|
hd — hip dysplasia
part 2. general information and statistics, etiology, pathological process developing
• general information / statistics
As we know Hip dysplasia (HD) is congenital disease based on heredity. It's quickly invades due to some common selection methods, for example, cross-breeding, line breeding, etc.
Main gravity issue of the disease is inheritance of so called flail hip joint which leads to acetabulum immaturity including immature and changed hip femoral head, additionally to different stresses affecting dog developing.
Hip joint is flexible bones junction composed by hip joint fovea (acetabulum) and hip femoral head. Hip joint is simple, triaxial, and globular.
General motions in the joint are flexing and rotation; they are limited and conditioned by ligament mechanism, joint relief structure and muscles. Joint capsule is wide and reinforced by mighty ligaments which limit movements in the joint.
Hip dysplasia had been first described in 1935. As Shales writes, up to 75% of German shepherds in USA had this fault (1959), while Henricson says about 7% (1969). Shuncard (1969) tells that 22,5% of 1.725 USA military German shepherds had been rejected due to this fault. Examination of German shepherds showed almost 50% rejection in most countries (Wamberg, 1967). Slaaf talks about 35,8% in GDR in 1971. Scandinavian statistics note about 90% of dogs with apparent HD signs.
Hip dysplasia is considerably spread between some breeds. Most often it hurts rottweilers, German shepherds, senbernars, newfoundlands — i.e. this disease takes mostly large dog breeds. There had been found no dependence to gender and age. In 89% of cases dysplasia hurts both hip joints, 3,3% — only right joint, 7,7% — only left one.
• etiology
Some authors suppose etiologic factor of incorrect hip joint development and related muscles is anlage fault, while others — late fetal hip joint development. Developing disorders some explain by vitamin balance changes, hormonal disorder, etc.
There's a suggestion that HD development goes due to lack of interaction of acetabulum and femoral head in fetal period. Sooner femoral head and acetabulum lose close contact, more distinct anatomic and clinical radiological dysplasia signs.
Many researches demonstratively proved that HD is inherited, i.e. is hereditable disease, while it's trigger is hereditable joint «hypoplasia factor».
All serious researchers state that parents with heavy degrees of disease give more percentage of puppies with heavy disorders either.
|
Parents' joints 
|
% descendants affected
|
|
Tarkevich (all breeds)
|
Robinson (all breeds)
|
|
• Both parents are healthy (HD free)
|
17,5
|
28,4
|
|
• Healthy Male / affected Bitch
|
41,4
|
48,2
|
|
• Affected Male / healthy Bitch
|
38,0
|
41,0
|
|
• Both parents are affected
|
45,0
|
84,0
|
table 1
Dependence of hip joint state of first generation descendants
from parents' hip joint state
Scientists' opinions on gender dependence differ. So, Wanderleep states that males (all breeds) are affected 1,2 times more often. Tarkevich mentions equal percentage of both genders affected (all breeds). Mitin (all breeds, 1982) found bitches being affected more. Though they refer not to coupling, but to hormonal influence. So, numbers demonstrated by different authors are commonly close, and affected bitches percentage is always higher. If both parents were HD-free (two-generation selection), healthy puppies percentage was up to 76. While if only one of the parents was HD-free, healthy puppies percent was between 47 and 50. Biorn-Fors supposes HD heredity type as autosome dominant with 60% chance to get phenotype gene in the population. Hereditable inclination is decisive in HD emergence. Though this fault may be found on dogs got from absolutely healthy parents. HD heredity degree, as Swedish authors show, is 55—60%. Statistical evaluation of fault in a whole dogs population is inconstant and depends on many factors.
As found, environmental factors effect appreciably final result of joint forming and clinical HD signs.
There is an opinion that large mighty dogs who eat well and grow fast are more inclined. These individuals muscular mass develops later than quickly growing skeleton, what leads to non-simultaneous achieving of functional maturity by these locomotor apparatus components and then to joint instability. Lines with higher muscular index, large and durable ligaments, fascies and tendons have less risk of being affected.
One more inclining factor is overload of growing youngster's hip joints. Critical development and stabilization period is age of puppy since birth till 60 days. In this period soft and elastic bones, cartilages, nerves and immature muscles are especially susceptible to stresses and weight load. Joint parts develop synchronically if load is properly distributed. 6-month-age joint ossification and muscular mass are enough to prevent HD in usual terms. From that angle «vendible» puppy of the best litter is going to HD-risk category. That's a fact to think about for clubs where excellent mark is mostly defined by «elephant weight», even though the puppy hardly moves.
By no means, exceeding weight appreciably increases hip joint load. Nutrition does matter either: proteinaceous food advantages muscular mass grow, balanced mineral supplement both with vitamins and microelements influences speed of grow and development of organism tissues, and skeleton forming and ossification. (You can check recommended balanced ration for rottweiler puppy here).
Lack or excess of minerals, microelements and vitamins may also lead to permanent changes of hip joints. So, some state that lack of ascorbic acid in the growing organism leads to HD developing on stress. Carbonated food (cereals) advantage fat formation which aggravates joints state. Rachitis wholly affects osteal tissue and may be start point for HD developing. Slow ossification of joint components caused by different factors also inclines to HD. The question, whether displaced joint state defines pelvic muscles weakness, or vice versa weakness is defining, is still open.
Some researchers mention relation between HD and special anatomic structure — straight hip position.
Swedish scientists found role of female sex hormones in HD emergence during period of grow and developing. They succeeded to incline litter to HD giving female sex hormones to parturient bitch and their puppies at their first months.
Important HD factor is excess of motion in the joint which increases joint load even with normal weight and muscular mass during period of grow and developing of long bones. Experiment to constrain puppies with initially slight degree let them appreciably stabilize their joints. Control group without constrains later had heavy forms of the disease.
We shall say then about popular now «exhibition training» system when 2—3-month-old puppy is led «leashed», made run a lot and almost yoked. This «training» not only shatters puppy's psychic, but also hip joint overload seems felonious. Renowned veterinary specialists recommend that main training method for 8—10 month old puppies shall be free motions, playing with other puppies and swimming — increasingly loading. Keep in mind that some «frisky» puppies go the limit while walking so the owner is that one who shall doze the load. Chase of galloping adult dog by a puppy hurts one's immature joints a lot. Early (before 10—12 months old) working with stuff (width, height and complexity don't matter) seem to be irrational. Joint overload and even some traumas on such exercises are stress factor and may affect.
• pathological process developing
The disease starts from osteochondral apparatus of hip joints, especially acetabulum top edge immaturity leading to it's consequent flattening. Fovea and femoral head matching is breached. Forces in the joint are redistributed, top and front acetabular surfaces are overloaded. Joint becomes flail affected by the body weight and pet's motions. Overloaded parts of femoral head are intensively deteriorated what isn't supplied by regenerative processes. Acetabular edges and femoral neck hyperostosis (exostosis) emerge. There are increasing degenerative changes in the cartilages. Deteriorated femoral head is deformed from globular to conical or mushroom shape. Bursa-ligament joint apparatus and adjoining tissues are changed. To hold the joint it's capsule is compacting. Calcipexy starts.
Weak musculature can't hold the joint. Joint tissues deterioration and degenerative processes inside lead to inflammation — acute or chronic with periodical flares arthritis with pains and limp. Motions are more and more limited, dog tries to favor injured ending. Increasingly all joint components are involved into this process. Femoral head blood circulation is hurt. Ligaments flail, nervous endings are hurt, causing pain. Subluxations and dislocations develop, joint configuration is breached. Femoral head always displaces up and out. Calcified capsule loses it's elasticity. Later full joint structure degeneration (arthrosis), joint capsule breach, joint stiffness or immobility (ankylosis), system affect and osteodystrophy may emerge. All listed above leads to dog's disability.
Pathogenesis of congenital hip dislocation is caused by subluxation and joint dysplasia characterized by acetabulum hypoplasia, small femoral head size and slow ossification, rotation of top hip end to the front, and hip joint nervous-muscular apparatus developing anomalies. Changes may occur in the flattened acetabulum form and structure, femoral head, joint cartilages, joint bursa, ligaments and muscles. Acetabulum may be not only flattened but also lengthened: it's top edge is immature, resulting to scullcapant roof and absence of top block for femoral head.
Acetabulum flattening is often being aggravated due to thickening of cartilage layer of acetabulum fundus and connective tissue formation on there. Dislocation increases these changes: top roof may totally disappear, acetabulum gets triangle shape, further flattening. Femoral neck developing without bone block is shortened, top end of femor together with femoral head rotate to the front. Femoral head is much more less than normal, deformed, ossification core appears later. Joint capsule gets sand-glass shape and suffers distinct morphological changes: it stretches, following femoral head displacing up and out.
|
|
Page 2 | 
