Development of medial coronoid disease in Labrador retrievers: Diagnostic and pathogenic studies

Abstract

Medial coronoid disease (MCD) of the canine elbow joint was first reported in 1974 as a developmental skeletal disease causing forelimb lameness in dogs. It is known as one of the most frequently diagnosed heritable disorders of dogs and usually affects young, large breed dogs, including Labrador retrievers. It has been described under a well-known umbrella disease i.e. elbow dysplasia together with entities such as ununited anconeal process, osteochondrosis or osteochondritis dissecans of the humeral trochlea, and joint incongruity. Diagnostic and pathogenic aspects were described in this thesis. Despite its variable sensitivity (10-62%), radiography is the first-line tool for diagnosing MCD due to its availability and easy access. In comparison with radiography, computed tomography (CT) is superior because it enables assessment of the medial coronoid process on multiplanar reconstructed images. We demonstrated wide ranges of radiographic, CT, and arthroscopic findings in Labrador retrievers in different age groups during their presentation to the clinic for lameness investigation. In a longitudinal study, following the development of incipient MCD, we demonstrated that MCD can be detected by means of CT in dogs as young as 14 weeks old (sensitivity, 30.8% ) and that the lesion mostly originates at the base of the MCP. Radiographically, incipient MCD was not detected. Subtrochlear sclerosis might develop in an advanced stage of MCD and should be regarded as a secondary change. Since MCD can occur without relevant radiographic and CT findings, a thorough physical examination and history taking remain essential to the diagnosis. In this thesis, we investigated the potential of a biomarker, namely, Col2-3/4Clong mono (C2C) in the plasma and synovial fluid from elbow joints of Labrador puppies to diagnose incipient MCD and found that the plasma and synovial C2C concentration is not useful as a biomarker to detect early stage of the MCD without signs of osteoarthritis.Regarding the pathogenesis, there was a significant depletion of GAG from articular cartilage in an early stage of MCD, before clinical signs are manifest.Due to the limitations of the study, e.g. single time point study, we cannot conclude that MCD develops as a result of changes in articular cartilage or that the GAG loss we observed was a consequence of MCD. We also postulated that it is unlikely that the joint incongruity was associated with the development of MCD in these Labrador retrievers.We documented that MCD development occurred due to a disturbance of endochondral ossification, and in particular delayed mineralization in the calcifying zone. We postulated that the retained hyaline cartilage could ultimately ossify during MCD progression, but weaker points might also develop into cracks between the retained hyaline cartilage and the subchondral bone of the MCP. Increased pressure or shearing forces during joint movement will lead to detachment of the coronoid process.