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Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

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Fragmented coronoid process in the dog is a common yet frustrating and poorly understood condition. Elbow joint incongruency, which refers to malalignment of the joint surfaces of the elbow, has been proposed as a key factor in the pathogenesis of fragmented coronoid process, and various surgical procedures have been devised to treat the proposed incongruency. However, precise characterisation of incongruency present in cases of fragmented coronoid process has not been reported consistently. In this article, the literature relating to the pathogenesis of fragmented coronoid process, the role of incongruency and its implications are reviewed.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

Elbow dysplasia, or abnormal development of the cubital joint, is a common condition in dogs (Morgan and others 1999). The term was originally used to describe a generalised arthrosis of the joint with or without an ununited anconeal process (UAP) (Corley and Carlson 1965). The umbrella term elbow dysplasia is now commonly used to represent a group of conditions affecting the elbow joint including fragmented medial coronoid process (FCP), osteochondritis dissecans (OCD) of the medial aspect of the humeral condyle and UAP (Schulz and Krotscheck 2003). Other less common abnormalities such as ununited medial epicondyle are also included by some authors (Walker 1998, Meyer-Lindenberg and others 2004).

FCP can occur alone or less commonly in conjunction with OCD (Bennett and others 1981, Guthrie and Pidduck 1990, Meyer-Lindenberg and others 2002) or UAP (Rovesti and others 2002, Meyer-Lindenberg and others 2006). FCP appears to be over-represented in certain breeds such as Labrador retrievers, golden retrievers, Rottweilers and Bernese mountain dogs (Morgan and others 2000, LaFond and others 2002) and is the most common cause of forelimb lameness in juvenile dogs in the majority of (Grøndalen 1976, 1979, Bojrab 1981) but not all (LaFond and others 2002) studies. Male dogs are affected more commonly than female dogs (Read and others 1990, Grøndalen and Lingaas 1991, Huibregste and others 1994). FCP has important financial and welfare implications because of its high prevalence in breeds used for working and guiding.

Development of the coronoid process

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

The coronoid process of the ulna is the distal articular extension of the trochlear notch. Medial and lateral parts of the coronoid process articulate with the humeral condyle proximally and the radial head cranially. The coronoid process develops from the same ossification centre as the proximal ulna (Guthrie and others 1992a).

Microcomputed tomography has been used to evaluate the trabecular alignment within the medial coronoid process and to determine the direction of forces within the bone during development. Primary trabecular alignment was found to be perpendicular to the humeroulnar articular surface in dogs aged four to 24 weeks, which matches the direction of forces produced by the humeroulnar joint during weight bearing (Wolschrijn and Weijs 2004). Secondary craniocaudal alignment corresponding to stresses from the annular ligaments was identified at 13 weeks of age. The bone volume fraction and definition of trabecular alignment was much higher than that observed in long bones or vertebrae at a similar age, which may reflect the early load-bearing function of the medial part of the coronoid process in the canine elbow. The subchondral bone layer of the medial coronoid process has also been evaluated by histology (Wolschrijn and Weijs 2005). The humeral surface of the medial coronoid process was observed to have remodelled from rough trabecular to smooth cortical bone more rapidly than the bone on the dorsal cortex (radial incisure), which again may reflect the stress placed on these areas of the coronoid process by weight bearing.

Aetiology of FCP

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

Various factors have been identified as contributing to the aetiology of FCP including genetics (Guthrie and Pidduck 1990, Maki and others 2000, Maki and others 2002), exercise and nutrition (Grøndalen 1982). However, the precise pathological mechanisms resulting in the development of FCP are poorly understood.

Genetics

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

A genetic basis to FCP is suggested by the strong breed predispositions associated with the development of the disease (LaFond and others 2002), although robust epidemiological data are lacking. The incidence of FCP in a population of 185 Dutch Labrador retrievers was reported to be (Salg and others 2006) 17·3 per cent (Ubbink and others 2000). FCP appears to show a polygenic mode of inheritance (Padgett and others 1995). However, most studies of the heritability of elbow dysplasia have used radiographic scoring for phenotype determination, and few radiographic scoring systems differentiate FCP from other component conditions of elbow dysplasia such as OCD and UAP. Therefore, although heritability estimates have been calculated for elbow dysplasia (0·10 per cent to 0·77 per cent) (Guthrie 1989, Guthrie and Pidduck 1990, Grøndalen and Lingaas 1991, Studdert and others 1991, Maki and others 2000), values for FCP in isolation from UAP and OCD are unknown. Indeed, two studies suggest that FCP is inherited independently from OCD (Padgett and others 1995, Janutta and others 2006) and UAP (Janutta and others 2006), which supports the view that the heritability of FCP alone cannot be ascertained from studies using the radiographic assessment of elbow dysplasia per se. Dogs can only be accurately phenotyped for FCP using computed tomography (CT) or direct visualisation. The expense of the former procedure and the invasiveness of the latter preclude their use routinely in clinical practice. Thus, alternative methods of identifying dogs at risk of developing FCP, such as those based on genotypic tests, are urgently required to allow more informed and effective breeding strategies.

To date, few genomic investigations of FCP have been reported. Evaluation of a population of Labrador retrievers indicated that FCP showed a sex predisposition (a male-to-female ratio of 2:1) (Salg and others 2006). This agrees with previous epidemiologic studies of the condition (Read and others 1990, Grøndalen and Lingaas 1991). Candidate genes encoding a wide variety of collagen subtypes known to be involved in bone formation, skeletal disorders or osteoarthritis in human beings were selected and evaluated using microsatellite markers in a cohort of dogs (Salg and others 2006). None of these genes were associated with the development of FCP within the Labrador retriever population studied.

Pathology of FCP

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

FCP is characterised by fissuring and fragmentation of the cartilage and bone over the craniolateral aspect of the medial coronoid process. Osteochondral fragments may remain in situ or may separate from the base of the coronoid process and become displaced (Grøndalen and Grøndalen 1981). Cartilaginous “kissing lesions” of the humeral condyle and secondary osteoarthritis are commonly seen (Grøndalen and Grøndalen 1981, Van Ryssen and Van Bree 1997). Cartilage erosion over the medial coronoid process and the medial aspect of the humeral condyle can occur in the absence of discrete bony coronoid fragmentation (Wind 1986b, Read and others 1990, Van Ryssen and Van Bree 1997, Schulz and Krotscheck 2003, Meyer-Lindenberg and Heinen 2004). FCP probably represents a specific lesion within a wider spectrum of pathology affecting the coronoid process and medial compartment of the elbow joint, which can be termed “medial compartment disease” (MCD) (Kramer and others 2006).

Initial reports that described FCP as “ununited coronoid process” (Olsson 1974, Tirgari 1974, Tirgari 1980) were shown to be inaccurate when it was subsequently recognised that the coronoid process does not develop from a separate centre of ossification to the remainder of the proximal ulna (Guthrie and others 1992a).

FCP was thought to represent a form of OCD (Bennett and others 1981, Olsson 1983). The medial coronoid process ossifies between 12 and 22 weeks (Hare 1961) and may be susceptible to OCD during this period. Histological features consistent with OCD have been reported in some dogs (Grøndalen and Grøndalen 1981, Wolschrijn and others 2005). However, other studies have not supported this theory and on the whole are more suggestive of an osteochondral fracture of the medial coronoid process. Guthrie and others (1992b) evaluated osteochondral fragments from 24 dogs with FCP. No microscopic evidence of OCD was found, and the histological picture was more consistent with a fibrous non-union. After treatment of clinical cases of FCP by subtotal coronoidectomy, Fitzpatrick and Reuter (2004) were able to evaluate both the loose fragments from the cranial aspect of the medial coronoid process and the caudal base of the coronoid process from where the fragments had originated. Again, no histological evidence of OCD was found, and the authors concluded that the histological appearance of FCP was most consistent with a non-healed osteochondral fracture (Fig 1).

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Figure 1. Histological images showing (A) subchondral microfractures (black arrow) and (B) fibrous tissue formation (black arrows) characteristic of osteochondral fracture of the coronoid process (courtesy of Mr Noel Fitzpatrick and Mr Tom Smith)

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Alternative hypotheses regarding the pathogenesis of the condition include the suggestion that affected dogs may be predisposed to fracture caused by metabolic or vascular anomalies of the coronoid process (Schulz K. S., personal communication) or by abnormalities in the anatomy of the radial incisure of the ulna and the annular ligament (Robbins G., personal communication). However, there is no published evidence to support these hypotheses at present.

The underlying molecular pathogenesis characterising FCP has been poorly investigated to date. Decreased levels of type X collagen in the cartilage of affected coronoid processes have been noted (Crouch and others 2000), but the implications of this finding were unclear.

Fragmentation of the coronoid process has also been recognised in skeletally mature dogs and may occur secondary to trauma in some cases. Interestingly, adult dogs suffering from traumatic coronoid process fracture which were treated by fragment excision appeared to have minimal progression of osteoarthritis, suggesting that the spectrum of pathology observed with FCP in younger dogs is not solely because of the fragmentation alone (Yovich and Read 1994).

Role of incongruency

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

Elbow incongruency is a term describing malalignment of the joint surfaces of the elbow (Samoy and others 2006). Developmental incongruency has been hypothesised as a pathogenic mechanism which may lead to FCP. Theoretically, incongruency may cause disproportionate load bearing through the medial compartment of the joint (Wind 1982), resulting in the development of cartilage lesions and coronoid process fracture (Hak and others 1998). This theory is supported by the experimental findings that increased loading of portions of an articular surface after fracture malreduction can cause osteochondral fragmentation (Llinas and others 1993). It has been hypothesised that the subchondral microfracture seen in dogs affected by FCP may be a consequence of increased loading (Danielson and others 2006) which may itself be subsequent to incongruency. Elbow joint incongruency and FCP have been reported to be frequent concurrent findings in Bernese mountain dogs (Ubbink and others 1999), and a strong association between joint incongruency and FCP was identified in another clinical study (Gemmill and others 2005).

Wind (1986a) suggested that under-development of the trochlear notch of the ulna could result in increased loading at the anconeus and the medial coronoid process. Incongruency was reported in nine dogs with FCP. The author suggested that the radius of curvature of the ulnar trochlear notch was decreased with respect to the radius of curvature of the humeral condyle, leading to a trochlear notch that was too small to accommodate the humeral condyle. This could in turn lead to increased loading of the anconeal and coronoid processes. Radiographic evidence published by the same author (Wind 1986b) showed an increase in the relative size of the proximal ulna in breeds affected by elbow dysplasia. It was concluded that this was because of the need for a larger trochlear notch to accommodate the humeral condyle and that a failure of development of the trochlear notch could lead to the proposed incongruency.

In a subsequent radiographic study, a decreased radius of curvature of the cranial aspect of the medial coronoid process was identified in Rottweilers, a breed commonly affected by FCP, when compared with that in greyhounds, a breed not predisposed to FCP (Collins and others 2001). Similar results have been reported for the contour of the trochlear notch of Bernese mountain dogs when compared with that of Rhodesian ridgebacks, namely that a decreased radius of curvature is found in breeds predisposed to FCP (Viehmann and others 1999). This suggests that the concept of bicentric concave humeroulnar incongruency (a mismatch between the radius of curvature of the humeral condyle with respect to the ulnar trochlear notch) may be a critical factor in the pathogenesis of the disease. However, other studies have indicated that humeroulnar incongruency may be a normal finding in both human beings (Eckstein and others 1994) and dogs (Preston and others 2000). In addition, osteoabsorptometry and joint contact area studies in normal elbows have indicated that the coronoid process may bear more load than the remainder of the semilunar notch (Maierl and others 2000), which supports the theory of a physiological humeroulnar incongruency being present in normal dogs.

A second hypothesis is that relative undergrowth of the radius with respect to the ulna may lead to the development of a step defect between the radial head and the coronoid process (Wind 1982, Morgan and others 2000). Cadaveric studies showed that an increase in loading of the medial coronoid process occurs during radial shortening, which supports this theory (Preston and others 2001). Likewise, the clinical finding of coronoid fractures in dogs suffering from radial shortening secondary to premature closure of the radial physes (MacPherson and others 1992) is also in agreement with this suggestion. However, as gross radial shortening is not commonly observed in most dogs with FCP, relative shortening is proposed to be a temporal phenomenon occurring and then resolving at some point during the growth phase of the elbow. Hence, incongruency is not necessarily evident at the time of investigation, but secondary pathologies such as fragmentation of the coronoid process, cartilage erosions and osteoarthritis persist. In addition, changes in joint loading secondary to incongruency could affect the development and eventual contour of the joint surfaces. As the radius then “catches up” with the ulna, contact with the humerus can be re-established in some areas, but the joint surfaces are left ultimately incongruent.

The role of incongruency in the development of FCP is further complicated by the observation that a significant proportion (25 of 155) of canine elbows being presented with UAP also have FCP identified within their affected joint (Meyer-Lindenberg and others 2006). Eight of these 25 cases appeared to have a short ulna syndrome, the opposite form of incongruency to that which would be expected. The remaining 17 cases had no evidence of incongruency. Clearly, the role of incongruency in the development of FCP may not be as straightforward as the earlier hypotheses suggested.

Diagnosis of FCP

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

Diagnosis of FCP is challenging when based on plain radiographs alone. Radiographic visualisation of the medial coronoid process is difficult (Robbins 1980, Henry 1984), and a presumptive diagnosis is often made indirectly based on the radiographic presence of osteophytes in the elbows of typically affected breeds (Denny and Gibb 1980, Bennett and others 1981) and the absence of radiographic evidence indicating the presence of any other component conditions of elbow dysplasia. However, up to 22 per cent of dogs with medial coronoid pathology do not have typical radiographic signs of osteoarthritis (Meyer-Lindenberg and others 2002) (Fig 2). A number of alternative radiographic projections have been proposed to improve visualisation of the medial coronoid process when compared with standard mediolateral and craniocaudal views. The craniolateral-15°-caudomedial oblique projection has been suggested to be the best radiographic view to allow evaluation of the cranial border of the medial coronoid process (Wosar and others 1999) and is the most sensitive view for the detection of FCP (Miyabayashi and others 1995). More recently, the distomedial-proximolateral oblique view was shown to be more reliable than standard mediolateral and craniocaudal projections for the detection of coronoid fragmentation (Haudiquet and others 2001). However, these oblique views can be difficult to interpret, and none are highly sensitive for the diagnosis of the disease.

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Figure 2. (A) Mediolateral radiograph of the elbow from a dog diagnosed with FCP arthroscopically but showing minimal osteophyte formation. A subtle increase in radiodensity in the subcoronoid region indicative of subchondral sclerosis is apparent. (B) More typical projection of the elbow from another dog diagnosed with FCP showing severe periarticular osteophyte formation. FCP Fragmented medial coronoid process

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Standard transverse CT images allow excellent visualisation of the coronoid process without superimposition of adjacent bony structures (Braden and others 1994, Reichle and others 2000, Ring and others 2002, Rovesti and others 2002). Displaced fragments and fissures in the coronoid process can be easily identified (Korbel and others 2001) (Fig 3), although smaller non-displaced fragments may not be identified on lower resolution scanners because of partial volume artefacts (Hathcock and Stickle 1993). It is unsurprising that CT evaluation of the elbow joint has been shown to have high sensitivity and specificity for the diagnosis of FCP (Carpenter and others 1993, Gielen and van Bree 2003).

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Figure 3. Transverse computed tomography scan through the medial coronoid process showing fragmentation of the coronoid process (arrow)

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Magnetic resonance imaging (MRI) has been used to image canine elbows (Snaps and others 1997, Snaps and others 1998, Snaps and others 1999), but its expense has limited widespread application. MRI is more accurate than plain radiography for the detection of FCP (Snaps and others 1997). Furthermore, although gross bone resolution with MRI is inferior to CT, subtle changes which are not evident on CT such as “bone bruising” can be appreciated (Mandalia and others 2005).

Arthrotomy or arthroscopy allows detailed, albeit more invasive, examination of the articular surface of the coronoid process (Read and others 1990, Van Ryssen and Van Bree 1997). These techniques allow diagnoses to be made in elbows with minimal radiographic changes but with significant cartilage pathology.

Diagnosis of incongruency

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

Diagnosis of elbow joint incongruency can be challenging. Plain radiographs are unreliable for the detection of elbow incongruency (Murphy and others 1998, Mason and others 2002). Arthroscopy can allow identification of incongruency (Beale 2002, Fitzpatrick and O’Riordan 2004), although the reliability of the technique has been questioned, as the introduction of the arthroscope into the elbow may induce or disguise the presence of incongruency in some cases. Furthermore, the technique is inherently invasive, limiting its usefulness as a screening tool.

CT has become well established as a diagnostic tool for the investigation of elbow pathology in both human beings (Franklin and others 1988, Holland and others 1994, Weber and Morrey 1999, Potter 2000, Edelson and others 2001) and dogs (Reichle and others 2000, Rovesti and others 2002). Some forms of elbow incongruency can be identified on transverse CT images. Boulay (1998) described an increase in the humeroulnar joint space at the centre of the trochlear notch in one affected elbow. However, the sensitivity and specificity of the technique was not evaluated.

Sagittal and dorsal plane images can be created from transverse CT scans, through computed reconstruction. These images allow good visualisation of elbow joint surfaces (Reichle and others 2000, De Rycke and others 2002, Holsworth and others 2005). In human elbows, accurate imaging of joint spaces has been reported (Seiler and others 1995). Direct measurement of radioulnar incongruency from reconstructed CT (rCT) images in canine elbows is possible, but the technique can be subjective and requires the use of geometric image analysis to diminish errors (Holsworth and others 2005).

The accuracy of rCT images for precise measurement of joint spaces in canine elbows has been investigated (Gemmill and others 2006). Using cadaver elbows, it was shown that measurements of humeroradial and humeroulnar joint spaces could be reliably obtained with low inter- and intra-observer variability. Using a cadaver model of elbow incongruency, a further study (Gemmill 2005) showed that similarly accurate measurements could be obtained in incongruent elbows. Dogs suffering from MCD were then studied in a retrospective fashion (Gemmill and others 2005). Diseased elbows were compared with control elbows, and a significant association was found between MCD and incongruency (Fig 4). However, incongruency was not identified in every diseased elbow. The study also showed that although radioulnar incongruency exists at the level of the coronoid apex in elbows affected by MCD, no incongruency was apparent at the level of the coronoid base.

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Figure 4. Dorsal plane reconstructed computed tomography images from a normal elbow (A) and an elbow diagnosed with FCP (B). Incongruency is evident affecting the diseased elbow (B) characterised by widening of the humeroradial joint space. The weight-bearing surface contour of the radius does not match that of the humeral condyle. FCP Fragmented medial coronoid process, H Humerus, R Radius, U Ulna

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The identification of an apical radioulnar incongruency supports the hypothesis that joint surface incongruency is involved in the pathogenesis of FCP in some dogs. In contrast, in a further study using rCT analysis (Kramer and others 2006), incongruency was identified at the level of the base, rather than at the apex, of the coronoid process in diseased elbows. The observation of incongruency in some, but not other, areas of the elbow supports the theory of a complex incongruency. The differences in the precise level of the incongruency as compared with the study by Gemmill and others (2005) may have been because of differences in the measurement technique used or may have been because a different cohort of dogs had been assessed.

MRI would also theoretically be suitable as a method of diagnosing and categorising elbow incongruency, although CT has both time and cost advantages in addition to providing improved bone resolution. To the authors’ knowledge, there are no studies evaluating incongruency using MRI published in the veterinary literature.

Treatment of FCP

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

Non-surgical management of FCP addresses the clinical signs associated with the condition and the secondary osteoarthritis. Strategies include exercise moderation (Read 1987), weight control (Kealy and others 2000), use of non-steroidal anti-inflammatory drugs and steroid medications (Read 1987), physical therapy (Conzemius 2004) and the use of slow-acting “disease-modifying” agents such as glucosamine, chondroitin, polysulphated glycosaminoglycans and pentosan polysulphate (Bouck and others 1995). Obviously, non-surgical management does not address the underlying incongruency of the elbow joint, if present.

Surgical treatment has traditionally consisted of fragment excision, either by open arthrotomy (Denny and Gibbs 1980, Bennett and others 1981, Read 1987, Read and others 1990) or arthroscopy (Bardet 1997, Meyer-Lindenberg and others 2002). However, the results of surgical management generally have been disappointing, with many authors noting that degenerative changes tend to progress irrespective of treatment (Bennett and others 1981, Huibregste and others 1994, Theyse and others 2000). When compared with those treated conservatively, some studies have reported an improved outcome in surgically treated patients (Henry 1984, Read and others 1990), but other studies have failed to show this improvement (Huibregste and others 1994, Bouck and others 1995); overall, the benefits of surgery have been marginal at best. The variable outcomes reported with surgical management of FCP imply that the fragmentation of the medial coronoid process alone is not always the sole cause of pathology associated with this condition. Other factors, such as osteoarthritis of the affected joint or underlying joint incongruency, may be more significant causes of lameness. The suboptimal results associated with surgical management have led some authors to question the benefits of fragment retrieval (Bennett and others 1981) and have prompted further investigations into the pathogenesis of the disease.

Treatment of incongruency

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

A variety of osteotomies have been described to address incongruencies associated with FCP, and these techniques have been reported to give good clinical results. Three studies (Thompson and Robbins 1995, Bardet and Bureau 1996, Ness 1998) have described a proximal ulnar osteotomy. The rationale for this technique is that the osteotomy allows slight shortening and rotation of the proximal ulna, which relieves abnormal loading on the medial coronoid process. Using an experimental model, incongruency induced by radial shortening can be corrected through the use of an ulna osteotomy stabilised with an intramedullary pin (Preston and others 2001). A radial lengthening osteotomy has also been described to relieve abnormal loading of the medial coronoid process by proximal elevation of the radial head (Slocum and Pfeil 2004).

However, the use of osteotomies for the treatment of FCP has been reported to result in significant postoperative morbidity in some cases (Meyer-Lindenberg and others 2001), and controlled large-scale studies evaluating the outcome of clinical cases after osteotomies are lacking. Furthermore, it has been suggested that in affected elbows, progressive collapse of the medial joint space may occur in the longer term (Schulz 2003). The mechanism of this collapse was proposed to have similarities to human unicompartmental knee osteoarthritis, in which an initial small decrease in joint space caused by cartilage atrophy leads to increased weight bearing through the diseased portion of the joint. This then subsequently leads to further cartilage loss and accelerating joint space collapse (Nagel and others 1996, Cameron and others 1997, Rees and others 2001). If medial joint collapse does occur in diseased canine elbows, radial lengthening or ulna shortening osteotomies may actually increase loading of the medial compartment of the joint in the long term, which may worsen the outcome.

We have reported (Gemmill and others 2005) that incongruency is not present in all dogs at the time of diagnosis, implying that osteotomy for every dog presenting with MCD is unjustified. In addition, this study suggested that if incongruency is present at the time of diagnosis, it is likely to be present only in certain areas of the joint. Correction of incongruency by osteotomy at one level may induce a subsequent incongruency at another level, which could lead to further problems. In cases where incongruency is diagnosed, an alternative procedure such as subtotal coronoidectomy may be more appropriate, as this may relieve abnormal humeroulnar loading through the medial aspect of the elbow without induction of further incongruency. Preliminary clinical results have suggested favourable outcomes in dogs treated with subtotal coronoidectomy (Fitzpatrick and O’Riordan 2004). However, to the authors’ knowledge, long-term objective studies regarding the efficacy of subtotal coronoidectomy for the treatment of FCP have not been published.

Rather than addressing underlying incongruency, some authors have suggested that osteotomy may represent a potential treatment for MCD by favourably altering transarticular loading and pressure within the joint (Mason and others 2003). Alternatively, osteotomy may have other advantageous effects such as relieving intra-osseous pressure. These proposals are based on the success of high tibial osteotomy for the treatment of human unicompartmental knee osteoarthritis (Nagel and others 1996).

For the canine elbow, a humeral osteotomy has been investigated (Fujita and others 2003, Mason and others 2003); subsequent to observations that cartilage loss appears to be predominantly centred on the medial aspect of the joint, the authors proposed that shifting transarticular loading towards the lateral aspect may be beneficial. Cadaver studies have confirmed that this can be achieved using either humeral wedge or humeral slide osteotomies (Mason and others 2003). However, the osteotomies also induced a decrease in the area of the proximal radial weight-bearing surface, and the long-term implications of this are unknown at the present time. The techniques have been applied to a limited number of clinical cases (Schulz K. S., personal communication; Fitzpatrick N., personal communication). Unpublished results indicate a favourable response to surgery in the short term, but severe complications have been encountered in some cases. Further investigation is required into the long-term biomechanical and physiological effects of these osteotomies, and studies to document outcomes in clinical cases are necessary before recommendations can be made regarding these procedures.

Conclusions

Although work to date has implicated developmental incongruency in the pathogenesis of FCP, understanding of the formation and progression of incongruency is incomplete. The role of incongruency will only be elucidated with certainty if the development of canine elbow joints affected and unaffected by FCP is evaluated throughout the growth period of the immature dog. Likewise, investigation into the genetic basis of FCP is in its infancy, and collaborative efforts are required if genotyping tests for the disease are to be developed. Finally, accurate characterisation of the prevalence and severity of incongruency in different cohorts of dogs and comparison of different treatments in a prospective fashion is urgently required to allow an evidence-based approach to FCP to be developed.

Acknowledgements

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References

The authors acknowledge BSAVA Petsavers who generously funded T. J. G.’s research into canine elbow joint incongruency, the staff at the University of Glasgow who assisted with the studies and the veterinary surgeons who referred cases of FCP that were used for the clinical research. The authors acknowledge Mr Tom Smith and Mr Noel Fitzpatrick who provided the histological images in Fig 1. D. N. C.’s current position at the University of Liverpool is funded by BBSRC.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Development of the coronoid process
  5. Aetiology of FCP
  6. Genetics
  7. Pathology of FCP
  8. Role of incongruency
  9. Diagnosis of FCP
  10. Diagnosis of incongruency
  11. Treatment of FCP
  12. Treatment of incongruency
  13. Acknowledgements
  14. References
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