Basic HTML Version
International Journal of Molecular Veterinary Research
2013, Vol.3, No.5, 13-22
http://ijmvr.sophiapublisher.com
19
day and housing outdoors in an open yard for several
hours daily. There was an increase in the 25(OH)
vitamin- D3 concentration in two pups <8 to 48 and
15 to 40 nmol/L, respectively, after treatment (Malik
et al., 1997). Vitamin-D dependent rickets in a Saint
Bernard dog was treated with 0.125 mg
dihydrotachysterol (AT-10, Winthrop Laboratories)
given orally every other day (Johnson et al., 1995).
Little (1973) opined that over supplementation with
vit D has to be avoided since that would lead to the
production of a scanty and defective matrix, which
might easily be destroyed by minor trauma. Sharma
(2002) treated 100 clinical cases of rickets in canine
by administering drugs like anthelmintic, Iron and
Vitamin-B complex and high oral dose of Ca and P.
He used plaster of Paris cast with well-padded
bamboo splints to straighten the already bent
forelimbs. Modified Thomas splints were applied in
some cases, which were, however, not so effective.
The POP casts were changed after every two weeks as
the splints were found to injure the bony prominences
of the rapidly growing pups. In the pups where the
bones were not grossly deformed, olive oil massage of
the limb and exposure to early morning sun, feeding
of calcium rich diet like cheese, milk etc. were
recommended. NSH has been treated by termination
of a meat-rich diet and feeding of a commercial,
nutritionally
balanced
diet
substituted
and
supplemented with calcium and phosphorus (Bennett,
1976). Milk and milk products are natural sources of
calcium and phosphorus. Dogs could be fed mineral
by providing chewing bones (Bennett, 1976). In case
of severe muscle pain, the intramuscular injection of a
combination of selenium and tocopherols has been
suggested (0.1ml/kg body weight once weekly)
(Miller, 1969). It has been confirmed experimentally
that the osteopenia in NSH is reversible provided the
pathology is not too advanced (Krook et al., 1971).
HOD affected dogs might recover in one to two
months with complete rest and elimination of
excessive vitamins and mineral supplements (Watson
et al., 1973). Dogs respond poorly to the vitamin C
therapy ( Holmes, 1962). Newton (1985) suggested
avoidance of minerals, vitamin C and vitamin D
supplements as they might accelerate the rate of
dystrophic calcification (Bennett, 1976 and Grondalen,
1976).
5.2 Hormones
Transforming Growth Factor Beta (TGF- β) is a
dimeric protein of 25 kDa molecular weight originally
isolated from platelets (Roberts and Sporn, 1993).
There are three distinct mammalian isoforms, TGF β1,
TGF β 2 and TGF β3, with TGF β1 being the most
abundant isoform. Allmost all cell types express TGF
β1 but the highest level of expression is in platelets
and bones (Assoian et al., 1983). Mature TGF β1
consists of two identical peptide chains, each
containing 112 aminoacids, linked by 9 disulphide
bonds (Sharples et al., 1987). TGF β1 is synthesized
as part of large, latent protein complex, unable to bind
to cellular receptors with mature active TGF β1
produced by cleavage (Miller et al.1990). TGF β1 has
a major role in chondroprotective mechanisms and is
known to promote matrix synthesis. A recent report
indicated that TGF β1 caused synovial hyperplasia
and osteophyte formation (Bakker, 2001). TGF beta 1
is a multifunctional cytokine that plays an important
role in immunomodulation, inflammation and tissue
repair (Sporn and Roberts, 1990). Many studies have
suggested that TGF β1 could be a potential therapeutic
reagent for the repair of soft tissue and bone following
ischemic injury. It may also have applications for the
treatment of chronic, inflammatory, fibrotic and
autoimmune diseases (Prudhomme and Piccirillo,
2000). In contrast; other studies demonstrated that
TGF β1 can cause inflammation and fibrosis (Shuler,
2000). The ability of transforming growth factor- TGF
β1 (TGF β1) to stimulate bone healing was evaluated
in a rat critical calvarial defect model. Both a low dose
and a high dose of TGF β1 were incorporated into two
different types of implants: one made from a
composite of poly (lactic-co-glycolic acid) (PLPG)
(50:50) and demineralized bone matrix (DBM), and
the other from calcium sulfate (CaSO
4
). These
preliminary studies show that TGF β1 is capable of
inducing new bone formation. Furthermore, the
materials used to deliver the growth factor can play a
significant role in the bone healing process (Gombotz
et al., 1994). TGF β1 has been used to treat
osteopaenia in rabbits (Parti et al., 2005) and in dogs
(Singh et al., 2011).The hormone calcitonin, which