Risk factors for hip-related clinical signs in a prospective cohort study of four large dog breeds in Norway
Introduction
Hip dysplasia and degenerative joint disease (DJD) in the hips are common causes of lameness and exercise intolerance in large-breed dogs (Vaughan, 1990, Roush, 2001). Canine hip dysplasia is a uni- or bilateral developmental disorder with a genetic predisposition, and the occurrence and severity of radiologically diagnosed hip dysplasia are influenced by environmental factors (Lust et al., 1973, Riser, 1974, Fry and Clark, 1992, Kealy et al., 1992, Zhu et al., 2009, Ginja et al., 2010, Krontveit et al., 2010, Krontveit et al., in press). DJD of the hips often occurs secondary to canine hip dysplasia, and both hip-joint laxity and increased bodyweight/body-condition score are risk factors for development of DJD in dogs with hip dysplasia (Smith et al., 1995, Smith et al., 2001, Runge et al., 2010). Hip instability allows the femoral head to subluxate during weight bearing which in turn alters the concentration of forces on the femoral head and acetabulum and results in DJD (characterized by loss of articular cartilage, fibrosis, bone remodeling, and loss of normal function) (Alexander, 1992, Fries and Remedios, 1995, Todhunter and Lust, 2003).
Clinical signs related to hip dysplasia can range from mild or intermittent lameness and stiffness with difficulty rising after rest, to nonambulation in severely affected dogs (Fry and Clark, 1992). Commonly, a bimodal age distribution is observed with affected younger dogs developing signs between age 3 and 12 mos and mature dogs displaying gradually increasing severity of signs due to progression of DJD (Riser, 1975, Vaughan, 1990, Dassler, 2003). The onset of signs in mature dogs varies from 2 to 12 yrs (Fry and Clark, 1992, Dassler, 2003, Ginja et al., 2010).
When relating clinical signs to the diagnosis of canine hip dysplasia, other causes of lameness or gait abnormalities must be ruled out (Fry and Clark, 1992). High frequencies of cranial cruciate-ligament ruptures have been found in dogs referred for lameness attributed to hip dysplasia (Roush, 2001, Powers et al., 2005). Additionally, both immature and mature dogs with hip dysplasia sometimes also have DJD in both shoulder and stifle joints which could contribute to lameness (Olsewski et al., 1983). Clinical tests can give information about hip joint-laxity and detect signs of DJD (Ginja et al., 2010). Standard radiographic examination of the coxofemoral joints might confirm the diagnosis of hip dysplasia through evaluation of hip-joint congruence and DJD, while stress radiography provides information about hip-joint laxity (Smith, 1997, Fluckiger et al., 1999, Ginja et al., 2010). Standard radiographic examination is used for official screening for canine hip dysplasia in many countries, including Norway, and the results of the radiographic screening are commonly registered in databases of national kennel clubs (e.g. the Norwegian Kennel Club (NKK)).
Aging, high birth weight, slippery pre-weaning floor cover, and neutering are risk factors for development of clinical signs related to canine hip dysplasia (van Hagen et al., 2005). The effect of neutering might be mediated by an increase in bodyweight (van Hagen et al., 2005). An association exists between radiological hip-dysplasia status at screening and incidence of veterinary insurance claims related to canine hip dysplasia (Malm et al., 2010). Not all dogs with a radiographic hip-dysplasia diagnosis develop clinical signs, and the severity of clinical signs will not always correspond with the radiographic findings (Brass, 1989, Fry and Clark, 1992, Dassler, 2003, Ginja et al., 2010).
In our analysis, a cohort of privately owned dogs from four large breeds was followed from birth until age 9 yrs. We wanted to investigate whether radiological hip-dysplasia status given at approximately age 12–18 mos and other factors during growth influenced development of clinical signs due to hip-joint disease necessitating veterinary consultation later in life. Whether or not such signs occurred due to hip dysplasia or due to secondary or primary DJD could not be distinguished, and we therefore used the term “owner-reported veterinary-diagnosed hip-related clinical signs” (also referred to as “the event”). The incidences over time under various exposures were studied. Specifically, our aims of the study were to describe breed differences in time to event and to evaluate potential risk factors by applying a Cox proportional-hazards model. The hypotheses were that radiological hip status at screening, bodyweight, and housing and exercise conditions during growth would influence time to the event.
Section snippets
Materials and methods
Our study was carried out in agreement with the provisions enforced by the National Animal Research Authority in Norway.
Descriptive statistics
The number of events, mean time to event or censoring, and total number of subjects in each category of dog data are provided in Table 2. Of the 494 dogs enrolled, 65 were lost to follow-up some time during the 9-yr observation period and 237 died or were euthanized. At the end of the study 46 NF, 85 LR, 53 LEO, and 8 IW were still alive.
Of the 46 dogs considered to have had the event (Table 3), 10 dogs were reported to have been euthanized due to hip dysplasia/hip-related problems without
Discussion
Our main findings were that there were breed differences in time to event, that dogs with radiographic hip status mild, moderate or severe had significantly shorter time to event (increased hazard) compared with dogs with radiographic hip status free, and that dogs exercised off-leash at 12 mos of age in garden and rough terrain had longer time to event (decreased hazard) compared to dogs not exercised this way.
The protective effect of being LR rather than NF disappeared by 4 yrs and by 2.5 yrs
Conclusion
Our findings supported our hypothesis that less severe radiological hip status at screening and provision of exercise during growth delayed the time to event. The LR and LEO breeds developed the event later than the NF. However, no effect of bodyweight was detected.
Conflict of interest statement
None of the authors of this paper has financial or personal relationship with other people or organizations that could inappropriately influence or bias the content of the paper.
Acknowledgements
The study was supported by grant no. 140541/110 from the Norwegian Research Council, the Norwegian School of Veterinary Science, and the Norwegian Kennel Club.
The authors thank the dog breeders, dog owners, kennel clubs, and veterinarians participating in this project for providing the material for the study. Professor Emeritus Jorunn Grøndalen, Professor Lars Moe, and Adjunct Professor Astrid Indrebø are thanked for their efforts in initiating the main study. A special “thank you” to Professor
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