Canine Hip Dysplasia –
Is early surgery the best choice to prevent arthritis?
Ken Ninomiya, DVM
AAVA.org maintenance staff
Canine hip dysplasia is
a multi-gene,
inherited, developmental malformation of the hip joint in dogs. The
malformation results in exessive laxity (looseness)
in the joint. This laxity causes excess stress on the joint structures
resulting, eventually, in osteoarthritis. Because the malformation is caused by
multiple genes, there can be variation in the degree of malformation between
affected individuals, even within the same blood line. In fact, there can even
be generations of seemingly normal individuals in affected blood lines.
The prediction of
developing canine hip dysplasia is now being determined as early as 4 months
old using a radiographic technique called PennHip. As
a result of early prediction of developing hip dysplasia, and therefore
potential osteoarthritis, there is an increasing trend by veterinarians to
recommend surgical methods to attempt to prevent, or reduce, the progression of
degenerative arthritis in the affected dog. However, an article in Compendium
on Continuing Education for the Practicing Veterinarian points out that
there is no scientific evidence that any currently recommended surgical
technique will prevent the development of degenerative arthritis in dogs with
hip dysplasia.1
There are non-surgical
methods that have scientific basis to support their use to delay the
progression of degenerative arthritis in dogs with early hip dysplasia.
Scientific evidence demonstrates that preventing over-nutrition and excess exercise in
at risk puppies can reduce the progression of degenerative arthritis.2,3,4,5,6 The use of chondroprotective
substances such as glucosamine and chondtroitin sulfates, have not
been scientifically proven to prevent or alter the development of degenerative
joint desease. However, some studies exist to suggest
that glucosamine and chondroitin
sulfate may effect cartilage metabolism in dogs.7
Other studies suggest that combinations of glucosamine hydrochloride, low molecular chondroitin sulfate, and
manganese ascorbate can retard cartilage damage.8
Until
scientific evidence exists that proves surgical intervention will reduce the
progression of canine hip dysplasia and subsequent arthritis, using non-surgical methods, that have been scientifically shown to
modify the progression of hip dysplasia or retard joint cartilage damage, would
be a better approach to treat dogs who have been diagnosed with hip dysplasia.
1. Kapatkin
AS, Mayhew PD, Smith GK: Canine Hip Dysplasia: Evidence-Based Treatment, The Compendium, Vol. 24, No. 8 August 2002
2. Arnbjerg
J: Recent information about hip dysplasia., Vet Clin North Am Small Anim Pract 1999 Jul;29(4):921-34
3.
4. Kealy
RD, Lawler DF, Ballam JM, Lust G, Smith GK, Biery DN, Olsson SE: Five-year longitudinal study on
limited food consumption and development of osteoarthritis in coxofemoral joints of dogs., J Am Vet Med Assoc 1997
Jan 15;210(2):222-5
5. Kealy
RD, Olsson SE, Monti KL, Lawler DF, Biery DN, Helms RW, Lust G, Smith GK: Effects of limited
food consumption on the incidence of hip dysplasia in growing dogs., J Am
Vet Med Assoc 1992 Sep 15;201(6):857-63
6. Kasstrom
H: Nutrition, weight gain and development of hip dysplasia. An experimental
investigation in growing dogs with special reference to the effect of feeding intensity., Acta Radiol Suppl 1975;344:135-79
7. Johnson KA, Hulse DA, Hart RC, Kochevar D, Chu Q: Effects of an orally administered mixture of chondroitin sulfate, glucosamine hydrochloride and manganese ascorbate
on synovial fluid chondroitin sulfate
3B3 and 7D4 epitope in a canine cruciate
ligament transection model of osteoarthritis., Osteoarthritis
Cartilage 2001 Jan;9(1):14-21
8. Lippiello L, Woodward
J, Karpman R, Hammad TA.:
In vivo chondroprotection and metabolic synergy of glucosamine and chondroitin sulfate.,
Clin Orthop
2000 Dec;(381):229-40