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Elbow Disorders in the Mastiff and Other Breeds Part II

By Fred Lanting

Fred Lanting is the author of "Canine Hip Dysplasia" and the soon-to-be published "Canine Or- thopedic Problems." The following is Part II of a three part article on elbow dysplasia written for The Mastiff Reporter. In Part I, an overview of the condition was presented, along with in- depth coverage of UAP (ununited anconeal 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 progres- sively more trouble in his geriatric years, even though he may have passed his middle years with little or no difficulty.


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, I feel, 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.


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.


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.


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.


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.

(Part III will discuss control through genetic selection and answers to some often-asked questions about elbow dysplasia).

For further discussion of the nutritional implications of OCD, HOD and Panosteitis refer to the articles by Linda Arndt in the MCOA Journal (1994 #2 & #3). If you do not receive the Journal, contact Sharon Krauss for copies of these articles.

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