Objective—To determine short- and long-term rates of successful outcomes of surgical and nonsurgical treatments for overweight dogs with cranial cruciate ligament rupture (CCLR).
Design—Prospective, randomized, clinical trial.
Animals—40 client-owned overweight dogs with unilateral CCLR.
Procedures—Dogs were randomly assigned to nonsurgical (physical therapy, weight loss, and NSAID administration) or surgical (tibial plateau leveling osteotomy) treatment groups; dogs in both groups received the same nonsurgical treatments. Dogs were evaluated immediately before and 6, 12, 24, and 52 weeks after initiation of treatments via owner questionnaires, gait analysis, and dual-energy x-ray absorptiometry. A successful outcome was defined as an affected limb net ground reaction force > 85% of the value for healthy dogs and a ≥ 10% improvement in values of questionnaire variables.
Results—Owner questionnaire responses indicated dogs in both groups improved during the study, but dogs in the surgical treatment group seemed to have greater improvement. Body fat percentages for dogs in both treatment groups significantly decreased during the study. Surgical treatment group dogs had significantly higher peak vertical force for affected limbs versus nonsurgical treatment group dogs at the 24- and 52-week evaluation times. Surgical treatment group dogs had a higher probability of a successful outcome (67.7%, 92.6%, and 75.0% for 12-, 24-, and 52-week evaluations, respectively) versus nonsurgical treatment group dogs (47.1%, 33.3%, and 63.6% for 12-, 24-, and 52-week evaluations, respectively).
Conclusions and Clinical Relevance—Overweight dogs with CCLR treated via surgical and nonsurgical methods had better outcomes than dogs treated via nonsurgical methods alone. However, almost two-thirds of the dogs in the nonsurgical treatment group had a successful outcome at the 52-week evaluation time.
Objective—To determine the relationship between serum cortisol concentration and pain severity as measured by force platform gait analysis in dogs with experimentally induced synovitis of the stifle joint.
Animals—10 healthy hound-type dogs.
Procedures—Dogs underwent 2 study phases. In the first phase, serum cortisol concentration, systolic arterial blood pressure, heart rate, and gait data were obtained at 0 (first sample), 2.5, 5, 7.5, and 10 hours. In the second phase, the same data were gathered immediately before (0 hours) and 2.5, 5, 7.5, and 10 hours after induction of acute urate synovitis in the left stifle joint. Data were statistically evaluated to compare changes in variable values over time and to determine the accuracy of serum cortisol measurements for diagnosis of acute orthopedic pain.
Results—Following induction of synovitis, ground reaction forces were significantly decreased relative to preinduction values at 2.5, 5.0, 7.5, and 10.0 hours and serum cortisol concentration was significantly increased at 2.5 hours. A cortisol concentration of ≥ 1.6 μg/dL indicated pain with a 91% sensitivity and 35% specificity.
Conclusions and Clinical Relevance—In this model, cortisol concentration may be useful for diagnosing pain in dogs. Although, with a cutoff of ≥ 1.6 μg/dL, pain would be detected in most dogs with pain, some pain-free dogs would also be identified as having pain. Conversely, dogs with a serum cortisol of < 1.6 μg/dL would be unlikely to have pain. Validation of this diagnostic test in a large, heterogeneous group of clinical patients is necessary.
Objective—To determine prevalence, level of inbreeding, heritability, and mode of inheritance for rupture of the cranial cruciate ligament (RCCL) in Newfoundlands.
Design—Retrospective and recruitment study.
Animals—574 client-owned Newfoundlands.
Procedure—Medical records from January 1, 1996, to December 31, 2002, were evaluated for prevalence of RCCL. A pedigree was constructed by use of recruited Newfoundlands with RCCL status based on results of veterinary examination; level of inbreeding, heritability, and mode of inheritance were calculated.
Results—Hospital prevalence for RCCL was 22%; dogs in the pedigree from the recruitment study had a mean level of inbreeding of 1.19 × 10−4, heritability of 0.27, and a possible recessive mode of inheritance with 51% penetrance for RCCL.
Conclusions and Clinical Relevance—Identification of a genetic basis for RCCL in Newfoundlands provided evidence that investigators can now focus on developing methods to identify carriers to reduce the prevalence of RCCL.
Objective—To compare tibial plateau angle (TPA)
between Greyhounds without damage to the cranial
cruciate ligaments and Labrador Retrievers with and
without damage to the cranial cruciate ligaments.
Animals—87 client-owned dogs and 15 research
Procedure—Standing position, horizontal-beam radiography
was performed on Greyhounds and unaffected
Labrador Retrievers to determine standing
TPA. Lateral radiography of the stifle joint was performed
on all dogs to determine traditional TPA. Age
and body weight were recorded for unaffected and
affected Labrador Retrievers.
Results—Greyhounds had mean standing TPA of
1.56° and mean traditional TPA of 22.50°. Unaffected
Labrador Retrievers had mean standing TPA of 3.52°
and traditional TPA of 27.97°. Affected Labrador
Retrievers had mean traditional TPA of 25.55°. No significant
difference was found in mean standing TPA
between Greyhounds and unaffected Labrador
Retrievers. Standing TPAs in Greyhounds and unaffected
Labrador Retrievers were not significantly different
from a plane drawn parallel to the ground.
Significant differences in traditional TPAs were
detected among all 3 groups.
Conclusions and Clinical Relevance—Greyhounds
had mean traditional TPA of 22.50°; similar angles
should be considered normal for dogs. Although
affected Labrador Retrievers had mean traditional
TPA that was significantly greater than that of
Greyhounds, the steepest TPA was found in unaffected
Labrador Retrievers. Because Greyhounds
and unaffected Labrador Retrievers had similar
standing TPAs, we conclude that although TPA may
be associated with damage to the cruciate ligaments,
many dogs with a steep TPA do not develop
cruciate ligament disease. (J Am Vet Med Assoc 2002;221:1426–1429)
Objective—To estimate the economic impact to veterinary
clients for the medical and surgical treatment
of rupture of the cranial cruciate ligament (RCCL) in
dogs for the year 2003.
Design—Economic impact survey.
Sample Population—501 diplomates of the
American College of Veterinary Surgeons (ACVS) indicating
that their area of surgical emphasis was small
animal orthopedic surgery or small animal general and
orthopedic surgery and 4,000 veterinarians indicating
to the AVMA that their professional area was small
animal practice exclusive or mixed animal practice (at
least 80% small animal).
Procedure—Veterinarians were surveyed concerning
the cost for medical and surgical treatment of RCCL
for 2003. The economic impact was calculated by
multiplying the number of RCCL surgeries performed
by the mean cost of surgery. This was added to the
number of RCCL cases managed medically multiplied
by the mean cost of medical management. This estimate
for survey responders was extrapolated to the
total number of veterinarians in the study population
for the ACVS or AVMA.
Results—Estimates for the total cost of surgery were
$171,730,134.72 and $1,020,167,907 for veterinarians
in the ACVS and AVMA populations, respectively. The
cost of medical management was $2,885,687.86 and
$126,558,155.16 for veterinarians in the ACVS and
AVMA populations, respectively. After combining the
ACVS and AVMA populations, we estimated that owners
spent $1.32 billion for the treatment of RCCL in the
United States in 2003.
Conclusions and Clinical Relevance—RCCL is a
prevalent, costly injury. Results may motivate veterinary
and consumer agencies to prioritize funding for a better
understanding of the injury. (J Am Vet Med Assoc 2005;
Objective—To identify chromosomal regions associated with cranial cruciate ligament rupture (CCLR) in a population of Newfoundlands.
Animals—90 client-owned Newfoundlands.
Procedures—A pedigree was constructed for dogs that did or did not have CCLR (determined on the basis of physical examination and radiographic findings). From this pedigree, affected and unaffected dogs were selected for genotyping on the basis of their predicted statistical likelihood of being homozygous CCLR-unaffected (n = 53) or homozygous CCLR-affected (37) dogs. Genotyping was performed for 532 microsatellite markers (MSATs). Comparisons of genotypes and allele frequencies were made between CCLR-affected and CCLR-unaffected dogs.
Results—In the selected population, 495 MSATs were informative with a mean interval between markers of 5.5 centimorgans. Eighty-six MSATs were significantly associated with the CCLR trait, whereas 4 markers (located on 4 chromosomes) were significantly associated with the trait when false discovery rate (q value) was controlled at the 0.05 level. Subsequent initial validation confirmed significant trait association for 3 of the 4 MSATs.
Conclusions and Clinical Relevance—In the population of Newfoundlands, 4 MSATs that were located on 4 chromosomes were significantly associated with the CCLR trait. Three of those markers were validated in part via genotyping additional closely located markers. The MSATs that were associated with the CCLR trait were identified in all regions (except for those on chromosome 24). Newfoundlands with CCLR could be used to study the disease process associated with anterior cruciate ligament injuries that occur in young female human athletes.
Objective—To characterize mucosal gene expression in dogs with chronic enteropathy (CE).
Animals—18 dogs with CE and 6 healthy control dogs.
Procedures—Small intestinal mucosal biopsy specimens were endoscopically obtained from dogs. Disease severity in dogs with CE was determined via inflammatory bowel index scores and histologic grading of biopsy specimens. Total RNA was extracted from biopsy specimens and microchip array analysis (approx 43,000 probe sets) and quantitative reverse transcriptase PCR assays were performed.
Results—1,875 genes were differentially expressed between dogs with CE and healthy control dogs; 1,582 (85%) genes were downregulated in dogs with CE, including neurotensin, fatty acid–binding protein 6, fatty acid synthase, aldehyde dehydrogenase 1 family member B1, metallothionein, and claudin 8, whereas few genes were upregulated in dogs with CE, including genes encoding products involved in extracellular matrix degradation (matrix metallopeptidases 1, 3, and 13), inflammation (tumor necrosis factor, interleukin-8, peroxisome proliferator–activated receptor γ, and S100 calcium-binding protein G), iron transport (solute carrier family 40 member 1), and immunity (CD96 and carcinoembryonic antigen–related cell adhesion molecule [CEACAM] 18). Dogs with CE and protein-losing enteropathy had the greatest number of differentially expressed genes. Results of quantitative reverse transcriptase PCR assay for select genes were similar to those for microchip array analysis.
Conclusions and Clinical Relevance—Expression of genes encoding products regulating mucosal inflammation was altered in dogs with CE and varied with disease severity.
Impact for Human Medicine—Molecular pathogenesis of CE in dogs may be similar to that in humans with inflammatory bowel disease.