Page 1611 - Clinical Small Animal Internal Medicine

174 Developmental Orthopedic Diseases 1549

Prognosis palpation. Systemic signs including fever, anorexia, leth-
VetBooks.ir age and until this time, supportive care is paramount. argy, and weight loss may accompany the lameness. The
The condition is often self‐limiting by 11–13 months of
signs may regress and reoccur, but rarely continue past 2
There are no predictive factors to determine if the bony
proliferations will regress partially or completely. For years of age.
owners who are unable to provide adequate care, for the Diagnosis
rare severe case, and for cases with intractable discom- Depending on the disease phase, radiographic findings
fort, euthanasia is an option. from orthogonal views of the affected bone(s) may vary
from completely normal to the classic blurring and inho-
mogeneity of the medullary cavity trabecular pattern.
Panosteitis
The first stage, rarely seen, is characterized by a decrease
Etiology and Pathophysiology of the radiodensity of the medullary cavity near the
Panosteitis is a self‐limiting disease of the bone marrow nutrient foramen. In the next stage, an increased medul-
of fore‐ and hindlimb long bones. Synonyms for panoste- lary opacity with a granular pattern or loss of trabecula-
itis include shifting leg lameness, enostosis, and eosino- tion, as well as periosteal bone formation, is seen. In a
philic panosteitis. later stage, changes in the medullary cavity become more
The earliest changes in affected long bones are seen diffuse and homogeneous. After 4–6 weeks the lesions
around the nutrient foramen. Vascular proliferation and regress and a coarse trabecular network develops. It
bone formation result in vascular congestion and increased should be noted that radiographic signs are not corre-
intraosseous pressure. In response to the increased intra- lated with patient discomfort or lameness.
osseous pressure, dogs develop lameness of the affected Differential diagnoses include elbow dysplasia, OCD,
limb and form bone in periosteum and medullary cavity. hip dysplasia, and HOD.
Eventually, the affected bone marrow is replaced by
normal, healthy adipose bone marrow. The etiology of Treatment
panosteitis is unknown but strong breed predispositions There are no known medical or surgical cures for this
(see Table 174.1) suggest a genetic component. condition. Treatment consists primarily of analgesics
(NSAIDs) and rest.
Epidemiology
The reported incidence of panosteitis is 2.6 per 1000 Prognosis
patients. The disease incidence is higher in north central The disease is self‐limiting, although recurrences are pos-
and northeastern regions of the United States, especially sible, reportedly even until the patient is 5 years of age.
in the summer and fall.

Hypertrophic Osteodystrophy
Signalment
Panosteitis is primarily a disease of medium‐ and large‐ Etiology and Pathophysiology
breed pure‐bred dogs. However, smaller dogs (either Hypertrophic osteodystrophy (HOD) is a disease of pre-
mixed breed or pure bred) such as the American cocker dominantly young, growing large‐breed dogs, character-
spaniel and the West Highland white terrier can also be ized by metaphyseal swelling of affected bones and
affected. Males are more frequently affected than females lameness. Synonyms for HOD include infantile scurvy,
(4:1), with patients most commonly affected between 5 Moller Barlow disease, juvenile scurvy, osteodystrophy
and 12 months of age. However, patients have been diag- II, skeletal scurvy, and metaphyseal osteopathy.
nosed as young as 2 months and as old as 5 years. In a The etiology of HOD is unknown. Proposed theories
study of 100 dogs, the median age of affected dogs was include overnutrition, vitamin C deficiency, infection,
12.4 months. vaccinations, and heritability. In more recent reports, the
etiologic roles of overnutrition and vitamin C deficiency
History and Clinical Signs have been questioned.
Panosteitis patients are often presented with a history of Many large dog breeds are predisposed to HOD (see
lameness, often shifting between limbs (shifting lame- Table 174.1) and therefore a genetic etiology has been
ness). Lameness ranges from mild to nonambulatory. suggested. In a litter of affected Weimaraners, the herit-
The occurrence can be acute in onset and may run a ability was estimated to be 0.68.
waxing–waning course. There is a 4:1 ratio of lesions in Several lines of evidence suggest an infectious etiology.
the forelimbs to hindlimbs, with 42%, 25%, 14%, 11%, and Specifically, many affected dogs have a history of, or
8% occurrence in the ulna, radius, humerus, femur, and actually are suffering from, a systemic illness (for instance,
tibia, respectively. The affected bones may be painful on a respiratory infection). Active bacteremia (E. coli) in an