Osteochondritis dissecans (OCD) is an uncommon manifestation of osteochondrosis of the articular surfaces of the distal femoral condyles, with the lateral condyle being more often involved. It is manifested by separation and then complete detachment of an osteochondral flap and consequent exposure of the subchrondral bone (Fig. 1). It affects medium, large and giant breeds of dogs during the growth period (5-9 months of age). Osteochondritis dissecans of the knee (stifle) causes varying degrees of lameness of the hind limbs and early onset of arthritis.
AETIOPATHOGENESIS
Osteochondrosis is a defect of endochondral ossification, which is the mechanism responsible for the longitudinal growth of long bones. The aetiopathogenesis of osteochondrosis is multifactorial, and predisposing factors and triggers can act simultaneously to cause the problem: overeating, too much integration, genetic predisposition, excessive movement associated with heavy body weight and rapid growth. During the course of osteochondrosis, the cells of the metaphyseal and epiphyseal growth cartilage fail to differentiate correctly and do not undergo normal calcification and ossification. The cartilage, therefore, continues to grow and becomes thicker and less resistant to mechanical stress. In the case of OCD, a crack first appears in the thickened part of the cartilage, the subchondral bone is exposed and an osteochondral flap separates from the underlying bone. Excessive movement or even only microtrauma from normal physical activity can lead to the osteochondral flap detaching completely, and becoming a loose body in the joint. Contact between the synovial fluid and subchondral bone triggers a series of biochemical and biological reactions which lead to the development of synovitis. It is usually at this point that the first clinical signs can be observed. The osteochondral flap floating free in the joint can be a source of continuous irritation and contribute to the development of the synovitis.
Malalignmentof the hind limbs may be an important aetiopathogenetic factor in the development of stifle OCD. Such a hypothesis, drawn from human medicine but not yet scientifically accepted and published in veterinary medicine, attributes the development of OCD to osteochondrosis in association with an unbalanced distribution of weight on the growing joint cartilage. In particular, OCD of the lateral femoral condyle can be seen in subjects with genu valgum with a resultant overburdening of the lateral condyle, while OCD of the medial femoral condyle can be associated with genu varum.
EPIDEMIOLOGY
Stifle OCDis found in medium, large and giant breeds of dogs in their growth phase between 5 and 9 months of age. There is no difference in prevalence according to gender. Not infrequently the disease is recognized in adult dogs because of the development of secondary arthritis or contemporary rupture of the cranial cruciate ligament. The breeds most affected are the German Shepherd, Boxer, Rottweiler, Great Dane, Newfoundland, Dobermann, Cane Corso and Saint Bernard.
CLINICAL SIGNS
Stifle OCDcauses various degrees of lameness of the hind limbs. This usually develops gradually and intermittently, and tends to worsen after physical exercise. The lameness tends to involve one limb more than the other, even in the case of bilateral lesions. When the diagnosis is made in adult dogs, the lameness is usually related to the development of arthritis and concomitant presence of lesions involving the cranial cruciate ligament and menisci.
DIAGNOSIS
An orthopaedic examination shows synovial ectasia, swelling of the medial compartment and pain on passive movement of the joints. As the lesion becomes chronic, there are various degrees of atrophy of the thigh muscles and greater peri-articular thickening. A diagnostic suspicion of OCD following the clinical examination can be confirmed by X-ray, under sedation or general anaesthesia. Stifle OCD is often bilateral and the contralateral limb should also be examined to detect lesions still producing few or no symptoms.
The X-ray projections necessary in order to make a diagnosis of stifle OCD are a medio-lateral projection without the condyles overlapping and a caudate-cranial projection with the knee flexed at an angle of approximately 100°-105° (Figs. 2 and 3). Cranial-caudate and caudate-cranial projections with the knee in extension may not reveal lesions in the most caudal part of the femoral condyle, hidden by the X-ray overlap with the cranial-distal part of the condyle. In patients with stifle OCD, a medio-lateral X-ray can reveal the presence of a defect in the articular profile of the affected condyle, which usually shows irregular flattening (Figs. 4 and 5). Small areas of radiolucency or a slight flattening of the profile in the absence of a joint effusion and clinical signs are suggestive of osteochondrosis and not OCD. A caudate-cranial projection with a flexed knee can provide information on the extent of the lesion and show its precise location (Figs. 6a/b).
The osteochondral flap is rarely seen on X-rays while an irregular articular profile associated with more or less marked areas of radiolucency of the subchondral bed are more commonly observed. In the case of a diagnosis of osteochondrosis, in the absence of a joint effusion and of clinical symptoms, X-ray monitoring of the lesion is recommended with follow-up visits approximately every 3 weeks to evaluate the development of the lesion. Besides X-rays, arthroscopy may be useful in the diagnosis of OCD of the knee: this technique enables therapy to be performed in the same session as the diagnosis is confirmed.
TREATMENT
Surgery is the usual treatment for OCD and involves removal of the osteochondral flap and treatment of the base of the lesion. This treatment consists in reactivating the base of the lesion, when this is sclerotic, by osteostixis, using a special spike to make holes a few millimetres apart from each other which penetrate the subchondral bone: this promotes vascularisation of the lesion and exposes mesenchymal cells. Any reparative fibrocartilage present should be conserved as this is a manifestation of early healing.
Both arthroscopic treatment and traditional surgery are management options for stifle OCD: a medial or lateral access is made depending on the site of the lesion. Recently, transplantation of autologous cartilage and subchondral bone has been proposed for large lesions with a less favourable prognosis. The graft is taken from the lateral or medial trochlear lip of the distal femur. This is easily accessed by mini-arthrotomy, and above all this is not a weight-bearing part of the joint (Figs. 7a/b/c and Figs. 8a/b/c/d). The advantage of this surgical technique is better repair of the lesion, with minimal formation of reparative fibrocartilage. The speed of functional recovery is another advantage, since this improves the poor prognosis of osteochondral lesions of the knee in dogs. Conservative treatment can be considered in cases of small, asymptomatic lesions, chronic lesions or in cases of early osteochondrosis in the absence of synovitis and clinical signs. Careful monitoring is essential until the lesion has healed spontaneously.
PROGNOSIS
Healing of the lesion is influenced by the extent of the joint damage, earliness of the treatment and site of the osteochondral defect. Large lesions on the surface of the condyle that takes the greatest weight, whether this is medial or lateral, have a poor prognosis. In contrast, small lesions that are either very caudal or very cranial heal better. As mentioned above, transplants of autologous cartilage and subchondral bone have led to better healing of even those lesions with a poorer prognosis. Early treatment and correct post-operative management are essential for good integration of the graft.
Suggested readings
- Palierne S, Bilmont A, Raymond-Letron I, Autefage A.“A case of stifle osteochondrosis treated by osteochondral autogenous grafting. One month morphological follow-up.”Vet Comp Orthop Traumatol 23(3): 190-5, 2010
- Mortellaro CM, Petazzoni M, Vezzoni A “Atlante BOA: approccio ortopedico orientato alla razza” Innovet ed, pp 56-57, 2008
- Cook JL, Hudson CC, Kuroki K.“Autogenous osteochondral grafting for treatment of stifle osteochondrosis in dogs.” Vet Surg Jun;37(4): 311-21, 2008
- LaFond E, Breur GJ, Austin CC.“Breed susceptibility for developmental orthopedic diseases in dogs.”J Am Anim Hosp Assoc Sep-Oct;38(5): 467-77, 2002
- Langley-Hobbs SJ.“Lateral meniscal tears and stifle osteochondrosis in three dogs.”Vet Rec Nov 10;149(19):592-4, 2001
- van Bree HJ, Van Ryssen B.“Diagnostic and surgical arthroscopy in osteochondrosis lesions.”Vet Clin North Am Small Anim Pract. Jan 28(1):161-89, 1998
- Kippenes H, Johnston G.“Diagnostic imaging of osteochondrosis.” Vet Clin North Am Small Anim Pract. Jan 28(1):137-60, 1998
- Harari J.“Osteochondrosis of the femur.”Vet Clin North Am Small Anim Pract. Jan 28(1): 87-94, 1998
- Bertrand SG, Lewis DD, Madison JB, de Haan JH, Stubbs WP, Stallings JT.“Arthroscopic examination and treatment of osteochondritis dissecans of the femoral condyle of six dogs.”J Am Anim Hosp Assoc Sep-Oct;33(5): 451-5, 1997