A number of questions were posed in the commission for an article on elbow dysplasia, and still this article will only dent the surface.

One of the questions asked was "Is it a problem in our breed?" indicating the need for breeder/fancier education on the subject. "Elbow dysplasia" is not a single disorder but a catch-all term for several abnormalities, with many separate genetic causes and overlapping environmental (nutritional) influences. One type of lesion may be more prevalent in certain breed types, a different disorder in another group of similar breeds, though nearly all breeds are at greater or lesser risk for almost any of them. In some breeds the incidence is of frightening magnitude. One in every 300 dogs seen at more than a dozen veterinary colleges in the USA from 1967 to 1979 had one of the elbow problems collectively and popularly known as elbow dysplasias. Depending partly upon breed susceptibility, these malformations may affect the anconeal or the coronoid portion of the olecranon or the humeral condyle, (the humerus is the upper arm, and its lower knobs are called condyles) with secondary effects on ligaments and synovium (lubricating fluid and membrane). There may also be OCD (osteochondritis dissecans, a loose piece of cartilage or bone irritating the joint), congenital dislocation, or subluxation (joint looseness) brought on by premature growth plate closure (either in the ulna or the radius). Already you can see that a thorough study and background is too large for magazine articles!

ANATOMY
The radius of the lower arm supports most of the dog's weight (75-80% of the bearing surface of the joint) while the ulna and its "processes" (the preferred term for the protruding bumps between which the condyle of the upper arm works in a hinge-like action) stabilizes and constrains the movement of the elbow's parts. The annular ligament (annular means ring-like) holds the head of the radius close to the ulna and the rest of the joint. Other ligaments also help maintain stability by means of their position and tautness in the joint. When the dog extends its elbow (straightens its arm), the anconeal process is inserted into the fossa, the deep depression above and between the back part of the humeral condyles, so that the hinge cannot fold sideways in the normal dog. When the arm is flexed (elbow is bent), the coronoid process rides into the groove at the bottom and between the condyles, also ensuring the normal stability of that hinge. Since before birth, the development of these parts is by endochondral ossification (bone replacing cartilage preferrably at a normal rate and manner). "Secondary" (other than the main part) bone or ossification centers are seen by about 10 weeks in most breeds, a little sooner in toys and slightly later in giant breeds. Although there are several of these centers, we'll discuss the ones of major interest here. Ossification of the anconeal process (the upper, beak-like protrusion in front of the olecranon) gradually proceeds until, somewhere in the 16-24 week timeframe, the center not only turns completely to bone, but also fuses with the ulna. The result is a stronger joint with more stability and weight- bearing ability than cartilage could offer. With the normal anconeal process in place (riding or inserting into the notch between the condyles of the humerus), there is stability in motion. Without it, there is a side-to-side action, with the olecranon (topmost point of elbow) rolling around in what is referred to as an "out at the elbows" gait.

Primary and secondary ossification centers in the elbow grow toward each other and eventually fuse. That is, if all goes according to plan. If adverse genetic and environmental factors work together, results could include one of a few elbow dysplasias. For example, dogs fed high-calcium, high-calorie diets can have a delayed development of these centers with concurrent lag or retention of cartilage in the growth plates between centers. At 16 weeks of age, the anconeal process of dogs on higher calcium rations is seen with X-rays as a partially ossified separate center, but in dogs on low-calcium food, it is typically fully ossified. It is about this age that this center begins to fuse with the olecranon, that top part of the ulna often referred to as the "point of the elbow." If it remains ununited, the dog has UAP (ununited anconeal process), and at some point around this age it will be too late for it to "heal" by itself, and the piece should be removed.

The growth rates of the two bones (radius and ulna) in the lower foreleg are not the same nor are they individually constant during maturation of the dog. Growth studies on young dogs of a variety of mostly mid-size and large breeds gave much information. Ossification of these bones occurred after about 16 weeks of age, but in the meantime, the bones not only grow at different and differing rates, but the ends of each bone change in growth rates, too. It may be that osteochondrosis-type defects in the growth plates cause disruptions in the lengthening of one of these two bones, which makes it too long or too short compared to its companion, and in turn puts uneven stresses on parts of the joint.

Gross differences in growth rates between ulna and radius can put great pressure on anconeal and coronoid "bumps," leading to UAP and FCP (fragmented coronoid process). In many dogs the lower forelimb is bowed as a result of those differences. If lameness does not develop, there may still be very variable amounts of ulnar growth retardation; many fiddle- fronted dogs are seen in the show rings, including Toys, Shar Pei, and many others. In the development of the normal elbow, there is good congruity (tight fit) between humeral condyles and the trochlear notch running from the ulna's anconeal and coronoid processes, and between humerus and radius. Likewise, there is a tight fit between the radius and the ulna, with the curve of the coronoid process continuing in an unbroken arc forming the articular top surface of the radius. In some elbows, the coronoid process is abnormally situated a bit higher than normal (or you could say the top of the radius isn't high enough because it has lagged in growth). This "step" is often accompanied by a crack in the coronoid process, or even a fragmentation. In some elbows with or without FCP, UAP, or OCD, there can be increased joint space between humerus and radius, humerus and ulna, or both. Studies at University of California-Davis showed that joint incongruity preceded FCP and since it is also seen in conjunction with UAP and OCD, the implication is strong that incongruity precedes these lesions as well.

UN-UNITED ANCONEAL PROCESS

We are certainly dealing with genes and how they are expressed, regardless of the type of elbow dysplasia. In UAP, as the dog grows, the anconeal process not being anchored continues to move in relation to the ulna, and the collagen fibers in the growth plate get torn in the constant vibration. This leads to trauma, evidenced by pain, lameness, and swelling. It can be major and sudden as in landing from a jump, or it might be a series of minor "events" such as the repetition of pivoting at the ends of the kennel run or along the driveway or yard fence. In any case, trauma brings on the complete fracture, breaking any partial bony bridge if it existed, but most of the time it's just cartilage that tears apart. The anconeal process breaks loose, floats around in the area, causing irritation and edema, and then may continue in that manner or become loosely attached to another part of the joint such as the humerus or perhaps new bone that has filled in the portion of the ulna where the loosened piece had come from. As time goes on, unless the piece is surgically removed, osteoarthritis sets in with its intensified remodeling and swollen look. The rest of the articular cartilage begins to degenerate, and osteophytes (abnormal bony, calcified growths) develop on the humeral con- dyles and often on the radius as well, but especially on the olecranon. At times, the dog may have episodes of severe pain and swelling until it is treated, euthanized, or dies of old age or other causes. If surgery is not used, synovial fluid volume increases, crepitus (that grinding noise or feeling like sand in the joint) is noticed, and ability to flex and extend the limb is reduced. Eventually, the dog is unable to climb even shallow stairs without swinging its stiff forelegs in wide arcs.

UAP Elbow

DIAGNOSIS of UAP

It is relatively easy to diagnose UAP through radiograph, with a couple of cautionary provisos. Your vet may also have OFA's directions on positioning. The dog doesn't need any chemical restraint for such a picture. It may not be easy for every veterinarian to distinguish in all cases, so have the film of a four-to-six month old pup looked at by an orthopodist/radiologist before rushing to surgery. Not every dog that stands "east-west" ("frenched," i.e. with pasterns turned inward and toes out) and stands or moves with elbows out has UAP or another elbow dysplasia, but in certain breeds these and the more obvious signs should be enough to move the owner to take the dog to a veterinarian familiar with these disorders. Relative stride length is a poor substitute for a radiographic diagnosis. Dog owners can find out, through OFA statistics (if enough films have been sent in), what elbow and other-joint disorders their breed is most at risk for, and then test first for that or those disorders before continuing with a sale, purchase, breeding, or training. While there are more shoulder arthroses than elbow problems when all canines are looked at, some breeds are especially susceptible to specific-joint problems. German Shepherd Dogs should be checked in adolescence for UAP and massive breeds such as Rottweilers and Bernese Mountain Dogs should be evaluated for FCP at least once during adolescence or early adulthood.

TREATMENT OF UAP

Even as late as the early 1980s, controversial forms of treatment were being promoted and practiced. Some advised rest, pain killers, and patience; others were experimenting with fixation with wires, screws, and the like; a fourth type of treatment proposed was surgical fusion of the elbow. All these have fallen out of favor as a result of comparisons, and removal of the offending particles is now generally agreed upon as the only reasonable treatment. As soon as UAP is diagnosed, the patient should be scheduled for surgery to remove the "loose" piece and thereby the movement, irritation, and worsening degenerative changes. If not diagnosed until gross changes in appearance and gait have become obvious, there may only be a 50/50 chance of improvement in gait and the rate of osteoarthritis development. Early correction is far better, and routine radiography of your young stock is cost-effective in the long run, as well as beneficial to your breed and your public image.

FRAGMENTED CORONOID PROCESS

FCP (fragmented or fractured coronoid process) is another genetically-based elbow disorder, this one secondarily caused by a retardation of longitudinal growth of the radius. With the resultant growth of the ulna outstripping that of the radius, this tends to press upon and fragment the coronoid process around the age of 4«-5« months, at least for Bernese Mountain Dogs, a not-very-distant relative of the Mastiff. An incongruity or subluxation develops out of the relative lack of stability.

Diagnosis of FCP is not that easy. Except in extremely well-developed pictures of dogs absolutely correctly positioned, FCP will usually be missed if the practitioner is looking for the coronoid process itself. Look for the tell-tale osteophytes on the anconeal process, and this will give a very strong indication that something is wrong with the coronoid process, which is hidden from radiographic view by the humeral condyles and the proximal end of the radius. While the highest degree of osteophyte production occurs when UAP is the lesion, the next most frequent cause is FCP. However, if the coronoid process only has a fissure because the dog hasn't had the condition that long or isn't very heavy, osteophyte formation will be low. Later, as irritation continues or the coronoid breaks off, deposits will be more easily seen, but again, mostly around the anconeal process. This is why FCP is usually diagnosed later than is possible with UAP.

FCP is probably much more common than UAP, especially if your statistics are tied to breed incidence, as more breeds have FCP than UAP. FCP is seen in a tremendous variety of breeds, but most often in those "built like a tank" with wide bodies, heavy musculature, and large intake of food. Among the breeds most afflicted are the Rotts and Bernese mentioned earlier, although with additional films submitted to OFA, you will see other molosser types increase in incidence and numbers. In a radiographic study on Rottweilers free of lameness, osteophytes were found in one or more elbows in 70% of the dogs! Imagine the percentage if limping dogs had been included. Another radiographic survey revealed elbow arthroses in 75% of 297 Rottweilers with or without foreleg lameness. Further work with more Rottweilers showed that 68% of 141 dogs over 12 months of age, reported by owners to not have been lame, had those osteophytes. I wouldn't be surprised to find a correlation between selection for massiveness and incidence of elbow arthroses. It appears many more dogs can better tolerate some coronoid problems than they can put up with UAP. Note what was said above about FCP-affected Rotties not limping and compare that with UAP's usual effects on gait and pain episodes, and it should be clearer. When individual elbow lesions were calculated, the Golden Retriever was shown to be most affected (67%) by osteochondritis dissecans of the humeral condyle, vs 12% for all breeds. The relevance of a genetic basis for these elbow problems is underscored by the fact that dogs with lesions obviously originating in trauma were excluded, as were old dogs with arthritis but no other signs of any of these 3 lesions. While it might be claimed that FCP is a disorder affecting mostly Rottweilers, it is a disorder that should be "checked for and checked." Overall, the incidence of elbow dysplasias may be less than 10% (some of the earlier work in Norway indicates about 8%, all breeds) but in specific breeds, there are alarmingly high peaks. They may not be always as dramatic as the 40, 55, or 90% incidences of HD in some breeds, but if you have ignored elbows while doing your best to reduce HD in your lines or breed, you will almost certainly run into some heartaches. Best to have your dog's elbows "done" when you bring him in to the vet's for any other reason, at the ages the lesions would be most likely to be detected (about 5 months or older for GSDs, over 1 year for Rotties, Mastiffs, etc.). In one study it was determined that 32% of Rotties which do not limp and have not limped or shown pain have the same problems (fragments or fissures) as those which do, which tells us that these dogs may shrug off discomfort for a while, but also it indicates that there are some dogs with defective elbows being bred and transmitting the diseases to future generations.

About 20-25% of the weight forces transmitted through the elbow are borne by the coronoid process. When the coronoid process "goes bad", several things can happen singly or in various combinations. The fragment may remain in place and/or attached to ligaments, may (rarely) be absorbed partially, or it may exist unattached and somewhat moveable. The coronoid's ossified fragment called an ossicle will almost never turn into a true "joint mouse" (cartilaginous loose body) and resorb. Therefore, because of the ossified nature of the fragment, actual spontaneous healing does not happen in FCP cases. However, craters may develop in the area of the remaining portion of the coronoid process, and may be partially filled with bone in an effort to repair or stabilize them. Fissures may form, yet some might never progress to fractures. When the joint of a limping dog, for example, is opened, erosion of the cartilage covering the coronoid may be the only finding.

A great deal of the dog's weight (approximately two-thirds) is supported by the head of the radius and the coronoid process of the ulna. Other forces on the process include rotation between ulna and radius and ligament tension. In the normal elbow, these stresses are well-handled, but inherited weakness magnified by nutritional and other environmental factors can overload the bearing capacity of that part of the joint. Although osteophytes form when OCD or FCP are the only lesions, the growth of new bone in UAP is much more prominent, and this goes along with the differences in pain and swelling between UAP and FCP or OCD. Whatever the elbow problem, osteophyte growth continues as the dog ages, so if you haven't discovered and taken care of the disorder earlier, your dog will have progressively more trouble in his geriatric years, even though he may have passed his middle years with little or no difficulty.

FCP DIAGNOSIS

The reasons FCP and OCD are frequently spoken of in the same breath are that they can be identified on the same radiograph, many times will be found in the same dog, and usually the same breeds are involved in regard to similar incidence. Since some measure of satisfaction (I hesitate to call it success) in the outcome of surgery is dependent on early treatment, then early diagnosis is paramount. Although UAP can be seen by about 5 months and OCD about 5-6 months, it is seldom that FCP can be radiographically detected until some time after 7 months of age, and then with difficulty. Because the condyles of the humerus "cover" and hide much of the anconeal process and all of the coronoid process when a radiograph is taken of the flexed arm in a "mediolateral" position (the dog on its side with upper and lower arms flat on the film cassette), joint mice or other defects on the coronoid process itself might not be noticed. However, the presence of osteophytes on the anconeal process is a tell-tale sign of something being wrong with the coronoid process. The same sort of body reaction that produces calcium deposits (osteophytes) on the pelvis and femur in cases of HD, is what puts those "distant signs" of FCP on the anconeus. If the elbow is not flexed to its maximum, the humeral condyles can interfere with observation of such osteophytes at the early ages when treatment can be most successful. If a dog of 6 or 7 months age is presented with foreleg lameness especially after exercise, or stiff front action after rest (even if very mild or transient), and no signs of OCD or UAP or even osteophytes are found, such a dog should be watched very carefully and brought back for more radiographs in another couple of months until the reason is discovered. Prognosis worsens with delay. Some have claimed that they've been able to see the coronoid fragment if the arm is exactly positioned, but they will miss far more than they will see. Many owners will entirely miss the subtle clinical signs of FCP or OCD in a young pup, and will be aware only when the dog is older and has pain, or if a pup sustains some injury during jumping or play. Trauma often is the motivation to have the dog examined, at which time radiographic signs may be noticed by a vet who is looking for these disorders. Sometimes the gait and posture will give a clue, as some dogs stand with their legs and feet slightly rotated outward (frenched), and in advanced cases the stride may be shortened and/or wide. Two reasons why young molosser-type dogs are not radiographed more frequently than is the case are:

1.That FCP is frequently bilateral so there is no difference in gait, right or left;
2.That some breeds' popularity has increased faster than has the education of the owners and breeders.

Other factors may include a great stoicism or high pain threshold and the tendency to show and "finish" them young without emphasis on working titles which are more demanding on joints and practical soundness. In the preliminary diagnosis, gait and case history should be considered, and the physical exam should include maximum extension and flexion of the arms to see if there is a pain response. Usually there is a definite pain response, but since the shoulder joint is extended and flexed at the same time the elbow is, it may be very difficult to tell where the pain is coming from. In those breeds with a propensity for shoulder OCD, this joint should also be radiographed during the elbow diagnosis visit. Because one side may show more signs than the other, it doesn't mean the other is normal; both sides should be examined. In many breeds, radiography for OCD of the condyles should be performed in the same visit as for FCP, since so often, these disorders are found in the same individuals or breeds. The dog which is being examined for FCP should be seen not only in the view used for UAP (maximum flexion), but also in what is called a "craniolateral to caudomedial, slightly oblique" position (your vet will know how to set up the dog). However, even this extra position may not discover the fragment from the coronoid process. As in UAP, sedation is not normally necessary.

TREATMENT OF FCP

According to Dr. Sten-Erik Olsson:
"...early removal of loose cartilage and ossicles, although not a panacea, seems to be the only rational treatment of FCP and OCD."
And, since early removal is needed, the veterinarian must become familiar with the signs and diagnosis of each as well as follow the procedures in his surgery textbooks. By the early 1980s surgical techniques were developed which will be sufficient today. In some few minor cases, only cartilage damage rather than coronoid fragmentation may exist, and in others, the fragment may reunite and the process heal.

OSTEOCHONDRITIS DISSECANS (OCD) OF THE HUMERAL CONDYLE

The typical growth plate is a uniformly thick set of layers of chondrocytes (cartilage cells) which ossify on the metaphyseal side. The disturbance of this activity which we call osteochondrosis gives a less regular arrangement of these cells and failure to ossify evenly makes for abnormally thick areas in the plate. If this happens on the main weight-bearing part of the distal (bottom end of) humerus, a fissure, flap, and possibly joint mouse (loose piece) can cause irritation and lameness. Healing is not possible if a piece of cartilage or bone remains in the joint, so surgery is strongly recommended unless no fragments can be demonstrated on the radiograph.

OCD at the humeral condyles begins the same way other forms of osteochondrosis do: cartilage loses some nutrient delivery either before or after misaligned stresses (with some obscure genetic origins) result in a fissure. This hairline crack propagates in a shallow, "horizontal" manner, or deeper and more perpendicular to the surface. Either way, a flap of cartilage develops early, with osseous (bone) tissue only secondarily involved.

FCP and elbow OCD are sometimes found together in the same joint, and some think they may be associated, while others find very few dogs with both. It may be that many cases of humeral condyle damage are caused by the fragment of the coronoid process rubbing or scratching the part of the humerus it articulates with. If no cartilage flap or chip of bone from the humerus is found, it may be called a "kissing lesion" of the FCP.

Disruption in the endochondral ossification of the medial humeral condyle in certain breeds and families, and often under certain conditions such as fast growth rates and high- energy diets, may have some connection with the facts that this condyle and the coronoid process have thicker cartilage, that they normally ossify later, and that they are subjected to higher stresses than found in most other areas. Relative growth rates of leg bones and even of the whole skeleton may be related to overfeeding, and the dog using more calories than is needed for normal growth. Disruption of ideal calcium balance with other elements results in many anomalies, including a continued thick cartilage up to perhaps 4 months or beyond. Retained or malnourished cartilage can result in osteochondrosis to the extent of fissures and fragments. A caveat here: keep away from high-energy, high-calcium diets for growing dogs. If OCD is the only lesion, or if the flap comes loose and becomes a joint mouse (and especially if it is very small or gets resorbed) there can be a sort of spontaneous healing. Dogs with both OCD and FCP in the same elbow suffer the most.

DIAGNOSIS

OCD can be seen as early as 5 months of age, though not always. It may become apparent in another month or two, or it may be that the position wasn't right the first time. To get a good view of the medial condyle and thus the lesion, a craniocaudal (front-to-back) position, may show the defect on the film as a depression in the condyle's shadow, indicating where the piece of cartilage was lost. Actually, the position is better described as a craniolateral to caudomedial, slightly oblique one. A slight change in the leg's rotation, and this may be covered up by the other dense material (bone and cartilage) in the region. Even before clinical signs, osteophytes on part of the anconeal process might appear, so when checking for OCD, it is a good idea to also look at the arm in the fully flexed position used to search for UAP and FCP.

TREATMENT of OCD

As in FCP, the only good way to handle OCD of the humeral condyle is by going in and removing the culprit responsible for the damage, and before much of that damage has been done. I can't emphasize the word "early" enough, especially in OCD, because in this lesion, delay gives a worse prognosis than it does in the other two elbow dysplasias. Get the minor cases treated early enough, and you can stop the progression of arthritis and overcome lameness. If the flap hasn't come loose yet, the results are best, and the size of the flap or mouse has a bearing on it, too. Because the two problems occur in the same articulation, the surgeon can look for both FCP and OCD at the same time. A typical approach is to saw through the epicondyle so the muscles and tendons attached to it can be pulled out of the way while the area of the fragment(s) can be scraped and washed out. The epicondyle is put back and held in place with a lag screw, and the joint closed.

Prognosis for surgical improvement of either FCP or OCD of the humerus is "guarded", with about 50% of those operated on being relieved from lameness. The extent of degen- erative change may have much to play in this scene, although some arthritis develops whether or not surgery is performed. Many of those who do not limp may not favor one bad elbow over the other, and decreased mobility of the joint is hard to objectively assess.

The ulna-to-radius ratio is greater in certain breeds than in others, and the size and shape of the trochlear notch is not sufficient for the size of the ulna. This disparity is mostly seen to be greatest in breeds such as the Newfoundland, Rottweiler, German Shepherd Dog, Bernese, and similar, mostly heavy breeds. Olsson disagreed with this (Wind & Packard) view of the pathogenesis of elbow arthroses, having not seen evidence of any connection between UAP and the other two diseases in his research. He believes that overgrowth of the ulna leads to FCP and OCD, but overgrowth in the radius is the culprit in UAP. The radius puts extra pressure on the humeral condyle, and the other (upper) side of the condyle has a notch called the "olecranon fossa of the humerus" which transmits this force to the anconeal process, distorting it as it develops. This idea was substantiated by experimentation and analysis. Whichever concept is more accurate, it is interesting to note that the breeds with the higher proximal ulna to radius ratios (PU:R) are also the ones with generally more elbow problems.

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:

** Elbow disease is of major concern in a variety of breeds;
**Screening and registration programs should be encouraged by the FCI (The FCI is the Federacion Cynologique Internationale, sort of a "world all-breed kennel club" with a few similarities to AKC or other national dog organizations.);
*Such a screening program should be performed in a uniform way in all member countries of FCI;
** The procedure should be practical (not difficult for vets to perform) and the results useful for selection of breeding stock. In Sweden, a ten-year screening program using radiographs of elbows in many breeds turned up some interesting conclusions:
** The elbow status of the parents significantly affected the incidence of arthrosis in the progeny, another indication that these are probably polygenic traits and certainly inherited weaknesses;
** Selection for normal elbows has resulted in gradually more dogs being screened and more being free from signs of arthroses, which is still further evidence of their being genetic disorders;
*Because of awareness and screening, incidence of all elbow arthroses in Bernese Mountain Dogs decreased from well above 50% to 35%, while that of Rottweilers decreased from well over 50% to 40%, with continued improvement expected;
** Data on the ability of different sires to produce certain effects on the elbow status of offspring has been very helpful. Good producers should be promoted preferentially over poor producers in regard to elbow quality;
** There is a positive cost-benefit advantage to paying fees for elbow screening, compared to the value of dogs which were saved from moderate to severe arthrosis and impairment of usefulness. Replacing a dog who is no longer able to function well as a companion or service dog is more expensive than prolonging its useful life by an operation performed in early life. The purpose of screening should be to help breeders avoid the use of animals that have high (genotype) risk for producing the disease, thus preventing the chain of conception, birth, sale, and heartbreak that marks the absence of such control.

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.

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(original article written by Fred Lanting, and editorialized to fit this site by the site owner)

Fred Lanting is the author of "Canine Hip Dysplasia" and "Canine Orthopedic Problems."