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International Journal of Molecular Veterinary Research
2013, Vol.3, No.5, 13-22
http://ijmvr.sophiapublisher.com
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commonly reported in dogs with the feeding of meat
products without bone (Bennett, 1976). The disease
also occurs in cats (Rowland et al., 1968) and
laboratory animals as well as in many farm animal
species (Gilka and Sugden, 1984). Osteogenesis
imperfecta, osteodystrophy fibrosa, juvenile osteoporosis,
nutritional osteoporosis, osteitis fibrosa and “all meat
syndrome” are synonyms to NSH, but have caused
confusion (Bennett, 1976).The basic underlying cause
is disturbance in mineral homeostasis induced by
nutritional imbalances, mainly calcium deficiency
(Bennett, 1976) or excessive phosphorus intake,
which stimulate the release of parathyroid hormone
(PTH) from the parathyroid glands (Bennett, 1976).
Hypocalcaemia may arise from inability to absorb
dietary calcium, lack of dietary calcium eg. in meat,
cereal, grains, fruits etc. (Miller, 1969). Excessive
dietary phosphorus (Miller, 1969) and several other
factors, which tend to reduce the availability of dietary
calcium like deficiency of Vitamin A and D, renal
insufficiency, dietary constituents such as magnesium,
phytate and fluorine and thyroid disease (Cardielhac,
1971). Hyperparathyroidism also occurs in cases of
rickets and osteomalacia, where a calcium deficiency
will result in increased PTH secretion (Miller, 1969).
NSH has been induced experimentally in 4 cross-bred
puppies of 7 week old, by Meier and Wild (1975), by
feeding 2/3 beef and 1/3rd cereal flakes, with 50 ml
milk and free access to water, giving a Ca:P ratio of
1:5. NSH was commonly seen in dogs reared on meat
rich diets containing little calcium and much
phosphorus, and clinically it was seen in growing dogs
of large breeds, where calcium requirements are
greater (Olsson, 1972), although the disease was
regularly seen in the small breed dogs and in cats
(Krook et al., 1971). NSH, osteoporosis and
osteomalacia markedly affect the material properties
and composition of bone, resulting in a fracture
(Schwarz, 1991). Healing of such fracture is delayed
(Bae and Bae, 1999). Bennett (1976) reported pain
(bone, joint and associated muscle), lameness, bone
deformity and pathological fracture (long bone and
vertebral body), abnormal tooth development and
deterioration of body attitudes in the diseased dogs.
Other signs were swollen metaphyses and
costo-chondral junctions, pyrexia, paresis or paralysis
from vertebral compression and constipation
following pelvic collapse . Blood analysis for calcium
and phosphorus levels generally reveal values in the
normal range since the metabolic control mechanism
endeavour to maintain normal mineral levels (Krook,
1971). Serum concentration of phosphorus and
alkaline phosphatase(AP) appear to increase. Meier
and Wild (1975) analysed serum Ca, P and AP at
weekly intervals in experimental cases of eight
cross-bred puppies aged 7 weeks (2 equal groups).
They found increased level of alkaline phosphatase in
serum of both groups in the first 5 weeks with values
for the test dogs clearly lower than for the controls.
Serum Ca and P contents in the 2 groups differed only
slightly after 10 weeks, although larger differences
had been recorded earlier.
The radiographic features of NSH, includes
generalized loss of bone density and thinning of
cortex. Growth plate appeared normal in most cases
and there was an area of increased radio-density in the
metaphysis adjacent to the growth plate, which
indicated area of preferential bone mineralization and
broadening of the metaphyses giving a “saucer” effect
rather than the “cupping” seen with rickets (Bennett,
1976). Changes were best appreciated in the distal
radius and ulna (Johnson et al., 1995).
3.4 Hypertrophic osterodystrophy (HOD)
Hypertrophic osterodystrophy (HOD) was first
described in the veterinary literature by Collett (1935).
Hypertrophic osteodystrophy primarily affects the
young, rapidly growing large and giant breed dogs
(Grondalen, 1976). Woodard (1982) studied HOD in a
Weimaraner littermate. Harrus et al. (2002) reported
the development of HOD and antibody response in a
litter of vaccinated Weimaraner puppies. A deficiency
of vitamin C has been implicated as an etiological
factor (Watson et al., 1973). Riser and Shirer (1965)
suggested mineral overloading as a cause of HOD.
Low levels of ascorbic acid have been reported in the
blood (Bosch et al., 1971) and urine (Holmes, 1962)
of affected dogs but this has not been a constant
finding. Hypertropic osteodystrophy may arise by
over supplementation of the diet with minerals and
vitamins rather than a hypovitaminosis (Bruyer, 1972).
Riser and Shirer (1965) suggested that excess of