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Health
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| 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. |
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| Here are some helpful links that should be of use to any dog owner. |
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