Cortical changes may also be indicative of the aggressive-ness of a lesion. Slow-growing processes tend to expand 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 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 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 osteomye litis where the exudate oozes from the medulla through the Volkmann’s canals to the subperiosteum, which is elevated, and stimulates osteoclasts to resorb bone subperiosteally (Figure 7.24).
Cortical defects: Endosteal scalloping may eventually result in a cortical defect, which is often associated with a cortical spike (Figures 7.25 and 7.26). This is a sign of a highly aggressive lesion. Cortical defects may also occur with chronic osteomyelitis, owing to cloaca formation.
Here, the cortical edges are rounded, indicative of a less aggressive and more chronic lesion (Figure 7.27).
The findings of new bone production or bone loss described above, are readily seen on radiographs but may be better defined on CT images which lack
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).
ate of c ange
Non-aggressive changes will show no or minimal changes on follow-up radiographs taken 10–14 days later, whereas aggressive lesions are likely to show progressive radio -log ical changes.
The rate of change, in combination with the aggressive-ness of the above-described new bone production, and the presence of bone loss and cortical defects, allows one to grade the aggressiveness of the pathology. Often, a range of changes will be present and the most aggressive of these must be used to classify the disease process (Figure 7.31). Figure 7.32 illustrates how these changes can be integrated. Aggressive changes require immediate veterinary intervention to optimize the chances of a favour-able outcome, whereas patients with more benign changes have time on their side for treatment and optimal recovery.
When interpreting all of the above changes it must be remembered that the changes described often take place simultaneously, with superimposition of periosteal 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.
Close-up ML view of the distal tibia with mild permeative lysis and marked
subperiosteal scalloping of the cranial cortex, indicative of osteomyelitis.
7.24
Close-up view of a post-mortem femur specimen showing endosteal scalloping resulting in a cortical spike proximally. Permeative lysis and a sunburst periosteal reaction are also present.
7.25
ighly aggressive osteosarcoma of the distal radius with a segmental pathological fracture (white arrows). Note how the medial radial cortex has been partly destroyed in the region of the endosteum (endosteal scalloping black arrow) and how the lateral cortex is almost completely destroyed, with total cortical destruction more distally. The solid periosteal reaction on the ulna is secondary to the surrounding neoplastic tissue.
7.26
CrCd view of a distal femur with chronic
osteomyelitis. Note the radiolucent cloaca with a cortical defect
and rounded edges (arrowed). A solid periosteal reaction is also present more proximally.
7.27
(a) Sagittal and (b) 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.
7.28
(a) (b) (c)
Dobermann with 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 canal and displacing the cord dorsally. The cord is surrounded by a thin layer of hyperattenuating
subarachnoid contrast medium from the
myelogram. CT is much more sensitive than radiographs for the detection of small amounts of contrast medium.
7.29
(a)
(b)
(c)
ltrasound image of the angular process area of the mandible that showed a draining tract and mild periosteal reaction on radiographs. The 26 mm inciting porcupine quill is readily seen between the markers.
7.30
ML view of a humeral osteosarcoma with a solid periosteal reaction caudally but with underlying permeative to moth-eaten lysis, making it overall an aggressive lesion despite the benign solid periosteal reaction.
7.31
Range of possible changes used to judge whether bone pathology is aggressive or non-aggressive.
7.32
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
sclerotic margin Well demarcated Poorly defined
Transition from lytic region to normal bone
Narrow transition zone Intermediate Wide transition zone
Cortical
destruction None to cortical thinning
and expansion Rounded cortical defects Cortical spikes accompanied by endosteal or subperiosteal scalloping
Rate of change
after 10–14 days None Mild Marked