Legg-Perthe's disease is a degeneration of the hip joint occurring in young
dogs. It is also known as Legg-Calve-Perthe's Disease, Perthe's disease,
Calve-Perthe's disease, or in medical terminology, avascular necrosis of the
femoral head and neck. The former names recognize the original researchers
in
the disease as it occurs in humans.
Legg-Perthe's disease (LPD) occurs most frequently in dogs 5 to 8 months of
age, with a reported range of 3 to 13 months. 1 It occurs primarily in small
dogs, and has been reported in many small and toy breeds, including Italian
greyhounds. Affected dogs are normal prior to the onset of the disease.
Symptoms of LPD are lameness, and pain in the area of the affected hip. In
some cases, the symptoms may be mild, and possibly go unnoticed. Upon
examination, pain can be elicited by a skilled examiner by moving the hip in
a variety of directions.
Definitive diagnosis is made by X-rays. As changes to bone occur slowly,
X-rays taken early in the course of the disease may appear normal. Repeating
the X-rays in 3 to 4 weeks will reveal the bony changes.
A dog affected with LPD suffers a loss of blood supply to an area of the
femur (thigh bone) known as the neck. Because the bone loses its blood
supply, it dies. As a result of the loss of bone tissue, the neck of the
femur collapses.
The neck attaches the head of the femur to the body of the femur. When the
neck collapses, the head of the femur is moved, and may also become
deformed.
These changes are readily apparent in X-rays. The head of the femur is the
"ball" which sits in the "socket" on the pelvis, making up the hip joint.
Therefore, changes to the head result in disruption of function of the hip
joint which causes the pain and lameness.
The term "avascular necrosis" means death of tissue due to lack of blood
supply. In most dogs, only one hip is affected, and males and females are
equally affected.(2) Why this loss of blood supply to the area occurs is not
known. What is known however, is the genetic nature of the condition.
The exact mode of inheritance of LPD has been debated among researchers.
Pidduck et al.,(3)working with toy poodles, proposed a simple (autosomal)
recessive mode of inheritance. Robinson,(4) working with data on West
Highland white terriers, Yorkshire terriers, miniature poodles and pugs,
also
suggested an autosomal recessive.
In an effort to clarify the mode of inheritance, Vasseur et al.,(5) working
with the Manchester terrier club, conducted a test breeding. Two affected
individuals were bred, and all five resulting puppies were X-rayed monthly
to
check for signs of LPD. If the disease were inherited as a simple recessive
in Manchester terriers, then the mating of two affected individuals should
have produced 100% affected puppies. At the seven month radiographic
examination, changes were noted in three of the puppies, and all three
subsequently became lame. The two remaining puppies had no radiographic
changes through nine months of age, and remained sound until 16 months when
they were placed in homes.
This study indicates that either LPD has a multigenic (more than one gene)
mode of inheritance in Manchester terriers, or that it is not completely
expressed. That is, an animal may have the affected genes, but not show
signs
of the disease. Regardless of the exact mode of inheritance, statistical
analysis of this and other studies reveals that LPD has a high degree of
heritability.
Treatment of LPD usually consists of surgery to remove the damaged femoral
head and neck (femoral head ostectomy). Mildly affected animals may recover
soundness with only cage rest. Affected animals will probably always have
some gait abnormalities, but make satisfactory pets after recovering from
surgery.
Prevention of the disease is only possible through genetic means. Affected
animals should not be bred. Breeding stock should have their hips X-rayed to
insure that they are not affected with mild LPD, the symptoms of which went
unnoticed during the dog's adolescence. Extreme caution should be used when
considering breeding animals that have produced LPD, or have LPD affected
littermates.
The Orthopedic Foundation of America (OFA) is a registry which examines
X-rays of hips and certifies that they are normal. The address for the OFA
is
2300 Nifong Boulevard
Columbia, MO 65201
(314) 442-0418.
Another
organization which also provides a similar service is the Institute for
Genetic Disease Control (GDC),
PO Box 222
Davis, CA 95617
(916) 756-6773
Bibliography
1. Brinker, Piermattei, and Flo.:Handbook of Small Animal Orthopedics &
Fracture Treatment. WB Saunders, Philadelphia, 1990.
2. Paatsama, S., Rissanan, P., et al.:Legg-Perthe's Disease in the Dog.
Journal of Small Animal Practice. 8:p215-220, 1967.
3. Pidduck, H., and Webbon, PM.:The Genetic Control of Perthe's Disease.
Journal of Small Animal Practice. 9:p-729-733, 1978.
4. Robinson, R.:Legg-Calve-Perthe's Disease in Dogs: Genetic Aetiology.
33:p275-6, 1992.
5. Vasseur, P., Foley, P. et al.:Mode of Inheritance of Perthe's Disease in
Manchester Terriers. Clinical Orthopaedics and Related Research.
244:p281-292, 1989.
Copyright The Italian Greyhound
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Legg Perthes
Legg-Perthes, also called Legg-Calve-Perthes (LCP) disease, is a disease of
the hip joints of small breeds of dogs. The head of the femur (the ball part
of the ball and socket) begins to die and disintegrate. This causes limping,
pain, and eventually arthritis. It usually appears between 6-12 months of
age. It is treated surgically by removing the head of the femur and letting
the muscles form a "false joint." It really does work.
Veterinarians have begun to address the heritability of this disease, and it
is generally agreed that although in very rare cases, the disease may be
brought on by trauma, it is probably genetic. It has been well documented in
terriers (Border Terrier, Lakeland Terrier, Jack Russell Terriers, Wheaten
Terrier), and has been proven to be hereditary in some breeds such as the
Wheaten Terrier. Bilateral cases (both hind legs affected) are not
considered to be the result of trauma, and are accepted to be hereditary.
(Source: Dr. John T. Payne, DVM (Diplomate, American College of Veterinary
Surgeons, College of Vet Med, University of Missouri at Columbia).