Elbow Disorders in the Mastiff and Other Breeds Part IIIBy Fred Lanting Mr.GSD@juno.com
Fred Lanting is the author of "Canine Hip Dysplasia" and the soon-to-be published "Canine Orthopedic Problems." The following is Part III of a three part article on elbow dysplasia written for The Mastiff Reporter. Parts I and II presented an overview of the condition, along with in-depth coverage of UAP (ununited anconeal process), FCP (fragmented or fractured coronoid process), and OCD (osteochondritis dissecans) of the humeral condyle.
CONTROL THROUGH GENETIC SELECTION
As we have gained more information about the incidence and course of elbow dysplasias, it becomes clear to scientists what many breeders and show fanciers have known all along: that these are genetic problems with environmental factors either making it worse or making it manifest. We don't have a good idea of how many genes are involved, but all of the above disorders are probably polygenic traits with fewer contributing genes than in HD. It is hard to imagine in this enlightened day that there is anyone left who does not acknowledge the genetic basis of orthopedic diseases, but there are indeed. It doesn't help the cause of improvement much to have laymen writing such things as "...it would be considered fairly strong evidence that UAP could have an inheritance factor" when a stronger statement would be both more accurate and more constructive. The real confusion comes about because the meaning of heritability isn't clear to everyone and the limited evidence available to the breeder and the average dog owner until quite recently.
In 1968 Dr. E.A.Corley (later best known for being head of OFA) considered the genetics of elbow arthroses. Using German Shepherd Dogs, he and his colleagues looked at the progeny of normal x normal, affected x affected, and normal x affected. In the second category, they found 57% normal offspring and 43% with arthritis or UAP. In the third group, 76% normal and 24% affected, and in the first category all normal offspring were recorded. This may be misleading, as the number was small and even normal dogs can produce dogs with elbow arthroses, since it appears these are polygenic disorders, as HD is, but the trend is obvious: the more "bad genes" you put together, the higher the incidence of affected dogs in the progeny. Crosses between affected GSDs and normal Greyhounds gave 84% with normal elbows, none with UAP, and 16% with some osteoarthritis.
Many others have also looked at the genetic aspects of elbow arthroses and the general consensus is that they are definitely controlled best by genetic selection. Studies in Norway strengthen this conclusion, as did the work by Guthrie and Pidduck on Labrador Retrievers in the UK in 1990. The estimates of heritability, sometimes being higher than in HD, indicate that there may be even less effect of environment in changing the ability of the genes to express themselves when it comes to the three elbow disorders. Whether these three are all parts of one syndrome is up for discussion; we do know that they share the effects of rapid early growth, high-energy nutrition, probably excess calcium, and perhaps selection for such things as massive size, all of which affect the expression (not the presence) of genes. Mason and Lavelle, in an Australian journal article, "Osteochondrosis in the Dog," mention the rapid expansion of the dog breeding industry in the 1970s and `80s with "selection for rapid growth, lack of critical selection of breeding stock, overfeeding, and generous use of calcium supplement" as having contributed to the apparent increase in osteochondrosis. Later work by Swenson, Wind, and others have lent additional weight to the growing certainty of elbow dysplasias being hereditary.
The "International Elbow Working Group,"* at their Vienna meeting concluded that:
It may be necessary to select breeding animals not only on the basis of information on the animals themselves, but also about their relatives. Although positive statistical correlation has been found between HD and elbow arthroses, this may be in part coincidental to dogs bred by some careless breeders: if someone is willing to overlook he'll probably overlook poor hips as well, or vice versa. Of course, there are also those who have been practicing HD control who are simply ignorant of the elbow problem. A study of over 2,000 Rotties, Berners, and Newfies showed that the relative risk for developing elbow arthroses (principally studied were FCP and OCD) in offspring of affected dogs compared to that of normal dogs was 1.6, which means that those progeny were 1.6 times as likely to develop elbow dysplasias than that of the non-affected parents. Because of the increased risk and the inescapable genetic link, elbow screening programs should be instituted and breeding candidates selected on the basis of their own, their parents, and other relatives' elbow status. It appears that noticeable progress, at least in populous breeds, may take several generations but this would be highly variable and based on the individuals chosen and how demanding the requirements. You can make faster progress in your own program than is possible on a breed club or national scale. A study I have mentioned in my new book indicated that frequency of elbow dysplasias in Rotties and Berners had been over 50%, and was reduced to 35 to 40% by the efforts of Swedish breeders and their national kennel club from 1981 to 1991. Better progress can be expected when leaders of various major breed clubs take their blinders off and encourage selection for control of these disorders of the elbow. The highest awards at a breed club's national specialty should be restricted to dogs that are orthopedically (and otherwise) sound. FCP is primarily a genetic disorder and secondarily a result of nutrition or environment. Consider pampered Great Danes in Holland; being a Dutchman myself, I can picture the owners sneaking those good Dutch butter cookies and cheese to their dogs. Three groups of Great Danes were fed diets with high, normal, and low calcium contents from 7 to 21 weeks of age. Those on the high-calcium diet developed severe changes across the entire distal ulnar metaphysis and had retarded development of the ulnar styloid process, the humeral medial epicondyle, the anconeal process, and the top physis of the olecranon. The experiment showed that the growth of the radius and several secondary ossification centers are retarded by the presence of excess dietary calcium.
ELBOW REGISTRY IN THE U.S.A.
The OFA has been evaluating elbow radiographs as a consulting service since 1969, and in 1990 began a separate registry for the use of breeders and clubs, with certification being awarded those dogs whose elbows appeared normal in all respects. Since elbow arthroses result in degenerative changes earlier than HD does, action can be taken sooner. However, since in some dogs radiographic evidence might not be obvious enough until later in life, the OFA decided to register dogs 24 months or older, while encouraging people to have their dogs screened much earlier. A pamphlet is available from OFA which explains the radiographic positions recommended to detect these disorders. However, the OFA was certainly not the only force for improvement in elbows, nor the best, according to many. There is now the Institute for Genetic Disease Control in Animals (GDC) started by Bernese Mountain Dog fanciers and vets in Sweden, Canada, Switzerland, the US, Canada, and the U.K. who came to realize that elbow dysplasias and other problems were very much genetic in nature, and that registry and control measures were needed. They formed an "open" registry (info on both normal and affected dogs being freely available to clubs and breeders). The GDC was formed not as competition for OFA, but as a complement and alternative for those who wanted faster progress more than confidentiality. This rapid progress with open registries has been proven many times over, such as in the progress made in hips in East and West Germany, Australia, Scandinavia, and other areas. Most body types are represented in the early lists of breeds affected by one or another of the elbow dysplasias, including Akita, Bouvier, Doberman, Fila Brasileiro, Springer, Irish Wolfhound, Shar Pei, and others in addition to the breeds discussed earlier. As more breeders participate and seek certifications to prove and increase the breeding value of their dogs and the quality of their produce, the list will expand greatly. In the December 1991 OFA elbow data, approximately 28% of the Bernese Mountain Dogs were dysplastic, 15% of the Goldens (though the sample was small), 15-19% of the German Shepherds, and 33-45% of the Rottweilers. No explanation was proffered as to why the percentages in Rotties and Berners were lower than those seen in Scandinavia. I might offer one possible idea: during the time the Norwegians and Swedes were emphasizing breeding dogs with normal elbows (and seeing progress in that joint) as well as normal hips, we in America were concentrating on promoting the preferential use of dogs with OFA numbers for hips only. If, as Dr. Olsson has said, osteochondrosis is the description of a general disorder in which HD is one manifestation, and elbow problems are others, then perhaps by selecting for normal hips, our better American breeders were unwittingly and unintentionally selecting dogs with fewer genes for osteochondrosis of any sort, including in elbows.
At least as pertains to FCP in the Rottweiler (and possibly a good guideline to other breeds), An estimate has been made that if both parents had been lame in the foreleg, or show osteophytes on radiographs, about 40% of their offspring will be lame (maybe not always, but part of the time). If only one parent is so affected, about 13% of the offspring will suffer from some elbow pain. If neither parent has had radiographic or clinical signs, chances are excellent (though certainly not 100%) that none of the pups will be lame during growth.
OTHER ELBOW PROBLEMS
Other, less common or less-publicized elbow disorders have been identified. Retarded growth or other disruptions in physis (growth plate) development such as early closure, a rarer form of elbow dysplasia called ununited medial epicondyle, a fragment from the immature medial epicondyle continuing to grow because it continues to get vascular nourishment via the tendons, dystrophic ossification of the synovial membrane, trauma triggering a calcification in the tendons of an immature dog (in immature humans it is called Little Leaguers' elbow), a weakness in the humeral condyle and nearby structures such as the supracondylar ridge and the epicondyle, osteoporosis, something which may still be called patella cubiti or ectopy ("solitary sesamoidal fragment on the lateral side of the radial head") arising from another location, osteochondrodysplasias (type of dwarfism), asynchronous (unequal) growth of the radius and ulna such as in Corgis, Bassets, Lhasa Apsos, and Pekingese, elbow subluxation, occasional or perhaps frequent abnormalities of the ligaments and joints in the elbow, micromelic dwarfism, Norwegian Elkhound chondrodysplasia (similar to the other canine dwarfisms as well as to human spondylometaphyseal dysplasia and maybe associated with glycosuria (sugar in the blood)), Akita dwarfism, and other dysplasias. Other elbow dislocations called congenital luxations and subluxations (also called arthrodysplasia) in the elbow have been described. So you see, this business of elbow abnormalities is not a simple problem; still, there is little cause for worry, since one or two may be all that you'll ever see in your breeding experience. Some of the reports of congenital elbow dislocations may have contributed to estimates of over 15% of the non-fracture elbow lamenesses but many of these may have been secondary to other elbow dysplasias. The few truly primary dislocations are probably genetic and may have their roots in the embryonic stage when the intra-articular ligaments are developing. Whether dislocation of the radius/humerus articulation is truly a congenital problem separate from other dysplasias, is a matter of uncertainty; many feel it is always secondary to growth plate disturbances. Other congenital luxations can be treated conservatively or with surgery, and this is likely the situation here.
Questions and Answers (from The Mastiff Reporter)