Bones – General PDF

Chapter 7 Bones – general Robert M. Kirberger minerals as well as haemopoietic tissue. Bone is relatively Terminology...

Chapter 7 Bones – general Robert M. Kirberger minerals as well as haemopoietic tissue. Bone is relatively Terminology light with a high tensile and compressive strength and at CT Computed tomography the same time retains an appropriate degree of elasticity. DECT Dual-energy computed tomography The bone surface, except where there is articular carti- DEXA Dual-energy X-ray absorptiometry lage, is covered by the periosteum. The periosteum con- MRI Magnetic resonance imaging sists of an outer fairly vascular connective tissue layer, which is attached to the underlying cortex by collagenous Sharpey fibres. The inner surface of the cortex is lined by endosteum, which is also made up of connective tissue. Between each of these layers and the underlying cortical Normal bone formation and bone there is a layer of osteoprogenitor cells and osteo- anatomy blasts that are required for osteogenesis. A long bone can be divided into several regions. The Bone is a dynamicfigorgan 2.1 that is constantly being renewed shaft, or diaphysis, has a distinct cortex and medulla and remodelled. It is responsive to mechanical stimuli and (Figure 7.1). The cortex is made up of compact bone and to metabolic, nutritional and endocrine influences. It acts should have smooth outer (periosteal) and inner (endo­ as a storage reservoir for calcium, phosphorus and other steal) surfaces, and should remain approximately even in Epiphyseal vessels from joint capsule Zone of resting or germinal cells Zone of proliferating cells Epiphysis Zone of maturing cells and columnation Physis Zone of hypertrophying vacuolated cells Metaphysis Zone of provisional calcification Zone of vascular invasion and ossification Diaphysis Vessels from tendons Nutrient vessel Metaphysis Epiphyseal vessels from joint capsule Epiphysis 7.1 Schematic representation of the different regions and blood supply of a long bone in an immature (top) and mature (bottom) long bone. Delivered by BSAVA to: 75 University College Dublin (7442) BSAVA Manual of Canine and Feline Musculoskeletal Imaging, second edition. Edited by Robert M. Kirberger and Fintan J. McEvoy. ©BSAVA 2016 IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04 BSAVA Manual of Canine and Feline Musculoskeletal Imaging thickness. A clearly defined channel may be seen running cartilage contributes to the growth of the epiphyses by at an angle through the cortex, usually from the periosteal endochondral ossification. There may be additional non- surface proximally to the endosteal surface distally articular cartilaginous protuberances, which ossify and (although this direction is reversed in the ulna). This is the form sites of attachment for tendons and ligaments. nutrient foramen, which provides passage for the blood These secondary centres of ossification are termed vessels going to and from the medulla. The nutrient fora­ apophyses; in the young animal (Figure 7.2) they are mina are most commonly seen in the long bones of larger sep­ arated from the main diaphysis or metaphysis by dog breeds and must not be mistaken for incomplete a radiolucent cartilaginous band, but they fuse in the fractures. The central medullary cavity has a reduced mature animal. opacity compared with the cortex, although the opacity is The blood supply to bones varies with the type of still usually greater than that of surrounding soft tissues. bone. In the immature long bone the physis is essentially Towards the end of each long bone is the metaphysis. The avascular, with the epiphysis and metaphysis supplied distinction between the cortex and medulla becomes less independently. Epiphyseal blood supply is mainly via clear here because of thinning of the cortices and the the joint capsule, and metaphyseal blood comes via the increasing amount of cancellous bone with its clear tra- vessels passing through the nutrient foramen (see Figure becular pattern. The main function of the cancellous bone 7.1). Vessels in both locations send branches towards the is to support the subchondral bone and transmit mechan­ physis with the metaphysis being particularly blood rich, ical forces to the diaphyseal cortex. Each end of the long making it the preferred location for haematogenous osteo- bone is termed the epiphysis and has an articular surface myelitis in the immature animal. The vertebral body can consisting of subchondral bone covered with cartilage. also be considered as a long bone with a central nutrient The radiopacity of the latter is uniform, and it is radiolucent foramen in the mid-body and numerous smaller vessels relative to bone. It does not contrast with synovial fluid and supplying the epiphyseal region. The neural arch is a flat is not seen as a discrete layer on radiographs. Between bone and, like other flat bones, has an extensive blood the epiphysis and metaphysis is the physis, or growth supply via numerous small nutrient foramina. plate. In the immature animal the growth plate is active and The periosteal blood supply is extensive in immature appears radiographically as a radiolucent band. As the bones to accommodate the intramembranous bone animal matures the physis disappears, although a faint formation, which increases cortical bone thickness. How­ radiopaque line, the physeal scar, may remain visible at the ever, in mature skeletal bone the periosteal blood supply site (for physeal closure times see Chapter 8). Besides is vesti­gial; blood supply is mainly via the nutrient artery long bones there are also short and irregular bones that as well as via the metaphyseal arteries, which anas­ have a cortex of compact bone with a central cancellous tomose with the nutrient artery. This medullary blood bone component, and flat bones. supplies the full thickness of the cortex except at sites of Most of the bones of the skeleton develop from a carti- fascial attachment, where the outer third of the cortex can lage model, which is converted over time to bone by endo- be supplied by arterioles entering by way of the fascial chondral ossification until in the adult only articular attachments. Medullary blood supply to the cortex is cartilage remains. Flat bones, particularly those of the normally centri­fugal, with cortical venous drainage taking skull, are formed by intramembranous bone directly from place via the periosteum and medullary drainage via the connective tissue. Bone development starts in utero with nutrient foramen. the formation of midshaft hyaline cartilage centres, which undergo endochondral ossification to form ossification ML view of the radius and 7.2 centres. These are surrounded by perichondral bone, the ulna from an immature first compact bone in the fetus. At birth, all the trabecular large-breed dog. Note the cutback bone of the ossification centres has been resorbed and zone of the distal ulnar metaphysis (arrowed) and the olecranon apophysis replaced by bone marrow. However, peripherally in the (*). metaphyseal region the lattice-like trabeculation remains. The physis (or growth plate) is responsible for the growth in length of the bone towards the diaphysis. The growth plate has distinct zones characterized by alter­ations in chondrocyte morphology (see Figure 7.1). Chondrocytes start as resting cells, which then proliferate and mature, forming columns. Here the cells hypertrophy, vacuolate and then undergo provisional calcification. Blood vessels and osteoprogenitor cells invade the cal­ cified longitudinal septa, and the osteoprogenitor cells differentiate into osteoblasts, which then lay down the bone matrix (osteoid). As the bone matures the osteoid becomes mineralized. Osteoid formation decreases with time and the osteoblasts become entrapped in the new bone to become osteocytes. Osteocytes form the majority of cells in mature compact bone and are interconnected by canaliculi and Volkmann’s canals to form the osteon or Haversian system. Osteoclasts are large multinucleated cells that are responsible for bone resorption by eroding mineralized bone. Bone formation and resorption are regu- lated systemically by parathyroid hormone, calcitonin and vitamin D (see Chapter 8). At predetermined times after birth, secondary ossifi- cation centres develop in the epiphyses. The articular Delivered by BSAVA to: 76 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04  Chapter 7 · Bones – general Modelling of bone is the process of moulding the bone to its functional adult shape and occurs particularly in growing bones. In the metaphysis the wide physeal region is modelled to the narrower diaphyseal bone by means of active subperiosteal osteoclastic activity. This results in a ‘cutback zone’, which is often quite irregular and must not be mistaken for pathology (see Figure 7.2). Re­- modelling of bone is the constant process of bone renewal by resorption and formation of new bone at endosteal and periosteal surfaces as well as at the osteonal surface. In pathological conditions an imbalance occurs between bone resorption and formation. Alternative imaging techniques 7.3 Polyostotic bone pathology involving both femoral shafts due to haematogenous fungal osteomyelitis. For information on alternative imaging techniques see Chapters 2 to 5. Bone mineral density is used in humans to detect Predilection sites for various conditions are common, osteoporosis but to date its measurement has not found and may be a specific bone or a region within that bone. much use in a small animal clinical setting. Dual-energy Some examples are: X-ray absorptiometry (DXA or DEXA) is the traditional method used to detect bone mineral density in humans Hypertrophic osteopathy results in periosteal reactions but cannot be done using routine X-ray equipment. Two starting distally in the limbs and then extending X-ray beams with different energy levels are used and the proximally (see Chapter 9) soft tissue X-ray absorption is subtracted from the whole Panosteitis affects the medulla of long bones, often body absorption, leaving the amount of X-rays absorbed starting in the region of the nutrient foramen (see by the bone, from which bone mineral density can be cal- Chapter 8) culated and expressed as grams per centimetre squared Growth abnormalities are often most marked at those (g/cm2). Quantitative CT can also be used to determine a physes that contribute the most to the overall length of volumetric bone mineral density (in cm3) and can separate a bone, and the distal radius and ulna will thus be cortical and trabecular bone densities. More recently, affected first (see Chapter 8) dual-energy CT (DECT) has come into use, but it requires Osteosarcoma favours the metaphyseal region of bone very expensive dual-head CT machines. With conven- because of the good blood supply and high metabolic tional CT, bone density can be calculated with minimal activity of these regions. Specific bones are commonly additional effort for patients undergoing CT examinations involved and include the distal radius and proximal for other medical problems. However, if a CT scan is humerus (see Chapter 9) performed specifically to quantify bone mineral density, it Prostatic neoplasia may metastasize to the caudal lumbar vertebrae (see Chapter 21). requires the use of a bone densitometry phantom and higher radiation exposure than required by DEXA. Aggressive versus non-aggressive changes The exact aetiology of specific radiological changes can Abnormal imaging findings rarely be determined from a radiograph alone. However, the type of lesion may assist in shortening the list of differential diagnoses. This is typically done by determining the aggres- Bone has limited response mechanisms when subjected to siveness of a lesion. An aggressive lesion is one with rapid pathological processes. Bone alignment or length may bony change where there is minimal time for the bone to be altered. More commonly, there may be a break in the respond and remodel. A non-aggressive lesion is a benign, continuity of the bone (see Chapter 10) or bone mass may slow-growing, more chronic process with time for bone to be increased or decreased. remodel. In between these two extremes lies a wide spec- trum of possible radiological changes. Aggressiveness can Classification of pathology be characterized by evaluating new bone production, bone loss or destruction, cortical changes and the rate at which Lesion distribution within the skeleton may be: change takes place. Varying degrees of aggressiveness may be present at the same time and the pathology is Monostotic – involving a single bone (e.g. an classified according to the most aggressive component. osteosarcoma) Polyostotic – multiple bones are involved (as seen with multiple myeloma or haematogenous osteomyelitis; New bone production Figure 7.3) Increased bone opacity may be: Focal – may involve a specific bone region (e.g. the metaphysis) Artefactual – due to superimposition of structures. This Generalized – involving all bones (as may be seen with could be one bone abnormally superimposed on metabolic conditions) another (e.g. often seen with fractures; Figure 7.4) or a Symmetrical (e.g. metaphyseal osteopathy) superficial soft tissue structure superimposed on bone Asymmetrical (as seen with a traumatic premature (e.g. a teat superimposed on the wing of the ilium on a physeal closure). ventrodorsal (VD) abdominal view) Delivered by BSAVA to: 77 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04 BSAVA Manual of Canine and Feline Musculoskeletal Imaging pathology (Figure 7.6). A fibrous matrix results in woven bone production. Initially the lesion will be radiolucent, but it changes to a more ground-glass appearance as bone is produced (Figure 7.7). Mineralization of a cartilage matrix has a stippled appearance which, when replaced by endo- chondral bone, develops circular or semicircular opacities. This process is typically seen in chrondrosarcomas. (a) (b) Artefactual increase in bone opacity due to superimposition 7.4 of fracture ends. (a) Craniocaudal (CrCd) view of the tibia with (a) (b) two transverse lines of increased opacity in the tibial diaphysis. (b) The ML view shows slight over-riding of the tibia fracture edges. Real – due to new bone production originating in the medulla, trabecula, endosteum or in the periosteum, individually or together. This may be monostotic or polyostotic. Generalized increased opacity is rare but is seen with osteopetrosis (see Chapter 8). According to Dobson and Friedman (2002), the radio- graphic features of localized new bone production (osteo- sclerosis in the medullary cavity) are dependent upon the nature of the matrix within which mineralization occurs. The matrix may be composed of osteoid, fibrous or carti- laginous tissue. An ivory-like opacity is seen with complete (c) (d) mineralization of the osteoid matrix, for example in osteo- Osteosarcoma of the distal tibia. (a) ML view of the distal tibia. mas (Figure 7.5). 7.6 Fairly solid periosteal reactions, permeative to moth-eaten Osteosarcoma may produce intra- or extramedullary lysis and neoplastic endosteal medullary new bone are seen at level b. osteoid, and the amount of mineralization of the osteoid (b–d) Transverse CT images made at the locations shown in (a). The fibula is on the left of the image and cranial is to the top. Note the will determine the opacity of the neoplasm. Intramedullary medullary new bone formation and solid periosteal reaction thickening osteoid may be difficult to appreciate on survey radio- the cortex in (b). In (c) and (d) the periosteal reaction ranges from thick graphs, particularly if there is a superimposed periosteal lamellar to immature solid. Note that medullary new bone clearly seen reaction. Here, cross-sectional imaging techniques, and in on the CT images is difficult to appreciate on the radiograph. Image (b) is particular CT, allow visualization of the intramedullary in a soft tissue window and (c) and (d) are in a bone window. ML view of a skeletally 7.7 immature canine distal radius and ulna with a fibrous cortical defect (ossifying fibroma) of the caudal metaphyseal ulna. The fibrous matrix results in the radiolucent defect, which will eventually fill up with bone. An ivory-like opacity is seen with complete mineralization of 7.5the osteoid matrix in an osteoma of the frontal bone. The radiograph was deliberately underexposed to show the peripheral pathology. Delivered by BSAVA to: 78 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04  Chapter 7 · Bones – general Endosteal and medullary osteosclerosis may occur with chronic osteomyelitis, or on the margins of an expan- sile neoplastic process, with panosteitis, bone infarction and neoplastic new bone formation (see Figure 7.6). Bone infarction in dogs may be associated with primary malig- nant neoplasia, particularly osteosarcoma (see Chapter 9). It has also been described in cats with feline leukaemia. All or most bones distal to the mid-femur are usually affected. Periosteal new bone formation usually takes place secondary to injury. The reactions are additions to the under­ lying cortex rather than replacements for the loss of cortical bone. However, the cortex may also be pen­ etrated by pathological processes originating from the medulla via enlarged Volkmann canals and Haversian spaces. This process may elevate the periosteum. Periosteal reactions (Figure 7.8) may be classified as con- tinuous or interrupted. The latter suggests an aggressive process. Types of periosteal reaction, from least to most aggressive, are as follows: Solid periosteal reaction Lamellar (parallel) periosteal reaction Lamellated periosteal reaction Brush-like periosteal reaction Sunburst periosteal reaction (a) (b) Amorphous bone production. (a) Focal anaerobic osteomyelitis of the caudal ulna with a 7.9 mature solid periosteal reaction. (b) Hypertrophic osteopathy Solid periosteal reaction: The periosteum is slowly lifted with immature solid periosteal reactions on the abaxial surfaces of over a period of time while laying down new bone. A solid metatarsals II and V. periosteal reaction may also develop from a lamellar reac- tion. The surface may be smooth, undulating or irregular and the opacity of the reaction is indicative of its duration. reactions are indicative of slow-growing benign processes. The more radiopaque the periosteal reaction, the longer Typical causes are fracture callus, chronic osteomyelitis it has been present (see Figure 7.6 and Figure 7.9). Solid and panosteitis. On the periphery of more aggressive perio­steal reactions (see below) the periosteum is lifted fig 2.8 more slowly and a triangular solid periosteal reaction known as a Codman’s triangle is often seen (see Figure Lamellar 7.15). It is usually present on the diaphyseal side of a meta- Solid Lamellated (parallel) physeal lesion and acts as a buttress for the cortex, which may have been partially or totally destroyed adjacent to it. It is often associated with malignant neoplasia but may also be seen with a variety of other causes. Lamellar (parallel) periosteal reaction: The periosteum is lifted by subperiosteal exudate, haematoma or, rarely, neoplastic cells. The periosteum produces a thin line of new bone which may be continuous, straight or undu­ lating and is separated from the underling cortex by a radiolucent line (Figure 7.10). This radiolucent line is better defined on CT (see Figure 7.6cd). With time the Continuous periosteal reactions radiolucent space between the thin line of new bone Amorphous and the cortex becomes filled with new bone, resulting Thick brush-like Thin brush-like Sunburst bone production in a solid periosteal reaction. The reaction is usually associated with a benign process. Lamellated periosteal reaction: This reaction is also known as an onion skin periosteal reaction and indicates a fairly slow process but it is more aggressive than the above two reactions. The periosteum is lifted repeatedly over a period of time by sequential insults. The reaction may be seen with osteomyelitis, particularly that of fungal origin, as well as with malignant neoplasia (Figure 7.11). Brush-like periosteal reaction: The periosteum is lifted Interrupted periosteal reactions fairly rapidly over an extensive area of the cortex with osteoblastic activity along the vertically orientated Schematic representation of periosteal reactions from least to Sharpey’s fibres. If the reaction is less aggressive and 7.8 most aggressive. slower growing, the spicules are thicker and it is known as Delivered by BSAVA to: 79 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04 BSAVA Manual of Canine and Feline Musculoskeletal Imaging Focal soft tissue Thick brush-like 7.10 swelling and lamellar 7.12 periosteal periosteal reaction cranially on reaction on the abaxial the radius. Radiograph surface of metacarpal V in a deliberately underexposed. dog with hypertrophic osteopathy. Post-mortem 7.11 specimen of a proximal femur with fungal osteomyelitis resulting in a Thin brush-like lamellated periosteal 7.13 periosteal reaction. reaction of the abaxial surface of metatarsals II and V in a case of hypertrophic osteopathy. a thick brush-like or palisade periosteal reaction (Figure 7.12). The thinner the reaction (thin brush-like or spiculated periosteal reaction), the more aggressive the process because there is less time for new bone production. This is more likely to be seen in neoplasia and acute haemato­ genous osteomyelitis but may also be seen in hypertrophic osteopathy (Figure 7.13). Sunburst periosteal reaction: This reaction is indicative of a highly aggressive process, and an osteosarcoma is the most likely cause although other neoplasms may also be involved occasionally. The periosteum is lifted rapidly over a focal area, resulting in a dome shape. The Sharpey fibres now have a radiating distribution with osteoblastic activity along the radiating fibres. Some of the new bone produced may also be neoplastic in origin (Figure 7.14). Amorphous bone production: This is not a periosteal reaction but neoplastic new bone production seen best beyond the confines of the periosteum, which has been destroyed. The amorphous bone may also be more cen- trally located but is then difficult to distinguish as such. The new bone may have a cotton wool or candyfloss appearance. Amorphous bone is highly suggestive of an Osteosarcoma of the frontal bone with a sunburst periosteal osteosarcoma (Figure 7.15). 7.14 reaction. Delivered by BSAVA to: 80 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04  Chapter 7 · Bones – general Proximal tibial CrCd view of the distal 7.15 osteosarcoma 7.16 radius of a dog with an with amorphous bone elongated radiolucency in the formation seen lateral to the distolateral radius adjacent to the proximal fibula. A solid ulna, which correlates to the soft periosteal reaction tissue depression seen in this region (Codman’s triangle, arrowed) of the limb. is present on the lateral cortex of the proximal tibial diaphysis. Bone loss or destruction Reduced bone opacity may be: Artefactual, due to: Superimposition of gas Superimposition of a defect in the superficial soft tissues A focal reduction in soft tissue thickness, e.g. of the Disuse osteoporosis of distolateral radius (Figure 7.16) 7.17 the manus. The Mach effect, which is a curious physiological phenomenon whereby the perception of edges is enhanced through exaggeration of local contrast (Grandage, 1976). Mach lines are optical illusions which mimic hairline fractures where two bones overlap. This is most commonly seen in extremity radiographs that have high contrast. Typical locations are the superimposing tibia and fibula, as well as the metacarpal and metatarsal bones (see Chapter 9). Real, due to generalized or focal bone loss. Increased osteoclast activity, stimulated by a pathological process (pressure and hyperaemia), results in bone destruction. This becomes radiologically visible only after 30–50% of bone is lost. This process will usually take at least 7–10 days and the only radiological evidence of possible pathology in this period may be soft tissue changes (see Chapter 6). A generalized decrease in bone radiopacity is known as osteopenia and is due to a reduction in bone mass. This may be due to osteoporosis or osteomalacia. Osteo­ porosis is bone atrophy, and this implies that there is less bone than normal but the composition of the bone that is present is normal. The number of trabeculae, how- ever, will be decreased and the remainder appear coarser and the cortex thinned. This may affect a single bone or Focal bone loss involves cancellous or cortical bone limb (e.g. with a fracture (Figure 7.17) or primary bone but is more readily seen in the latter owing to the greater neoplasm resulting in disuse atrophy), or involve the contrast. Lysis is a result of increased osteoclastic activity whole skeleton, when metabolic disease is more likely. secondary to the pathological insult. Focal bone destruc- Osteomalacia is a decrease in bone mass with con­ - tion may be classified as follows (Figure 7.18): co­mitant disturbance in bone composition due to insuffi- cient or abnormal osteoid mineralization. Osteomalacia Geographic lysis may affect the entire skeleton and is usually also of meta- Moth-eaten lysis bolic origin (see Chapter 9). Permeative lysis. Delivered by BSAVA to: 81 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04 BSAVA Manual of Canine and Feline Musculoskeletal Imaging Geographic bone lysis 7.19 of the distal fourth Geographic lysis Geographic lysis metatarsal bone. Note also the – least aggressive – more aggressive cortical thinning and expansion. Moth-eaten lysis Permeative lysis Graphic representation of focal bone destruction from least 7.18 to most aggressive. Geographic bone lysis: Geographic bone lysis is the least aggressive form of lysis and is generally seen with slower- (a) (b) growing lesions. It is usually seen in cancellous bone at the extremities and consists of a single or several large Proximal tibial ossifying 7.20 fibroma with more radiolucent areas, cortical expansion and thinning (Figure aggressive geographic bone lysis 7.19). There is usually a sclerotic rim and possibly sclerotic than in Figure 7.19. There is still a septa, as seen in osteoclastomas and enchondromas. If large focal lytic lesion but with there is no sclerotic rim and the margin is well defined the cortical destruction (white arrows) lesion is more aggressive and is known as a ‘punched out’ and minimal sclerosis. (a) ML view; lesion. Peripherally the cortex may be destroyed (Figure (b) CrCd view; (c) sagittal ultrasonographic image over the 7.20). This is typically seen in multiple myeloma and medial aspect of the tibia with the metastatic bone disease. The margin of the lytic area is white arrows corresponding to narrow and the transitional zone between affected and those in (b) and the black arrow normal tissue is also narrow. A slightly wider and more indicating the normal solid cortex indistinct margin is an indication of a more rapidly growing more distally. Note that the lesion and thus more aggressive lesion that is locally infiltrative, has not extended into the adjacent soft tissues and that the thin such as a fibrosarcoma. remnant cortical bone allows transmission of the sound waves into Moth-eaten bone lysis: There are multiple separate foci the subcortical neoplastic tissue (*). of lysis, usually slightly greater than 2–3 mm in diameter, with more ill-defined and wider margins than geographic bone lysis (Figure 7.21). These are typically seen in (c) the cortex because of greater contrast and are usually Delivered by BSAVA to: 82 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04  Chapter 7 · Bones – general 7.21 Proximal Permeative bone lysis: Permeative lysis is the most humerus aggressive form of bone destruction and is seen with osteosarcoma in an rapidly growing lesions. Numerous lytic areas, 1–2 mm in 11-year-old dog. Note the areas of moth- diameter, with poorly defined borders are seen in the eaten lysis and cortex and there is a wide indistinct transitional zone minimally displaced (Figure 7.23). Permeative lysis is often associated with pathological fracture. cortical scalloping or defects (see below). Osteolytic osteo­ The focal lytic area at sarcomas and haematogenous osteomyelitis are likely to the caudal show permeative lysis. supraglenoid tuberosity is unlikely to be part of the ML view of the 7.23 proximal tumour. humerus with a highly aggressive osteosarcoma and pathological fracture. Note the permeative lysis in the proximal diaphysis extending into the meta- and epiphyseal regions where the foci of fig 2.22 lysis coalesce to form a large lytic defect. endo­ steal in origin (Figure 7.22). These lesions have intermed­iate aggressiveness and may be accompanied by visible cortical destruction. The transitional zone between fig 2.22 affected and non-affected bone is fairly wide. The lytic areas may eventually coalesce. Endosteal Subperiosteal scalloping scalloping Cortical changes Cortical changes may also be indicative of the aggressive- ness of a lesion. Slow-growing processes tend to expand Endosteal Subperiosteal scalloping scalloping the cortex, whereas more rapid changes will erode or destroy the cortex. Cortical expansion: Geographic bone lysis is often seen with an associated expanding cortex that may also be thinned. The expansion results from endosteal resorption due to pressure from an impinging growth or hyperaemia, and may be accompanied by periosteal new bone form­ ation. Eventually the whole cortex may be destroyed with only a shell of periosteal new bone remaining (see Figure 7.19). The shell may be thick, thin or, if there is a focal (a) variation in growth rate, lobulated. Cortical scalloping: These are focal erosions of the cor- tex due to moth-eaten or permeative lysis. Intramedullary neoplasia results in endosteal scalloping, which destroys a more and more of the cortex towards the centre of the neoplasm (see Figures 7.21 to 7.23). Subperiosteal scalloping is usually associated with haematogenous c osteomye­litis where the exudate oozes from the medulla through the Volkmann’s canals to the subperiosteum, which is elevated, and stimulates osteoclasts to resorb a b bone subperiosteally (Figure 7.24). Cortical defects: Endosteal scalloping may eventually (b) c result in a cortical defect, which is often associated with Schematic representation of the location of lysis in cortical a cortical spike (Figures 7.25 and 7.26). This is a sign of a 7.22 bone destruction (e.g. moth-eaten or permeative) and highly aggressive lesion. Cortical defects may also occur b Lateral view of a long-bone diaphysis. The lytic areas scalloping. (a) with chronic osteomyelitis, owing to cloaca formation. appear to be in the medulla but are in the superimposed cortex. Here, the cortical edges are rounded, indicative of a less (b) Cross-section of the bone in (a). The lytic areas are actually in the cortex but are superimposed on the medulla. Bear in mind that opacity is aggressive and more chronic lesion (Figure 7.27). influenced by tissue thickness. Thus, as distances a and b combined are The findings of new bone production or bone about half of distance c (radiologically seen cortex) they appear loss described above, are readily seen on radiographs relatively radiolucent on the lateral view. but may be better defined on CT images which lack Delivered by BSAVA to: 83 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04 BSAVA Manual of Canine and Feline Musculoskeletal Imaging Close-up ML CrCd view of a 7.24 view of the distal 7.27 distal femur tibia with mild permeative with chronic lysis and marked osteomyelitis. Note the subperiosteal scalloping of radiolucent cloaca with a the cranial cortex, cortical defect indicative of osteomyelitis. and rounded edges (arrowed). A solid periosteal reaction is also present more proximally. Close-up view of 7.25 a post-mortem femur specimen showing endosteal scalloping resulting in a cortical spike proximally. Permeative lysis and a sunburst periosteal reaction are also present. superimposition of the osseous changes (Figure 7.28). Bone loss or production is seen much earlier on CT than on radiographs (Figure 7.29) and lack of radiological changes does not exclude the possibility of bone loss. Diagnostic ultrasonography is also an ideal modality to detect early new bone production and to a lesser extent, bone loss. Additionally, surrounding soft tissue abnormal­ ities such as neoplastic invasion, spread of infection or regional lymph node involvement can be assessed and ultrasound-guided tissue samples taken. Foreign bodies causing fistulous tracts and secondary periosteal reaction can also be diagnosed (Figure 7.30). Rate of change Non-aggressive changes will show no or minimal changes on follow-up radiographs taken 10–14 days later, whereas 7.26 Highly aggressive lesions are likely to show progressive radio­ - aggressive log­ical changes.­ osteosarcoma of the distal radius with a segmental The rate of change, in combination with the aggressive- pathological fracture ness of the above-described new bone production, and (white arrows). Note how the presence of bone loss and cortical defects, allows the medial radial cortex has one to grade the aggressiveness of the pathology. Often, a been partly destroyed in range of changes will be present and the most aggressive the region of the of these must be used to classify the disease process endosteum (endosteal scalloping: black arrow) (Figure 7.31). Figure 7.32 illustrates how these changes and how the lateral cortex can be integrated. Aggressive changes require immediate is almost completely veterinary intervention to optimize the chances of a favour­ destroyed, with total able outcome, whereas patients with more benign changes cortical destruction more have time on their side for treatment and optimal recovery. distally. The solid periosteal When interpreting all of the above changes it must reaction on the ulna is secondary to the be remembered that the changes described often take surrounding neoplastic place simultaneously, with superimposition of periosteal tissue. reactions masking minor underlying lytic lesions or the differences in opacity of irregular superimposing perio­ steal reactions mimicking underlying bone lysis. In these cases CT is very valuable to best define the degree and extent of pathology present (see Figure 7.6 and Figure 7.28). Thoracic radiographs to look for metastasis may also assist in deciding whether a skeletal lesion is a malignant neoplasm. Delivered by BSAVA to: 84 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04  Chapter 7 · Bones – general (a) Sagittal and (b) 7.28 transverse CT images in a bone window of the tibial osteosarcoma in Figure 7.15. Note how well defined the tibial moth-eaten lysis is, when compared with the radiograph. (c) Vascular enhancing (reddish hue) volume-rendered CT image of the same area, showing the vascularity of the neoplastic tissue that has invaded the surrounding soft tissues from the tibia. (a) (b) (c) Dobermann with 7.29 progressive pelvic limb spastic paresis. (a) Lateral view of cranial thoracic vertebrae (* = T2), which look normal. Myelography showed that the contrast column stopped at T2 (image not shown). (b) Sagittal reconstructed CT image in a bone window shows marked lysis of the T2 vertebral body. (c) Transverse CT image of T2 with hypoattenuating neoplastic tissue invading the vertebral Ultrasound image of the angular process area of the mandible canal and displacing the cord 7.30 that showed a draining tract and mild periosteal reaction on dorsally. The cord is radiographs. The 26 mm inciting porcupine quill is readily seen between surrounded by a thin layer of the markers. hyperattenuating (a) subarachnoid contrast medium from the myelogram. CT is much more sensitive than radiographs for the detection of small amounts of contrast medium. (b) ML view of a humeral osteosarcoma with a solid periosteal 7.31 reaction caudally but with underlying permeative to moth- (c) eaten lysis, making it overall an aggressive lesion despite the benign solid periosteal reaction. Delivered by BSAVA to: 85 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04 BSAVA Manual of Canine and Feline Musculoskeletal Imaging Characteristic Non-aggressive Aggressive Bone destruction Geographic Moth-eaten Permeative Periosteal reaction Solid Lamellar Lamellated Thick brush-like Thin brush-like Sunburst Amorphous Edge of lytic focus Well demarcated and Well demarcated Poorly defined sclerotic margin Transition from Narrow transition zone Intermediate Wide transition zone lytic region to normal bone Cortical None to cortical thinning Rounded cortical defects Cortical spikes accompanied by endosteal or destruction and expansion subperiosteal scalloping Rate of change None Mild Marked after 10–14 days 7.32 Range of possible changes used to judge whether bone pathology is aggressive or non-aggressive. Differentiating neoplasia from osteomyelitis Grandage J (1976) Interpretation of bone radiographs: some hazards for the unwary. Australian Veterinary Journal 52, 305–311 For information on how to differentiate neoplasia from Madewel JE, Ragsdale BD and Sweet DE (1981) Radiologic and pathologic analysis of solitary bone lesions. Part I: Internal margins. Radiologic Clinics of osteomyelitits see Chapter 9. North America 19, 715–748 Olsson S-E and Ekman S (2002) Morphology and physiology of the growth cartilage under normal and pathologic conditions. In: Bone in Clinical Orthopedics, 2nd edn, ed. G Sumner-Smith, pp. 117–124 Thieme, Stuttgart References and further reading Ragsdale BD, Madewel JE and Sweet DE (1981) Radiologic and pathologic analysis of solitary bone lesions. Part II: Periosteal reactions. Radiologic Clinics of North America 19, 749–783 Dennis R, Kirberger RM, Barr FJ et al. (2010) Appendicular skeleton. In: Handbook of Small Animal Radiology and Ultrasound: Techniques and Summerlee AJS (2002) Bone formation and development. In: Bone in Clinical Differential Diagnosis, 2nd edn, pp. 1–9. Churchill Livingstone Elsevier, Orthopedics, 2nd edn, ed. G Sumner-Smith, pp. 1–21. Thieme, Stuttgart London Wilson JW (2002) Blood supply to developing, mature and healing bone. In: Bone Dobson H and Friedman L (2002) Radiologic interpretation of bone. In: Bone in in Clinical Orthopedics, 2nd edn, ed. G Sumner-Smith, pp. 23–43. Thieme, Stuttgart Clinical Orthopedics, 2nd edn, ed. G Sumner-Smith, pp. 175–204. Thieme, Wrigley RH (2000) Malignant versus non-malignant bone disease. Veterinary Stuttgart Clinics of North America: Small Animal Practice 30, 315–347 Delivered by BSAVA to: 86 University College Dublin (7442) IP: 137.43.79.141 On: Wed, 22 Nov 2023 10:49:04