunion is caused by loss of blood supply to one or both fragments. The end of the affected fragment remains sharp, well‐defined, and pointed due to a lack of bone remodeling. If the blood supply is only diminished and not completely lost, some remodeling may occur and the fracture ends may appear more rounded and sclerotic (called a nonviable nonunion). Complete loss of blood supply is called a necrotic nonunion.

Malunion fractures are those that are healed but with abnormal bone geometry (Figure 5.38). Abnormal geometry can lead to increased stress at the proximal or/and distal joint and may impair limb function. The healed bone fragments may be angled, rotated, shortened, or otherwise malaligned. Comparison radiographs of the contralateral limb may be useful to assess the degree of limb deformity.

A sequestrum is a fragment of bone that is no longer viable due to loss of its blood supply. It appears as a sharply‐defined, sclerotic piece of bone that is not incorporated in the callus and exhibits little or no remodeling (Figure 5.39). A sequestrum may be located within its bone of origin or separate from it. Fragments that remain in the bone sometimes are located in a lacuna, which is a pocket of necrotic soft tissue. The lacuna often is surrounded by a rim of sclerotic bone called an involucrum. In some cases, a draining tract extends from the involucrum to the skin surface where it opens as a cloaca. The tract may be demonstrated in radiographs using fistulography (Figure 2.96). Sequestra are more likely to occur as a complication of osteomyelitis or in a necrotic nonunion, and rarely with neoplasia (i.e., osteosarcoma).

A pseudoarthrosis or “false joint” sometimes develops at a nonunion fracture site. It occurs when the fibrocartilage between the fracture fragments forms into a capsule that fills with serum. The pseudoarthrosis may allow the patient some use of the limb.

Occasionally a bone fragment will fuse to an adjacent bone. This is called a synostosis and can result in loss of movement.

Physeal injuries and limb deformities

Any physis in any bone can be injured and may lead to a growth deformity in the bone. The degree of the deformity depends on the age of the animal at the time of injury, which physis was affected, and the severity of the damage. Physeal injuries that lead to limb deformities may be unilateral or bilateral. Bilateral conditions may or may not be symmetrical.

Damage to a physis most often is due to trauma. The traumatic incident may or may not be known at the time of diagnosis. The younger the patient when the damage occurs, the greater the potential for limb deformity. In many cases, the severity of physeal damage is not evident until bone growth stops (i.e., all the physes are closed). Therefore, the earlier a damaged physis is detected, the greater the possibility for successful treatment.

Physeal damage affects the rate of bone growth. If the entire physis is damaged, growth may either be delayed or stopped completely. If only part of a physis is damaged, that side may grow more slowly than the other. Abnormal rates of growth are most significant when paired bones are involved (i.e., radius and ulna, tibia and fibula). It is important to realize that complete cessation of long bone growth is not necessary to produce a limb deformity, merely a differential in the rate of growth between the two bones. Asynchronous growth can lead to abnormal shortening, bowing, and angulation of one or both bones. Limb deformities can lead to abnormal joint stresses, subluxation, and degenerative joint disease. Clinical signs tend to be more significant in young, large, and giant breed dogs due to their greater and faster bone growth. Certain dog breeds are deliberately bred to exhibit asynchronous growth as a desired trait (e.g., Bassett Hound, Dachshund).

In radiographs, the damaged part of a physis may or may not be visible. When visible, the damaged physis typically appears thinner and more opaque than the other physes, a finding commonly referred to as “premature closure” of the physis. Note: be cautious when interpreting subtle signs of a thinner, more opaque than expected physis because the normal physes can vary in appearance, even when comparing contralateral limbs. Experience is needed to recognize normal physeal variations and avoid overdiagnosis. Serial radiographs sometimes are needed. The important point is to carefully inspect the physes in a deformed limb to determine whether physeal damage and asynchronous growth might be the cause of the deformity. Asynchronous growth is discussed in greater detail in this chapter with Congenital and Developmental Abnormalities. If a physis is not visible at all, it likely is “closed,” and no further growth should be expected from that site.

Osteomyelitis

Inflammation of bone tissue is called osteitis. If inflammation includes the medullary cavity, it is called osteomyelitis. Inflammation sometimes starts in the medullary cavity, especially if the cause is hematogenous in origin. If due to a penetrating wound, inflammation can start anywhere from the skin to the medullary cavity.

Osteomyelitis most often is caused by an infection, either bacterial, mycotic, or protozoal. Infection may be monostotic (all lesions in one bone), regional (all lesions in one limb), or polyostotic (lesions in multiple bones and multiple limbs).

The earliest radiographic sign of osteomyelitis is soft tissue swelling. Bone lesions may become visible after about 1–2 weeks, sometimes sooner in very young animals. Bone lesions caused by active inflammation typically appear as an ill‐defined periosteal response. Osteolysis may develop if inflammation remains active and unchecked by either body defenses or appropriate therapy. Bone weakened by osteolysis is susceptible to pathologic fracture. In chronic cases, osteosclerosis surrounds the lytic areas as the body attempts to wall‐off the infection. Osteomyelitis, whether due to a bacterial or mycotic infection, rarely extends into the joints.

Bacterial osteomyelitis tends to stimulate a greater periosteal response than a mycotic infection or a tumor.

Elevation of the periosteum is caused by subperiosteal accumulation of fluid (e.g., purulent, hemorrhagic, serous). In radiographs, the subperiosteal fluid may separate the periosteal new bone from the underlying cortex. Bacterial infections tend to result in a more rapid accumulation of subperiosteal fluid which can spread proximally and distally along the diaphyses of the long bones (Figure 5.40). In some cases, the entire diaphysis will be involved.

Bacterial osteomyelitis typically affects a single limb, but multiple bones in that limb may be involved (Figure 5.41). Bacterial infection can result from a penetrating wound, extension of an infection in the adjacent tissues, or hematogenous spread. Polyostotic bacterial infections are less common, typically resulting from a systemic infection. Lesions can occur in any part of any bone, but they are more likely in areas with a rich blood flow, such as the metaphyses in immature animals and the vertebrae and ribs in older animals. Occasionally a bone abscess develops, appearing as a focal, sharply marginated area of decreased opacity. Chronic infections can lead to development of a fistulous tract.

Mycotic osteomyelitis usually is hematogenous in origin and polyostotic in distribution. Mycosis in a single bone is uncommon, but when it occurs the ends of the bone (metaphyseal or epiphyseal region) are more likely to be affected. Mycotic infection at the end of a bone often is indistinguishable from a bone tumor, although mycoses tend to more osteoproductive and neoplasms more osteolytic. Mycotic osteomyelitis tends to produce a smaller and better defined periosteal response that bacterial infections and rarely involves the entire diaphysis, as often is seen with bacterial infections. Fungal infections typically grow more slowly and periosteal elevation is more gradual.

Mycotic osteomyelitis is more common in endemic regions. It is reported more often in dogs than in cats, particularly in young adult, large‐breed dogs used for hunting. Animals that are immunocompromised are at increased risk.

Protozoal osteomyelitis is uncommon in dogs and cats. Parasites that may infect bone include hepatozoonosis, leishmaniasis, and neosporosis. Protozoa may enter bone via hematogenous spread or from the adjacent soft tissues. Lesions usually are polyostotic and aggressive. Any bone may be affected, but the long bones most often are involved. Periosteal new bone may be ill‐defined (active process) or well‐defined (inactive disease) and varies in appearance from smooth and laminar to very irregular and proliferative.