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Hip dysplasia

Hip dysplasia is a congenital disease that, in its more severe form, can eventually cause lameness and painful arthritis of the joints. It is caused by a combination of genetic and environmental factors. It can be found in many animals and occasionally in humans, but is common in many dog breeds, particularly the larger breeds. more...

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Description

In the normal anatomy of the hip joint, the thigh bone (femur) joins the hip in the hip joint, specifically the caput ossis femoris. The almost spherical end of the femur articulates with the hip bone acetabulum, a partly cartilaginous mold into which the caput neatly fits. It is important that the weight of the body is carried on the bony part of the acetabulum, not on the cartilage part, because otherwise the caput can glide out of the acetabulum, which is very painful. Such a condition also may lead to maladaptation of the respective bones and poor articulation of the joint.

In dogs, the problem almost always appears by the time the dog is 18 months old. The defect can be anywhere from mild to severely crippling. It can cause severe osteoarthritis eventually.

Causes

In dogs, there is considerable evidence that genetics plays a large role in the development of this defect. There might be several contributing genetic factors, including a femur that does not fit correctly into the pelvic socket, or poorly developed muscles in the pelvic area. Large and giant breeds are susceptible to hip dysplasia, and cocker spaniels and Shetland sheepdogs are also known to suffer from it. Cats are also known to have this condition, especially Siamese.

Detection

The classic diagnostic technique is with appropriate X-Rays and hip scoring tests. These should be done at an appropriate age, and perhaps repeated at adulthood - if done too young they will not show anything. Since the condition is to a large degree inherited, the hip scores of parents should be professionally checked before buying a pup, and the hip scores of dogs should be checked before relying upon them for breeding.

Prevention

Overfeeding puppies and young dogs, particularly in the giant breeds, might aggravate the problem or bring it on earlier, because pups tend to be more active, less aware of their physical limitations, and have immature bones and supporting structures carrying their weight. Dogs from breeds which are known to be prone to dysplasia, can be kept slightly leaner than normal until around 2 years old, by which time the bones are full strength and the animal can be easily brought up to its normal adult weight. Overexercising young dogs whose bones and muscles have not yet fully developed might also be a contributing factor.

Symptoms

Dogs might exhibit signs of stiffness after rising from rest, reluctance to exercise, bunny-hopping gait, lameness, pain, or wasting away of the muscle mass in the hip area. Radiographs often confirm the presence of hip dysplasia, but radiographic features may not be present until two years of age in some dogs. Moreover, many affected dogs do not show clinical signs, but some dogs manifest the problem before seven months of age, while others do not show it until well into adulthood.

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Meyer Dysplasia as a Cause of Hip Pain in Children
From American Family Physician, 2/1/00 by Jeffrey T. Kirchner

Meyer dysplasia is a rare condition that affects the femoral epiphysis in young children. This developmental disorder of the hip is characterized by delayed, irregular ossification of the femoral epiphyseal nucleus. Onset usually occurs in the second year of life, and the disorder usually disappears by the end of the sixth year. Harel and colleagues review the features of this dysplasia and describe five cases that were initially misdiagnosed.

The five cases included four males and one female who ranged from nine to 48 months of age at the time of presentation. Each child had a history of acute onset of limping of two to 30 days' duration. Three of the children had decreased range of motion on physical examination, and one patient had a fever. The erythrocyte sedimentation rate was elevated in two patients. The initial diagnosis was osteomyelitis in two children and Perthes disease in three children.

Radiographs of the hips revealed epiphyseal changes compatible with Meyer dysplasia. Two children had unilateral involvement, and three had bilateral involvement. Bone scans were normal in all five cases. Magnetic resonance imaging was performed in one child and revealed multiple centers of ossification and no evidence of ischemia or edema. In all patients, limping resolved within one to three weeks without specific treatment.

The authors note that Meyer dysplasia is most often bilateral. Meyer, in 1964, reported that this disorder occurs bilaterally in 42 percent of patients. In contrast, 7 percent of patients with Perthes disease have bilateral involvement. Previous studies indicate that boys are affected five times more often than girls. Patients show continuous improvement, with steady unification and growth of the epiphysis, usually over a three-year period.

Meyer dysplasia likely represents a physiologic variant of ossification of the femoral head. In most cases, the disorder is asymptomatic and is discovered incidentally on radiographs obtained for other reasons. Radiographic features include radiolucent defects in the femoral head and fragmentation of the femoral head. The authors point out that epiphyseal dysplasia and hypothyroidism should be included in the differential diagnosis whenever bilateral changes are visualized on plain radiographs of the hips. Bone scans are normal in patients with Meyer dysplasia. The authors note that Meyer dysplasia may be easily confused with more serious conditions such as osteomyelitis and Perthes disease, but knowledge of this condition can prevent unnecessary hospitalization and treatment.

Harel L, et al. Meyer dysplasia in the differential diagnosis of hip disease in young children. Arch Pediatr Adolesc Med September 1999;153:942-5.

COPYRIGHT 2000 American Academy of Family Physicians
COPYRIGHT 2000 Gale Group

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