Consangvinizari gresite la mioritic

Theories of Pathogenesis

Canine hip dysplasia is a complex disease. It 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. The degree of involvement varies from minute changes in bone structure to total destruction of the hip joint. Investigators have searched intensively for genetic, chemical, and metabolic defects, but the cause has remained obscure.

Hip dysplasia affects humans and all other domestic mammals. In humans, 1.3 children in 1000 are affected. In dogs the prevalence may run over 50% in large dogs if control measures have not been practiced. Few data are available on the prevalence of hip dysplasia in other mammals, but it is thought to be low. The disease is undoubtedly rare in undomesticated animals.

No specific genetic pattern of inheritance has been demonstrated in this variable disease. It has been demonstrated that both genetic and environmental influences contribute to development, regardless of the species affected.(15,31, 32,40,74,76) Consequently, the disease has been designated as polygenic or multigenic.(28) As in most polygenic diseases, there are both major and minor causative factors. 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.(31,32) 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.(53) No other malformations are associated with the disease.(79) A causal relationship between muscles and soft tissue defects or pathologic changes other than lack of muscle mass or strength has not been established.(40,41)

Experimentally, hip dysplasia may be produced in many ways.(43,56,74,76,87,88) These include any circumstances that contribute to an unstable hip joint, namely, adductor forces, lack of muscle strength, chemical relaxation of the pelvic soft tissues, traumatic injury to the hip joint, and overloading of the joint by weight. 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.

The general cause of hip dysplasia, when defined, must be broad enough to explain its development, not only in dogs, but also in all other affected animals. Many genetic and environmental factors can trigger events that bring about the condition secondarily.(74,77,79,88) Hip dysplasia, therefore, is not one disease but many diseases that result in common degenerative lesions of the hip joints.(77)

Hip dysplasia has been observed in cats (27,35) and in most breeds of dogs; however, it is a greater problem in some breeds(65) than in others. The true prevalence of hip dysplasia among breeds of purebred dogs is not known, but data from the Orthopedic Foundation for Animals (OFA) on the first 36,000 pelvic radiographs evaluated has given insight into answering this question (Table 83-1).

The percentage of dogs of various breeds affected by hip dysplasia is not a true representation of the prevalence of the disease in these breeds because radiographs depicting obvious dysplasia were screened by referring veterinarians and not submitted. Therefore, the overall prevalence of hip dysplasia is higher than that represented in the analysis (Table 83-1). The rankings of the breeds are consistent with those obtained previously from smaller populations.(36) All breeds were screened in a similar manner.

Table 83-1 Pelvic Radiographic Diagnosis
Body Size

The breeds with the lowest prevalence of hip dysplasia are near the size of the ancestral dog. The bones are small in diameter and smooth, the feet are small and well arched, and the shape of the head is long and narrow.

The giant breeds with the highest prevalence of hip dysplasia are two to three times larger than the ancestral dog. Their bones are coarse and large in diameter, with prominent protrusions and depressions. The feet are large and splayed, and the head is wide and oversized.

Body Type

In general, the body conformation of the breeds with the lowest prevalence of hip dysplasia is slender and trim. The skin is thin, smooth, and stretched tightly over the underlying tissues. The muscles are prominent, hard, and full-bellied. At dissection in these breeds, the skin and subcutaneous tissues and fascia rarely contain over 1% to 2% fat by weight. The joint ligaments are well developed; the fibers are coarse, closely packed, and relatively free of fat. The well-formed pelvic and thigh muscles are attached to broad, coarse tendons that are attached securely to the bones. These dogs are fleet-footed and well-coordinated in their movements.

Of the high-risk group, the four breeds of the giant type are not only two to three times the size of the ancestral dog, but their body conformation is heavy, round, and stocky. Acromegalic characteristics are present to some extent in all four breeds. Fat is abundant in the subcutaneous and fascial spaces and commonly accounts for 5% to 10% of the weight of the soft tissues of the hindquarters. In comparison with the low-dysplasia group, the muscles are less prominent and less developed. Fat is infiltrated into the tendons and ligaments. The fibers of these two structures are smaller in diameter than those of the low-risk group. The gait of the giant breeds is less graceful and slower than that of the smaller breeds.

Growth Pattern

Breeds with the highest prevalence of hip dysplasia grow and mature more rapidly than those in the low-risk group. Starting at birth, this group gains rapidly. The pups of these breeds are aggressive eaters, both as they nurse and as they take supplemental food. In a study involving 222 German shepherds, 63% of the dogs that weighed more than the mean of this group at 60 days of age were dysplastic at 1 year of age, whereas only 37% of those less than the mean became dysplastic. The same rapid rise in weight in other breeds of the group at high-risk for dysplasia has been observed.(63)

Hip dysplasia has not been reported in the wild undomesticated carnivorous animals, such as wolves and foxes. A study of their pattern of growth found that the pups were slow-growing and late maturing. The young pups were whelped in dens. As newborns, they received their nourishment by nursing during the first few weeks. When more food was required, the mother killed rodents and either brought them to the den or ate the animal where it was killed and then returned to the den where the ingested rodents were regurgitated for the young to eat.(61) Young carnivores were quite mature and 6 to 10 months old before they began to hunt. The amount of food available for the growing members of a litter was limited. This caused the young to mature slowly and remain thin and light for their body size. Such an environment favored the completion of ossification and developmental maturity of the joint before the hips could be subjected to possible injury, incongruity, or subluxation from excessive extrinsic forces (e.g., excessive body weight) (65,69)

Genetic Influences and Heritability

Few genes analyzed thus far directly affect osseous structures.(17) The shape of bones reflects changes by biomechanical stresses.(15)

In the dog no clear-cut pattern of inheritance has been recognized.(23,28,30) This means that many genes are affected, and polygenic traits are subject to environmental modifications. New data have substantiated these findings.(29)

The spread of hip dysplasia centers around the genetic transmission and heritability of a particular body size, type, conformation, movement, growth pattern, and temperament. This conclusion is based on the facts that the prevalence of hip dysplasia is approximately the same in a number of breeds with similar body characteristics and there is no gene flow between these purebred breeds. Since these facts must be respected, biomechanical and environmental factors associated with certain body conformation and size must be considered as causes.(69)

Critical evaluation of the heritability of hip dysplasia has been made in the German shepherd in 244 offspring from 54 full subfamilies. In one report, "heritability was defined as a property not only of the character (trait) but also the population and the environmental circumstances to which individuals are subjected. Heritability, because it represents the proportion of the total phenotypical variance, receives the attributes of a positive number which may range from 0 to 1.0 in magnitude".(29) On this scale and based on evaluations of radiographs from 2 year-old dogs, the heritability was given an average estimate of 0.25. The conclusions were that canine hip dysplasia be termed a moderately heritable diseased.(30)

In a study involving 236 German shepherds, it was demonstrated that the most reliable way to eliminate canine hip dysplasia was through the establishment of "pedigree depth," that is, by the use of ancestral lines of dogs radiographically free of hip dysplasia.(33)

Results of controlled breeding programs in Sweden further indicated that the prevalence of hip dysplasia in the German shepherd was substantially reduced by mating only dogs with radiographically normal hips.(7,50) Similar decreases in prevalence have occurred in another controlled breeding program in a colony of guide dogs (Seeing Eye, Inc. Morristown, NJ).

In another account, with 584 progeny in a closed colony of German shepherds, it was shown that the prevalence of hip dysplasia was noticeably reduced by selectively breeding dogs proved radiographically to have normal hips at 1 year of age or older. In 3-1/2 years the incidence of hip dysplasia was lowered from 39% to less than 17%.(64) The male dogs in this colony had a wide variation in their ability to transmit normal hips to their progeny. For example, only 8.7% of the progeny of one dog with radiographically normal hips at 2 years of age developed hip dysplasia, whereas 37.8% of the pups of another dog with similar radiologic evaluation mated to the same bitches developed hip dysplasia.(20)

Environmental and Man-Made Influences

Embryologically, articular joints are differentiated as units in situ from a mass of skeletal mesenchyme.(90) Development progresses normally in each joint as long as there is full congruity between the parts. The congruity remains as long as the supporting tissues are strong enough to withstand the mechanical or physiological factors that tend to pull them apart.(77)

In humans, intrauterine stress has been cited as contributing to hip dysplasia, particularly if the fetus is positioned with the legs in adduction and extension.

Hip dysplasia in humans is rarely associated with teratology abnormalities. Other hip abnormalities distinctive from dysplasia, however, are frequently associated with such deformities as clubfoot, hyperextension of the knees, spinal deformities, arthrogryposis multiplex, and chondro-osteodystrophy.(22)

In the young child, the position of the legs during infant care is found to be very important to normal hip development.(71,73,75) Abduction and flexion of the legs has a stabilizing effect on the hip joints. The square diaper favors greater abduction of the legs than does the three cornered diaper. The Bantu baby, who is carried with its front side bound to the mother's back with its legs in acute abduction and flexion, seldom has abnormal hip joints.(71,75) In contrast, the Navajo Indian baby, who spends its first years of life strapped to a cradleboard with the legs in abduction and extension, has a high rate of hip joint instability.(70)

Other factors such as femoral anteversion and spastic shortening of the psoas muscle have been shown to favor acetabular dislocation when the leg was extended.(44) These observations indicate that both environmental and hereditary influences are important.(28,42)

In the dog, the hip joints are normal at birth.(43,68) The long bones of the pup are short during prenatal life, and mechanical stresses that bring about dislocation of the femoral heads are minimal. Teratologic abnormalities of the joints are rare in the dog, except for congenitally dislocated elbows and an occasional clubfoot deformity. Congenital malformation of the hips is also rare.

Extrauterine Influences

EARLY WEIGHT GAIN

In 222 German shepherds born consecutively, 100 were dysplastic, and the prevalence of hip dysplasia at 1 year had a direct correlation with their weight at 60 days of age. The heavier dogs, that is, the heaviest males and heaviest females at 60 days of age, had the highest incidence of hip dysplasia at maturity.(63) (See Fig. 83-2.)

These data suggested a number of indirect genetic factors influencing the rate of hip dysplasia. The aggressiveness in nursing may be inherited, as may be the quality and quantity of the supporting tissues around the hip joint. It was concluded that when growth, gain in weight, and nursing aggressiveness exceeded the strength of the supporting tissues, subluxation and hip dysplasia occurred.(63)

The first subluxating stress on the hips occurs when the pup supports itself while nursing, and the hindlegs are in forceful adduction and extension. The heaviest pups were the more aggressive, worked the hardest while nursing, and spent the most time feeding.(63)

PELVIC MUSCLE MASS

Data indicate that here is a positive correlation between the amount of pelvic muscle mass and the prevalence of hip dysplasia. Of three large breeds of dogs, the greyhound is relatively free of hip dysplasia; over half of the German shepherds are affected with hip dysplasia, and nearly all the July foxhounds are dysplastic.(69)

These data further emphasize that hip dysplasia encompasses biologic height, weight, and muscle bracing. The builder, before architecture was a science, learned that when the height of a structure was doubled, the bracing had to be tripled or the structure would fall of its own weight.(82) This basic rule, learned many years ago, illustrates clearly why a low foot stool fits solidly on the floor and the tall stool of the same area wobbles when supporting weight.(82) Similarly, it has been found that dogs less than 30.5 cm in height and less than 11.3 kg in weight (dachshund) are relatively free of hip dysplasia. On the other hand, at least half the large dogs, those 34 kg or more in weight and more than 50.8 cm in height, are affected with dysplasia.(66)

MUSCLE MYOPATHIES

All newborn mammals, including human infants, undergo many metabolic changes during their transition from intrauterine to extrauterine life. The muscle tissues are relatively immature both anatomically and biochemically at birth. Lack of muscular maturation in the newborn influences the manner in which the newborn responds to function. This immaturity accounts for the failure of many mammals, including the human, dog, and cat, to walk at birth.(88)

There is evidence that the wide range of acetabular and femoral changes occurring in hip dysplasia is the consequence of joint laxity. The possibility that this may be associated with or influenced by the rate of muscle maturation has not been explored. The rate of muscle maturation may be an inherited factor.(12,43) Consequently, the degree of subluxation in the young may be influenced by subnormal muscular function. In humans, the possibility of iliopsoas muscle spasm in the infant has been explored. (41,44)

In the adult dog, the light microscope was used to examine histologically the individual pelvic muscles associated with hip joint motion. Evidence of muscle disease was not recognized. In dogs with advanced hip dysplasia and associated osteoarthritis, atrophy of the pelvic muscles was present but changes such as muscular necrosis, inflammation, and extensive fibrosis were not found.(66,69)

One observer suggested that in young dogs with developing dysplasia, the pectineus muscles were in spasm and contained a degenerative lesion.(4) The pectineus muscle (an adductor), when in spasm, was thought to favor forcing the femoral heads out of the acetabula. This observer further suggested that if the pectineus were cut in the dog at an early age, the occurrence of hip dysplasia would be drastically lowered.(4)

A causal relationship between the pectineus muscles and hip dysplasia was not established in an experiment using the pelvic muscles from Labrador retrievers, German shepherds, Alaskan malamutes, and beagles.(40) Pectineus muscles in these dogs with both normal and dysplastic hips were examined and compared. The relationship between pectineus muscle abnormality and hip dysplasia remains undefined. The pectineus muscles from some young pups showed both hypotrophic and hypertrophic changes. It was suggested that the alterations seen in the pectineus muscles of dysplastic dogs probably represented secondary manifestations associated with a disease of developing hip joints (hip dysplasia).(4,12) The available evidence does not support the concept that abnormal pectineus muscle behavior is a cause of hip dysplasia. (39)

Developmental myopathy with type II fiber hypotrophy has been described in the pectineus muscles of very young dysplastic German Shepherds These investigators failed to establish a relationship between this muscle change, joint laxity, and dysplasia but have suggested the possibility of such a relationship. In their experiments using an enzyme stain, the small fibers stained as type I (white) and the large fibers as type II (dark). They considered the differentiation between small and large fibers in young dogs to be a myopathy. No myopathies were present in either the normal or dysplastic adult dogs in their study.(12) This change in the young dog resembles muscle fiber hypotrophy, which follows the cutting of the nerve to a muscle. These hypotrophied muscles become functional again and the fibers become normal in size when the nerve unites and use is restored.(34) Atrophied muscle due to a severed nerve and immature muscle are similar in appearance. (34)

Metabolic Influences

SEX

In humans, the female is affected with hip dysplasia four to eight times more often than the male.(22) In the dog an equal number of females and males are affected. The reasons for this difference have not been explained. Of 100 dysplastic German shepherds at the Armens Hund Skula (Sweden), 49 were males and 51 were females.(63)

CHEMICAL AND HORMONAL INFLUENCES

Pelvic tissue relaxation is a well-known physiological phenomenon that occurs during the terminal phase of pregnancy in mammals. This reaction has been associated with the female hormone, estrogen. Experimentally, this reaction has been studied by injecting ovarian extracts into dogs to produce pelvic tissue relaxation resembling that seen at the termination of pregnancy. The specific polypeptide hormone that is commonly used is called relaxin. Male and spayed and virgin females when "primed" with estrogen before relaxin was administered responded sufficiently to relax pelvic tissues around the hip joints.(43,55)

The urine of newborns was examined to see if there was a correlation between high estrogen levels and the unstable hip. From the first tests, it appeared that such a correlation existed, but the use of more refined tests failed to verify these findings. (1,3,81) The conclusion is that hormonal influence is not associated with the development of congenital hip dysplasia in humans or animals.(1,3,71,81)

In the dog it has been possible to increase the incidence of hip dysplasia by giving relaxin to newborn pups and to produce hip dysplasia in the greyhound. (18,43,51,55) "It does not prove, however, that estrogens have anything to do with etiology and pathogenesis of spontaneously occurring hip dysplasia."(19) There is no evidence that estrogen levels within the biologic range have a relationship to the incidence of hip dysplasia in dogs.(19,52,55,81)

Defective protein biosynthesis of collagen was suggested as a cause for increasing articular cartilage degradation in osteoarthritic joints. Soluble collagen was reported to be found in the acetabular cartilage of dysplastic dogs, while predominantly insoluble collagen was present in dogs with normal hip joints. It was not possible to relate these changes to hip dysplasia or to osteoarthritis.(39,40)

Inborn metabolic errors of chemical or hormonal origin have not been found in human or canine hip dysplasia.(39,40,52,87)

DIET

A variety of nutritional and mineral supplements have been used in attempts to alter or prevent the course of hip dysplasia in the dog. Diet has not affected the occurrence or course of the disease other than the mechanical effect of increased or decreased weight upon the hip joint.(66)

Prevention

In the child the development of hip dysplasia can be stopped and the condition can be reversed to a stable normal hip if it is discovered early before remodeling has begun. The key to treatment is the restoration of full congruity between the femoral head and acetabulum by placing the legs in an abductor-flexed position.(76,88)

In the young dog genetically conditioned to develop hip dysplasia, confinement to a small cage (1 m3) where the dog spends most of his time sitting on his haunches (abductor-flexed position) will prevent the development of hip dysplasia.(66,68) Surgical improvement of joint congruity can also be very beneficial.

Linkul catre documentul intreg cal.vet.upenn.edu/projects/saortho/chapter_83/83mast.htm

Esti un mare mincinos si invidios pui din cuibul cu acest mascul sunt prezenti in expozitii si nu au probleme. Iar daca nu ai loc de masculul meu te dau in judcata pentru calomnie. Veziti de treba ta si nu mai minti lumea.

Buna ziua,
Tin sa adaug parerea unui amator(adica eu).
Nu am nimic cu domnul Osiceanu, defapt nu am cumparat de la dansul nici un mioritic. Tin doar sa adaug din postura unui amator de mioritici ca are perfecta dreptate. Scopul nu este de a avea cat mai multi mioritici, ci de a avea mioritici de calitate. Exemplarele enumerate mai sus lasa de dorit din multe puncte de vedere. Am participat anul(2012) acesta la expozitia de la Romexpo de mioritici, vreau doar sa adaug ca am vazut cativa caine care erau mioritici si restul care isi doreau sa fie mioritici. Culmea este ca Tender Ebony era foarte apreciat de arbitru si nu numai, sincer adaug, nu as tine acel caine nici daca mi l-ar da cineva gratis. Sincer am ramas suprins pentru aprecierea unor exemplare, pentru care eu din punctul de vedere al unui amator, mentionez ca nu au ceea ce ar trebui sa urmareasca o linie de mioritic, in special o linie de campioni, asa cum se doresc cei care erau la expozitie. Din cauza defectelor enumerate mai sus am vazut mioritici cu un comportament complet deviat. Am vazut mioritici speriati, timorati, coafati si parfumati, am ramas putin socat de ceea ce am vazut(cu exceptia unor exemplare). Eu intelesesem ca in trecut mioriticul parca se lupta cu lupul, ursu si alte animale salbatice. Cu siguranta mentionez ca 85% din exemplarele vizionate la Romexpo 2012, nu erau decat niste javre timorate, unele dintre ele considerate campioni. As dorii sa adaug ca o exceptia mi s-a parut canisa de runc, avand din punctul meu de vedere exemplare de exceptie cu un temperament echilibrat si puternic. Astfel promovarea unor exemplare care au abaterii grave de la standard fac un deserviciu acestei rase. Cunosc multi oameni care nu vor sa auda de acesta ras, tocmai pentru ca au achizitionat sau au vazut exemplare timorate si fricoase in ograda multor oameni. Am incercat sa explic acestor oameni ca exemplarele respective erau doar niste caini mari cu parul lung, dar nu erau 100% mioritici, ci proveneau din tot felul de incrucisari in trecutul indepartat. In speranta ca vom avea in romania exemplare deosebite de mioritici va salut!