The Etiology of Medial Coronoid Disease

Introduction

Medial coronoid disease (MCD) is one of the most frequently diagnosed heritable orthopaedic disorders of dogs and usually affects young, large-breed dogs. This disease of the medial coronoid process (MCP) was first called "ununited medial coronoid process" of the canine elbow joint and was described as the presence of an ossified bone loosely attached to the MCP of the ulna (Tirgari 1974). In later years, it became known as "fragmented medial coronoid process (FMCP)". The term "medial coronoid disease (MCD)" was introduced in 2008 as being a more representative term for FMCP, as it encompasses lesions of both articular cartilage and subchondral bone (Moores et al. 2008; Fitzpatrick et al. 2009). Despite the extensive research, the etiology of MCD remains uncertain. Different theories regarding the etiology of MCD have been postulated.

Etiology of MCD

Although MCD has been recognized as a heritable disease for more than 30 years, its mode of inheritance is still unclear. The disease is suggested to have a multifactorial and polygenic origin (Guthrie, Pidduck 1990). Salg et al. (2006) hypothesized that the disturbance of one or more collagen genes in an indirect manner (disturbance in expression or alteration in posttranslational modification) may cause MCD. The causative genes have not yet been identified and more disease- and breed-specific research is recommended.

MCD was also believed to be caused by osteochondrosis (OC), which is defined as a focal disturbance of endochondral ossification of articular cartilage in growing animals (Olsson 1981). The presence of retained cartilage is thought to serve as a weak starting point for fissures to develop in the articular cartilage layer. The occurrence of osteochondrotic lesions has been associated with chondronecrosis, caused by a failure of blood supply to growing cartilage.

In the 1990s and 2000s, results from histological studies were more supportive of MCD to be caused by abnormalities of the underlying subchondral bone. Danielson et al. (2006) reported the size of fatigue microcracks increased by an increase of disease severity and damage being more severe at the fragmented site than at the rest of the bone. The loss of osteocytes with more pronounced osteoporosis of the fragmented MCP has also been reported. Later studies with dual-energy x-ray absorptiometry (DEXA) showed the mean bone mineral density of the MCP to be lower in MCD-positive animals than in controls. In both groups, bone mineral density was 50% lower at the axial border of the MCP than at the abaxial border. This suggests that the abaxial border might be more resistant to compressive loading than the axial border, and that this difference might predisposes the axial border of the MCP to develop microcracks.

The opposite - i.e., an increase in bone density at the MCP and ulnar trochlear notch - was also suggested to contribute to the development of MCD (Smith et al. 2009). Subtrochlear notch sclerosis (STS), which is characterized by increased radiopacity adjacent to the ulnar trochlear notch and caudal to the coronoid process, is an important indicator in diagnosing MCD radiographically. Although there is evidence that there is a relationship between STS and MCD, it is still debated whether STS is the cause of MCD or the result of secondary degenerative changes. It was postulated as a cause of MCD with the explanation that increased stiffness of subchondral bone would cause the overlying articular cartilage layer to become more vulnerable to injury.

Another postulated important cause of MCD was abnormal mechanical loading, which might be due to changes in joint alignment and spaces that result in radioulnar incongruence (RUI) because of a disparity in the length of the radius and ulna, underdevelopment of the ulnar trochlear notch, or physiological incongruity during loading. Although RUI in conjunction with MCD is a typical finding in Bernese Mountain dogs (in 50% of the cases of ED; Lavrijsen et al. 2012), RUI has been reported in Labrador retrievers in a much lower frequency. Labrador retrievers with MCD are believed not to have significant RUI at the medial coronoid region at the time of diagnosis. Other possible causes or factors contributing to MCD development include changes in the magnitude and topographic distribution of loading, pressure or forces within the joint, such as tensile forces originating from the annular ligament, and shear stress between the contact area of the proximal radial head and the axial border of the MCP during pronation and supination. It has been suggested that biceps brachii/brachialis muscle complex in relation to the bony anatomy might lead to rotational instability, and give rise to shear planes between the radial head and the radial incisure of the MCP. This may result in micro-damage or even fragmentation of the MCP.

Several studies have investigated the role of the shape of the MCP, trochlear notch, and the articular contact areas in the development of MCD. Compared between the different breeds, there is high variability between growth in the length and width of the MCP. Large-breed dogs are believed to have a less pronounced growth in length of the MCP in comparison to the width of the MCP during growth of the elbow joint, resulting in a more obtuse shape of the MCP in comparison with small-breed dogs. Hence, loading and forces acting on the MCP might be larger in large-breed dogs than expected. A difference in the rate of ossification between small and large-breed dogs is suggested to predispose large-breed dogs to MCD: Ossification of the MCP is completed significantly earlier in small-breed dogs than in large-breed dogs, and slow maturation of the MCP is believed to be a cause of MCD in larger dogs.

In one of the studies following the development of incipient MCD (Lau et al. 2013) by using radiograph and computed radiography, the histological results showed that MCD in Labrador retrievers is most likely the product of delayed endochondral ossification at the lateral aspect of the MCP at the level of the base of the MCP, with focus on the delay in calcification of the calcifying zone without concurrent abnormalities in the superficial layers of the joint cartilage. The persistence of retained cartilage provides a weak point at the cartilage-bone interface, where biomechanical forces may initiate cleft formation. In the same study also, there was no evidence of STS found radiographically in the MCD positive dogs. This suggests that STS develops in an advanced stage of MCD and should be regarded as secondary changes. In addition, other environmental factors such as nutrition, exercise, and microtrauma cannot be ruled out as playing a role in MCD development, and this has yet to be investigated.

References

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