Osteochondrosis
Osteochondrosis (OC) is a focal disturbance of endochondral ossification due to a failure of blood supply to the epiphyseal growth cartilage and associated ischemic chondronecrosis.
Osteochondritis dissecans (OCD) is a form of osteochondrosis. Any disturbance affecting the differentiation of growth cartilage is considered osteochondrosis. When this disturbance affects the articular cartilage and results in detachment of cartilage fragments, the condition is then called OCD. Osteochondritis dissecans is a well-recognized condition but the etiology remains unclear. Osteochondritis dissecans is highly found in the shoulder but can occur in other joints.
Most commonly affects joints are the shoulder joint, followed by the elbow, tarsal, and stifle joints. There is still more to learn regarding the disease’s definition, etiology and pathogenesis.
The term osteochondrosis has been used to describe a wide range of lesions and disorders that affect the growing skeleton.
It has been suggested to refine this terminology and add the following modifiers:
latens (lesion confined to epiphyseal cartilage)
manifesta (lesion accompanied by delay in endochondral ossification)
dissecans (cleft formation through articular cartilage).
Etiology
OC is defined as a focal disturbance of endochondral ossification and is considered as having a multifactorial etiology. The most cited etiologic factors are heredity, rapid weight gain and/or accelerated growth rate, anatomic conformation, activity levels, trauma, dietary factors and a defect in vascular supply to epiphyseal cartilage. Yet only heredity and anatomic conformation are well supported by scientific literature.
OC is a complex disease, and it is still unclear what determines the initiation of the disease. However, several events have been proposed, such as the formation of fragile cartilage, failure of chondrocyte differentiation, subchondral bone necrosis, and failure of blood supply to the growth cartilage, which recent literature strongly suggests it might be the most likely cause of disease initiation.
Epidemiology
The actual estimates of the incidence of OC in dogs in the literature are scarce, probably because these estimates are based on OC causing clinical or radiographic signs, which represent chronic stages of the disease rather than the primary process. Therefore, the actual prevalence and incidence of all stages of OC is probably higher than previously reported.
Breed-related differences in the risk of OC suggest a genetic component to the disease etiology. Reported high-risk breeds varies depending on the affected joint. Some of the overrepresented breeds are Bernese Mountain dog, Irish wolfhound, and Pyrenean Mountain dog, Newfoundland, Rottweiler, Labrador retriever, Mastiff, Great Dane, and Bullmastiff
There is a higher prevalence of OC in large-size heavy breeds compared to small-sized light weight breeds, presumably due to their size, body weight, growth rate and activity pattern. The median age at first diagnosis of OC is usually 7-8 months. male dogs seem to have a higher risk of OC than female dogs.
Clinical signs
Clinical signs of OC/OCD include stiffness, joint pain, joint effusion, which are generally recognized before the age of one year. Overtime clinical signs will evolve in lameness (variable from mild to non-weight bearing lameness) on affected leg or legs, in some cases an affected joint is warm and swollen on palpation.
Diagnosis
Diagnosis of OCD is based on signalment (age, breed, and sex), patient history, clinical signs, physical examination and radiographic or advanced imaging evidence.
Locations of the lesions include the head of the humerus (shoulder), medial aspect of the humeral condyle (elbow), femoral condyles (stifle) and trochlear ridges of the talus (tarsus). Radiographic findings include flattening of joint surfaces, sclerosis or subchondral bone radiolucency, osteophytosis, joint effusion, and “joint mice”. arthrography can be used to outline cartilage flaps. CT scan can be used to identify subchondral bone changes and arthroscopy is used for both diagnosis and therapeutic purposes and can be executed to identify and treat cartilage or joint lesions.
Some studies suggested that lesions sometimes undergo spontaneous resolution. Further CT and histological observations indicated that this occurs by filling of radiolucent defects with bone from separate centers of endochondral ossification.
Treatment
The recommended treatment varies depending on several factors such as the affected joint, the severity of the clinical signs, and owner’s financial possibilities. Treatment can be conservative or surgical. Conservative treatment consists in NSAIDs, joint supplements and more. Surgical treatment of OCD consists in surgical excision the cartilage flap or free-floating fragments in the joint and stimulating defect healing by curetting the cartilage defect. Therapy is subjective and based on the patient's symptoms.
Prognosis:
The prognosis varies depending on the affected joint. The prognosis is considered good to excellent for shoulder joint OC, good in the elbow joint, fair to guarded for OC in the stifle and tarsal joints. Recent treatment methods with autografts or allografts to resurface the joint contour or fill the defect have shown promising results and are now under evaluation.
Research is currently focused on identifying the cause of the vascular failure in osteochondrosis. Future challenges are to distinguish between different causes of vascular failure and to understand better the nature of the heritable predisposition for osteochondrosis.
Sources:
Engdahl K, Höglund O, Hedhammar Å, Hanson J, Bergström A. The epidemiology of osteochondrosis in an insured Swedish dog population. Prev Vet Med. 2024 Jul;228:106229.
Olstad, K., Ekman, S., Carlson, C.S., 2015. An update on the pathogenesis of osteochondrosis. Vet. Pathol. 52, 785–802.
Ytrehus, B., Carlson, C.S., Ekman, S., 2007. Etiology and pathogenesis of osteochondrosis. Vet. Pathol. 44, 429–448.
LaFond, E., Breur, G.J., Austin, C.C., 2002. Breed susceptibility for developmental orthopedic diseases in dogs. J. Am. Anim. Hosp. Assoc. 38, 467–477
Demko, J., McLaughlin, R., 2005. Developmental orthopedic disease. Vet. Clin. North Am. Small Anim. Pract. 35, 1111–1135.
van der Peijl, G.J., Schaeffer, I.G., Theyse, L.F., Dijkshoorn, N.A., Schwencke, M., Hazewinkel, H.A., 2012. Osteochondrosis dissecans of the tarsus in Labrador Retrievers: Clinical signs, radiological data and force plate gait evaluation after surgical treatment. Vet. Comp. Orthop. Traumatol. 25, 126–134.
Franklin, S.P., Stoker, A.M., Murphy, S.M., Kowaleski, M.P., Gillick, M., Kim, S.E., Karlin, M., Cross, A., Cook, J.L., 2021. Outcomes associated with osteochondral allograft transplantation in dogs. Front Vet. Sci. 8, 759610
