Orthopedic Foundation for Animals

OFA founded and originally incorporated as a private not for profit foundation in 1966, this year the Orthopedic Foundation for Animals (OFA) celebrates its 40th anniversary.

Credit for the formation of the OFA is generally attributed to John M. Olin, well known inventor, industrialist, philanthropist, conservationist, and sportsman. John Olin was an avid sportsman, hunter, and field trial participant. When hip dysplasia began to impact the performance of Olin’s dogs, he organized an initial meeting with representatives of the veterinary community, the Golden Retriever Club of America, and the German Shepherd Dog Club of America to discuss means of limiting the disease. This ultimately led to the formation and incorporation of the OFA in 1966. Its initial mission: To provide radiographic evaluation, data management, and genetic counseling for canine hip dysplasia.

While the OFA continues to focus on hip dysplasia, today’s OFA Mission, “To improve the health and well being of companion animals through a reduction in the incidence of genetic disease,” reflects the organization’s expansion into other inherited diseases and other companion animals such as cats.

The OFA is guided by the following four specific objectives:

1. To collate and disseminate information concerning orthopedic and genetic diseases of animals.

2. To advise, encourage and establish control programs to lower the incidence of orthopedic and genetic diseases.

3. To encourage and finance research in orthopedic and genetic disease in animals. 4. To receive funds and make grants to carry out these objectives.

• General Hip Dysplasia Information
• OFA's Handling Procedures
• Other Radiographic Findings

General Hip Dysplasia Information

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.

RETURN TO TOP

OFA's Handling Procedures

When a radiograph arrives at the OFA, the information on the radiograph is checked against information on the application. The age of the dog is calculated, and the submitted fee is recorded. The board-certified veterinary radiologist on staff at the OFA screens the radiographs for diagnostic quality. If it is not suitable for diagnostic quality (poor positioning, too light, too dark or image blurring from motion), it is returned to the referring veterinarian with a written request that it be repeated.

An application number is assigned. Radiographs of animals 24 months of age or older are independently evaluated by three randomly selected, board-certified veterinary radiologists from a pool of 20 to 25 consulting radiologists throughout the USA in private practice and academia. Each radiologist evaluates the animal's hip status considering the breed, sex, and age. There are approximately 9 different anatomic areas of the hip that are evaluated (Figure 1). View the graphic below.

1. Craniolateral acetabular rim

2. Cranial acetabular margin

3. Femoral head (hip ball)

4. Fovea capitus (normal flattened are on hip ball)

5. Acetabular notch

6. Caudal acetabular rim

7. Dorsal acetabular margin

8. Junction of femoral head and neck

9. Trochanteric fossa

Seven classifications are needed in order to establish heritability information (indexes) for a given breed of dog. Definition of these phenotypic classifications are as follows:

1. Excellent 2. Good 3. Fair 4. Borderline 5. Mild 6. Moderate 7. Severe

The hip grades of excellent, good and fair are within normal limits and are given OFA numbers. This information is accepted by AKC on dogs with permanent identification and is in the public domain. Radiographs of borderline, mild, moderate and severely dysplastic hip grades are reviewed by the OFA radiologist and a radiographic report is generated documenting the abnormal radiographic findings. Unless the owner has chosen the open database, dysplastic hip grades are closed to public information.

RETURN TO TOP

Other Radiographic Findings

In addition to assessing the dog's hip conformation, the veterinary radiologist reports other radiographic findings that could have familial, inherited causes such as transitional vertebrae or spondylosis. Transitional vertebrae are a congenital malformation of the spine that occur at the junctions of major divisions of the spine (usually between the thoracic and lumbar vertebral junction and the lumbar and sacral vertebral junction). Transitional vertebrae take on anatomic characteristics of both divisions of the spine it occurs between. The most common type of transitional vertebrae in dogs is in the lumbo-sacral area where the last lumbar vertebral body takes on anatomic characteristics of the sacrum. Transitional vertebrae are usually not associated with clinical signs and the dog can be used in a breeding program. The OFA recommends breeding the dog to another dog that does not have transitional vertebrae.

Spondylosis is another incidental radiographic finding where smooth new bone production is visualized between vertebral bodies at the intervertebral disc spaces. The new bone production can vary in extent from formation of small bone spurs to complete bridging of adjacent vertebral bodies. Spondylosis may occur secondary to spinal instability but often it is of unknown cause and clinically insignificant. A familial basis for its development has been reported. Like transitional vertebrae, dogs with spondylosis can be used in a breeding program.

RETURN TO TOP