Small Animal Radiology and Ultrasound: A Diagnostic Atlas and Text

Chapter Five The Skull 639
disease has been reported in Siamese and domestic short-haired cats. Abnormal nasal
turbinate development and aplasia or hypoplasia of the frontal and sphenoid sinuses have
been described. The nasal and ethmoid turbinates are short and tortuous. The vertebrae
are wide and asymmetric, with irregular epiphyses present when the cat is young. Widened
wedge-shaped disc spaces and periarticular osteophytes also are present. Coxofemoral joint
subluxation with femoral head remodeling is observed also in this disease. There is
decreased bone density with thin cortices and a coarse trabecular pattern. Degenerative
joint disease is present, with the changes being more severe in the hips and shoulders than
in the stifles or tarsi. There is hypoplasia of the hyoid bones and hypoplasia or fragmentation
of the odontoid process of the second cervical vertebra. Fragmentation or abnormal
ossification of the patella was observed. The radiographic diagnosis usually is made after
examination of vertebral or pelvic radiographs rather than skull radiographs. In dogs, the
changes are similar, with facial deformity and brachygnathia. Narrowed intervertebral disc
spaces, cervical disc prolapse, vertebral articular facet irregularities, subluxation of vertebral
bodies, and subchondral bone lysis with narrow joint spaces have been reported. 96
Craniomandibular Osteopathy. This condition affects young dogs, primarily the
Highland Terriers (Scottish, Cairn, West Highland White). It has been reported infrequently
in a large range of other breeds (e.g., Great Danes, Labrador Retrievers, Boston
Terriers, Doberman Pinchers, Pyrenean mountain dogs). 46,97-100 In West Highland White
Terriers, the disease has been shown to be an autosomal recessive trait. 100,101 The primary
radiographic change is the presence of palisading periosteal new bone involving the
mandible and increased width and density of the tympanic bulla and the frontal, parietal,
and temporal bones (Fig. 5-35). The bony proliferation is most often symmetric; however,
unilateral involvement has been observed. The bone lesions usually are self-limiting, with
regression of the lesions occurring after skeletal maturity is reached. However, some produce
enough reactive new bone that they encroach upon important adjacent structures
(e.g., temporomandibular joints, orbit). 102 Some dogs may not survive because they are
unable to open their mouths to eat. As the disease regresses, the new bone will remodel and
have smooth margins, with the residual change appearing as particularly thick mandibular
cortices. In some affected dogs the condition is not limited to the skull and involvement of
the appendicular skeleton has been described, which also may be associated with a defect
in canine leucocyte adhesion. 103 The bony lesions consist of a metaphyseal periosteal proliferation,
which extends into the diaphysis. The physis is not affected, and the metaphyseal
lucencies seen in hypertrophic osteodystrophy are not observed in this disease. This permits
discrimination between the lesions of the appendicular skeleton that were observed
Fig. 5-35 A 6-month-old male
Scottish Terrier with swelling of both
mandibles. The lateral radiograph
revealed a large amount of palisading
periosteal new bone formation
involving the bodies of both
mandibles. Diagnosis: Craniomandibular
osteopathy.