Page 5 - IJMVR 2013 Vol.3 No.5

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International Journal of Molecular Veterinary Research
2013, Vol.3, No.5, 13-22
http://ijmvr.sophiapublisher.com
14
minerals, especially calcium-phosphate in the form of
hydroxyapatite [Ca
10
(PO
4
)
6
(OH)
2
]. At birth, long
bones of an animal mostly look like poorly
mineralized tiny cartilaginous models of woven bone.
In dogs, especially in large breeds, longitudinal bone
growth is rapid during the first 3 months and
exponential during the first 6 months of life (Olsson,
1993), which is largely dependent on the process of
physeal growth including multiplication, maturation
and orientation of chondroblasts/chondrocytes in
columns, their mineralization and replacement of
woven bone by a process called endochondral
ossification. Simultaneously bone remodeling takes
place by bone resorption and formation at the
metaphyseal, periosteal and endosteal sites in response
to mechanical stress (Ekman and Carlson, 1998).
Changes in bone structure and conformation can occur
very rapidly in growing dogs, as most of the skeletal
growth occurs during the first year of life. Hence,
during this period decreased mineralization ,
thinning of cortices of long bones and defect in
endochondral ossification may lead to angular limb
deformities (Kushwaha, 2003).
Angular limb deformity disorders occurring during
bone growth are either developmental or metabolic in
nature and frequently the result of growth plate
pathology or abnormalities in bone remodeling (Thorp,
1994).
Bone growth disturbances are mostly originate in the
growth plate and are commonly manifested as skeletal
abnormalities (Prasad et al., 1972) bone deformity
(Poulos, 1978). Etiopathology of angular deformities
of the foreleg can occur for various reasons. The
two-bone system of the ante-bracheum is predisposed
to deformity caused by the continued growth of one
bone after premature growth cessation of the other.
The bones normally elongate through the process of
endochondral ossification, which occurs in growth
plate or physis (Fox et al., 2006).
Total or partial premature closure of growth plates can
lead to angular limb deformities (Guthrie and Pead,
1992). Ulnar and radial growth plate defects occur
most commonly affected (Fox and Bray, 1993). The
premature closure of the radius and ulna growth plates
resulting in deformity of canine fore limbs has been
described (Fox, 1984). Any type of trauma to the limb
may lead to such closures, and the premature closure
of distal ulnar physis and its resultant deformities is
the most frequently (O’ Brien et al., 1971). Angular
limb deformities may also be associated with
metabolic bone diseases such as hypertrophic
osteodystrophy, retained cartilage core and nutritional
secondary hyperparathyroidism (Riser and Shirer,
1965).
2 Premature Closure of Physis
Growth plates, peripheral extensions of the primary
center of ossification, are responsible for the
longitudinal growth of a long bone (Newton, 1985). In
dogs, growth plate closure is completed within the
first year of life and as in other species, the time of
fusion varies between the different ossification centers.
Disorders of the growth plate in immature animals
will result in shortening and/or angulations of the limb
and this can result in secondary joint disorders. The
most growth plate disorders involve the radius and
ulna, because it receives a disproportionate amount of
stress, its growth comes from several physes and it is
composed of two parallel long bones, which must
grow in unison if the limb is to remain straight
(Bennett, 1990).The most common growth plate
defect is its premature closure leading to shortening of
limb with angular deformity (Fox et al., 2006). The
type of defect produced varies according to the plate
affected, to the growth potential of the plate, and to
the extent of the cellular damage (Vaughan, 1976). It
was more common in fore limbs and growth plates
involved in decreasing order of prevalence were the
distal ulna, distal radius and proximal radius as
reported by Fox et al (2006). They also found
predominance of unilateral cases. The most common
cause of premature growth cessation is trauma to one
of the physeal plates (Singh et al., 2012). These
injuries to the physes have been classified into five
groups by Salter and Harris, based on the fractures and
anatomical configurations (Salter and Harris, 1963). A
transverse fracture through the weak region of the
hypertrophied and degenerating cartilage, which is
being invaded by the capillaries and chondroblasts, is
called Salter I fracture. A similar fracture that extends