Increased bone opacity may be:
• Artefactual – due to superimposition of structures. This could be one bone abnormally superimposed on another (e.g. often seen with fractures; Figure 7.4) or a superficial soft tissue structure superimposed on bone (e.g. a teat superimposed on the wing of the ilium on a ventrodorsal (VD) abdominal view)
Polyostotic bone pathology involving both femoral shafts due to haematogenous fungal osteomyelitis.
7.3
• 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 mineralization of the osteoid matrix, for example in osteo-mas (Figure 7.5).
Osteosarcoma may produce intra- or extramedullary osteoid, and the amount of mineralization of the osteoid will determine the opacity of the neoplasm. Intramedullary osteoid may be difficult to appreciate on survey radio-graphs, particularly if there is a superimposed periosteal reaction. Here, cross-sectional imaging techniques, and in particular CT, allow visualization of the intramedullary
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.
Artefactual increase in bone opacity due to superimposition of fracture ends. (a) Craniocaudal (CrCd) view of the tibia with two transverse lines of increased opacity in the tibial diaphysis. (b) The ML view shows slight over-riding of the tibia fracture edges.
7.4
(a) (b)
An ivory-like opacity is seen with complete mineralization of the osteoid matrix in an osteoma of the frontal bone. The radiograph was deliberately underexposed to show the peripheral pathology.
7.5
Osteosarcoma of the distal tibia. (a) ML view of the distal tibia.
Fairly solid periosteal reactions, permeative to moth-eaten lysis and neoplastic endosteal medullary new bone are seen at level b.
(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 medullary new bone formation and solid periosteal reaction thickening the cortex in (b). In (c) and (d) the periosteal reaction ranges from thick lamellar to immature solid. Note that medullary new bone clearly seen on the CT images is di cult to appreciate on the radiograph. Image (b) is in a soft tissue window and (c) and (d) are in a bone window.
7.6
(a) (b)
(c) (d)
ML view of a skeletally 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.
7.7
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
• Amorphous bone production.
Solid periosteal reaction: The periosteum is slowly lifted over a period of time while laying down new bone. A solid 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.
The more radiopaque the periosteal reaction, the longer it has been present (see Figure 7.6 and Figure 7.9). Solid
fig 2.8
Continuous periosteal reactions Solid Lamellar
(parallel) Lamellated
Interrupted periosteal reactions
Thick brush-like Thin brush-like Sunburst Amorphous bone production
Schematic representation of periosteal reactions from least to most aggressive.
7.8
reactions are indicative of slow-growing benign processes.
Typical causes are fracture callus, chronic osteomyelitis and panosteitis. On the periphery of more aggressive perio steal reactions (see below) the periosteum is lifted more slowly and a triangular solid periosteal reaction known as a Codman’s triangle is often seen (see Figure 7.15). It is usually present on the diaphyseal side of a meta-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 radiolucent space between the thin line of new bone and the cortex becomes filled with new bone, resulting 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 fairly rapidly over an extensive area of the cortex with osteoblastic activity along the vertically orientated Sharpey’s fibres. If the reaction is less aggressive and slower growing, the spicules are thicker and it is known as
(a) Focal anaerobic osteomyelitis of the caudal ulna with a mature solid periosteal reaction. (b) ypertrophic osteopathy with immature solid periosteal reactions on the abaxial surfaces of metatarsals II and V.
7.9
(a) (b)
Focal soft tissue swelling and lamellar periosteal reaction cranially on the radius. Radiograph deliberately underexposed.
7.10
Post-mortem specimen of a proximal femur with fungal osteomyelitis resulting in a lamellated periosteal reaction.
7.11
Thick brush-like periosteal reaction on the abaxial surface of metacarpal V in a dog with hypertrophic osteopathy.
7.12
Thin brush-like periosteal reaction of the abaxial surface of metatarsals II and V in a case of hypertrophic osteopathy.
7.13
Osteosarcoma of the frontal bone with a sunburst periosteal reaction.
7.14 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 (Figure 7.15).