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Canine hip dysplasia: Another perspective
The Veterinary Journal 183 (2010) 247–248
Contents lists available at ScienceDirect
The Veterinary Journal journal homepage: www.elsevier.com/locate/tvjl
Guest Editorial
Canine hip dysplasia: Another perspective
Hip dysplasia in dogs is a complex genetic disease characterized by joint instability and osteoarthritis (Lust, 1997). Factors that affect development of the disease include the amount of food consumption, bodyweight, age, and even hormones in milk during nursing (Kealy et al., 1992; Steinetz et al., 2008). The disease has been conventionally thought to be an abnormality involving only the tissues in the region of the hip joint, but evidence has shown that osteoarthritic changes often occur in shoulder, stifle and in vertebral joints of 6-month old, hip dysplastic dogs (Olsewski et al., 1983). This observation suggests that hip dysplasia is simply a conspicuous manifestation of a more generalized abnormality affecting the diarthrodial joints. It long has been known that hip dysplasia is a quantitative genetic trait and scientists have begun to define the regions on the dog genome that contain the genes that contribute to hip dysplasia. These regions are known as quantitative trait loci (QTL) and recent publications provide evidence that there are at least two and possibly as many as twelve canine chromosomes that harbor QTL for hip dysplasia (Marschall and Distl, 2007; Todhunter et al., 2005). Radiographic examination procedures developed to control the occurrence by selective breeding have reduced the frequency of hip dysplasia in strictly controlled populations of dogs (Swenson et al., 1997; Leighton, 1997). However, selective breeding has been less successful in the overall dog population; the disease has not been eliminated and still represents a major health problem for dogs. The reason for the lack of success in controlling hip dysplasia in part can be ascribed to non-compliance of breeders using dysplastic dogs, or using dogs for breeding without knowledge of their hip joint status. For example, the American Kennel Club does not require that dogs be certified as dysplasia-free for registration. Optimal or reduced feed intake, and possibly other treatments, and a proper understanding of the nature of the underlying genetics also may have a role and are more difficult to assess. Other characteristics or traits, besides hip joint status, also influence the use of dogs in breeding decisions. Aggressive behavior, intelligence, coat color, skeletal (bone) structure, and other disease risks are considered as selection criteria. These traits can be evaluated subjectively by owners and by veterinarians, and also by judges at dog shows in the process of identifying certain dogs for special recognition. Judges examine bone structure in the head and also the height and length of dogs and choose those that conform to specific breed standards. Yet, the effects of the selection of a skeletal form favored by judges on the health of dogs and their progeny have not been explored extensively. 1090-0233/$ - see front matter Ó 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.tvjl.2009.12.017
A report by Roberts and McGreevy (2010), published in this issue of The Veterinary Journal, addresses the role of the body length and height of dogs as related to the appearance of hip dysplasia. The conclusion of their study of 30 breeds of dogs was that the ratio of body length to body height (L/H) of the best-of-breed dogs in a breed was strongly correlated with a published percent of hip dysplasia as based on radiographic diagnosis. Stated differently, their findings were that a correlation existed between published percentages of hip dysplasia for a breed and a high L/H ratio derived from a picture of champion dogs in the breeds. On the other hand a low L/H ratio was associated with a low percentage of hip dysplasia. They identified an L/H ratio of 1.06 above which hip dysplasia occurred more frequently and below which more normal hip joints would be expected. They determined that the L/H ratio relationship by comparing breeds was observed in three national registries that evaluated hip status radiographically. The authors proposed that by selecting dogs with longer body lengths than heights judges at shows might be choosing dogs with an increased predisposition for hip dysplasia and perhaps promoting hip dysplasia in progeny. The discovery that higher L/H ratios in dogs are associated with a high percentage of dysplastic dogs and that lower L/H ratios favor good joints is new and ultimately may be of practical utility. If the observation is substantiated by further studies, and if judges do select long-bodied dogs for prizes, more hip dysplasia might be an unintended result. Two concerns should be considered before the concept is established with confidence. The authors’ data used L/ H ratios and it can be reasoned that the terms ‘long bodied appearance’ or ‘relative body length’ are not equivalent to a high L/H ratio. ‘Long bodied’ implies that length alone is associated with a higher percentage of hip dysplasia; however, no correlations with length alone were presented in the article. Also, the use of L/H ratios complicates interpretations because two measurements (L and H) are involved. It might be that judges sometimes favor shorter forelimbs, or smaller rib cages (i.e. chests), which also could result in higher L/H ratios. Taller dogs would promote lower L/H ratios. The authors of the study alert us to another important point. Data presented were generated by comparing 30 different breeds. Strong support for their proposal would be that dogs within a breed as well as mixed breed dogs have the same relationships. In other words, do unaffected dogs have low L/H ratios and dysplastic dogs have high ratios? The results presented in the article by Roberts and McGreevy (2010) are interesting and tentatively support their conclusions and recommendations. But, in the final analysis more information
248
Guest Editorial / The Veterinary Journal 183 (2010) 247–248
is needed to confirm or refute their hypothesis. If confirmed, L/H ratios might be considered as another environmental factor that influences the pathogenesis of hip dysplasia. How the environmental factors interact with the genes that cause the disease also requires additional research. George Lust College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA E-mail address: [email protected]
References Kealy, R.D., Olsson, S.E., Monti, K.L., Lawler, D.F., Helms, R., Biery, D., Lust, G., Smith, G.K., 1992. Effects of limited food consumption on the incidence of hip dysplasia in growing dogs. Journal of the American Veterinary Medical Association 201, 857–863.
Leighton, E.A., 1997. Genetics of canine hip dysplasia. Journal of the American Veterinary Medical Association 210, 1474–1479. Lust, G., 1997. An overview of the pathogenesis of canine hip dysplasia. Journal of the American Veterinary Medical Association 210, 1443–1445. Marschall, Y., Distl, O., 2007. Mapping QTLs for canine hip dysplasia in German Shepherd dogs. Mammalian Genome 38, 661–670. Olsewski, J.M., Lust, G., Rendano, V.T., Summers, B.A., 1983. Degenerative joint disease in multiple joints of young and mature dogs. American Journal of Veterinary Research 44, 1300–1308. Roberts, T., McGreevy, P.D., 2010. Selection for breed-specific long-bodied phenotypes is associated with increased expression of canine hip dysplasia. The Veterinary Journal. 183, 266–272. Steinetz, B.G., Williams, A.J., Lust, G., Schwabe, C., Büllesbach, E.E., Goldsmith, L.T., 2008. Transmission of relaxin and estrogens to suckling pups via milk and possible association with hip joint laxity. American Journal of Veterinary Research 69, 59–67. Swenson, L., Audell, L., Hedhammar, A., 1997. Prevalence and inheritance of and selection for hip dysplasia in seven breeds of dogs in Sweden and benefit: cost analysis of a screening and control program. Journal of the American Veterinary Medical Association 210, 207–214. Todhunter, R.J., Mateescu, R., Lust, G., Burton-Wurster, N., Dykes, N.L., Bliss, S.P., Williams, A.J., Vernier-Singer, M., Corey, E., Harjes, C., Quaas, R.L., Zhang, Z., Gilbert, R.O., Volkman, D., Casella, G., Wu, R., Acland, G.M., 2005. Quantitative trait loci for hip dysplasia in a crossbreed canine pedigree. Mammalian Genome 16, 720–730.
Contents lists available at ScienceDirect
The Veterinary Journal journal homepage: www.elsevier.com/locate/tvjl
Guest Editorial
Canine hip dysplasia: Another perspective
Hip dysplasia in dogs is a complex genetic disease characterized by joint instability and osteoarthritis (Lust, 1997). Factors that affect development of the disease include the amount of food consumption, bodyweight, age, and even hormones in milk during nursing (Kealy et al., 1992; Steinetz et al., 2008). The disease has been conventionally thought to be an abnormality involving only the tissues in the region of the hip joint, but evidence has shown that osteoarthritic changes often occur in shoulder, stifle and in vertebral joints of 6-month old, hip dysplastic dogs (Olsewski et al., 1983). This observation suggests that hip dysplasia is simply a conspicuous manifestation of a more generalized abnormality affecting the diarthrodial joints. It long has been known that hip dysplasia is a quantitative genetic trait and scientists have begun to define the regions on the dog genome that contain the genes that contribute to hip dysplasia. These regions are known as quantitative trait loci (QTL) and recent publications provide evidence that there are at least two and possibly as many as twelve canine chromosomes that harbor QTL for hip dysplasia (Marschall and Distl, 2007; Todhunter et al., 2005). Radiographic examination procedures developed to control the occurrence by selective breeding have reduced the frequency of hip dysplasia in strictly controlled populations of dogs (Swenson et al., 1997; Leighton, 1997). However, selective breeding has been less successful in the overall dog population; the disease has not been eliminated and still represents a major health problem for dogs. The reason for the lack of success in controlling hip dysplasia in part can be ascribed to non-compliance of breeders using dysplastic dogs, or using dogs for breeding without knowledge of their hip joint status. For example, the American Kennel Club does not require that dogs be certified as dysplasia-free for registration. Optimal or reduced feed intake, and possibly other treatments, and a proper understanding of the nature of the underlying genetics also may have a role and are more difficult to assess. Other characteristics or traits, besides hip joint status, also influence the use of dogs in breeding decisions. Aggressive behavior, intelligence, coat color, skeletal (bone) structure, and other disease risks are considered as selection criteria. These traits can be evaluated subjectively by owners and by veterinarians, and also by judges at dog shows in the process of identifying certain dogs for special recognition. Judges examine bone structure in the head and also the height and length of dogs and choose those that conform to specific breed standards. Yet, the effects of the selection of a skeletal form favored by judges on the health of dogs and their progeny have not been explored extensively. 1090-0233/$ - see front matter Ó 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.tvjl.2009.12.017
A report by Roberts and McGreevy (2010), published in this issue of The Veterinary Journal, addresses the role of the body length and height of dogs as related to the appearance of hip dysplasia. The conclusion of their study of 30 breeds of dogs was that the ratio of body length to body height (L/H) of the best-of-breed dogs in a breed was strongly correlated with a published percent of hip dysplasia as based on radiographic diagnosis. Stated differently, their findings were that a correlation existed between published percentages of hip dysplasia for a breed and a high L/H ratio derived from a picture of champion dogs in the breeds. On the other hand a low L/H ratio was associated with a low percentage of hip dysplasia. They identified an L/H ratio of 1.06 above which hip dysplasia occurred more frequently and below which more normal hip joints would be expected. They determined that the L/H ratio relationship by comparing breeds was observed in three national registries that evaluated hip status radiographically. The authors proposed that by selecting dogs with longer body lengths than heights judges at shows might be choosing dogs with an increased predisposition for hip dysplasia and perhaps promoting hip dysplasia in progeny. The discovery that higher L/H ratios in dogs are associated with a high percentage of dysplastic dogs and that lower L/H ratios favor good joints is new and ultimately may be of practical utility. If the observation is substantiated by further studies, and if judges do select long-bodied dogs for prizes, more hip dysplasia might be an unintended result. Two concerns should be considered before the concept is established with confidence. The authors’ data used L/ H ratios and it can be reasoned that the terms ‘long bodied appearance’ or ‘relative body length’ are not equivalent to a high L/H ratio. ‘Long bodied’ implies that length alone is associated with a higher percentage of hip dysplasia; however, no correlations with length alone were presented in the article. Also, the use of L/H ratios complicates interpretations because two measurements (L and H) are involved. It might be that judges sometimes favor shorter forelimbs, or smaller rib cages (i.e. chests), which also could result in higher L/H ratios. Taller dogs would promote lower L/H ratios. The authors of the study alert us to another important point. Data presented were generated by comparing 30 different breeds. Strong support for their proposal would be that dogs within a breed as well as mixed breed dogs have the same relationships. In other words, do unaffected dogs have low L/H ratios and dysplastic dogs have high ratios? The results presented in the article by Roberts and McGreevy (2010) are interesting and tentatively support their conclusions and recommendations. But, in the final analysis more information
248
Guest Editorial / The Veterinary Journal 183 (2010) 247–248
is needed to confirm or refute their hypothesis. If confirmed, L/H ratios might be considered as another environmental factor that influences the pathogenesis of hip dysplasia. How the environmental factors interact with the genes that cause the disease also requires additional research. George Lust College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA E-mail address: [email protected]
References Kealy, R.D., Olsson, S.E., Monti, K.L., Lawler, D.F., Helms, R., Biery, D., Lust, G., Smith, G.K., 1992. Effects of limited food consumption on the incidence of hip dysplasia in growing dogs. Journal of the American Veterinary Medical Association 201, 857–863.
Leighton, E.A., 1997. Genetics of canine hip dysplasia. Journal of the American Veterinary Medical Association 210, 1474–1479. Lust, G., 1997. An overview of the pathogenesis of canine hip dysplasia. Journal of the American Veterinary Medical Association 210, 1443–1445. Marschall, Y., Distl, O., 2007. Mapping QTLs for canine hip dysplasia in German Shepherd dogs. Mammalian Genome 38, 661–670. Olsewski, J.M., Lust, G., Rendano, V.T., Summers, B.A., 1983. Degenerative joint disease in multiple joints of young and mature dogs. American Journal of Veterinary Research 44, 1300–1308. Roberts, T., McGreevy, P.D., 2010. Selection for breed-specific long-bodied phenotypes is associated with increased expression of canine hip dysplasia. The Veterinary Journal. 183, 266–272. Steinetz, B.G., Williams, A.J., Lust, G., Schwabe, C., Büllesbach, E.E., Goldsmith, L.T., 2008. Transmission of relaxin and estrogens to suckling pups via milk and possible association with hip joint laxity. American Journal of Veterinary Research 69, 59–67. Swenson, L., Audell, L., Hedhammar, A., 1997. Prevalence and inheritance of and selection for hip dysplasia in seven breeds of dogs in Sweden and benefit: cost analysis of a screening and control program. Journal of the American Veterinary Medical Association 210, 207–214. Todhunter, R.J., Mateescu, R., Lust, G., Burton-Wurster, N., Dykes, N.L., Bliss, S.P., Williams, A.J., Vernier-Singer, M., Corey, E., Harjes, C., Quaas, R.L., Zhang, Z., Gilbert, R.O., Volkman, D., Casella, G., Wu, R., Acland, G.M., 2005. Quantitative trait loci for hip dysplasia in a crossbreed canine pedigree. Mammalian Genome 16, 720–730.