Content uploaded by Emma R Schachner
Author content
All content in this area was uploaded by Emma R Schachner on May 20, 2015
Content may be subject to copyright.
© 2015 Schachner and Lopez. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0)
License. The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further
permission from Dove Medical Press Limited, provided the work is properly attributed. Permissions beyond the scope of the License are administered by Dove Medical Press Limited. Information on
how to request permission may be found at: http://www.dovepress.com/permissions.php
Veterinary Medicine: Research and Reports 2015:6 181–192
Veterinary Medicine: Research and Reports Dovepress
submit your manuscript | www.dovepress.com
Dovepress 181
REVIEW
open access to scientific and medical research
Open Access Full Text Article
http://dx.doi.org/10.2147/VMRR.S53266
Diagnosis, prevention, and management
of canine hip dysplasia: a review
Emma R Schachner
Mandi J Lopez
Department of Veterinary Clinical
Sciences, School of Veterinary
Medicine, Louisiana State
University, Baton Rouge, LA, USA
Correspondence: Mandi J Lopez
Department of Veterinary Clinical
Sciences, School of Veterinary Medicine,
Louisiana State University, Skip Bertman
Drive, Baton Rouge, LA 70803, USA
Tel +1 225 578 9918
Email mlopez@lsu.edu
Abstract: Canine hip dysplasia (CHD) is a polygenic and multifactorial developmental disorder
characterized by coxofemoral (hip) joint laxity, degeneration, and osteoarthritis (OA). Current
diagnostic techniques are largely subjective measures of joint conformation performed at dif-
ferent stages of development. Recently, measures on three-dimensional images generated from
computed tomography scans predicted the development of OA associated with CHD. Continued
refinement of similar imaging methods may improve diagnostic imaging techniques to iden-
tify dogs predisposed to degenerative hip joint changes. By current consensus, joint changes
consistent with CHD are influenced by genetic predisposition as well as environmental and
biomechanical factors; however, despite decades of work, the relative contributions of each
to the development and extent of CHD signs remain elusive. Similarly, despite considerable
effort to decipher the genetic underpinnings of CHD for selective breeding programs, relevant
genetic loci remain equivocal. As such, prevention of CHD within domestic canine popula-
tions is marginally successful. Conservative management is often employed to manage signs of
CHD, with lifelong maintenance of body mass as one of the most promising methods. Surgical
intervention is often employed to prevent joint changes or restore joint function, but there are
no gold standards for either goal. To date, all CHD phenotypes are considered as a single entity
in spite of recognized differences in expression and response to environmental conditions and
treatment. Identification of distinct CHD phenotypes and targeting evidence-based conservative
and invasive treatments for each may significantly advance prevention and management of a
prevalent, debilitating condition in canine companions.
Keywords: canine hip dysplasia, orthopedics, joint, osteoarthritis
Introduction
Canine hip dysplasia (CHD) is a complex developmental disorder characterized by joint
laxity and osteoarthritis (OA) in one or both coxofemoral (hip) joints (Figure 1A–C).1
The polygenic, multifactorial etiology2 of CHD has challenged veterinarians and
researchers since the condition was described in the 1930s.3 Joint changes characteristic
of CHD are also associated with environmental factors such as nutrition,4–6 exercise,7
and the process of skeletal ossification.8,9 The condition affects essentially all breeds,
with an estimated prevalence ranging from 1% to 80% according to the Orthopedic
Foundation for Animals. It appears to occur at a relatively high rate in large-bodied
and brachycephalic dogs as well as those with high body length to height ratios.10,11
The periodic appearance of OA in joints other than the coxofemoral joint12,13 has led
some to propose systemic contributions to CHD expression.1 These complexities,
among others, complicate attempts to manage the CHD by selective breeding despite
strict reporting and guidelines.14
Number of times this article has been viewed
This article was published in the following Dove Press journal:
Veterinary Medicine: Research and Reports
19 May 2015
Veterinary Medicine: Research and Reports 2015:6
submit your manuscript | www.dovepress.com
Dovepress
Dovepress
182
Schachner and Lopez
There are many theories to explain CHD joint degenera-
tion, but joint laxity and irregular or delayed endochondral
ossification are among the most popular. The conditions are
not mutually exclusive, and their phenotypic expression is
variable within and among breeds.15 Partially ossified hip
structures may become distorted during development due
to mechanical stresses in joints with delayed endochondral
ossification.8,16 Joint components may be more vulnerable to
deformation and damage from normal joint kinetics before
they are fully ossified.8,9,17 Abnormal and delayed endochon-
dral ossification in the coxofemoral joint has been identified
in 15-day-old dogs that developed CHD by the time they were
12 months old,8,9,18 and in Great Danes with experimentally
induced hip dysplasia.19 In contrast, comparably earlier joint
ossification appears to occur in Greyhounds, a breed with
one of the lowest incidences of CHD. While it is clear that
variation in the process of endochondral ossification may play
a role in the development of CHD, the exact relationships
between ossification patterns, abnormal joint structure, and
development of OA remain unclear.20
Affected joints usually develop varying degrees
of synovial inflammation, articular cartilage damage
( Figure 1), osteophytes, and subchondral bone sclerosis and
remodeling.21–23 While there is no single, overarching descrip-
tion of the sequence of events in the process, there are changes
that occur in many forms of dysplasia. Recently, the dorsal
acetabular rim angle (a measure of the dorsal slope [angle] of
the subchondral articular acetabular surface relative to hori-
zontal) was reported to be significantly larger (less femoral
head coverage by the acetabulum) in dogs with coxofemoral
joint laxity versus normal dogs as early as 1 week of age.17
Subluxation of the femoral head and delays in ossification
Figure 1 Anatomy of canine hip dysplasia.
Notes: (A–C) Canine hip-extended radiographs, and corresponding images of the joints (D–F) from different individuals demonstrating mild (A and D), moderate (B and E),
and severe (C and F) joint changes. Light photomicrographs of normal (G) and brillated (H, arrow) articular cartilage.
Veterinary Medicine: Research and Reports 2015:6 submit your manuscript | www.dovepress.com
Dovepress
Dovepress
183
Canine hip dysplasia
of the craniodorsal acetabular margin are often visible by
8 weeks, and, in many cases, subluxation of the femoral
head increases by around 12 weeks of age.18 Degeneration
and microfractures of the articular cartilage, and thickening,
inflammation, and deterioration of the joint capsule, tendi-
nous insertions, and ligaments are often apparent by 5 months
of age.18 Despite the presence of these degenerative traits in
many dogs with degenerative coxofemoral joint changes,
clinical signs are variable.21
A direct relationship between joint capsular collagen
composition and mechanical properties was proposed over
30 years ago.24 Altered capsular collagen composition has
been identified in children with congenitally dislocated
hips25 and dogs with hip joint laxity.26 Joint capsular collagen
fibrils were found to be more heterogeneous in 8-month-old
Labrador Retriever puppies with severe coxofemoral joint
laxity than those with normal joints.15 Abnormal collagen
composition is thought to contribute to reduced joint capsule
stiffness, which contributes to excess femoral head motion
and abnormal mechanical stresses on the femoral greater
trochanter and acetabular margins and cartilage.15 Over time,
the abnormal forces are thought to result in deformation of
the articulating structures and an incongruous joint.18
Despite almost a century of work, many aspects of the
development and progression of joint changes and OA associ-
ated with CHD remain elusive. This makes establishment of a
gold standard for treatment a challenge. The lack of a single,
predictable pattern of joint degeneration is likely a reflection
of natural variability, including individual responses to exter-
nal environmental influences. However, ambiguity in disease
progression may also reflect distinct disease processes that
have yet to be recognized. Continued efforts to identify and
characterize patterns in joint changes may lead to identification
of CHD phenotypes, which will, in turn, contribute to earlier
disease identification and more effective targeted treatments.
Diagnosis
Despite some recognized patterns of joint degeneration
characteristic of CHD, there is significant variability in the
progression and ultimate severity of the disease as well as
inconsistent relationships between gross and radiographic
joint changes and clinical signs.21 There are, however, two
general behaviors often attributed to CHD, including lame-
ness in young dogs (under 1 year), that increases with activity
or trauma, and gait abnormalities and hind limb muscle atro-
phy in older dogs.27 Notably, hind limb lameness can be due
to reasons other than CHD joint changes, including pelvic,
distal hind limb, and neurological pathologies, metabolic
bone disease, ligament rupture, patellar luxation, and spine
disorders.27 Hence, a thorough, comprehensive assessment is
paramount to identification of the source of discomfort.
Subjective laxity examinations
The Ortolani test is a subjective evaluation of coxofemoral joint
laxity originally designed for diagnosis of human congenital
hip dislocation in the 1930s.28,29 The test is also used as a CHD
screening test.28 Dogs are placed in lateral recumbency; one
hand of the examiner is used to apply force along the length of
the femur from the stifle toward the pelvis as the other braces
the back just above the sacrum (Figure 2).27 This maneuver is
intended to displace the femoral head. The stifle is then slowly
abducted to reduce the joint.29 An audible or palpable pop as the
femur slips back into the acetabulum is considered a positive
Ortolani sign indicative of joint laxity. Lack of an Ortolani
sign does not necessarily mean that the hip is normal. Joint
changes associated with dysplasia, like thickening of the joint
capsule and joint tissue, may interfere with the displacement
required for a positive sign.28,30 Bardens’ test,31 an examination
technique designed to evaluate the hips of babies (aged younger
than 6 months), is thought to be more sensitive for detecting
coxofemoral joint laxity and/or shallow acetabula in puppies
6–8 weeks of age.29 With the dog in lateral recumbency, the
proximal femur is elevated laterally from the body. With the
femur elevated, the index finger of the other hand is used to
push the femur away from the joint in a dorsal direction with
pressure on the greater trochanter. More than 2 mm of displace-
ment is considered a positive sign.31 In general, these and other
palpation techniques may be used as part of a comprehensive
examination on puppies or dogs suspected to have excessive
joint laxity characteristic of CHD. However, the tests alone are
not sufficient for diagnosis of CHD.
Radiography
Radiography has long been the gold standard to assess
and quantify joint changes associated with CHD joint
remodeling.32,33 Worldwide, there are five popular, standard-
ized evaluation systems with distinct metrics that are used to
grade canine radiographic coxofemoral joint conformation
and degenerative changes.
Orthopedic Foundation for Animals
The Orthopedic Foundation for Animals evaluation is
performed on hip-extended radiographs performed under
heavy sedation or general anesthesia by three independent
board-certified radiologists.10 Based on subjective assess-
ment of nine joint parameters (Figure 3A), conformation
Veterinary Medicine: Research and Reports 2015:6
submit your manuscript | www.dovepress.com
Dovepress
Dovepress
184
Schachner and Lopez
is categorized as excellent, good, fair, borderline, mild,
moderate, or severe. The first three categories are considered
to be normal while the last three are dysplastic.10 Metrics
are largely subjective assessments of hip conformation and
evidence of degenerative joint disease.
British Veterinary Association/Kennel Club
The British Veterinary Association/Kennel Club maintains a
“pass/fail” evaluation system that was instituted in 1965 and
updated in 1984.34 For scoring, dogs must be at least 1 year
of age, microchipped (or tattooed), and, if registered with the
Kennel Club, the registration number must be included on the
radiograph.35 Each dog has one opportunity to be scored by the
system. Joints are individually scored on nine criteria from 0 to
5 or from 0 to 6 on hip-extended radiographs by two qualified
radiologists on a British Veterinary Association/ Kennel Club
panel, with 0 being the best score and 106 the worst (53 possible
points for each hip).34 The nine criteria ( Figure 3B) include the
Norberg angle (Figure 3C) and subjective assessments includ-
ing subluxation, dorsal acetabular edge, cranial acetabular
edge, cranial effective acetabular rim, acetabular fossa, femoral
head recontouring, and femoral head and neck exostosis.34,35
An average score for each individual dog breed is published,
ie, the breed mean score, and it is recommended that only
animals with total scores well below the breed mean be used
for breeding purposes.35
Fédération Cynologique Internationale
The Fédération Cynologique Internationale (FCI)36 is one
of the largest canine organizations in the world and includes
kennel clubs from across Europe, Asia, Africa, and South
America. Extended hip and abducted hind limb radiographs
performed at 1 year of age (18 months for large breed dogs)
are scored according to the official FCI system by radiologists
approved by breed-specific kennel clubs.36 Scoring includes
the Norberg angle, formed by a horizontal line connecting
the centers of the right and left femoral heads and a line con-
necting each center to the cranial margin of the corresponding
acetabulum (Figure 3C)37 as well as subjective hip conforma-
tion parameters. Each joint is assigned a grade of A–E, with
A representing healthy and E representing severe dysplasia.
The more dysplastic of the two joint scores is considered the
A
Acetabulum
Ligamentum
teres
Cartilaginous labrum
B
DC
Femoral head
Joint capsule
Figure 2 Schematic illustration of the Ortolani test.
Notes: Image demonstrates the coxofemoral joint prior to distraction (A), while force is applied from the stie toward the hip along the axis of the femur to displace the
femoral head (B), during abduction of the femur to reduce the joint (C), and with the femoral head snapping back into place with an audible click, ie, the Ortolani sign (D).
Arrows indicate the direction of the applied force. Adapted from Chalman JA, Butler HC. Coxofemoral joint laxity and the Ortolani sign. Journal of American Animal Hospital
Association. 1985;21:671–676.28
Veterinary Medicine: Research and Reports 2015:6 submit your manuscript | www.dovepress.com
Dovepress
Dovepress
185
Canine hip dysplasia
final score for the individual dog. The same grading scale can
also be applied to computed tomography (CT) scans.
Pennsylvania Hip Improvement Program
University of Pennsylvania researchers developed a quantita-
tive method to evaluate canine hip conformation38–40 that was
implemented in 1994.41 The primary distinction of the Penn-
sylvania Hip Improvement Program (PennHIP) method is that
passive hip joint laxity is measured in addition to subjective
radiographic conformation.38–40 Three radiographic views
are evaluated by PennHIP-certified radiologists: a standard
hip-extended view for evidence of degenerative joint disease;
a compression view for congruity between the femoral head
and acetabulum; and a distraction view, for joint laxity. The
distraction index is the ratio of the distance between the
centers of the femoral head and acetabulum (d) and the radius
of the femoral head (r), as shown in Figure 3D. The closer the
score is to 0, the better the fit, ie, minimal femoral distrac-
tion, but a score of 1 indicates severe laxity and associated
femoral distraction.41 Recently, the PennHIP distraction index
and OA scores were found to have strong correlations with
microstructural changes in the articular cartilage,42 potentially
indicating a relationship between joint laxity measured by
this technique and articular surface degeneration.
Dorsolateral subluxation
Dorsolateral subluxation is used to quantify joint laxity in
a position to simulate weight-bearing (Figure 3E). During
Figure 3 Representations of anatomical landmarks and evaluation mechanisms to assess canine hip dysplasia.
Notes: Coxofemoral joint anatomical characteristics considered by the Orthopedic Foundation for Animals (A): craniolateral acetabular rim (1), cranial acetabular margin
(2), femoral head (3), fovea capitis (4), acetabular notch (5), caudal acetabular margin (6), dorsal acetabular margin (7), junction of femoral head and neck (8), and trochanteric
fossa (9). (B) British Veterinary Association/Kennel Club canine coxofemoral joint characteristics scored during evaluation.10,34 Schematic superimposed on a hip-extended
radiograph demonstrating the Norberg angle (C, arrow). Illustration of the Pennsylvania Hip Improvement Program (distraction index, the distance between the centers of
the femoral head and acetabulum during distraction (D) divided by the radius (r) of the femoral head (d).41 Depiction of the dorsolateral subluxation score (E) calculated as
100 multiplied by the percentage of femoral head medial to the cranial acetabular rim (d) divided by the femoral head diameter (θ), d/θ ×100%).
Abbreviations: AF, acetabular fossa; An, acetabular notch; CaAE, caudal acetabular edge; CrAE, cranial acetabular edge; CrEAR, cranial effective acetabular rim; DAE, dorsal
acetabular edge; Fh, femoral head; Fv, foveal defect.
Veterinary Medicine: Research and Reports 2015:6
submit your manuscript | www.dovepress.com
Dovepress
Dovepress
186
Schachner and Lopez
general anesthesia, pressure is applied to the femur at the level
of the stifle while imaging the dog in ventral recumbency.43
Joints with less than 45% coverage of the femoral head
by the lateral aspect of the cranial acetabular rim have an
increased chance of developing joint changes and OA over
time compared with those with a higher percentage (.55%)
of coverage.43
Subjective radiographic evaluations are limited by
the inherent variability associated with examiners, image
quality, and differences between animals including periar-
ticular soft tissue changes and muscle atrophy. Variation in
the degree of muscle relaxation associated with sedation
or anesthesia during imaging can influence the ability to
identify joint abnormalities by as much as 50%.44 Further,
each evaluation system is distinct, so results are based on
slightly different criteria. Recently, the Orthopedic Founda-
tion for Animals score was reported to underestimate the
likelihood of developing coxofemoral joint OA compared
to the PennHIP distraction index.45 Reporting mechanisms
also vary widely in public access to individual scores for
reproduction decisions. As with any measure, radiographic
hip scores should not be used in isolation to evaluate and
predict current and future joint structure and function. It
is possible that the presence of OA at a young age may be
indicative of rapidly progressive joint disease, and, given
recognition of the genetic basis for the disease, consider-
ation of the presence and extent of CHD signs in related
individuals is likely warranted. Based on this information,
it is clear that continued efforts to identify mechanisms for
early and accurate CHD diagnosis are of utmost importance.
Adaptation of knowledge from decades of research to emerg-
ing imaging modalities will, no doubt, continue to improve
upon current standards.
Computed tomography
CT technology for pelvic imaging has improved consider-
ably over the past few decades. While radiographs remain
the primary method used to image canine coxofemoral
joints, CT is becoming increasingly popular. Using three-
dimensional CT models, a recent longitudinal study showed
that volumetric changes in the acetabulum and proximal
femur occurred in a predictable manner during skeletal
growth in a colony of dogs with coxofemoral joint laxity.46
Another study demonstrated that two-dimensional CT images
and three-dimensional models created from CT images
can be used to predict the presence of joint OA at matu-
rity.47 Two-dimensional CT measures included the percent
femoral head coverage, acetabular index, and the following
angles: acetabular anteversion, ventral, dorsal, and horizontal
acetabular sector, center edge, and horizontal toit externe
(Figure 4). Measures on three-dimensional models included
femoral head and neck volumes, femoral head and neck radii
and femoral neck angle (Figure 4). The 16-week distraction
index and center edge angle combination was the best pre-
dictor of mature OA, whereas the 32-week dorsal acetabular
sector angle and Norberg angle combination was the most
effective predictor of the presence of OA at maturity. Hence,
combined measures were the best mechanism for predicting
development of OA, and the combinations varied with age.
In a separate study, numerous measures were performed on
pelvic CT scans of beagles and mixed breed dogs at various
time points between the ages of 2 months and 1 year to assess
the relationship of the measures with joint laxity.17 The dorsal
acetabular rim angle and center distance index (the distance
between the femoral head and the center of the acetabulum,
divided by the radius of the femoral head, or the PennHIP41
distraction index) were found to be good indicators of joint
laxity and dysplastic changes.17 Magnetic resonance imag-
ing is used to evaluate the three-dimensional structure of
human articular soft tissues, and relatively recently, canine
articular soft tissues,48 but CT is best for bone structure,49
and the cost of magnetic resonance imaging for screening
may be prohibitive. As technology advances, and CT and
magnetic resonance imaging become more readily available
and affordable, use of three-dimensional imaging method-
ologies will likely become an integral part of diagnosis and
assessment of CHD.
Therapeutic management
and intervention
Conservative management
There are numerous descriptions of multifactorial systems,
with numeric, visual analog, and descriptive scales to repro-
ducibly evaluate joint pain associated with CHD.50 Many of
the assessments within the systems are subjective evalua-
tions of individual behavior or responses, and there is no
single gold standard with which to quantify hip pain in the
dog.50 While efforts continue to establish a uniform, standard
evaluation system for canine hip joint pain, those systems
that include multiple subjective and objective assessments
by individuals who are not aware of specific treatments or
conditions, are often informative.
Conservative management of CHD generally consists
of a combination of mechanisms to reduce progression of
joint damage and alleviate discomfort.51 Nonsteroidal anti-
inflammatory drugs are commonly used for pain associated
Veterinary Medicine: Research and Reports 2015:6 submit your manuscript | www.dovepress.com
Dovepress
Dovepress
187
Canine hip dysplasia
Figure 4 Measurements and three-dimensional models for evaluating the dysplastic canine hip.
Notes: (A) Volume rendered model of the canine pelvis generated from two-dimensional computed tomography images (B and C). The blue line in (A) indicates the level
of the cross-sectional image in (B) and (C). (B) and (C) Representative measures performed on two-dimensional computed tomographic images of the canine coxofemoral
joint. Acetabular index is the ratio between the width and the depth of the acetabulum; d/w ×100. For further information see Lopez et al42 and Andronescu et al.47 For
details on these measures see Lopez et al.42
Abbreviations: AAA, acetabular anteversion angle; AI, acetabular index; CEA, center edge angle; CPC, percentage of femoral head coverage; DASA, dorsal acetabular
sector angle (dorsal coverage of the femoral head); HASA, horizontal acetabular sector angle (total acetabular coverage of the femoral head); HTEA, horizontal toit externe
angle (orientation of the acetabulum); VASA, ventral acetabular sector angle (ventral coverage of the femoral head).
with severely arthritic joints in dogs.52 Numerous studies
indicate that achieving and maintaining a healthy body
weight contributes to delayed onset and reduced clinical signs
associated with hip joint pain.4,5,53 Various food supplements
reported to alleviate signs of coxofemoral joint pain from OA
range from green-lipped mussels (Perna canaliculus)54 to
fish oil.55 Polysulfated glycosaminoglycan supplements and
injections have been recommended for prevention and treat-
ment of OA in dogs and other mammals.56–59 Intramuscular57
and intra-articular administration has also been reported,56
but responses vary.51 Alternative methods that have also been
investigated for the treatment of painful CHD joints include
acupuncture and gold bead implantation, among others. The
implantation of gold beads at acupuncture points was devel-
oped in the USA in the 1970s and implemented to a limited
degree in veterinary medicine in the 1990s for degenerative
joint disease pain.60,61 Results are mixed, with some studies
showing clinical improvement61,62 and others showing no
discernible effect.63
Maintenance of optimum body weight has long been
considered one of the most effective methods for reducing the
signs associated with dysplasia and OA.4 A lifelong dietary
restriction of 25% delayed the appearance of OA as well as the
intensity of clinical signs in Labrador Retrievers compared
with feeding ad libitum.53 Weight loss in conjunction with
physiotherapy that included transcutaneous electrical nerve
stimulation improved the clinical outcome for obese dogs
with radiographic signs of OA.64 Recently, intra-articular
botulinum toxin A was reported to reduce the pain associated
with OA based on improvements in limb use (ie, gait pat-
terns) measured with a force platform.65 At present, there are
few reports of long-term studies concerning the efficacy of
nonsurgical or conservative treatment of CHD joint changes.
These studies can be limited by the challenges of consistent
monitoring and reporting by multiple and individual owners,
as well as a wide range of disease severity and canine per-
sonalities.66 However, a recent retrospective report indicates
that conservative and nonsurgical management (ie, weight
Veterinary Medicine: Research and Reports 2015:6
submit your manuscript | www.dovepress.com
Dovepress
Dovepress
188
Schachner and Lopez
control, reduced exercise, and analgesics) of 74 dogs over the
span of 13 years did not improve quality of life as anticipated
from previous reports.66
There is significant interest in the use of regenerative
medicine to treat signs of CHD and OA; however, much of
the information reported is subjective in nature. Currently,
numerous controlled, preclinical and clinical trials are under-
way that may provide some perspective on the value of this
emerging technology. Intra-articular injection of adipose-
derived stem cells has been found to be a safe therapeutic
approach for the treatment of symptoms associated with
OA.67 Preliminary studies show that injection of adipose-
derived stem cells into affected joints may reduce clinical
signs of hip pain (ie, lameness) based on subjective clinical
evaluations67 and force platform gait analysis.68,69 A random-
ized comparison between a single intra-articular injection of
adipose-derived stem cells or plasma rich in growth factors
showed that both treatments reduced behavior associated with
pain, but that the adipose-derived stem cells appeared to be
more effective for up to 6 months post-treatment based upon
owner assessments.70 This information clearly demonstrates
that there is more work to be done on the efficacy of conserva-
tive and alternative methods to manage signs of CHD.
Surgery
Despite the prevalence of CHD, a gold standard surgical pro-
cedure has yet to be identified.71 As such, there are numerous
surgeries to prevent progression of degenerative joint changes
or alleviate pain and restore joint function.
Some surgical procedures designed to prevent onset of OA
in hips identified as being predisposed to development of OA72
include double and triple pelvic osteotomy, acetabular shelf
and excision arthroplasty, femoral osteotomy, and juvenile
pubic symphysiodesis.73 Both juvenile pubic symphysiodesis
and triple pelvic osteotomy are designed to increase femoral
head coverage by ventrolateral rotation of the acetabulum. The
juvenile pubic symphysiodesis procedure involves premature
closure of the pubic symphysis.72,74 Resulting reduction in
the pelvic inlet width causes ventrolateral rotation of the
acetabulum during pelvic growth, and is thought to result in
a 40%–46% improvement in acetabular and dorsal acetabu-
lar rim angles compared to no treatment.73–75 Juvenile pubic
symphysiodesis appears to have the best outcomes when per-
formed in puppies that are 12–16 weeks old.73 Triple pelvic
osteotomy is a much more extensive procedure, and involves
osteotomies of the ilium, pubis, and ischium to allow manual
rotation of the acetabulum for better femoral head coverage.76
The ilial osteotomy is stabilized with bone plates customized
to accommodate the rotation.77 This procedure is generally
recommended for young dogs without irreversible (or with
mild) degeneration of the coxofemoral joint.77,78 Information
about long-term outcomes of the various surgical treatments
is limited. Preliminary reports indicate that juvenile pubic
symphysiodesis and triple pelvic osteotomy minimally affect
laxity and femoral head coverage when performed at 5 months
or older72 compared with earlier reports indicating that the
procedure performed slightly earlier (15 weeks) improved
acetabular coverage of the femur.75 Mechanisms to reduce the
OA characteristic of CHD will undoubtedly improve quality of
life for affected dogs. Long-term outcomes will help identify
treatments toward this end.
Total hip replacement (Figure 5) is often applied in
advanced cases of joint degeneration and is considered a
salvage procedure.79 There are no clear guidelines for the
best time to implement total hip replacement, but the aver-
age time between onset of signs and surgery is 10 months.80
Total hip replacement procedures in dogs began in the 1970s,
and a modular system was introduced in the mid 1990s that
coupled a fixed monobloc cobalt-chromium alloy femoral
implant with an acetabular cup for cemented fixation.81
Further refinements to total hip replacement implants have
contributed to a high clinical recovery rate, with loosening of
the acetabular cup and cup wear reported as some of the most
common complications.81 More recently, cementless fixation
has been developed, and is reported to have positive results.79
As the name implies, femoral and acetabular implants are
cemented to bone for cemented total hip replacement. In
contrast, cementless fixation or uncemented implants are
designed so that the bone grows into or onto the prosthesis
without the need for cement at the bone–implant interface.
Implant loosening is reported to be less than for cemented
implants.79,82 A primary concern associated with total hip
replacement is the potential for an inflammatory response
Figure 5 Radiograph illustrating a bilateral total hip replacement.
Notes: Blue line indicates femoral implant, pink line indicates acetabular implant.
Image courtesy of Dr Jeffrey D Brourman.
Veterinary Medicine: Research and Reports 2015:6 submit your manuscript | www.dovepress.com
Dovepress
Dovepress
189
Canine hip dysplasia
to implant particulate wear debris from aseptic implant
loosening.83 Another consideration is that the persistence
of joint laxity may influence the outcomes of total hip
replacement.84 Efforts continue to improve upon available
total hip replacement implants for dogs. A hybrid system of
a cementless acetabular cup and a cemented femoral implant
has been successfully applied in dogs relatively recently.85
Hip resurfacing to replace only joint surfaces versus the
entire joint86 in dogs is under development, but clinical
trials have yet to be reported.81 Unfortunately, large-scale,
prospective randomized studies have yet to be conducted
for comparison of long-term outcomes for various surgical
procedures and nonsurgical management. Hence, individu-
alized care remains largely based on clinician preference
and experience.71
Genetics
While diagnosis and treatment of CHD are central to indi-
vidual patient care, prevention by selective breeding will help
obviate the presence of a debilitating condition in canine
companions. With this in mind, there has been significant
effort focused on identifying specific genes, genetic muta-
tions, and quantitative trait loci (regions of chromosomes
containing DNA for a specific trait), to use in conjunction
with standard imaging methods for identification of CHD
carriers.87,88 Genetic screening programs are complicated
by the polygenic nature of CHD and related OA, as well as
environmental influences on phenotypic expression. A few
promising quantitative trait loci for OA associated with
CHD89 and the CHD phenotype in German shepherds90
have been identified relatively recently. Additionally, several
chromosomal markers for CHD have been reported for a
population of cross-bred Labrador Retriever–Greyhounds.91
Notably, several specific single nucleotide polymorphisms
and positional candidate genes in dogs with CHD have been
found to correlate with genes associated with the expression
of OA and developmental dysplasia of the hip in humans.87
While the genomic underpinnings of CHD remain largely
elusive, significant progress has been made and will continue,
with expanding knowledge of the canine genome and interac-
tions among genes that influence their expression.
Future directions
Despite almost a century of research, the complex etiology
and optimal treatment paradigm for CHD remain elusive.
As originally proposed by Schnelle at a meeting of the
Veterinary Medical Society of New York City in the 1930s,92
CHD is not likely a single affliction but an array of heritable
and environmentally induced degenerative disorders that
differentially affect the morphology and function of the
canine hip. The variable phenotypic expression of CHD
makes development and implementation of standard iden-
tification procedures difficult. It may be possible to identify
specific phenotypes within the broad spectrum of CHD
similar to those of the human hip, like acetabular rim syn-
drome, acetabular retroversion, and femoral head necrosis.
The relationship between articular damage in the human
hip with morphology suggests a need to evaluate similar
relationships in the dog.93 Identification and characteriza-
tion of CHD phenotypes at the genetic, microstructural, and
macrostructural levels will likely contribute to early detec-
tion and informed breeding decisions. Another area that will
continue to promote progress in both imaging and treatment
is development of novel measures on images obtained with
contemporary imaging modalities like CT and magnetic
resonance imaging. As evidence-based assessments of CHD
prevention and treatment strategies become available, their
selection and implementation will improve and facilitate
the development of novel clinical approaches and surgical
procedures. Incremental advances in the diagnosis, treat-
ment, and prevention of the joint degeneration and pain
associated with CHD through focused research and clinical
evidence will continue to progress toward diminishing and
eradicating CHD from our canine companions.
Disclosure
The authors report no conflicts of interest in this work.
References
1. Lust G. An overview of the pathogenesis of canine hip dysplasia. J Am
Vet Med Assoc. 1997;210:1443–1445.
2. Zhang ZW, Zhu L, Sandler J, et al. Estimation of heritabilities, genetic
correlations, and breeding values of four traits that collectively define
hip dysplasia in dogs. Am J Vet Res. 2009;70:483–492.
3. Schnelle GB. Bilateral congenital subluxation of the coxo-femoral
joints in a dog. University of Pennsylvania Bulletin School of Veterinary
Medicine Veterinary Extension Quarterly. 1937;37:15–16.
4. Impellizeri JA, Tetrick MA, Muir P. Effect of weight reduction on clinical
signs of lameness in dogs with hip osteoarthritis. J Am Vet Med Assoc.
2001;216:1089–1091.
5. Kealy RD, Lawler DF, Ballam JM, et al. Evaluation of the effect of
limited food consumption on radiographic evidence of osteoarthritis in
dogs. J Am Vet Med Assoc. 2000;217:1678–1680.
6. Steinetz BG, Williams AJ, Lust G, Schwabe C, Büllesbach EE,
Goldsmith LT. Transmission of relaxin and estrogens to suckling canine
pups via milk and possible association with hip joint laxity. Am J Vet
Res. 2008;69:59–67.
7. Greene LM, Marcellin-Little DJ, Lascelles BD. Associations among exer-
cise duration, lameness severity, and hip joint range of motion in Labrador
retrievers with hip dysplasia. J Am Vet Med Assoc. 2013;242: 1528–1533.
8. Madsen JS, Reimann I, Svalastoga E. Delayed ossification of the femoral
head in dogs with hip dysplasia. J Small Anim Pract. 1991;32: 351–354.
9. Todhunter RJ, Zachos TA, Gilbert RO, et al. Onset of epiphyseal mineral-
ization and growth plate closure in radiographically normal and dysplastic
Labrador retrievers. J Am Vet Med Assoc. 1997;210: 1458–1462.
Veterinary Medicine: Research and Reports 2015:6
submit your manuscript | www.dovepress.com
Dovepress
Dovepress
190
Schachner and Lopez
10. The Orthopedic Foundation for Animals [webpage on the Internet].
The OFA’s Hip Radiograph Procedures. Available from: http://www.
offa.org/hd_procedures.html. Accessed January 10, 2015.
11. Roberts T, McGreevy PD. Selection for breed-specific long-bodied phe-
notypes is associated with increased expression of canine hip dysplasia.
Vet J. 2010;183:266–272.
12. Farquhar T, Bertram J, Todhunter RJ, Burton-Warster N, Lust G.
Variations in composition of cartilage from shoulder joints of young
dogs at risk for developing canine hip dysplasia. J Am Vet Med Assoc.
1997;210:1483–1485.
13. Olsewski JM, Lust G, Rendano VT, Summers BA. Degenerative joint
disease: multiple joint involvement in young and mature dogs. Am J
Vet Res. 1983;44:1300–1308.
14. Leppänen M, Mäki K, Juga J, Saloniemi H. Factors affecting hip
dysplasia in German shepherd dogs in Finland: efficacy of the current
improvement programme. J Small Anim Pract. 2000;41:19–23.
15. Todhunter RJ, Lust G. Hip dysplasia: pathogenesis. In: Slatter ED,
editor. Textbook of Small Animal Surgery. Philadelphia, PA, USA:
Saunders; 2003.
16. Vanden Berg-Foels WS, Todhunter RJ, Schwager SJ, Reeves AP. Effect
of early postnatal body weight on femoral head ossification onset and
hip osteoarthritis in a canine model of developmental dysplasia of the
hip. Pediatr Res. 2006;60:549–554.
17. Fujiki M, Kurima Y, Yamanokuchi K, Misumi K, Sakamoto H.
Computed tomographic evaluation of growth-related changes in the
hip joints of young dogs. Am J Vet Res. 2007;68:730–734.
18. Riser WH. The dysplastic hip joint: radiologic and histologic
development. Vet Pathol. 1975;12:279–305.
19. Wu FM, Hedhammar Å, Krook L. Overnutrition and skeletal disease.
An experimental study in growing Great Dane dogs. IX. The long bones.
Cornell Vet. 1974;64:83–114.
20. Chalmers HJ, Dykes NL, Lust G, et al. Assessment of bone mineral
density of the femoral head in dogs with early osteoarthritis. Am J Vet
Res. 2006;67:796–800.
21. Barr ARS, Benny HR, Gibbs C. Clinical hip dysplasia in growing dogs:
the long-term results of conservative management. J Small Anim Pract.
1987;28:243–252.
22. Bijlsma JW, Berenbaum F, Lafeber FP. Osteoarthritis: an update with
relevance for clinical practice. Lancet. 2011;377:2115–2126.
23. Buckwalter JA, Martin JA. Osteoarthritis. Adv Drug Deliv Rev. 2006;58:
150–167.
24. Grant ME, Prockop DJ. The biosynthesis of collagen. N Engl J Med.
1972;286:194–199.
25. Skirving AP, Sims TJ, Bailey AJ. Congenital dislocation of the hip:
a possible inborn error of collagen metabolism. J Inherit Metab Dis.
1984;7:27–31.
26. Madsen JS. The joint capsule and joint laxity in dogs with hip dysplasia.
J Am Vet Med Assoc. 1997;210:1463–1465.
27. Fry TR, Clark DM. Canine hip dysplasia: clinical signs and physical
diagnosis. Vet Clin North Am Small Anim Pract. 1992;22:551–558.
28. Chalman JA, Butler HC. Coxofemoral joint laxity and the Ortolani sign.
J Am Anim Hosp Assoc. 1985;21:671–676.
29. Ginja MMD, Silvestre AM, Gonzalo-Orden JM, Ferreira AJ. Diagnosis,
genetic control and preventive management of canine hip dysplasia:
a review. Vet J. 2010;184:269–276.
30. Puerto DA, Smith GK, Gregor TP, et al. Relationship between results of
the Ortolani method of hip joint palpation and distraction index, Norberg
angle, and hip score in dogs. J Am Vet Med Assoc. 1999;214: 497–501.
31. Bardens JW, Hardwick H. New observations on the diagnosis and cause
of hip dysplasia. Vet Med Small Anim Clin. 1968;63:238–245.
32. Risler A, Klauer JM, Keuler NS, Adams WM. Puppy line, metaphyseal
sclerosis, and caudolateral curvilinear and circumferential femoral
head osteophytes in early detection of canine hip dysplasia. Vet Radiol
Ultrasound. 2009;50:157–166.
33. Szabo SD, Biery DN, Lawler DF, et al. Evaluation of a circumferential
femoral head osteophyte as an early indicator of osteoarthritis charac-
teristic of canine hip dysplasia in dogs. J Am Vet Med Assoc. 2007;231:
889–892.
34. Gibbs C. The BVA/KC scoring scheme for control of hip dysplasia:
interpretation of criteria. Vet Rec. 1997;141:275–284.
35. Dennis R. Interpretation and use of BVA/KC hip scores in dogs. In
Practice. 2012;34:178–194.
36. Fédération Cynologique Internationale [webpage on the Internet]. FCI
Scientific Commission. Available from: http://www.fci.be/en/FCI-
Scientific-Commission-71.html. Accessed January 10, 2015.
37. Comhaire FH, Criel ACC, Dassy CAA, Guévar PGJ, Snaps FR.
Precision, reproducibility, and clinical usefulness of measuring the
Norberg angle by means of computerized image analysis. Am J Vet
Res. 2009;70:228–235.
38. Smith GK, Gregor TP, Rhodes WH, Biery DN. 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 radiography. Am J Vet Res.
1993;54:1021–1042.
39. Smith GK, Biery DN, Gregor TP. New concepts of coxofemoral joint
stability and development of a clinical stress-radiographic method for
quantitating hip joint laxity in the dog. J Am Vet Med Assoc. 1990;196:
59–70.
40. Lust G, Williams A, Burton-Warster N, et al. Joint laxity and its associa-
tion with hip dysplasia in Labrador retrievers. Am J Vet Res. 1993;54:
1990–1999.
41. PennHIP [webpage on the Internet]. PennHIP Method: Measuring
Hip Joint Laxity. http://info.antechimagingservices.com/pennhip/
navigation/penn-HIP-method/distraction-index-measuring-laxity.html.
Accessed January 10, 2015.
42. Lopez MJ, Lewis BP, Swaab ME, Markel MD. Relationships among
measurements obtained by use of computed tomography and radiogra-
phy and scores of cartilage and microdamage in hip joints with moderate
to severe joint laxity of adult dogs. Am J Vet Res. 2008;69:362–370.
43. Farese JP, Todhunter RJ, Lust G, Williams AJ, Dykes NL. Dorsolateral
subluxation of hip joints in dogs measured in a weight-bearing position with
radiography and computed tomography. Vet Surg. 1998;27: 393–405.
44. Malm S, Strandberg E, Danell B, Audell L, Swenson L, Hedhammar Å.
Impact of sedation method on the diagnosis of hip and elbow dysplasia
in Swedish dogs. Prev Vet Med. 2007;78:196–209.
45. Powers MY, Karbe GT, Gregor TP, et al. Evaluation of the relation-
ship between Orthopedic Foundation for Animals’ hip joint scores
and PennHIP distraction index values in dogs. J Am Vet Med Assoc.
2010;237:532–541.
46. D’Amico LL, Xie L, Abell LK, Brown KT, Lopez MJ. Relationships
of hip joint volume ratios with degrees of joint laxity and degenerative
disease from youth to maturity in a canine population predisposed to
hip joint osteoarthritis. Am J Vet Res. 2011;72:376–383.
47. Andronescu AA, Kelly L, Kearney MT, Lopez MJ. Associations between
early radiographic and computed tomographic measures and canine hip
joint osteoarthritis at maturity. Am J Vet Res. 2015;76:19–27.
48. Ginja MMD, Ferreira AJ, Jesus SS, et al. Comparison of clinical,
radiographic, computed tomographic and magnetic resonance imag-
ing methods for early prediction of canine hip laxity and dysplasia. Vet
Radiol Ultrasound. 2009;50:135–143.
49. Preidler KW, Resnick D. Imaging of osteoarthritis. Radiol Clin North
Am. 1996;34:259–271.
50. Hielm-Björkman AK, Kuusela E, Liman A, et al. Evaluation of methods
for assessment of pain associated with chronic osteoarthritis in dogs.
J Am Vet Med Assoc. 2003;222:1552–1558.
51. Kirkby KA, Lewis DD. Canine hip dysplasia: reviewing the evidence
for nonsurgical management. Vet Surg. 2012;41:2–9.
52. Pollmeier M, Toulemonde C, Fleishman C, Hanson PD. Clinical
evaluation of firocoxib and carprofen for the treatment of dogs with
osteoarthritis. Vet Rec. 2006;159:547–551.
53. Smith GK, Paster ER, Powers MY, et al. Lifelong diet restriction and
radiographic evidence of osteoarthritis of the hip joint in dogs. J Am
Vet Med Assoc. 2006;229:690–693.
54. Rialland P, Bichot S, Lussier B, et al. Effect of a diet enriched with
green-lipped mussel on pain behavior and functioning in dogs with
clinical osteoarthritis. Can J Vet Res. 2013;77:66–74.
Veterinary Medicine: Research and Reports 2015:6 submit your manuscript | www.dovepress.com
Dovepress
Dovepress
191
Canine hip dysplasia
55. Hielm-Björkman A, Roine J, Elo K, Lappalainen A, Junnila J, Laitinen-
Vapaavuori O. An un-commissioned randomized, placebo-controlled
double-blind study to test the effect of deep sea fish oil as a pain reliever
for dogs suffering from canine OA. BMC Vet Res. 2012;8:157.
56. Fujiki M, Shineha J, Yamanokuchi K, Misumi K, Sakamoto H. Effects
of treatment with polysulfated glycosaminoglycan on serum cartilage
oligomeric matrix protein and C-reactive protein concentrations, serum
matrix metalloproteinase- 2 and -9 activities, and lameness in dogs with
osteoarthritis. Am J Vet Res. 2007;68:827–833.
57. Lust G, Williams AJ, Burton-Warster N, Beck KA, Rubin G. Effects
of intramuscular administration of glycosaminoglycan polysulfates on
signs of incipient hip dysplasia in growing pups. Am J Vet Res. 1992;53:
1836–1843.
58. Todhunter RJ, Lust G. Polysulfated glycosaminoglycan in the treatment
of osteoarthritis. J Am Vet Med Assoc. 1994;204:1245–1251.
59. White GW, Fregin GF, Selden JR. Effect of prophylactic intramuscular
administration of polysulfated glycosaminoglycan on developmental
and traumatic joint injuries in thoroughbred foals. J Equine Vet Sci.
2007;27:107–111.
60. Durkes TE. Gold bead implants. Probl Ved Med. 1992;4:207–211.
61. Jaeger GT, Larsen S, Søli N, Moe L. Double-blind, placebo-controlled
trial of the pain-relieving effects of the implantation of gold beads into
dogs with hip dysplasia. Vet Rec. 2006;158:722–726.
62. Jaeger GT, Larsen S, Søli N, Moe L. Two years follow-up study of the
pain-relieving effect of gold bead implantation in dogs with hip-joint
arthritis. Acta Vet Scand. 2007;49:9.
63. Bollinger C, Decamp CE, Stajich M, et al. Gait analysis of dogs with hip
dysplasia treated with gold bead implantation acupuncture. Vet Comp
Orthop Traumatol. 2002;15:116–122.
64. Mlacnik E, Bockstahler BA, Müller M, Tetrick MA, Nap RC, Zentek J.
Effects of caloric restriction and a moderate or intense physio-
therapy program for treatment of lameness in overweight dogs with
osteoarthritis. J Am Vet Med Assoc. 2006;229:1756–1760.
65. Heikklä HM, Hielm-Björkman AK, Morelius M, et al. Intra-articular
botulinum toxin A for the treatment of osteoarthritic joint pain in dogs:
a randomized, double-blinded, placebo-controlled clinical trial. Vet J.
2014;200:162–169.
66. Farrell M, Clements DN, Mellor D, et al. Retrospective evaluation of
the long-term outcome of non-surgical management of 74 dogs with
clinical hip dysplasia. Vet Rec. 2007;160:506–511.
67. Marx C, Silverira MD, Selbach I, et al. Acupoint injection of autologous
stromal vascular fraction and allogeneic adipose-derived stem cells to
treat hip dysplasia in dogs. Stem Cells Int. 2014;2014:391274.
68. Vilar JM, Batista M, Morales M, et al. Assessment of the effect of
intraarticular injection of autologous adipose-derived mesenchymal
stem cells in osteoarthritic dogs using a double blinded force platform
analysis. BMC Vet Res. 2014;10:143.
69. Vilar JM, Morales M, Santana A, et al. Controlled, blinded force
platform analysis of the effect of intraarticular injection of autologous
adipose-derived mesenchymal stem cells associated to PRGF-Endoret
in osteoarthritic dogs. BMC Vet Res. 2013;9:131.
70. Cuervo B, Rubio M, Sopena J, et al. Hip osteoarthritis in dogs:
a randomized study using mesenchymal stem cells from adipose
tissue and plasma rich in growth factors. Int J Mol Sci. 2014;15:
13437–13460.
71. Bergh MS, Budsberg SC. A systematic review of the literature describing
the efficacy of surgical treatments for canine hip dysplasia. Vet Surg.
2014;43:501–506.
72. Manley PA, Adams WM, Danielson KC, Dueland RT, Linn KA.
Long-term outcome of juvenile pubic symphysiodesis and triple pelvic
osteotomy in dogs with hip dysplasia. J Am Vet Med Assoc. 2007;230:
206–210.
73. Dueland RT, Adams WM, Patricelli AJ, Linn KA, Crump PM. Canine
hip dysplasia treated by juvenile pubic symphysiodesis. Part I: two
year results of computed tomography and distraction index. Vet Comp
Orthop Traumatol. 2010;23:306–317.
74. Dueland RT, Adams WM, Fialkowski JP, Patricelli AJ, Mathews KG,
Nordheim EV. Effects of pubic symphysiodesis in dysplastic puppies.
Vet Surg. 2001;30:201–217.
75. Patricelli AJ, Dueland RT, Adams WM, Fialkowski JP, Linn KA,
Nordheim EV. Juvenile pubic symphysiodesis in dysplastic puppies at
15 and 20 weeks of age. Vet Surg. 2002;31:435–444.
76. Slocum B, Devine T. Pelvic osteotomy technique for axial rotation
of the acetabular segment in dogs. J Am Anim Hosp Assoc. 1986;22:
331–338.
77. Borostyankoi F, Rooks RL, Kobluk CN, Reed AL, Littledike ET. Results
of single-session bilateral triple pelvic osteotomy with an eight-hole iliac
bone plate in dogs: 95 cases (1996–1999). J Am Vet Med Assoc. 2003;222:
54–59.
78. Rose SA, Bruecker KA, Petersen SW, Uddin N. Use of locking plate
and screws for triple pelvic osteotomy. Vet Surg. 2012;41:114–120.
79. Fitzpatrick N, Law AY, Bielecki MB, Girling S. Cementless total
hip replacement in 20 juveniles using BFX™ arthroplasty. Vet Surg.
2014;43:715–725.
80. Lockwood AA, Liska WD. Duration of clinical signs prior to total hip
replacement in dogs. J Am Vet Med Assoc. 2011;238:905–908.
81. Allen MJ. Advances in total joint replacement in small animals. J Small
Anim Pract. 2012;53:495–506.
82. Morshed S, Bozic KJ, Ries MD, Malchau H, Colford JM. Comparison
of cemented and uncemented fixation in total hip replacement. Acta
Orthop. 2007;78:315–326.
83. Harris WH. Wear and periprosthetic osteolysis: the problem. Clin Orthop
Relat Res. 2001;393:66–70.
84. Hayes GM, Ramirez J, Hobbs JL. Does the degree of preoperative
subluxation or soft tissue tension affect the incidence of postoperative
luxation in dogs after total hip replacement? Vet Surg. 2009;40:6–13.
85. Gemmill TJ, Pink J, Renwick A, et al. Hybrid cemented/cementless total
hip replacement in dogs: seventy-eight consecutive joint replacements.
Vet Surg. 2010;40:621–630.
86. Bozic KJ, Pui CM, Ludeman MJ, Vail TP, Silverstein MD. Do the
potential benefits of metal-on-metal hip resurfacing justify the increased
cost and risk of complications? Clin Orthop Relat Res. 2010;468:
2301–2312.
87. Zhou Z, Sheng X, Zhang Z, et al. Differential genetic regulation of
canine hip dysplasia and osteoarthritis. PLoS One. 2010;5:e13219.
88. Zhu L, Zhang Z, Friedenberg SS, et al. The long (and winding) road to
gene discovery for canine hip dysplasia. Vet J. 2009;181:97–110.
89. Mateescu RG, Burton-Warster N, Tsai K, Phavaphutanon J, Zhang Z,
Murphy KE. Identification of quantitative trait loci for osteoarthritis
of hip joints in dogs. Am J Vet Res. 2008;69:1294–1300.
90. Fels L, Distl O. Identification and validation of quantitative trait loci
(QTL) for canine hip dysplasia (CHD) in German shepherd dogs. PLoS
One. 2014;9:e96618.
91. Todhunter RJ, Mateescu RG, Lust G, et al. Quantitative trait loci for hip
dysplasia in a cross breed canine pedigree. Mamm Genome. 2005;16:
720–730.
92. Noble H. What radiology does for dogs: through x-ray pictures, vet-
erinarians have been able to catalogue canine ills. American Kennel
Gazette. 1935;1935:25–27.
93. Kaya M, Suzuki T, Emori M, Yamashita T. Hip morphology influences
the pattern of articular cartilage damage. Knee Surg Sports Traumatol
Arthrosc. September 11, 2014. [Epub ahead of print.]
Veterinary Medicine: Research and Reports
Publish your work in this journal
Submit your manuscript here: http://www.dovepress.com/veterinary-medicine-research-and-reports-journal
Veterinary Medicine: Research and Reports is an international,
peer-reviewed, open access journal publishing original research,
case reports, editorials, reviews and commentaries on all areas of
veterinary medicine. The manuscript management system is com-
pletely online and includes a very quick and fair peer-review system.
Visit http://www.dovepress.com/testimonials.php to read real quotes
from published authors.
Veterinary Medicine: Research and Reports 2015:6
submit your manuscript | www.dovepress.com
Dovepress
Dovepress
Dovepress
192
Schachner and Lopez