Page 1586 - Clinical Small Animal Internal Medicine

1524 Section 13 Diseases of Bone and Joint

(a) (b) remodeling process, the poor‐quality woven bone and
VetBooks.ir fibrous tissue laid down will be replaced with well‐
mineralized trabeculae and the bones will return to
normal strength.

Rickets and Osteomalacia

Rickets is a disease of young animals and is due to a
failure of mineralization of osteoid and cartilage at the
provisional zone of calcification in the growth plate.
Osteomalacia is essentially the same condition but in
adult animals. Since adult animals do not have growth
plates, in osteomalacia only new osteoid laid down
during the normal remodeling process is poorly
mineralized. Both conditions are rare in dogs and cats.

Etiology/Pathophysiology
Rickets and osteomalacia are due to either dietary vita­
Figure 172.1 Radiograph from 12‐week‐old greyhound puppy min D deficiency or phosphorus deficiency. Phosphorus
with fibrous osteodystrophy. (a) Tibia/fibula showing osteopenia, deficiency is very rare in dogs and cats, and as described
with normal growth plate width, sclerosis of the metaphysis in the FOD section, phosphorus excess is far more
beneath the physis, and a folding fracture. (b) Mandible showing common.
loss of alveolar bone surrounding the teeth. Source: Courtesy of Dogs and cats are unusual in mammalian species in that
K.G. Thompson.
they do not appear to produce vitamin D in the skin under
the influence of ultraviolet light. In most animals, ultravio­
plain radiographs. DEXA and CT may be useful for let B light results in the conversion of 7‐dehydrocholes­
monitoring the success of treatment. In one study, bone terol, in keratinocytes and the dermis, to previtamin D3
mineral density, as measured by both DEXA and CT, which then undergoes thermal isomerization to vitamin
showed substantial improvement once the diet had D3. However, cats and dogs have been shown to have only
been corrected. 10% of the 7‐dehydrocholesterol in their skin that rats do,
7
and cat skin contains a 7‐dehydrocholesterol‐delta ‐
reductase which breaks down 7‐dehydrocholesterol.
Therapy
Therefore, irradiation of cat and dog skin with ultraviolet
Animals with nutritional FOD should be fed a commer­ light does not cause an increase in plasma vitamin D
cial balanced diet with the recommended 1:1 ratio of concentration. Cats and dogs are, for that reason, reliant
Ca:P. Affected animals may also benefit from receiving on their diet for their vitamin D requirements. However,
additional calcium, enough to raise the total Ca:P ratio of there are few reports of naturally occurring rickets in dogs
the diet to 2:1. The additional calcium may be in lactate, and cats in the literature, likely due to the widespread
carbonate or gluconate forms and should be continued feeding of commercial pet food. In addition, the most
for two months, after which time the animal can be common inappropriate diet fed to puppies and kittens is
maintained on a commercial balanced diet. Animals meat and offal, which contain high levels of phosphorus
with microfractures or infractions may require pain and adequate vitamin D.
relief. An important component of treatment is confin­ Vitamin D deficiency leads to decreased absorption
ing affected animals for the first 3–4 weeks of treatment of calcium and phosphorus from the intestine and
in order to decrease the risk of further pathologic decreased reabsorption of calcium and phosphorus
fractures. from the kidney, leading to hypocalcemia and
hypophosphatemia. Animals that have rickets due to
vitamin D deficiency will often have concurrent FOD
Prognosis
due to hypocalcemia. Decreased plasma ionized cal­
With correction of the diet, and provided catastrophic cium concentration leads to increased PTH secretion
fracture does not occur, the prognosis for a return to and therefore increased osteoclastic resorption of bone
normality is excellent. With time and the normal and FOD.