HIP & ELBOW DYSPLASIA - PART III

by:  Greg Keller, DVM, MS, DACVR

Elbow Dysplasia Database

Anchor Jump Menu:
 Etiology Clinical
Presentation
OFA Elbow
Protocol
 Elbow
Classifications
Rationale for
Selective Breeding
 Application
Information
 Preliminary
Evaluations
 References    

Elbow dysplasia was originally described as a developmental disease manifested as degenerative joint disease (DJD) with or without an ununited anconeal process (UAP). Over time, two other inherited diseases, osteochondrosis (OCD) and fragmented medial coronoid process (FCP), were identified as part of the DJD complex collectively referred to as elbow dysplasia.

 

Etiology

Multiple theories on the cause of these abnormalities have been proposed. Olsson suggested a unitarian theory that UAP, OCD and FCP were all due to osteochondrosis. Osteochondrosis is a disturbance in endochondral ossification (the process by which bone is formed from a cartilage mold). Osteochondrosis results from a reduction in nutrients to the chondrocytes of the cartilage mold beneath articular cartilage. This loss of chondrocytes produces a weakened foundation under the articular cartilage, resulting in fracturing of the cartilage.

Wind suggested that asynchronous growth of the ulna and radius, or insufficient development of the ulnar trochlear notch, results in abnormal loading forces on the anconeal process or medial coronoid process.

Numerous studies suggest that the three diseases (UAP, OCD and FCP) are independent, inherited diseases.

 

Clinical presentation

The radiographic evidence of elbow dysplasia (ED), the presence of secondary degenerative joint disease (DJD), and the clinical presentation do not correlate directly. Grondalen reported on a population of 207 Rottweilers of which 141 were not lame. Yet 68% of the non-lame dogs had degenerative joint disease of the elbow. Another study by Read reported on serial radiographic and physical examination of 55 Rottweilers at 6 and 12 months of age. At 6 months of age the majority of lame dogs did not have radiographic evidence of ED; however, by 12 months of age the radiographic changes were apparent. But the majority of dogs remained sound.

The elbow is a complex joint with overlapping osseous structures which often makes a definitive diagnosis difficult especially when dealing with pathology involving the medial coronoid process. To increase the probability of achieving an accurate diagnosis, the routine radiographic examination of the elbow (cranial-caudal and neutral medial-lateral projections) can be supplemented with the craniolateral caudomedial oblique and an extreme flexed mediolateral projection. Even then, a definitive diagnosis can be difficult without linear tomography, computerized tomography or surgical exploration of the joint.

 

OFA elbow protocol

The International Elbow Working Group, (IEWG) a consortium of experts from around the world, was founded in 1989 to lower the incidence of elbow dysplasia by coordinating worldwide efforts. The OFA started its elbow database in 1990 using a modified protocol of the IEWG. The diagnosis of elbow dysplasia is based on the presence of degenerative joint disease/osteoarthrosis. Radiographically, the primary finding is sclerosis in the area of the trochlear notch and a periosteal response on the anconeal process which is best visualized on the extreme flexed mediolateral projection (Fig. 7). Although in and of itself, secondary degenerative joint disease is not an inherited disease, it is the end result found in dogs with elbow dysplasia.

Therefore, OFA requires one view of each elbow clearly labeled left and right in the extreme flexed medial-lateral position (Fig. 7). Inclusion of additional views is at the discretion of the attending veterinarian. A permanent clearance can be obtained at 24 months of age, and dogs between 5 and 24 months of age can receive a preliminary evaluation. The elbow radiographs are required to contain permanent dog identification in the emulsion. Nongrid, table top technique using high MaS and low Kvp is recommended.

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Figure 7

Figure 8

Note the remodeling of the proximal surface of the anconeal process (thick arrow, top) and sclerosis in the area of the trochlear notch (thin arrow). Irregularly formed medial coronoid process (thin arrow) and fracture of the articular cartilage (thick arrow). These changes are difficult, if not impossible, to visualize radiographically.

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Elbow classifications

The OFA reports elbows as normal or dysplastic. While there is no subdivision classification of normal, dysplastic elbows are graded 1 through 3, with grade 3 being the most severe. Differences between dysplastic grades are based on the severity of degenerative joint disease present.

Normal  - No evidence of inherited pathologic change

Dysplastic -
    Grade 1 - mild DJD - osteophytes less than 2 mm in height
    Grade 2 - moderate DJD - osteophytes 2 to5 mm in height
    Grade3 - severe DJD - osteophytes greater than 5 mm

There can be pathology involving the medial coronoid process without a distinct fracture fragment. As seen in Fig. 8 the malformed medial coronoid process and a fissure fracture of the articular cartilage could not be ascertained from the radiographic image, but created sufficient joint instability to produce secondary degenerative joint disease (Fig. 7).

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Rationale for selective breeding

There are multiple studies supporting the theory that the various components of ED have a polygenic mode of inheritance. Further, it appears that environmental factors also contribute to expression of the disease. Selective breeding of phenotypically normal dogs has been shown to reduce the incidence of elbow dysplasia. In 1965, Corley reported on the inheritance of ununited anconeal process. Swenson reported on a study which included 4,515 dogs registered by the Swedish Kennel Club. As selective pressure was applied toward identifying and breeding dogs with normal elbows, there was a corresponding increase in the percentage of normal progeny.

There are a number of papers reporting on the inheritance of osteochondrosis and fragmented medial coronoid process. A recent report by Padgett classifies these as separate diseases that may occur alone or in combination. In this study, the initial breeding pair of Labrador Retrievers had surgically confirmed osteochondrosis and fragmented medial coronoid process in both elbows. The male dog was subsequently bred to two of his fi rst and second generation daughters. There was a total of 31 progeny produced of which 83.9% had osteochondrosis, fragmented coronoid process or both.

Table 7 illustrates the outcome of matings based on information extracted from the OFA database. A total of 13,151 progeny were identified in which both parents had elbow dysplasia evaluations. The percentages of progeny with elbow dysplasia more than doubled if either parent had ED, and more than tripled if both parents had ED, as compared to when both parents were normal. Results of selective breeding practices indicate that elbow dysplasia should be considered in the moderate to high heritability estimate category (See discussion on genetics).

 

Table 7: Elbow scores

Scores on 13,151 progeny from sires and dams with known elbow scores.

Dam

Sire

 

Normal

Dysplastic

Normal

T = 10,245
D = 12.2%
T = 1,345
D = 31.3%

Dysplastic

T = 1,289
D = 26.1%
T = 272
D = 41.5%

T = total number of progeny; D = the percentage of progeny with elbow dysplasia


Application information

The owner or agent should complete and sign the OFA application form, and the information is best obtained directly from the animal's certificate or registration papers. It is also important to record the animal's tattoo or microchip number, and registration numbers of the sire and dam. Application forms are available on request from the OFA or can be downloaded from the OFA web site (www.offa.org). The radiograph, signed application form (which should include the owner's choice of open or semi-open database), and the service fee should be mailed to: Orthopedic Foundation for Animals, Inc., 2300 E. Nifong Blvd., Columbia, MO 65201-3856. All radiographic images are retained by the OFA for research and reference purposes.

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Preliminary hip and elbow evaluations

This service is offered to evaluate the hip status of an animal as young as 4 months of age. Many owners choose to breed their animals prior to 24 months or need to know the hip status of progeny produced by a particular sire and dam before using them in a repeat breeding. The evaluation is performed by one radiologist, and the response time is usually five days. Use the same application procedure as described under "Hip Dysplasia" in Part 1.

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References

  1. Bennett D: Hip Dysplasia and Ascorbate Therapy: Fact or Fancy? Seminars in Vet. Med. And Surg., Vol. 2, No. 2, 1987, p. 152-157.
  2. Corley EA, Carlson W: Radiographic, Genetic, and Pathologic Aspects of Elbow Dysplasia. J Am Vet Med Assoc, 1965;147:1651.
  3. Corley EA, et al: Reliability of Early Radiographic Evaluation for Canine Hip Dysplasia Obtained from the Standard Ventrodorsal Radiographic Projection. JAVMA, Vol. 211, No. 9, November 1997, pp. 1142-1146.
  4. Grondalen J, Grondalen T: Arthrosis in the Elbow Joint of Young, Rapidly Growing dogs. Nordish Veterinarmedicin, 1981:33:1-16.
  5. Grondalen J: Arthrosis in the Elbow Joint of Young, Rapidly Growing Dogs: Interrelation between Clinical Radiological, and Pathoanatomical Findings. Nordish Veterinarmedicin, 1982; 34:65-75.
  6. Kasstrom H: Nutrition, Weight Gain, and Development of Hip Dysplasia: An Experimental Investigation in Growing Dogs with Special Reference to the Effect of Feeding Intensity. Acta Radiol. Suppl.,  Vol 344: 135-179, 1975.
  7. Kealy RD, et al: Effects of Limited Food Consumption on the Incidence of Hip Dysplasia in Growing Dogs. JAVMA, Vol. 201, No. 6, 1992, p.857-863.
  8. Kealy RD, et al: Effect of Diet Restriction on Life Span and Age-related Changes in Dogs. JAVMA, 2002; 220: p.1315-1320.
  9. Leighton EA: Genetics of Canine Hip Dysplasia. JAVMA, Vol. 210, No. 10, 1997, pp. 1474-1479.
  10. Lust G et al: Joint Laxity and its Association with Hip Dysplasia in Labrador Retrievers. AJVR, Vol. 54, No. 12, 1993, p.1990-1999.
  11. Lust, G et al: Comparison of Three Radiographic Methods for Diagnosis of Hip Dysplasia in Eight-month Old Dogs. JAVMA, 2001; 219: p.1242-1246.
  12. Olsson SE: Osteochondrosis in Domestic Animals. ACTA Radiologic Suppl., 358, 1978, pp.299-305.
  13. Olsson SE: The Early Diagnosis of Fragmented Coronoid Process and Osteochondritis Dissecans of the Canine Elbow Joint. JAAHA, 1983:19(5):616-626.
  14. Padgett GA, et al: The Inheritance of Osteochondritis Dissecans and Fragmented Coronoid Process of the Elbow Joint in Labrador Re­triever. JAAHA, 1995; 31: 327-330.
  15. Read RA, et al: Fragmentation of the Medical Coronoid Process of the Ulna in Dogs: A Study of 109 Cases. J. Sm. Anim. Prac., 1990; 32(7), 330-334.
  16. Reed AL, et al: Effect of Dam and Sire Qualitative Hip Conformation Scores on Progeny Hip Conformation. JAVMA, 2000; 217: 675-680.
  17. Rettenmaier JL, Keller GG, et al: Prevalence of Canine Hip Dysplasia in a Veterinary Teaching Hospital Population. Vet. Rad. & Ultra­sound, Vol. 43, No. 4, 2002, p. 313-318.
  18. Smith, GK et al: Coxofemoral Joint Laxity from Distraction Radiography and its Contemporaneous and Prospective Correlation with Lax­ity, Subjective Score, and Evidence of Degenerative Joint Disease from Conventional Hip-Extended Radiograph in Dogs. AJVR, Vol 54: 1021-1042, No. 7, July, 1993.
  19. Swenson L, Audell L, Hedhammar A: Prevalence and Inheritance of and Selection for Elbow Arthrosis in Bernese Mountain Dogs and Rottweilers in Sweden and Benefit: Cost Analysis of a Screening and Control Program. JAVMA, 1997; 210: 215 - 221.
  20. Tomlinson JL: Quantification of Measurement of Femoral Head Cover­age and Norberg Angle within and among four breeds of dogs. AJVR, 2000; 61: p.1492-1498.
  21. Willis MB: Practical Genetics for Dog Breeders. H. F. & G. Witherby Ltd, Great Britain, 1992.
  22. Wind A: Elbow Incongruity and Development Elbow Dysplasia in the Dog (Part 1). J Amer Anim Hosp Assoc 1986:22:711-724.

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CREDITS:

G. G. Keller, D.V.M., MS, Diplomate of A.V.C.R., is the Executive Director of Orthopedic Foundation for Animals, Inc. Dr. Keller received his Doctorate in Veterinary Medicine in 1973 and was in a small animal private practice until 1987 at which time he accepted the Associate Director position for the Orthopedic Foundation for Animals. He received the Masters degree in Veterinary Medicine and Surgery in 1990 and Diplomate status in the American College of Veterinary Radiology in 1994. He assumed the role of Executive Director for the Orthopedic Foundation for Animals in January, 1997.

This article was originally printed on the OFA web site as part of its introductory article, "The use of health databases and selective breeding", and may be viewed in its entirety at http://www.offa.org/. Copyright © 2003 with all rights reserved. This publication cannot be reproduced in any form or by any means without prior written approval from the author(s).