Fragmented coronoid process (FCP), ununited anconeal process (UAP), osteochondritis dessicans (OCD) of the medial humeral condyle, ununited medial epicondyle (UME), and elbow joint incongruity have all been described as components of elbow dysplasia (1,2,3,4). Orthopedic enthusiasts have advanced some interesting theories on the pathogenesis of elbow dysplasia and how some or all of the aforementioned components may develop along the same pathogenetic line. Two theories are currently the most popular. The first is that elbow dysplasia is a variation of OCD; abnormal cartilage development prevents the anconeal process and the medial humeral epicondyle from fusing properly, and the coronoid process from ossifying to the body of the ulna, and it can produce a cartilage flap on the joint surface of the medial humeral condyle. The second is that all these phenomena arise due to asynchronous growth of the radius and ulna and the resulting incongruity of the elbow joint. When the humerus, ulna, and radius don't fit together properly at the elbow, weight-bearing forces are distributed abnormally, thus preventing fusion or ossification of the medial humeral epicondyle, the anconeal process, or the coronoid process.
These theories are particularly interesting when viewed in light of an uncommon elbow condition described here that has been reported in the literature infrequently.
A 17-month-old, 22 kg, spayed female German short-haired pointer was presented due to a lameness of the right front leg. There was no history of trauma. Physical examination revealed minimal weight-bearing, swelling of the elbow, and pain on elbow manipulation. Radiographs were judged to be normal. The dog was placed on nonsteroidal antiinflammatory medication and rest. Thirty weeks later, the dog had a recurrence of the lameness, which responded to nonsteroidal antiinflammatory medication. Fifty-six weeks after the initial presentation, the dog was evaluated again for lameness. Mild atrophy of the biceps and triceps musculature was noted, along with occasional crepitus on flexion of the elbow. Radiographs showed degenerative joint disease of the elbow and 2 mineralized densities medial to the joint (Figure 1). Radiographs of the contralateral leg were normal. These densities were removed surgically from amidst the origins of the flexor tendons on the medial aspect of the elbow. A round osteophyte, 11 mm in diameter, was found to be adherent to the joint capsule, while a linear osteophyte, 16.5 mm in length, was removed from among the flexor tendons. Postoperatively, the dog was treated with pentosan polysulfate (Cartrophen Vet; Arthropharm Pharmaceuticals, Ottawa, Ontario), 4 mg/kg bodyweight, SC, once weekly for 4 treatments. One week postoperatively, the dog was using the leg normally and has not had any additional problems during the ensuing 4 y.

Figure 1. Craniocaudal radiographic view of the elbow of German shorthaired pointer with 2 densities on the medial side.
What was this elbow condition, how did it develop, and why was it not detected radiographically at the time of the first visit? Review of the radiographs taken originally revealed that there were, in fact, changes visible at the time of the first visit (Figure 2). A very small osteophyte could be seen distal to the caudal aspect of the medial humeral condyle on the lateral projection. The most important lesson learned came in reviewing the dorsopalmar view of the elbow. This view was significantly oblique as sometimes happens when one is struggling to position an active young dog! Without a true dorsopalmar view, the minimal changes that were present at that time on the medial side of the joint were obscured by the head of the radius (Figure 3).

Figure 2. Reexamination of Figure 1 showing a small osteophyte (arrow) superimposed on the proximal region of the ulna.

Figure 3. Oblique view of the elbow in Figure 1 such that the densities on the medial side are obscured.
Classically, these elbow changes have been referred to as UME. The explanation has been that the ossification center associated with the medial epicondyle of the humerus has failed to fuse; an event that normally occurs around 10 wk of age (1). This explanation has not rested well with some authors, however. They point to the fact that there is no good radiographic correlation between the bony densities and the location of the medial epicondyle. In the case of a UAP, for example, it is clear, even to the casual observer, where the UAP is supposed to fit, while such was not the case with these densities. If such densities involve the medial epicondyle at all, most reports describe them as being associated with only its distal portion (1). Some authors have even gone so far as to question the existence of UME in the dog (1). If not a UME, then what? At least 4 theories have been advanced in the literature:
This represents a variation of OCD associated with the medial humeral condyle. The origins of 5 flexor tendons are located on the medial humeral condyle. If pieces of abnormal cartilage are pulled off in these flexor tendons, they may undergo bony metaplasia and produce osteophytes, such as those seen in this case. Support for this theory includes the observation that this condition is frequently bilateral, and that the area of concern is very near a site of known OCD on the joint surface of the medial humeral condyle (2).
Traumatic avulsion of all or a portion of the medial humeral epicondyle in the immature dog may be a factor in some cases (1). Although many cases are not associated with a known trauma, such an episode would presumably have to occur before the fusion of the growth center at 10 wk and there may be some lag time before lameness develops. However, this theory is of questionable value in explaining the lameness in our case at 17 mo or in others that have occurred in dogs of 4 or 5 y old (2,3).
Some have attributed this lesion to dystrophic calcification of flexor tendons due to chronic inflam mation (1,3). The presence of other forms of elbow dysplasia, joint incongruity, or injury have all been proposed as sources of inflammation. In this light, the presence of degenerative joint disease (DJD) on the medial side of our dog's elbow joint is interesting and raises the question: Did the DJD produce the bony densities or did the irritation of the densities produce the DJD?
It has been proposed that the formation of these densities occurs at the site of an aberrant ossification center, in much the same way that a sesamoid bone is formed (4).
Bony densities on the medial aspect of the elbow joint may be present asymptomatically in some dogs. If and when they are associated with lameness, surgical excision seems to produce resolution (1,2,3,4).
References
- 1.Zontine WJ, Weitkamp RA, Lippincott CL. Redefined type of elbow dysplasia involving calcified flexor tendons attached to the medial humeral epicondyle in three dogs. J Am Vet Med Assoc 1989;194: 1082–1085. [PubMed]
- 2.Piermattei DL, Flo GL. Handbook of Small Animal Orthopedics and Fracture Repair, 3rd ed. Philadelphia: WB Saunders, 1997:314–317.
- 3.Walker TM. A redefined type of elbow dysplasia in the dog-2 cases. Can Vet J 1998;39:573–575. [PMC free article] [PubMed]
- 4.Grondalen J, Braut T. Lameness in two young dogs caused by a calcified body in the joint capsule of the elbow. J Small Anim Pract 1976;17:681–684. [DOI] [PubMed]
