Legg- Calve- Perthes Disease (LCP) is a disorder of hip joint conformation occurring in
both humans and dogs. In dogs, it is most often seen in the miniature and toy breeds
between the ages of 4 months to a year.
LCP results when the blood supply to the femoral head is interrupted resulting in
vascular necrosis, or the death of the bone cells. Followed by a period of
re-vascularization, the femoral head is subject to remodeling and/or collapse creating
an irregular fit in the acetabulum, or socket. This process of bone cells dying and
fracturing followed by new bone growth and remodeling of the femoral head and
neck, can lead to stiffness and pain.
LCP is believed to be an inherited disease, although the mode of inheritance is not
known. Because there is a genetic component, it is recommended that dogs affected
with LCP not be used in breeding programs.
What is Patella Luxation? The patella, or kneecap, is part of the stifle joint (knee). In
patella luxation, the kneecap luxates, or pops out of place, either in a medial or lateral
position.
Bilateral involvement is most common, but unilateral is not uncommon. Animals can be
affected by the time they are 8 weeks of age. The most notable finding is a knock-knee
(genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral
ligament may be evident. The medial retinacular tissues of the stifle joint are often
thickened, and the foot can be seen to twist laterally as weight is placed on the limb.
MPS VI disease is due to an arylsulfatase B deficiency and has been reported in Siamese
and domestic shorthair cats, as well as Miniature Pinschers, Miniature Schnauzers,
Welsh Corgis, and Chesapeake Bay Retrievers. A DNA based test is available to screen
Siamese cats, in other cats an enzyme activity test is required (metabolic screening).
Similarly, a DNA test has recently been developed for Miniature Pinschers with MPS VI.
In mucopolysaccharidosis, certain large sugars (polysaccharides) of the body are not
properly broken down. In MPS VI, the deficient enzyme is arylsulfatase B, which is
responsible for degrading dermatin sulfate. MPS VI is autosomal recessively inherited
and has been seen in humans, cats and, more recently, dogs.
Clinical Signs:
The ensuing cellular accumulation results in skeletal deformities, including defects in
the sternum, vertebrae and particularly the hip joints. To varying degrees they may
also experience corneal cloudiness and facial dysmorphia.
The discovery of a disease-causing mutation in the arylsulfatase gene in Miniature
Pinschers enabled the development of a DNA test which allows the identification of
MPS affected, carrier, and normal (clear) animals. Affected Miniature Pinschers have not
only been found in various states in the US, but also abroad. Thus, it is believed to be
more wide spread and under-diagnosed than previously thought.
both humans and dogs. In dogs, it is most often seen in the miniature and toy breeds
between the ages of 4 months to a year.
LCP results when the blood supply to the femoral head is interrupted resulting in
vascular necrosis, or the death of the bone cells. Followed by a period of
re-vascularization, the femoral head is subject to remodeling and/or collapse creating
an irregular fit in the acetabulum, or socket. This process of bone cells dying and
fracturing followed by new bone growth and remodeling of the femoral head and
neck, can lead to stiffness and pain.
LCP is believed to be an inherited disease, although the mode of inheritance is not
known. Because there is a genetic component, it is recommended that dogs affected
with LCP not be used in breeding programs.
What is Patella Luxation? The patella, or kneecap, is part of the stifle joint (knee). In
patella luxation, the kneecap luxates, or pops out of place, either in a medial or lateral
position.
Bilateral involvement is most common, but unilateral is not uncommon. Animals can be
affected by the time they are 8 weeks of age. The most notable finding is a knock-knee
(genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral
ligament may be evident. The medial retinacular tissues of the stifle joint are often
thickened, and the foot can be seen to twist laterally as weight is placed on the limb.
MPS VI disease is due to an arylsulfatase B deficiency and has been reported in Siamese
and domestic shorthair cats, as well as Miniature Pinschers, Miniature Schnauzers,
Welsh Corgis, and Chesapeake Bay Retrievers. A DNA based test is available to screen
Siamese cats, in other cats an enzyme activity test is required (metabolic screening).
Similarly, a DNA test has recently been developed for Miniature Pinschers with MPS VI.
In mucopolysaccharidosis, certain large sugars (polysaccharides) of the body are not
properly broken down. In MPS VI, the deficient enzyme is arylsulfatase B, which is
responsible for degrading dermatin sulfate. MPS VI is autosomal recessively inherited
and has been seen in humans, cats and, more recently, dogs.
Clinical Signs:
The ensuing cellular accumulation results in skeletal deformities, including defects in
the sternum, vertebrae and particularly the hip joints. To varying degrees they may
also experience corneal cloudiness and facial dysmorphia.
The discovery of a disease-causing mutation in the arylsulfatase gene in Miniature
Pinschers enabled the development of a DNA test which allows the identification of
MPS affected, carrier, and normal (clear) animals. Affected Miniature Pinschers have not
only been found in various states in the US, but also abroad. Thus, it is believed to be
more wide spread and under-diagnosed than previously thought.
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