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Comparing Hip Dysplasia in Dogs and Humans: A Review
Article in Frontiers in Veterinary Science · December 2021
DOI: 10.3389/fvets.2021.791434

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REVIEW
published: 15 December 2021
doi: 10.3389/fvets.2021.791434

Comparing Hip Dysplasia in Dogs
and Humans: A Review
Koen Willemsen 1,2 , Michelle M. Möring 2 , Netanja I. Harlianto 2 , Marianna A. Tryfonidou 3 ,Bart C. H. van der Wal 2 , Harrie Weinans 2,4*, Björn P. Meij 3 and Ralph J. B. Sakkers 2
1

3D Lab, Division of Surgical Specialties, University Medical Center Utrecht, Utrecht, Netherlands, 2 Department ofOrthopedics, University Medical Center Utrecht, Utrecht, Netherlands, 3 Department of Clinical Sciences, Faculty of
Veterinary Medicine, Utrecht University, Utrecht, Netherlands, 4 Department of Biomechanical Engineering, Delft University ofTechnology, Delft, Netherlands

Edited by:
Jan H. Spaas,
Boehringer Ingelheim, Germany
Reviewed by:
Wanda J. Gordon-Evans,
University of Minnesota Twin Cities,
United States
Carlien Brondeel,
Ghent University, Belgium*Correspondence:
Harrie Weinansh.h.weinans@umcutrecht.nl
Specialty section:
This article was submitted to
Veterinary Regenerative Medicine,a section of the journal
Frontiers in Veterinary Science
Received: 08 October 2021
Accepted: 17 November 2021
Published: 15 December 2021
Citation:
Willemsen K, Möring MM,
Harlianto NI, Tryfonidou MA, van der
Wal BCH, Weinans H, Meij BP and
Sakkers RJB (2021) Comparing Hip
Dysplasia in Dogs and Humans: A
Review. Front. Vet. Sci. 8:791434.
doi: 10.3389/fvets.2021.791434

Hip dysplasia (HD) is common in both humans and dogs. This interconnection is because
humans and dogs descended from a common ancestor and therefore have a similar
anatomy at micro- and macroscopic levels. Furthermore, dogs are the animals of choicefor testing new treatments for human hip dysplasia and orthopedic surgery in general.
However, little literature exists comparing HD between the two species. Therefore, theaim of this review is to describe the anatomy, etiology, pathogenesis, diagnostics, andtreatment of HD in humans and dogs. HD as an orthopedic condition has many common
characteristics in terms of etiology and pathogenesis and most of the differences canbe explained by the evolutionary differences between dogs and humans. Likewise, thetreatment of HD shows many commonalities between humans and dogs. Conservative
treatment and surgical interventions such as femoral osteotomy, pelvic osteotomy andtotal hip arthroplasty are very similar between humans and dogs. Therefore, future
integration of knowledge and experiences for HD between dogs and humans could be
beneficial for both species.
Keywords: hip dysplasia, one health, treatment, translational, comparative, acetabulum

INTRODUCTION
Dogs and humans have developed from a common ancestor. Both species are vertebrates andterrestrial mammals, with a very similar homologous musculoskeletal structure (Figure 1). Becauseof this resemblance in body structure, certain diseases in both species have a common ground. Oneof these diseases is hip dysplasia (HD). HD was first described in dogs in the 1930’s (1) and in
humans as early as Hippocrates (2). HD is better known as canine hip dysplasia (CHD) in dogs,
and developmental dysplasia of the hip (DDH) in humans. The prevalence of HD in humans varies
between 0.1and 10%, depending on the population and definition (3, 4). In dogs, the prevalence
varies between 0 and 73.4%, depending on the breed (5–8).
There are similar characteristics for HD in humans and dogs. In both species the acetabular
cover of the femoral head is insufficient, either because the acetabulum (5, 9, 10) or the femoral head(5, 9, 10) is deformed, or joint laxity (2, 5) is present. This disturbed femuro-acetabular relationshipcauses abnormally high peak forces (1, 6, 10) with or without joint instability and (sub)luxation(2, 5, 9) resulting in osteoarthritic changes (2, 5, 9). The body tries to counter the sequela of HD in
both species by thickening and stiffening of the joint capsule (10–12) in order to reduce the laxity(11, 12). However, HD will eventually induce osteoarthritis (OA) resulting in pain (6, 13), lameness(14), and loss of limb function (6, 13), reducing quality of life.

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FIGURE 1 | Comparison skeletal structure between dog and human.

While CHD and DDH show numerous similar characteristics,
disease management is not always the same for both
species. In this review we give an overview of the anatomy,
etiology, development, diagnostics and treatment of HD
in humans and dogs. This will provide veterinarians andphysicians a perspective and incentive to share the combinedtranslational knowledge.

Humans can also reduce load on the affected sides by using
instruments such as a cane or a stroller (23).
The canine and human anatomy is not just similar on amacroscopic level. Human and canine hips have a similar cortical
microstructure (24, 25) and long bone vascularization (25, 26).
Because of these external and internal similarities, the dog haslong since been (one of) the animal(s) of choice for orthopedic
research aimed at humans (24, 27, 28).

ANATOMYETIOLOGY AND PATHOGENESIS

Initially, the anatomy of humans and dogs may seem very
different. For instance, an obvious difference between dogs andhumans is that dogs have a quadruped (four-legged) gait while
humans have adopted a bipedal (two-legged) gait. While someanatomical differences have developed due to this difference in
gait, dogs and humans have more in common than one might
think (Figure 1).
The human biped gait has a smaller base of support (lesspoint of ground contact) and an elevated center of mass (15, 16).
To balance the body, humans have developed a lumbar lordosis
so the center of mass (head, arms and trunk) is directly above
the point of ground contact. This is also more energy efficient(17, 18). Similarly, a wider pelvis with more laterally oriented iliac
crests (as opposed to the coronal plane in dogs) allowed for somechanges in musculature, improving balance on one leg, energy
efficiency, and increasing stride length (16–18).
While the load orientation (19) of the hip is very similar indogs and humans, the difference between biped and quadrupedgait gives different load distribution between limbs. Humans
distribute their bodyweight between two legs while dogs
distribute their weight over four legs, with the front legs carrying
approximately 60–65% of the bodyweight (20–22). Because of thedominance of the front legs over the hind legs, dogs are capableof compensating for hip abnormalities (e.g., HD) by lowering
their neck and increasing the load on the non-affected side (20).

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While the exact etiology of HD for both humans and dogs
remains unknown (10, 29), the general agreement is that both
genetic and environmental factors influence the developmentof CHD and DDH (4, 8). First the genetic factors are
discussed, followed by environmental factors and finished withthe pathogenesis.
Some examples of common genetic factors that influence theoccurrence of HD in both species include breed (1, 6) ethnicity(29), increased anteversion angle of the femur (2, 30, 31), neckshaft angle of the femur (2, 31), and collagen composition(1, 4). Because of these high genetic factors, family anamnesis
is important for discovering HD in humans and improving
breeding programs in dogs. However, not all genetic factors havean known influence on both species, e.g., a clear genetic factor
such as female sex in humans is known for a higher incidence ofHD (4:1, Female:Male) (3, 9), while no such relation is known fordogs (8, 32).
Besides genetic factors there are many different environmental
factors influencing the development and incidence of HD. Somecommon environmental factors concern the nutritional statesuch as diet (33), obesity (14, 34, 35) and high birth weight(5, 36). Furthermore, environmental factors such as to seasonal
influence (4, 7) and hormone levels have an association with HD

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have developed and implemented screening programs aimed at
diagnosing DDH in infancy (51). In dogs early detection of HD
is usually driven by the occurrence of clinical signs from age of
4 to 5 months, which will stimulate owners to seek veterinary
advice for diagnostic testing, usually with radiography. However,screening programs for CHD in dogs are recommended forbreeding, and is globally implemented. However, the minimum
age for screening using radiographs is commonly set at skeletally
mature age of 1 year for most breeds and at 18 months for selectedlarge to giant breeds. Since HD in young dogs is commonly
asymptomatic this will prevent early detection of HD in dogs.
While the details might differ, the clinical diagnostics in dogs
and humans are very comparable, generally consisting of physicalexamination and imaging.

(4, 37). Other environmental factors concern disturbances of thebiomechanical equilibrium in the pelvic area, e.g., transitionalvertebrae (38) can change the forces flowing through the hip.
This also happens with restrictive swaddling of babies whichis common in certain human cultures. Swaddling limits the
abduction and therefore reduces the required force on thetriradiate growth plate (39, 40).
Most of previous mentioned factors are identical between both
species, however factors surrounding birth do differ between
species. Humans have only one baby at a time, while dogs haveseveral pups in their litter, meaning intra-uterine mechanicalfactors are different. For instance, breech presentation in humans
is associated with a high incidence of DDH in single childpregnancies, but no relation has been found in twin pregnancies(3, 41). Similarly, other factors like oligohydramnios (42), breachposition, being first born (3, 4) and even the preference for the left
hip are commonly described in humans, but not in dogs who are
typically born in a litter. The preference for the left hip in humans
might be explained as the left hip is often positioned against themother’s spine in the womb, which limits abduction (5, 9) andreduces force on the developing triradiate cartilage.
Besides genetic and environmental factors, there is a clear
developmental aspect in both DDH and CHD. Both species need
the femoral head to be centered on the triradiate cartilage ofthe acetabulum in order to develop normal joint morphology(5, 9, 10). Well balanced supporting structures of the joint likethe pelvic muscles (2, 43), the joint capsule, and the femoral
head ligament are important to maintain joint congruity (5). A
larger amount of pelvic muscle mass is associated with a lower
incidence of CHD (2, 10). Similarly, weak pelvic muscles in dogs
are associated with adverse joint changes (2). For humans, weakpelvic muscles have also been theorized to cause dysplasia anddegenerative joint change (43).
Human newborns with normal hips might develop HD later inlife (44). Of newborns with perceptible HD, 88% will develop into
normal hip joints by the age of 8 weeks, without any intervention(9, 39, 45). However, the older the infant is, the less likely it will bethat natural normalization occurs (9). The abnormal stress on the
hip joint caused by HD can cause pain even before degenerativechanges start. Patients with HD can already present with OA
in adolescents and young adults (46). In CHD, the hips are
typically normal at birth (2, 10). However, early signs such as
edematous and slightly torn ligaments of the femoral head canalready be seen around 4 weeks of age (47, 48). Subsequently,
further dysplastic joint changes develop such as joint laxity anddeformity of the acetabulum and femur (47). This deformity
eventually leads to cartilage changes, pain and lameness. Somedogs start showing clinical signs around 3–12 months of age(10, 49), while other dogs remain asymptomatic and present longafter full maturation.

Physical Examination
Early observational findings during physical examination inhumans are restricted abduction and difference in leg length
in case of hip (sub)luxation (9, 39). Asymmetric gluteal folds
who were once thought to be of high clinical significance did
not have a high predictive value and are therefore not usedanymore (52). In a child of walking age the Trendelenburg sign
can be seen with or without asymmetries, like a proximal thighcrease, posterior knee crease, wide perineum, prominent hip
curvature, and limping (39, 53). With bilaterally affected hips
this asymmetry is usually absent, but bilateral Trendelenburg
sign, waddling gait (9, 39) and bilateral limited abduction (9)can be seen. Dogs should be observed in rest, during activity,
and after exercise (54). The main finding in young dogs withhip joint laxity is lameness that increases during exercise (1),but also hip atrophy, reduced range of motion and pain duringflexion and extension may be present. Hip pain in dogs is
usually noted by abnormal behavior like bunny hopping withpelvic limbs, difficulty to rise, and less playfulness together
with grunting, whimpering, or whining (55). The combined
pain assessment by both the owner and the veterinarian seems
to work best (55), but there is no consensus on a gold
standard (1, 55). Furthermore, dogs do not need a pain free
full range of motion for a normal gait (11), typically dogs
with no or minimal clinical signs could have severe dysplastic
hips (12).
For examining the depth of the acetabulum and joint laxity,
the following clinical tests are performed: the Barlow test, theBarden test, the Galeazzi test, and the Ortolani test, all of whichwere originally developed for use in humans (1, 9). The Ortolani
test is most commonly used in both humans (9, 51) (Figure 2)
and dogs (1, 54) (Figure 3). The Barlow test is also commonlyused in dogs (1, 54). It should be noted that while on humaninfants and dogs these tests can be directly performed, these tests
often require sedation or general anesthesia when dogs are notcooperative (54) (Figures 2, 3).
Since DDH and CHD develop at different rates, a positive
result has slightly different implications. In humans a positive
result indicates subluxation or dislocation of the femoral head
typically due to decreased coverage (9, 51). A positive Ortolani
test in young dogs usually points to joint laxity (1, 54) which is asign of HD in development (58).

DIAGNOSIS
Early detection of HD in humans and dogs can lead to earlierinterventions, which is important for disease management (9,50). To ensure early detection in humans, many countries

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FIGURE 2 | The Barlow and Ortolani test in dogs. (A) “Barlow” (subluxation)
test. The dog is positioned in lateral or dorsal recumbency. In lateralrecumbency, the examiner is caudal to the dog with one hand on the distal
stifle (flexed to 90 degrees) and the other is dorsal to the pelvis, with the thumb
resting over the greater trochanter. The limb is in an adducted position, andforce is applied toward the dorsum of the dog up through the femur (green
arrow), causing dorsal subluxation in a hip with joint laxity. (B) Ortolani(reduction) test. The limb is slowly abducted (yellow arrow) while force along
the axis of the femur is maintained. A positive Ortolani sign is felt when a click
or clunk is heard or palpated as the subluxated femoral head reduces into theacetabulum (red arrow). Figure reproduced without modification from (56)under the Creative Commons Attribution 4.0 International License ().

FIGURE 3 | The Barlow and Ortolani test in Humans. The Barlow test fordevelopmental dislocation of the hip in a neonate. (A) With the infant supine,
the examiner holds both of the child’s knees and gently adducts one hip andpushes posteriorly. (B) When the examination is positive, the examiner will feelthe femoral head make a small jump (arrow) out of the acetabulum (Barlow’ssign). When the pressure is released, the head is felt to slip back into place
The Ortolani test for developmental dislocation of the hip in a neonate. (C) The
examiner holds the infant’s knees and gently abducts the hip while lifting up on
the greater trochanter with two fingers. (D) When the test is positive, thedislocated femoral head will fall back into the acetabulum (arrow) with apalpable (but not audible) “clunk” as the hip is abducted. [Reprinted withpermission from Tachdjian’s Pediatric Orthopedics (57), Elsevier Publishing].

humans the radiographs are taken in ventrodorsal and anteriorposterior position to measure the center-edge (CE)-angle andthe Norberg angle (Figure 4)(59, 62–64). Besides the CE-angle
and the Norberg angle, other radiographic parameters can bemeasured to increase the validity of the diagnosis. However the
CE-angle is the most renown (65).

Imaging
Radiography is the golden standard for diagnosing HD in dogs(1). Historically, pelvic and hip radiography has been used for
diagnosing HD in humans (9, 59). However, in some parts of
the worlds X-rays have been partially replaced by ultrasoundimaging for young patients (60) as classification of HD on Xrays is currently considered less reliable before ossification of
the femoral head center occurs at 4–6 months (9, 39). Although
there are widely accepted ultrasound classifications, ultrasoundimages still has drawbacks, such as: high variability and low
agreement (61). In dogs the ossification starts at 8 weeks, whichmakes ultrasound less useful as the ossification distorts the viewof the acetabulum on ultrasound (54). The way radiographs are
attained and measured is remarkably alike, both in dogs andFrontiers in Veterinary Science | www.frontiersin.org

TREATMENTThe available treatments for HD in humans and dogs change
when patients develop toward skeletal maturity (39). Youngpatients have soft and pliable bone with good remodelingcapabilities due to growth. Therefore, HD treatment can focus
on stimulating growth by redirecting the femoral head to the4

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FIGURE 4 | Radiographic diagnostics. Left: Norberg-Angle, take the center of each femoral head (hip ball) and draw a line between them. Then take the center of thefemoral head and draw a line to the outer point of the pelvis. The angle between these lines is the Norberg angle. The Norberg angle is calculated for each hip joint. A
normal Norberg Angle ranges from 100/105 to 115 degrees. <100 degrees is dysplastic. Right: CE-angle, take the center of each femoral head (hip ball) and draw aline between them. Then take the center of the femoral head and draw a line to the outer point of the pelvis. The angle between these lines is the CE angle. The
CE-angle is calculated for each hip joint. A normal CE Angle ranges from 110/115 to 130 degrees. <110 degrees is dysplastic.

been described for dogs, since they do not easily accept external
hip coaptation devices. However, a somewhat similar concept
was used in puppies with genetic predisposition for CHD thatwere raised in a small cage (1 m3 ) until they finished growing.
This caused them to sit more often with their hind limbs spread(flexion and abduction) and reduced the prevalence of CHD. Thismethod prevents dogs from socializing and is therefore not usedin daily practice (48, 54).
In young dogs with CHD that start to show clinical signs,
usually from age 4 to 5 months, the non-surgical treatment
measures are similar to those at older age and therefore will be
discussed in more detail in section Late Non-surgical Treatment.

center of the triradiate growth plate of the acetabulum in order tocreate a stable well-covered hip joint (9). As the patient matures
the growth potential of bone decreases and the ability to correct
the joint relationships with it. When forming a congruent wellcovered joint is no longer an option, osteoarthritis might develop.
Skeletal maturity is reached around 15–18 years in humans(43) and 1–1.5 years in dogs (66). The triradiate cartilage(acetabular growth plate) closes around 14 years of age inhumans (67) and around 6 months of age in dogs. There is noclearly defined separation between treatment options for certain
ages and stages of bone development. Therefore, in order toaccommodate this review a separation is made between “early”
and “late” treatment.

Early Surgical Treatment

Early Non-surgical Treatment

If non-surgical treatments are ineffective or the child gets older
than 9–18 months, open reduction of the hip joint can be
performed (9, 46). Open reduction focuses on reducing the
subluxated or dislocated hip and creating a stable hip joint,
similar to closed reduction. Open reduction of the hip is usuallycombined with capsular reefing and the release of the transverse
acetabular ligament, and may be combined with an acetabularor femoral osteotomy in order to create a stable well-centeredhip (9). After the open reduction, the child is treated with aspica cast to maintain the position of the hips (9). In dogs open
reduction for a luxated hip due to severe HD is never performed.
Hip luxation in young dogs with HD, called the luxoid hip, isusually an indication for early euthanasia, femoral head and neckresection or total hip replacement from age 7–9 months.
In the older child with residual hip dysplasia, an
acetabuloplasty, e.g., the Dega, or Pemberton acetabuloplasty iscommonly used to improve centering and acetabular coverage ofthe femoral head (70, 71). While both procedures are different,
both are curved partial osteotomies of the ilium, with a small(bone) graft placed in the osteotomy. This partial osteotomy

Early treatment of hip dysplasia in humans distinguishes betweena (sub-)luxated and a non-luxated hip. A luxated hip needs
repositioning first before the acetabular dysplasia can be treated.
When a dysplastic hip is diagnosed with (sub)luxation of thefemoral head, a Pavlik harness is most often applied as firsttreatment. The Pavlik harness uses several straps to flex thehips and knees and prevent adduction, while movement is still
possible (9, 68). In a child treated within the 1 weeks after birth
this position forces the femoral head into the acetabular socket
and onto the triradiate cartilage. After creation of a stable joint,
the harness is still worn for 23 h per day until a morphologicallynormal hip joint is found on imaging (39, 68). When a stablereduction of the hip is not reached within 3–4 weeks, repositionof the hip under full relaxation under anesthesia might be tried,with or without adductor tenotomy, followed by a plaster castusually for 3 months (9, 68). If repositioning of the hip fails underanesthesia, open reposition of the hip should follow, usually
after the age of 6–9 months (9). There is no consensus about
optimal treatment length (9, 69). The Pavlik harness has not

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causes a hinging effect in the horizontal line of the triradiate
cartilage and will reshape the acetabulum, reducing its diameter,
yet increasing depth (72). The Pemberton acetabuloplasty
improves anterior and lateral femoral head coverage, but notcoverage of the posterior femoral head. The Dega acetabuloplasty
increases the anterior, lateral, and posterior femoral head
coverage (72). Acetabuloplasties give the best results when usedon patients 2–8 years old (46).
Another common technique for pelvic osteotomies in young
children is the Salter osteotomy (9, 72). This technique is basedon a complete osteotomy of the ilium bone just superior of theacetabulum and redirection of the existing acetabulum (73, 74).
Therefore, the Salter osteotomy does not alter the shape of
the acetabulum. A possible complication described in the Salter
osteotomy is instability (71, 74) and another complication for
the Salter and Pemberton acetabuloplasty (71) is overcorrection,
leading to excessive coverage of the femoral head resulting infemoral acetabular impingement (71, 74).
The majority of early surgical treatments, like the Pemberton
and Salter osteotomy used in humans are not applicable in dogs
simply because CHD is not detected early enough in the dog’slife. The only comparable treatment in dogs is juvenile pubic
symphysiodesis (JPS). The JPS is an early surgical treatment
for CHD, and to our knowledge has not been used in humans.
JPS is a relatively simple surgery in which the cartilage of the
pubic symphysis is destroyed through electrocauterization. The
heat causes the chondrocytes to become necrotic, resulting inpremature closure of the pubic symphysis. Since other parts of thepelvis continue to grow, the acetabulum is rotated ventrolateral,similarly to the human Pemberton and Salter osteotomy, whichallows for greater femoral head coverage (12, 54, 66). To beeffective, JPS should be performed before week 18 in small dogs
or week 22 in large breed dogs (12, 66).
Osteotomies of the femur are frequently used in humans
and infrequently in dogs. In dogs aged ½−2 years theintertrochanteric femoral osteotomy is used to reduce the neckshaft angle (varisation) and anteversion angle, which are often
increased in dysplastic hips. The femoral head is moved more
medially (12, 75, 76) which helps redirect the femoral head into
the acetabulum (75, 76). This is achieved by removing a bonewedge from the proximal femur and the bone is then stabilized
by a hook plate (12, 75, 76). In humans, a femoral osteotomy canbe performed sub- or intertrochanteric. The osteotomy also aims
to reduce the anteversion (also called derotational osteotomy)
and neck-shaft angle. Femoral osteotomies in humans are often
combined with open reduction and acetabular osteotomies,
between the ages of 2–14 years (69).

3 years (10) and in overweight dogs and humans 10% bodyweight reduction is associated with a relieve in symptoms
and signs (14, 77). Another non-surgical intervention is thenutraceutical market, which is especially big in the veterinary
market. Nutraceuticals are food additives or supplements thatare purported to have a disease modifying potential in hip
dysplasia and osteoarthritis, but also other conditions. An
example of a nutraceutical is Polysulfanated glycosaminoglycans(PSGAGs) which proposedly stimulates collagen synthesis andinhibits the breakdown of collagen (13) which may help reduce
subluxation (54).
Another option for early non-surgical treatment is
physiotherapy (78, 79). In both dogs and humans physiotherapy
and hydrotherapy is an important component first as aconservative treatment option but also as an important aspect inpost-surgical rehabilitation (78, 79).

Late Surgical Treatment
Originally designed for humans with HD, triple pelvic osteotomy(TPO) has also become a successful procedure for dogs with HD(12, 80)(Figure 5). This surgery can be used in young dogs (1, 54,81), but more often in adolescents (46, 82, 83) and young adults(82, 83) without or with minimal degenerative joint damage(1, 49, 54, 83). In dogs, the surgery is preferably performed
before full skeletal maturity is reached, while in humans it can beused both before and after the triradiate cartilage closes (9, 83).
However, humans have more early surgical treatments available(e.g., Salter & Pemberton), deferring the more invasive TPO toolder patients. Over the years there have been many changes
in specific surgical techniques, but the general outline of TPO
remains the same. Osteotomies are made in the pubic, ischial, andiliac bones, and the acetabulum is subsequently rotated ventrally
to improve femoral head coverage and increase the load bearing
area (80) (Figure 5). The acetabulum is then fixated in place byplates, screws, or K-wire. Clinical reduction of lameness after
TPO, and improvement in weight bearing of 86–92% is reported
in dogs (75, 76, 81). The joint laxity is reduced following TPO
in dogs (80, 81), but degenerative changes cannot be stopped
completely (81). In humans, TPO causes a long term reductionof pain and improvement of function (84) and a (total hip free)survival of 68% after 25 years is reported. Recently, dual pelvic
osteotomy (DPO) has been recommended in dogs (75, 85), it has
also been described in humans (72). DPO is similar to TPO, witha faster post-operative recovery, as there is no osteotomy of theischium and therefore no pelvic discontinuity (75, 85).
Shelf arthroplasty is a commonly used salvage procedure for
HD in humans (86). It involves the placement of an autologous
bone graft outside of the joint capsule superior to the acetabulum(87, 88). The graft can be impacted into the bone or be heldin place by a screw (88), improving the support structure of
the joint (9). Capsular metaplasia causes the improvement of
the articulating surface. The improved support and improved
femoral head coverage helps improve the weight bearing surface(9) and delays the progression of OA. This procedure ispreferably performed in younger patients with minimal arthritic
changes, however it is mostly reserved as a salvage procedure
as other treatments are not eligible. The survival of the shelf

Late Non-surgical Treatment
There are various late non-surgical treatments for dogs andhumans with hip dysplasia. To decrease pain (1, 77), reduce
lameness (14), and delay onset of osteoarthrosis (1, 66) a varietyof treatments are available including medication like NSAIDs(1), reducing body weight (34, 77), life style changes including
training of pelvic muscles, exercise programs and the limiting
sudden explosive movements (like throwing a ball for dogs).
On average, weight loss in dogs delays surgery for another

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FIGURE 5 | Canine left and human right triple pelvic osteotomies (purple planes) are made in the pubic, ischial and iliac bones and subsequently the acetabulum isrotated ventrally (dogs) or anteriorly (humans) to improve femoral head coverage and increase the load bearing area.

procedure can be up to 72% at 35 years of follow-up (86).
A similar procedure called the biocompatible osteoconductive
polymer (BOP) procedure has been described as an alternativeto TPO in adolescent dogs (12, 75, 76). Instead of autologous
bone graft, biocompatible osteoconductive fibers were used toincrease coverage, because the fibers were expected to promotebony ingrowth (12, 75, 76). Despite that the shelf procedure was
successful in humans, BOP in dogs never became a common
procedure because of uncontrolled bone growth (75, 76). New
procedures involving 3D-printed titanium shelfs (89) or 3Dprinted biodegradable magnesium phosphate shelfs (90) are still
being developed in dogs and when successful these procedures
hopefully find their way back to the human clinic.
While being one of the most effective procedures, total hip
arthroplasty (THA) in humans and dogs (12) is often postponed
as the last treatment option (Figure 6). When young patientswith a demanding lifestyle receive a THA they may need one ormore revisions in their lifetime due to implant wear. However,every revision is more difficult to perform due to fibrosis in the
perioperative area. Therefore, in humans, the need for THA is
preferably postponed beyond the age of 60 to prevent revisions
in the long term. Although THA has been available for dogs
for three decades, it remains an expensive treatment option,
especially when the owners have no insurance (49). Also, THA
in humans can become technically demanding due to anatomicaldifferences in dysplastic hips making it difficult to ream a large
enough bony bed to support an acetabular cup (91). In dogs
the procedure is technically demanding due to breed anatomic
differences but can be used in dogs of any size or shape when
aged 9 months or older (12).
It is good to note that implant improvements have benefited
for cross species research. For example, due to the active natureof dogs, the THA materials demand is high and companies
specializing in canine THA have benefited from the prosthetic
knowledge being researched and developed for human medicine.
For example, similar durable materials developed for humancups and stems are translated to the dog THA allowing dogs to
perform without the need for revision beyond a decade lifetime,

Frontiers in Veterinary Science | www.frontiersin.org

FIGURE 6 | The comparable set-up of the total hip arthroplasty in humans anddogs. On the left the set-up in dogs and on the right the set-up in humans.

with a biomechanically demanding lifestyle asking for morecyclic loading of their implants than humans. Vice versa, in dogs
new products are developed e.g., to decrease stem loosening,
because dogs demand immediate full weightbearing after surgery
due to there non-compliance to life style restrictions. One
example of a successful concept in THA surgery in dogs (Zürich
cementless THA) is the immediate stem screw fixation at themedial femoral cortex instead of press fit fixation (92). Likewise,
in a few years more developments might be translated back fromthe veterinary to the human market.
One of the least performed in humans but most commonly
executed salvage procedures in dogs is the femoral head andneck excision (75, 76). The surgery is relatively easy to performand has low costs, and is most effective in dogs with low bodyweight (75, 93). The removal of the femoral head and neck7

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Willemsen et al.

Human and Dog’s Hip Dysplasia

We suggest that further exchange between research on HD in
humans and dogs can be beneficial for the treatment of HD in
humans and dogs.

leads to a fibrotic pseudoarthrosis (false joint), allowing for
relative pain free movement (12, 49). Femoral head and neckexcision generally has good results in relieving pain, however
possible side effects are extensive rehabilitation, decreased rangeof motion, muscle atrophy and limping due to decreased limb
length (12, 75, 76, 93). Important factors in the outcome arebody size (12, 75, 76), dog temperament and activity (12, 94).
This procedure performed in humans is called a “Girdle stone”
procedure, but only as the last option (94).

AUTHOR CONTRIBUTIONS
BW, BM, RS, HW, and KW: conceptualized the study. KW,
MM, and NH: collected the data. KW, MT, MM, NH, and RS:
analyzed the data. HW, BM, MT, and BW: supervised the project.
KW, MT, RS, NH, MM, HW, BM, and BW: wrote, edited andreviewed the paper. All authors have read and approved the final
submitted manuscript.

CONCLUSION
In this review we described the anatomy, etiology, development,
diagnostics and treatment of HD in humans and dogs. Humans
and dogs have similar anatomy on micro- and macroscopic
levels. HD as an orthopedic condition has many overlying
characteristics in humans and dogs in terms of etiology
and pathogenesis. Likewise, treatment of HD shows many
similarities. There is much parallel use of early and after growth(conservative) treatments and interventions. Moreover, many of
the surgical treatments for HD that were developed for humans
have first been tested in experimental dogs. Procedures that
became successful in humans found their way to the veterinary
field and are now commonly used in companion animal clinics.

FUNDINGKW and HW report a Governmental research grant fromInterreg VA Flanders—The Netherlands program, during the
conduct of the study; KW and HW report grants from the Smart
industry project 15479 funded through governmental grant by
NWO domain TTW, during the conduct of the study; MT,
HW, and BM report funding from the Dutch Arthritis Society(LLP12/22). The funding sources played no role in the study
design, data analysis and interpretation, nor drafting of themanuscript or the decision to submit it for publication.

REFERENCES

12. Anderson A. Treatment of hip dysplasia. J Small Anim Pract. (2011) 52:182–
9. doi: 10.1111/j.1748-5827.2011.01049.x
13. Kirkby KA, Lewis DD. Canine hip dysplasia: reviewing theevidence for nonsurgical management. Vet Surg. (2012) 41:2–
9. doi: 10.1111/j.1532-950X.2011.00928.x
14. Impellizeri JA, Tetrick MA, Muir P. Effect of weight reduction on clinicalsigns of lameness in dogs with hip osteoarthritis. J Am Vet Med Assoc. (2000)
216:1089–91. doi: 10.2460/javma.2000.216.1089
15. Bonneau N, Baylac M, Gagey O, Tardieu C. Functional integrative analysisof the human hip joint: the three-dimensional orientation of the acetabulum
and its relation with the orientation of the femoral neck. J Hum Evol. (2014)
69:55–69. doi: 10.1016/j.jhevol.2013.12.013
16. Hogervorst T, Bouma HW, De Vos J. Evolution of the hip and pelvis. Acta
Orthop. (2009) 80:1–39. doi: 10.1080/17453690610046620
17. Lovejoy CO. The natural history of human gait and posture. Part 1
Spine and pelvis Gait Posture. (2005) 21:95–112. doi: 10.1016/j.gaitpost.2004.
01.001
18. Gruss LT, Schmitt D. The evolution of the human pelvis: changing adaptations
to bipedalism, obstetrics and thermoregulation. Philos Trans R Soc Lond B Biol
Sci. (2015) 370:20140063. doi: 10.1098/rstb.2014.0063
19. Bergmann G, Siraky J, Rohlmann A, Koelbel R. A comparison of
hip joint forces in sheep, dog and man. J Biomech. (1984) 17:907–
21. doi: 10.1016/0021-9290(84)90004-6
20. Soontornvipart K, Chalayon P, Tangwongsan C. Standing analysis ofhealthy and abnormal canines using force platform system. In: 2013 10th
International Conference on Electrical Engineering/Electronics, Computer,
Telecommunications and Information Technology. IEEE (2013) p. 1–6.
21. Brookhart JM, Parmeggiani PL, Petersen WA, Stone SA.
Postural Stability in the Dog. Am J Physiol. (1965) 208:1047–
57. doi: 10.1152/ajplegacy.1965.208.6.1047
22. Nunamaker DM, Blauner PD. Normal and Abnormal Gait. Textb Small Anim
Orthop. Ithaca, NY: International Veterinary Information Services (IVIS)(1985).
23. Byrne DP, Mulhall KJ, Baker JF. Anatomy & Biomechanics of the Hip. OpenSport Med J. (2010) (4):51–7. doi: 10.2174/1874387001004010051

1. Lopez M, Schachner E. Diagnosis, prevention, and managementof canine hip dysplasia: a review. Vet Med Res Reports. (2015)
6:181. doi: 10.2147/VMRR.S53266
2. Olmstead ML, Linda LD. Small Animal Orthopedics. St. Louis: Mosby (1995).
p. 365–8.
3. Stein-Zamir C, Volovik I, Rishpon S, Sabi R. Developmental dysplasia of
the hip: risk markers, clinical screening and outcome. Pediatr Int. (2008)
50:341–5. doi: 10.1111/j.1442-200X.2008.02575.x
4. Rhodes AML, Clarke NMP. A review of environmental factors implicatedin human developmental dysplasia of the hip. J Child Orthop. (2014) 8:375–
9. doi: 10.1007/s11832-014-0615-y
5. Vanden Berg-Foels WS, Todhunter RJ, Schwager SJ, Reeves AP. Effect ofearly postnatal body weight on femoral head ossification onset and hip
osteoarthritis in a canine model of developmental dysplasia of the hip. Pediatr
Res. (2006) 60:549–54. doi: 10.1203/01.pdr.0000243546.97830.a0
6. Roberts T, McGreevy PD. Selection for breed-specific long-bodied phenotypes
is associated with increased expression of canine hip dysplasia. Vet J. (2010)
183:266–72. doi: 10.1016/j.tvjl.2009.11.005
7. Worth AJ, Bridges JP, Cave NJ, Jones G. Seasonal variation in the hip scoreof dogs as assessed by the New Zealand Veterinary Association hip dysplasia
scheme. N Z Vet J. (2012) 60:110–4. doi: 10.1080/00480169.2011.636730
8. Rettenmaier JL, Keller GG, Lattimer JC, Corley EA, Ellersieck MR. Prevalenceof canine hip dysplasia in a veterinary teaching hospital population. Vet Radiol
Ultrasound. (2002) 43:313–8. doi: 10.1111/j.1740-8261.2002.tb01010.x
9. Kotlarsky P, Haber R, Bialik V, Eidelman M. Developmental dysplasia of
the hip: what has changed in the last 20 years? World J Orthop. (2015)
6:886–901. doi: 10.5312/wjo.v6.i11.886
10. Smith GK, Karbe GT, Agnello KA, McDonald-Lynch MB. Pathogenesis,
diagnosis and control of canine hip dysplasia. In: Veterinary Surgery: Small
Animal. 1st ed. St. Louis: Elsevier (2012). p. 824–48.
11. Barr ARS, Denny HR, Gibbs DC. Clinical hip dysplasia in growing dogs : thelong-term results of conservative management. J Small Anim Pract. (1987)
28:243–52. doi: 10.1111/j.1748-5827.1987.tb03879.x

Frontiers in Veterinary Science | www.frontiersin.org

8

December 2021 | Volume 8 | Article 791434

Willemsen et al.

Human and Dog’s Hip Dysplasia

44. Klisic PJ. Congenital dislocation of the hip–a misleading term: brief report. J
Bone Joint Surg Br. (1989) 71:136. doi: 10.1302/0301-620X.71B1.2914985
45. Sakkers R, Pollet V. The natural history of abnormal ultrasound findings
in hips of infants under six months of age. J Child Orthop. (2018) 12:302–
7. doi: 10.1302/1863-2548.12.180056
46. Wenger DR, Bomar JD. Human hip dysplasia: evolution of current treatment
concepts. J Orthop Sci. (2003) 8:264–71. doi: 10.1007/s007760300046
47. Tobias KM, Johnston SA. Veterinary surgery: small animal-E-BOOK: 2volume set. Elsevier Health Sciences. (2013).
48. Read RA. Conservative management of juvenile canine hip dysplasia. Aust Vet
J. (2000) 78:818–9. doi: 10.1111/j.1751-0813.2000.tb10494.x
49. Rawson EA, Aronsohn MG, Burk RL. Simultaneous bilateral femoral headand neck ostectomy for the treatment of canine hip dysplasia. J Am Anim Hosp
Assoc. (2005) 41:166–70. doi: 10.5326/0410166
50. Gatineau M, Dupuis J, Beauregard G, Charette B, Breton L, BeauchampG, et al. Palpation and dorsal acetabular rim radiographic projection forearly detection of canine hip dysplasia: a prospective study. Vet Surg. (2012)
41:42–53. doi: 10.1111/j.1532-950X.2011.00926.x
51. Shorter D, Hong T, Osborn DA. Screening programmes for developmental
dysplasia of the hip in newborn infants. Cochrane database Syst Rev. (2011)(9):CD004595. doi: 10.1002/14651858.CD004595.pub2
52. Kang MS, Han GW, Kam M, Park S-S. Clinical significance ofasymmetric skin folds in the medial thigh for the infantile screeningof developmental dysplasia of the hip. Pediatr Neonatol. (2019)60:570–6. doi: 10.1016/j.pedneo.2019.02.004
53. Kamath SU, Bennet GC. Does developmental dysplasia of
the hip cause a delay in walking? J Pediatr Orthop. (2004)
24:265. doi: 10.1097/01241398-200405000-00005
54. Ginja MMD, Silvestre AM, Gonzalo-Orden JM, Ferreira AJA. Diagnosis,
genetic control and preventive management of canine hip dysplasia: a review.
Vet J. (2010) 184:269–76. doi: 10.1016/j.tvjl.2009.04.009
55. Hielm-Björkman AK, Kuusela E, Liman A, Markkola A, Saarto E, Huttunen
P, et al. Evaluation of methods for assessment of pain associated withchronic osteoarthritis in dogs. J Am Vet Med Assoc. (2003) 222:1552–
8. doi: 10.2460/javma.2003.222.1552
56. Kyriazis A, Prassinos NN. Canine hip dysplasia: part i: aetiopathogenesis &diagnostic approach. Hell J Companion Anim Med. (2016) 5:22–47.
57. Herring JA. Tachdjian’s Pediatric Orthopaedics: From the Texas Scottish Rite
Hospital for Children E-Book. Philadelphia, PA: Elsevier (2020).
58. Ginja MMD, Ferreira AJ, Jesus SS, Melo-Pinto P, Bulas-Cruz J,
Orden MA, et al. Comparison of clinical, radiographic, computed
tomographic, and magnetic resonance imaging methods for early
prediction of canine hip laxity and dysplasia. Vet Radiol Ultrasound.
(2009) 50:135–43. doi: 10.1111/j.1740-8261.2009.01506.x
59. Wiberg G. Studies on dysplastic acetabula and congenital subluxation of the
hip joint: with special reference to the complication of osteoarthritis. Acta Chir
Scand. (1939) 83:53–68.
60. Storer SK, Skaggs DL. Developmental dysplasia of the hip. Am Fam Physician.
(2006) 74:1310–6.
61. Quader N, Schaeffer EK, Hodgson AJ, Abugharbieh R, Mulpuri K, A.
systematic review and meta-analysis on the reproducibility of ultrasoundbased metrics for assessing developmental dysplasia of the hip. J Pediatr
Orthop. (2018) 38:e305–11. doi: 10.1097/BPO.0000000000001179
62. Murphy SB, Ganz R, Müller ME. The prognosis in untreated dysplasia of thehip. A study of radiographic factors that predict the outcome. J Bone Jt Surg
Am. (1995) 77:985–9. doi: 10.2106/00004623-199507000-00002
63. Murphy SB, kijewski PK, Millis MB, Harless A. Acetabular dysplasia in
the adolescent and young adult. Clin Orthop Relat Res. (1990) 261:214–
23. doi: 10.1097/00003086-199012000-00023
64. Werner CML, Ramseier LE, Ruckstuhl T, Stromberg J, Copeland CE, Turen
CH, et al. Normal values of Wiberg’s lateral center-edge angle and Lequesne’s
acetabular index–a coxometric update. Skeletal Radiol. (2012) 41:1273–
8. doi: 10.1007/s00256-012-1420-7
65. Monazzam S, Bomar JD, Cidambi K, Kruk P, Hosalkar H. Lateral center-edge
angle on conventional radiography and computed tomography. Clin Orthop
Relat Res. (2013) 471:2233–7. doi: 10.1007/s11999-012-2651-6
66. Vezzoni A, Dravelli G, Vezzoni L, De Lorenzi M, Corbari A, Cirla A, et al.
Comparison of conservative management and juvenile pubic symphysiodesis

24. Pearce AI, Richards RG, Milz S, Schneider E, Pearce SG. Animal models
for implant biomaterial research in bone: a review. Eur Cell Mater. (2007)
13:1–10. doi: 10.22203/eCM.v013a01
25. Eitel F, Klapp F, Jacobson W, Schweiberer L. Bone regeneration in animals
and in man. A contribution to understanding the relative value of animal
experiments to human pathophysiology. Arch Orthop Trauma Surgery. (1981)
99:59–64. doi: 10.1007/BF00400911
26. Rhinelander FW, Nelson CL, Stewart RD, Stewart CL. Experimental
reaming of the proximal femur and acrylic cement implantation:
vascular and histologic effects. Clin Orthop Relat Res. (1979)(141):74–89. doi: 10.1097/00003086-197906000-00009
27. Goel VK, Drinker H, Panjabi MM, Strongwater A. Selection of an animalmodel for implant fixation studies: anatomical aspects. Yale J Biol Med.
(1982) 55:113–22.
28. Aerssens J, Boonen S, Lowet G, Dequeker J. Interspecies differences in bonecomposition, density, and quality: potential implications for in vivo bone
research. Endocrinology. (1998) 139:663–70. doi: 10.1210/endo.139.2.5751
29. Ibrahim T, Riaz M, Hegazy A. The prevalence of developmental dysplasiaof the hip in idiopathic clubfoot: a systematic review and meta-analysis. Int
Orthop. (2015) 39:1371–8. doi: 10.1007/s00264-015-2757-z
30. Sankar WN, Neubuerger CO, Moseley CF. Femoral anteversion indevelopmental dysplasia of the hip. J Pediatr Orthop. (2009) 29:885–
8. doi: 10.1097/BPO.0b013e3181c1e961
31. Sugano N, Noble PC, Kamaric E, Salama JK, Ochi T, Tullos HS.
The morphology of the femur in developmental dysplasia of the hip.
J Bone Joint Surg Br. (1998) 80:711–9. doi: 10.1302/0301-620X.80B4.
0800711
32. Krontveit RI, Nødtvedt A, Sævik BK, Ropstad E, Skogmo HK, Trangerud
C, et al. Prospective study on canine hip dysplasia and growth in a cohortof four large breeds in Norway (1998-2001). Prev Vet Med. (2010) 97:252–
63. doi: 10.1016/j.prevetmed.2010.09.015
33. Kealy RD, Olsson SE, Monti KL, Lawler DF, Biery DN, Helms RW, et al. Effects
of limited food consumption on the incidence of hip dysplasia in growing
dogs. Journal-American Vet Med Assoc. (1992) 201:857.
34. Karlson EW, Mandl LA, Aweh GN, Sangha O, Liang MH, Grodstein
F. Total hip replacement due to osteoarthritis: the importance of age,
obesity, and other modifiable risk factors. Am J Med. (2003) 114:93–
8. doi: 10.1016/S0002-9343(02)01447-X
35. Smith GK, Paster ER, Powers MY, Lawler DF, Biery DN, Shofer FS,
et al. Lifelong diet restriction and radiographic evidence of osteoarthritisof the hip joint in dogs. J Am Vet Med Assoc. (2006) 229:690–
3. doi: 10.2460/javma.229.5.690
36. Atalar H, Gunay C, Yavuz OY, Camurdan AD, Uras I, Eren A. Maternalheight and infant body mass index are possible risk factors for developmental
dysplasia of the hip in female infants. Acta Med Okayama. (2015) 69:349–51.
37. 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. doi: 10.2460/ajvr.69.1.59
38. Flückiger MA, Steffen F, Hässig M, Morgan JP. Asymmetrical
lumbosacral transitional vertebrae in dogs may promote asymmetricalhip joint development. Vet Comp Orthop Traumatol. (2017)30:137–42. doi: 10.3415/VCOT-16-05-0072
39. Schwend RM, Shaw BA, Segal LS. Evaluation and treatment of developmental
hip dysplasia in the newborn and infant. Pediatr Clin North Am. (2014)
61:1095–107. doi: 10.1016/j.pcl.2014.08.008
40. Kutlu A, Memik R, Mutlu M, Kutlu R, Arslan A. Congenital dislocation of
the hip and its relation to swaddling used in Turkey. J Pediatr Orthop. (1992)
12:598–602. doi: 10.1097/01241398-199209000-00006
41. De Pellegrin M, Moharamzadeh D. Developmental dysplasia of the hip in
twins: the importance of mechanical factors in the etiology of DDH. J Pediatr
Orthop. (2010) 30:774–8. doi: 10.1097/BPO.0b013e3181fc35c0
42. Manoukian D, Rehm A. Oligohydramnios: Should it be considered a risk
factor for developmental dysplasia of the hip? J Pediatr Orthop Part B. (2019)28:442–5. doi: 10.1097/BPB.0000000000000624
43. Ford CA, Nowlan NC, Thomopoulos S, Killian ML. Effects of imbalanced
muscle loading on hip joint development and maturation. J Orthop Res. (2016)35:1128–36 doi: 10.1002/jor.23361

Frontiers in Veterinary Science | www.frontiersin.org

9

December 2021 | Volume 8 | Article 791434

Willemsen et al.

Human and Dog’s Hip Dysplasia

84. van Stralen RA, van Hellemondt GG, Ramrattan NN, de Visser E, de Kleuver
M. Can a triple pelvic osteotomy for adult symptomatic hip dysplasia provide
relief of symptoms for 25 years? Clin Orthop Relat Res. (2013) 471:584–
90. doi: 10.1007/s11999-012-2701-0
85. Vezzoni A, Boiocchi S, Vezzoni L, Vanelli AB, Bronzo V. Double pelvic
osteotomy for the treatment of hip dysplasia in young dogs. Vet Comp Orthop
Traumatol. (2010) 23:444–52. doi: 10.3415/VCOT-10-03-0034
86. Willemsen K, Doelman CJ, Sam ASY, Seevinck PR, Sakkers RJB, Weinans H,
et al. Long-term outcomes of the hip shelf arthroplasty in adolescents andadults with residual hip dysplasia: a systematic review. Acta Orthop. (2020)
91:383–9. doi: 10.1080/17453674.2020.1747210
87. Migaud H, Chantelot C, Giraud F, Fontaine C, Duquennoy A. Long-term
survivorship of hip shelf arthroplasty and Chiari osteotomy in adults. Clin
Orthop Relat Res. (2004) (418):81–6. doi: 10.1097/00003086-200401000-00014
88. Bartoníček J, Vávra J, Chochola A. Bosworth hip shelf arthroplasty in adultdysplastic hips: ten to twenty three year results. Int Orthop. (2012) 36:2425–
31. doi: 10.1007/s00264-012-1665-8
89. Willemsen K, Tryfonidou M, Sakkers R, Castelein RM, Zadpoor AA, Seevinck
P, et al. Patient-specific 3D-printed shelf implant for the treatment of hip
dysplasia: Anatomical and biomechanical outcomes in a canine model. J
Orthop Res. (2021). doi: 10.1002/jor.25133
90. Golafshan N, Willemsen K, Kadumudi FB, Vorndran E, Dolatshahi-Pirouz
A, Weinans H, et al. 3D-printed regenerative magnesium phosphate implant
ensures stability and restoration of hip dysplasia. Adv Healthc Mater. 10:e
101051. doi: 10.1002/adhm.202101051
91. Bicanic G, Barbaric K, Bohacek I, Aljinovic A, Delimar D. Current concept
in dysplastic hip arthroplasty: Techniques for acetabular and femoral
reconstruction. World J Orthop. (2014) 5:412–24. doi: 10.5312/wjo.v5.i4.412
92. Vezzoni L, Vezzoni A, Boudrieau RJ. Long-term outcome of Zürich
cementless total hip arthroplasty in 439 cases. Vet Surg. (2015) 44:921–
9. doi: 10.1111/vsu.12371
93. Off W, Matis U. Excision arthroplasty of the hip joint in dogs and cats. clinical,
radiographic, and gait analysis findings from the department of surgery,veterinary faculty of the ludwig-maximilians-university of munich, germany.
1997. Vet Comp Orthop Traumatol. (2010) 23:297–305.
94. Olsson SE, Figarola F, Suzuki K. Femoral head excision arthroplasty. A salvage
operation in severe hip dysplasia in dogs. Clin Orthop Relat Res. (1969)
62:104–12. doi: 10.1097/00003086-196901000-00013

in the early treatment of canine hip dysplasia. Vet Comp Orthop Traumatol.
(2008) 21:267–79. doi: 10.1055/s-0037-1617372
67. Parvaresh KC, Pennock AT, Bomar JD, Wenger DR, Upasani VV. Analysis ofacetabular ossification from the triradiate cartilage and secondary centers. J
Pediatr Orthop. (2018) 38:e145–50. doi: 10.1097/BPO.0000000000001120
68. Tibrewal S, Gulati V, Ramachandran M. The Pavlik method: asystematic review of current concepts. J Pediatr Orthop B. (2013)
22:516–20. doi: 10.1097/BPB.0b013e328365760e
69. Cooper AP, Doddabasappa SN, Mulpuri K. Evidence-based management ofdevelopmental dysplasia of the hip. Orthop Clin North Am. (2014) 45:341–
54. doi: 10.1016/j.ocl.2014.03.005
70. López-Carreño E, Carillo H, Gutiérrez M. Dega vs. Salter osteotomy for thetreatment of developmental dysplasia of the hip. J Pediatr Orthop B. (2008)
17:213–21. doi: 10.1097/BPB.0b013e32830850eb
71. Castañeda P, Vidal-Ruiz C, Méndez A, Salazar DP, Torres A. How
often does femoroacetabular impingement occur after an innominate
osteotomy for acetabular dysplasia? Clin Orthop Relat Res. (2016) 474:1209–
15. doi: 10.1007/s11999-016-4721-7
72. Sales de. Gauzy J. Pelvic reorientation osteotomies and acetabuloplasties
in children Surgical technique. Orthop Traumatol Surg Res. (2010) 96:793–
9. doi: 10.1016/j.otsr.2010.07.004
73. Wang CW, Wang TM, Wu KW, Huang SC, Kuo KN. The comparative,
long-term effect of the salter osteotomy and pemberton acetabuloplasty on
pelvic height, scoliosis and functional outcome. Bone Joint J. (2016) 98:1145–
50. doi: 10.1302/0301-620X.98B8.37215
74. Wang C-W, Wu K-W, Wang T-M, Huang S-C, Kuo KN. Comparisonof acetabular anterior coverage after salter osteotomy and pemberton
acetabuloplasty: a long-term followup. Clin Orthop Relat Res. (2014)
472:1001–9. doi: 10.1007/s11999-013-3319-6
75. Raghuvir HB, Shivrajsinh KJ, Dipak NS, Harit DB, Chirag AB, Naresh HK.
Treatment of canine hip dysplasia: a review. J Anim Sci Adv. (2013) 3:589–97.
76. Remedios AM, Fries CL. Treatment of canine hip dysplasia: a review. Can Vet
J = La Rev vétérinaire Can. (1995) 36:503–9.
77. Bliddal H, Leeds AR, Christensen R. Osteoarthritis, obesity and weight loss:
evidence, hypotheses and horizons - a scoping review. Obes Rev. (2014)
15:578–86. doi: 10.1111/obr.12173
78. Bockstahler B, Levine D, Maierl J, Millis D, Wittek K. Essential Facts ofPhysical Medicine, Rehabilitation and Sports Medicine in Companion Animals.
Babenhausen: VBS GmbH (2019).
79. Retchford TH, Crossley KM, Grimaldi A, Kemp JL, Cowan SM. Can
local muscles augment stability in the hip? A narrative literature review. J
Musculoskelet Neuronal Interact. (2013) 13:1−12.
80. Hara Y, Harada Y, Fujita Y, Taoda T, Nezu Y, Yamaguchi S, et al. Changes of
hip joint congruity after triple pelvic osteotomy in the dog with hip dysplasia.
J Vet Med Sci. (2002) 64:933–6. doi: 10.1292/jvms.64.933
81. McLaughlin RM, Miller CW, Taves CL, Hearn TC, Palmer NC, Anderson GI.
Force plate analysis of triple pelvic osteotomy for the treatment of canine
hip dysplasia. Vet Surg. (1991) 20:291–7. doi: 10.1111/j.1532-950X.1991.
tb01270.x
82. de Kleuver M, Kapitein PJ, Kooijman MA, van Limbeek J, Pavlov
PW, Veth RP. Acetabular coverage of the femoral head after triple
pelvic osteotomy: no relation to outcome in 51 hips followed for 815 years. Acta Orthop Scand. (1999) 70:583–8. doi: 10.3109/17453679908
997846
83. Mimura T, Mori K, Kawasaki T, Imai S, Matsusue Y. Triple pelvic osteotomy:
Report of our mid-term results and review of literature. World J Orthop.
(2014) 5:14–22. doi: 10.5312/wjo.v5.i1.14

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