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What are the OFA, & Hip Dysplasia?

Photo : Youth Male by VKW Rottweilers

 

German Rottweilers are susceptible to hip dysplasia While the Rottweiler puppies from a back yard breeder may appear healthy, the degradation of the hip joint can take years to cause noticeable discomfort to the dog. The condition often leads to severe pain that requires a complete hip replacement. Ethical Rottweiler breeders will have their breeding stock evaluated by the OFA prior to any breeding.  By eliminating dogs of inferior hip configuration from the gene pool, the incidence of dysplasia is being greatly reduced in the Rottweiler today. Vom Keiser Wappen breeds Rottweilers which have been evaluated as having a Good or Excellent hip by the OFA.

The OFA is a most prized resource by identifying those with the condition and keeping a database which breeders can use freely to evaluate potential breeding combinations.

 

An introduction to the OFA

John M. Olin was a well-known industrialist, philanthropist and sportsman. His commitment to the welfare of dogs was first evidenced in his founding of Nilo Kennels, where he bred, trained and campaigned outstanding examples of the sporting breeds.

Olin recognized that hip dysplasia was a common and debilitating orthopedic disease in dogs, and in the fall of 1964 gathered a group of individuals to discuss means of limiting hip dysplasia. This initial meeting, which included representatives of the Golden Retriever Club of America, German Shepherd Dog Club of American, and the veterinary community led to the organization of the Orthopedic Foundation for Animals (OFA).

The OFA was incorporated as a not-for-profit corporation by the state of Illinois on July 7, 1966. The original purpose of the organization was providing radiographic evaluation, database maintenance, and breeding advice to reduce the incidence of canine hip dysplasia.

Over the past 10 to 15 years the OFA has recognized that a variety of heritable diseases impact animal health. As scientific advancements enhanced the ability to diagnose heritable diseases, the OFA has supported development of diagnostic criteria and databases for a number of genetic diseases in addition to hip dysplasia.


Hip Dysplasia

Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.

The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases.

No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.

See the XRAYS

 

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