THE DYSPLASIA : Reminders & advices during puppy growth

« La dys­plasie provient d'une mal­for­ma­tion de l'articulation coxo-fémorale qui appa­raît durant la crois­sance et qui entraîne une insta­bil­ité artic­u­laire et le développe­ment d'arthrose. Toutes les races peu­vent être con­cernées par cette affec­tion, mais les plus touchées sont les races lour­des et char­p­en­tées (ex : St-Bernard, Terre Neuve, Rot­tweil­er, Bou­vi­er bernois) ain­si que cer­taines races moyennes à grandes (ex: Berg­er Alle­mand, Gold­en Retriev­er, …). Le plus sou­vent, les deux hanch­es sont atteintes.» Charles René Sain­tRemy (Source SCC)

Il est qua­si­ment impos­si­ble de savoir si un chiot est atteint de dys­plasie de la hanche en obser­vant sa seule démarche. Les « appren­tis experts » qui dis­pensent leurs con­seils à tort et à tra­vers, affolant de cré­d­ules maîtres ren­con­trés en prom­e­nade avec leur chiot, par des diag­nos­tics com­plète­ment erronés, se lais­sent sou­vent leur­rer par une oscil­la­tion des jar­rets ou par cer­tains mou­ve­ments sac­cadés du postérieur : ces phénomènes sont dus à la crois­sance et né sont en aucun cas liés à une quel­conque patholo­gie.

Plusieurs degrés de grav­ité sont con­statés. Ils don­nent lieu à un classe­ment offi­ciel :

  • Classe A : Chien non dys­plasique avec artic­u­la­tion par­faite et un angle de N‑O supérieur à 105º : aucun signe de dys­plasie.
  • Classe B : Chien non dys­plasique avec artic­u­la­tion impar­faite et un angle de N‑O com­pris entre 90º et 105 : état des hanch­es presque nor­mal.
  • Classe C : Chien dys­plasique avec pince­ment artic­u­laire, un acétab­u­lum trop peu creusé ou une tête fémorale aplatie et un angle N‑O com­pris entre 80º et 90º : dys­plasie légère.
  • Classe D : Chien dys­plasique avec une artic­u­la­tion sub­luxée et un angle de N‑O inférieur à 90º.
  • Classe E : Chien dys­plasique grave avec lux­a­tion totale de l'articulation et un angle de N‑O inférieur à 90°.

« La dys­plasie de la hanche n'est pas une patholo­gie bien cernée, beau­coup de fac­teurs entrent en jeu, cer­tains con­trôlables, d'autres non. Face à elle, chaque chien est unique. » Cour­toisie UMES, doc­teur vétéri­naire, San­drine PAWLOWIEZ

S'il né fait aucun doute que la dys­plasie est dans la majorité des cas hérédi­taire, ce n'est pas le seul fac­teur en cause, la dys­plasie est en fait mul­ti­fac­to­rielle !

  1. Le GENE HEREDITAIRE est très com­plexe. La dys­plasie né dépend pas d’un seul gène mais de l’influence com­binée de plusieurs gènes. Il faut l’addition d’un cer­tain nom­bre de gènes défa­vor­ables pour que la mal­adie s’exprime. Tous les ani­maux por­teurs n’expriment pas la mal­adie. Il y a donc une dif­fi­culté cer­taine à l’éradiquer par la sélec­tion géné­tique.

Encore là, il est pos­si­ble que les gènes fau­tifs né se soient pas man­i­festés chez les par­ents mais qu’ils se déclar­ent chez le chiot.

  1. Les CONDITIONS OF VIE inter­vi­en­nent égale­ment dans une pro­por­tion très impor­tante autant pour l’apparition que pour la pro­gres­sion et la sévérité de la mal­adie :
    • l'alimentation est un fac­teur déclen­chant très impor­tant.
    • l'exercice physique. Il faut éviter de trop forcer sur l’exercice physique durant toute la péri­ode de crois­sance du chiot.
    • Eviter les exer­ci­ces vio­lents (comme grimper un escalier) et lim­iter les risques de trau­ma­tismes pou­vant entraîn­er des défor­ma­tions artic­u­laires défini­tives.

Voici pourquoi on né doit jamais laiss­er les chiots sauter, mon­ter, descen­dre les escaliers, au cours de leur crois­sance :

  1. L'alimentation né doit être ni trop riche en énergie, ni défi­ciente durant la crois­sance
    • préfér­er une crois­sance lente et har­monieuse à une crois­sance trop rapi­de due à une ali­men­ta­tion trop énergé­tique ou avec excès de cal­ci­um ou de vit­a­mine
    • éviter un excès de poids. Une ali­men­ta­tion adap­tée et bien équili­brée per­me­t­tra le main­tien strict du poids nor­mal du
  2. Les exer­ci­ces pro­duisant des efforts exces­sifs notam­ment pen­dant la péri­ode de crois­sance doivent être lim­ités
    • pour dévelop­per les mass­es mus­cu­laires, priv­ilégi­er des balades tran­quilles et la nata­tion sans excès, adap­tées à l’envie du chiot.
    • d’une manière générale, pour chaque activ­ité physique (c’est à dire prom­e­nade, for­ma­tion, jeux, course, jeux avec les autres chiens), lim­iter la durée à 5 min­utes par mois de vie.
      • par exem­ple, pour un chiot de 8 semaines, seule­ment 10 min­utes d'activité physique par jour !
      • pour un pup­py de 6 mois, seule­ment 30 min­utes d'activité physique par jour !
    • éviter toute forme de sauts qui pour­raient trau­ma­tis­er votre com­pagnon ou nuire à ses artic­u­la­tions sur le long terme. Ain­si, éviter de le faire utilis­er les march­es d’un escalier, ou de le faire entr­er ou descen­dre d’un véhicule, mon­ter sur le canapé,
    • éviter les sols glis­sants comme linoléum, car­relage… qui sont sources de chutes.
  3. Com­porte­ment. Empêch­er que votre chien né se tienne sur ses pattes arrière.

Sources divers­es : SCC. Point Vétéri­naire. Didi­er Jaminet & Char­ly St Remy. Dr Alain Fournier. Dr Guil­laume Raget­ly. Dr Lebernard. Dr Sébastien Mirkovic (L’Hormet — 42210 Saint-Cyr les vignes).

10 Things important SUR THE DYSPLASIA CANINE OF THE HIP by Carole BEUCHAT — PhD

Hip dysplasia is a hot topic in dogs, if it's possible to stay "hot" for 50 years. Researchers have been working hard for decades looking for solutions, and breeders have been doing their best to reduce the risk of producing affected puppies. But still the problem remains.

There are some simple things we could do to reduce the incidence of hip dysplasia now if we understand a few basic things. Here are the 10 most important things you need to know.

Hip dysplasia is not a congenital defect; it is not present at birth. Multiple studies have demonstrated that all normal puppies are born with "perfect" hips; that is, they are "normal" for a newborn with no signs of dysplasia. The structures of the hip joint are cartilage at birth and only become bone as the puppy grows. If a puppy is going to develop hip dysplasia, the process begins shortly after birth.

This is the hip joint of a 1 day old puppy. The cartilage tissue does not show up on an x-ray until the minerals are deposited that form bone. Proper development of the joint depends on maintaining the proper fit between the head of the femur and the socket (acetabulum).

""The hip joints of all dogs are normal at birth. The joints continue to develop normally as long as full congruity is maintained between the acetabulum and the femoral head... The acetabular rims are stimulated to grow by mild traction applied by the joint capsule and gluteal muscles attached along their dorsal borders, and from pressure by the femoral heads upon the articular surfaces... The morphologic characteristics of the complex hip structure show that biomechanical behavior is the prime influence in the growth of this joint." (Riser 1985) " (Ris­er 1985)

Hip dysplasia tends to be more common in some breeds than others and in some lines than others, which indicates that there is a genetic component to the disorder. However, scientists have been looking for genes that are responsible for the development of hip dysplasia in dogs for decades without success.

Genes that are associated with hip dysplasia have been identified in some breeds, but they are breed-specific; that is, the assortment of genes is different in every breed. (For example, see studies on the German Shepherd dog (Marschall & Distl 2007, Fells & Distl 2014, and Fels et al 2014), Bernese Mountain Dog (Pfahler & Distl 2012), and Labrador Retriever (Phavaphutanon et al 2008). Genes that could cause hip dysplasia have not been found in any breed. & Dis­tl 2007, Fells & Dis­tl 2014 et Fels et al 2014), Le Bou­vi­er Bernois (Pfahler & Dis­tl 2012) et le Labrador (Phava­phutanon et al 2008). Jamais les gènes qui pour­raient causer une dys­plasie de la hanche n'ont été trou­vés dans aucune race.

It's unlikely that researchers are going to discover an easy genetic solution to the problem of hip dysplasia. It is a complex trait that is influenced by both genes and environment, and there is no simple solution just over the horizon. We should be able to improve genetic progress by using selection strategies that are as efficient and effective as possible such as estimated breeding values, EBVs. One great advantage of using EBVs is that the genes responsible for a trait don't need to be known; you need only a pedigree database and information about affected animals. EBV (Esti­mat­ed Breed­ing Val­ues). L'un des grands avan­tages de l'utilisation des EBV est qu'il n'est pas néces­saire de con­naître les gènes respon­s­ables d'un trait. vous n'avez besoin que d'une base de don­nées généalogiques et d'informations sur les ani­maux affec­tés.

Although there is a genetic influence on hip dysplasia, the heritability of the trait is rather low. Many studies have shown that genetic variation accounts for only a modest fraction of the variation in hip scores, usually 15-40%. This means that some fraction of the variation in the quality of the hips is the result of non-genetic, or "environmental" influences. This is one reason why decades of strong selection has resulted in only modest reductions in hip dysplasia in some breeds. At the current rate of progress and selecting only by phenotype, it could take decades to achieve a meaningful reduction in the incidence of hip dysplasia (Lewis et al 2013).

Understanding the specific environmental factors that play a role in the development of hip dysplasia should allow us to reduce the number of animals affected by hip dysplasia even if the genetic basis is not yet understood. This would reduce significant pain and suffering as well as the expense and heartache endured by owners of an afflicted dog. There is no reason why we should not be taking active steps to do this now.

The top three environmental factors that have been found to play a significant role in the develop of dysplastic hips are: a) joint laxity, b) weight, and c) exercise (see below). ​

Puppies are born with perfect hips, and if the hips do not develop laxity the dog does not develop hip dysplasia (Riser 1985). Joint laxity occurs when the head of the femur does not fit snugly into the acetabulum. This could be the result of traumatic injury, overloading of the joint by weight, lack of muscle strength, or adductor forces (e.g., bringing the legs together). Joint laxity is the primary factor that predisposes a dog to the development of hip dysplasia.

In dogs as well as many other vertebrates (including humans), the head of the femur in newborns is held securely in place by a strong ligament variously called the "round ligament" or "teres ligament".

Une extrémité de ce lig­a­ment est attachée à la tête du fémur et l'autre extrémité à la paroi interne de l'acétabulum (la cupule du bassin).

You can see the teres ligament in this illustration (labeled "LIGAM TERES").

One end of this ligament is attached to the head of the femur and the other end to the inner wall of the acetabulum (the cup-like socket on the pelvis).

If the femoral head is not positioned properly in the socket, the forces on the hip will be abnormal. Instead of being distributed across the inner surface of the socket, the forces on the joint will be concentrated in a smaller area on the weaker rim of the acetabulum. The result will be damage to the rim of the socket when a load is placed on the hip joint.

The teres ligament should hold the head of the femur securely in the socket of the growing puppy while the muscles that will support the hip develop and grow stronger. But in some puppies, the ligament shows evidence of damage before they are even a month old (Riser 1985).

"The teres ligaments of the hip joints were edematous [swollen], a few ligament fibers were torn, and capillary hemorrhage dotted the surface of the ligaments at the point of the tears. These changes were considered the first findings that might be linked to hip dysplasia." "

The abnormal forces on the femur and acetabulum that are caused by joint laxity result in the trauma that causes hip dysplasia and osteoarthritis of the hip.

""There is no evidence that a primary defect of bone exists but rather the disease is a failure of the muscles and other soft tissues to hold the hip joint in full congruity. This is further supported by the fact that bony dysplasia can be increased, decreased, or prevented by controlling the degree of joint instability and incongruity. No other malformations are associated with the disease. A causal relationship between muscles and soft tissue defects or pathologic changes other than lack of muscle mass or strength has not been established... Hip dysplasia is a concentration of factors from a pool of genetic weaknesses and environmental stresses that fall into a programmed pattern of progressive remodeling and degenerative joint disease." (Riser 1985) " (Ris­er 1985)

If there is laxity in the hip joint, the amount of damage done to the femur and acetabulum will depend on the magnitude of the forces in the hip joint. The heavier the dog, the greater the forces will be and also therefore the higher the risk of hip dysplasia and osteoarthritis.

Puppies that weigh more at birth as well as those with higher growth rates (so they get heavier sooner) have a higher risk
of degenerative changes in the hip joint (Vanden Berg-Foels et al 2006).

As this graph shows, puppies kept on a restricted diet (gray line) have a dramatically lower risk of dysplasia and it develops much later in life than in puppies kept on normal rations (black line) (Smith et al 2006).

At four years old, less than 10% of dogs kept on a restricted diet (25% less than the control diet) were dysplastic, while at the same time more than 30% of the dogs in the control group were dysplastic. As an added advantage, dogs on restricted diets live longer, too (Kealy et al 2002)!
Unfortunately, many dogs (including show dogs!) are overweight (McGreevy et al 2005, Corbee 2013), and obesity could well be the single most significant environmental factor affecting the development of hip dysplasia and osteoarthritis. But body weight is a factor that we can control.

Although progress from genetic selection will take many generations, the incidence of hip dysplasia in dogs could be immediately and dramatically reduced simply by practicing better weight management. l’incidence de la dys­plasie de la hanche chez le chien pour­rait être immé­di­ate­ment et con­sid­érable­ment réduite sim­ple­ment en pra­ti­quant une meilleure ges­tion du poids.

Exercise strengthens the muscles of the legs and pelvis, and this will increase the stability of the hip joint. But all exercise is not created equal.

Puppies raised on slippery surfaces or with access to stairs when they are less than 3 months old have a higher risk of hip dysplasia,while those who are allowed off-lead exercise on soft, uneven ground (such as in a park) have a lower risk (Krontveit et al 2012). Dogs born in summer have a lower risk of hip dysplasia, presumably because they have more opportunity for exercise outdoors (Ktontveit et al 2012). On the other hand, dogs from 12-24 months old that regularly chase a ball or stick thrown by the owner have an higher risk of developing dysplastic hips (Sallander et al 2006).

The most critical period for proper growth and development of the hip in dogs is from birth to 8 weeks old, so the type of exercise the puppies are exposed to is most important during this time.

While puppies are growing rapidly, it is critically important to get their nutrition right.

Growing puppies need to eat enough to support growth but they should not be fat, because any extra weight can increase the risk of developing hip dysplasia (Hedhammar et al 1975, Kasstrom 1975). An additional problem is that puppies getting too much food could also consume too much of specific nutrients. Puppies provided a quality commercial puppy food that is fed in the proper amount will have a nutritionally balanced diet and should not receive any supplements. Dietary supplements, especially of calcium, are not only unnecessary but could cause serious problems. There is no evidence that supplemental protein or vitamins will reduce the risk of hip dysplasia (Kealy et al 1991, Nap et al 1991, Richardson & Zentek 1998). aucun com­plé­ment. Les com­plé­ments ali­men­taires, en par­ti­c­uli­er le cal­ci­um, né sont pas seule­ment inutiles, mais peu­vent égale­ment causer de graves prob­lèmes. Il n'y a aucune preuve qu'un apport sup­plé­men­taire en pro­téines ou en vit­a­mines réduise le risqué de dys­plasie de hanche (Kealy et al. 1991, Nap et al. 1991, Richard­son & Zen­tek, 1998).

Most treatments for hip dysplasia are easier and more successful in younger dogs. If early symptoms are overlooked and screening is done only after 24 months or more, the window of time with the best prognosis in response to treatment will have passed (Morgan et al 2000). Signs of lameness usually first appear when the puppy is 4 to 6 months old, but after a month or two the dog will often seem better. This is because damage to the acetabular rim such as microfractures will have healed and the dog is no longer in pain, but development of dysplasia and osteoarthritis will continue. From there, the dog might not display clinical signs again for years while the pathological damage progresses.

Laxity in the joint can be determined as early as 4 months old (either by palpation or PennHIP). If detected early, intervention to mitigate additional damage can include weight loss, modifying exercise and activities, or surgery - but it must be done early before skeletal growth is complete. Breeders should educate new puppy owners about the factors that can increase the risk of developing hip dysplasia and also advise them to get a veterinary examination immediately if there is any sign of lameness.

Genetic selection should continue to produce modest progress in the reduction of hip dysplasia. But a significant and immediate reduction in the number of afflicted animals could be achieved by better control of non-genetic, environmental factors. Weight management, appropriate exercise, proper nutrition, and early intervention at the first sign of lameness are simple steps we can take that will dramatically reduce the pain and suffering caused by hip dysplasia. The research will surely continue, but we already have the information we need to tackle this problem.

Cor­bee RJ. 2012. Obe­si­ty in show dogs. Anim. Phys­i­ol. Anim. Nut. DOI: 10.1111/j.1439–0396.2012.01336.x

Fels L, Y Marschall, U Philipp, & O Dis­tl. 2014. Mul­ti­ple loci asso­ci­at­ed with canine h.ip dys­pla­sia (CHD) in Ger­man shep­herd dogs. Mamm. Genome. DOI 10.1007/s00335-014‑9507‑1.

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