SHOULDER OSTEOCHONDROSIS
Shoulder osteochondrosis is a disturbance of endochondral ossification in the humeral head cartilage, which may lead to a clinical problem, the appropriate term for which is "osteochondritis dissecans." It is seen in young dogs (4 to 10 months of age), of large size and rapid growth (generally with individuals weighing more than 20kg), though the condition has seldom been described in the beagle and the miniature poodle, males are more often affected than females (ratio 2/1). The condition is generally bilateral (27 to 68% depending on the authors), though only 5% of radiographically affected dogs present with bilateral forlimb lameness.
Pathogenesis
The increase of epiphyseal volume, in growing animals, occurs through endochondral ossification within the epiphyseal cartilage. Multiplication of cartilage cells within a germinal layer leads to thickening of the growth cartilage towards the metaphysis. As the cartilage grows, the cells left in the newly formed matrix undergo a maturation, or degenerative process, while the ground substance becomes mineralised. Capillary buds then invade the mineralised cartilage from the metaphysis, following a front of chondroclasts that remove the cartilage. The latter is then replaced by bony tissue, synthetized by osteoblasts around the buds. Thus, normal growth of long bones results from a precise balance between cartilage growth and its gradual replacement by bone. Chondrodystrophy (or "osteochondrosis") in any particular point within the cartilage lead to a failure of the phenomena allowing capillary invasion and replacement of the cartilage by bone. Consequently, the cartilage tissue becomes abnormally thickened in that area. The process can be self-limiting. In this case, it remains clinically silent, although it may be detected as an incidental finding on survey radiographs. It may, on the other hand, evolve into a more significant lesion, associated with inflammation and clinical symptoms: this is referred to as "osteochondritis dissecans" (OCD).In shoulder OCD, the caudal aspect of the humeral head is usually affected. The epiphyseal cartilage is avascular, so that it only receives its nutrition via osmosis from the synovial fluid. When the cartilage thickens markedly, in osteochondrosis, diffusion of nutrients in its deeper portion in poor, leading to degeneration and necrosis of cartilage cells. A fissure may develop at the necrotic site. Initially limited to the depth of the cartilage, it gradually extends towards the articular surface.This microfracture corresponds to the «osteochondritis» stage and is referred to as 'dissecans' ('dissecting') due to the formation of cartilage flaps separating from the subchondral bone. If a flap is completely detached, it may become free within the joint, forming one or more 'joint mice,' which may become localised in any joint recesses, though more particularly in the caudal recess or in the bicipital groove in the shoulder. A joint mouse can occasionally be gradually resorbed, or increase in size and become mineralised. Cartilage fissuring releases degradation products that have a pro-inflammatory effect. Invasion of the cracks by synovial fluid, thus coming into contact with subchondral bone also promotes inflammation. The latter leads to the initial signs of the clinical condition.
Etiology
This is more likely multifactorial. Several hypotheses have been proposed. The growth rate and weight gain appear to be major predisposing factors, underlying factors being frequently suggested: Genetic factors: a hereditary predisposition is frequently suggested, as an increased occurrence is observed among certain family lines.
Nutritional factors in growing pups: overfeeding, i.e., excess energy, protein, calcium, phosphorus and vitamin D intake (HEDHAMMAR et al. 1974) causes an increased incidence of OCD when compared to a a normal diet. Neither excess energy (LAVELLE 1989) nor excess protein (NAP et al. 1993) in the diet appear to be involved. Excess calcium, conversely, has been shown to be a significant factor (HAZEWINKEL 1985). It has been suggested to cause increased calcitonin activity, thus leading to delayed cartilage mineralisation, necessary for subsequent endochondral ossification. The potential roles of excess phosphorus and vitamin D have not been demonstrated.
The involvement of traumatic factors has been reported. A primary involvement of trauma is, however, unlikely. The thickened cartilage is admittedly a 'weak point,' which may be particularly prone to injury from mechanical stress, especially once fissures have developped.
Structural alterations in the various cartilage layers (KINCAID et al. 1985) have been associated with variations of mechanical strength. Finally, metabolic disturbances have been reported in cells within OCD lesions (KINCAID et al. 1985).
Clinical and Diagnostic Significance
Clinically, it is most commonly diagnosed in young animals, aged 6-8 months. A sudden or more insidious onset forelimb lameness is observed. There may be episodes of spontaneous improvement for one or several weeks but the pain persists despite anti-inflammatory or analgesic therapy. Rapid muscle atrophy develops in shoulder muscles. Manipulation of the limb yields marked pain upon hyperextension of the scapulo-humeral joint and, to a lesser degree, upon forced flexion or deep palpation of the caudal joint recess. Diagnosis is based upon radiography, a mediolateral projection being most useful. The shoulder joint should be isolated as well as possible to improve visualization of the caudal aspect of the humeral head. The following technique is prefered:
The affected limb should be pulled forward. This may be painful and can necessitate sedation or short-acting anesthesia.
Pull the contralateral limb as far back as possible.
Lift the head and neck away from the shoulder.
If no lesions are detected on this view, a caudomedial location should be suspected. The procedure should be repeated while rotating the humerus medially to bring the lesion into a caudal position. Both shoulders should be radiographed.
The typical radiographic appearance of OCD consists of an altered subchondral bone contour in the caudal aspect of the humeral head: an 1 to 2cm area of decreased radiodensity and irregular contour is observed. It may be surrounded by a sclerotic bone area characterised by increased radiodensity and loss of trabecular pattern.
Occasionally, a thin radiopaque line, corresponding to mineralisation of the cartilage flap, is visible.
The radiographic image only translates the failure of mineralisation of the epiphyseal bone but yields little information regarding the nature and severity of cartilage damage.
If osteochondrosis without osteochondritis is suspected, arthrography or arthroscopy may be necessary to confirm or rule out the presence of cartilage flaps.
Treatment
It is a general agreement that the only rational treatment of an OCD is a surgical one, possibly after a 6-week maximum conservative treatment. The caudo-lateral approach (between the acromial and the scapular part of the deltoid muscle, with dissection and cranial retraction of the teres minor, and a caudal incision of the joint capsule, parallel to the joint space) is sufficient to provide adequate visualization of the lesion, if the capsule is adequately retracted and if an assistant rotates the leg internally. The minimal surgical trauma caused by this approach allows a good and rapid post-operative recovery. Other more traumatic approaches can be used if the surgeon works alone (osteotomy of the acromial process, tenotomy of infraspinatus and teres minor...), but they are associated with higher post-operative morbidity. The cartilage flap is cut free and all the abnormal cartilage around the lesion must be trimmed with a curette to create vertical walls. The curetage of the floor of the lesion is very questionable, and we avoid it, performing multiple drill holes in the bed of the lesion with a 1mm drill or a kirschner wire. A forcefull lavage of the joint helps to flush out any remaining debris, including free fragments of cartilage which should always be looked for in the caudal cul-de-sac of the joint. If joint mice have been identified in the bicipital groove, a cranial approach is performed to remove them.
The leg is usually left unbandaged and very minimal activity (house confinement and short leash walking) is suggested for 4 to 6 weeks after surgery.
Usually the results are quite good, particularly if the treatment has been performed precociously. In some rare cases (most often with big lesions) it may take up to 6 months before the dog becomes sound.
Some animals, seemingly hyperactive ones, develop a seroma, all of them clearing spontaneously (we never aspire nor drain even the largest ones).
If the equipment and skills are available, arthroscopic treatment of OCD can be performed.
SHOULDER SYNOVIAL OSTEOCHONDROMATOSIS
Shoulder synovial osteochondromatosis (or synovial chondrometaplasia) is a rare diesase, in which the synovial lining of the shoulder joint or the bicipital tendon bursa undergo a nodular cartilaginous metaplasia, the cartilage being sometimes replaced by cancellous bone. Both primary (idopathic) and secondary (maybe as a response to chronic irritation of the joint synovium) forms of synovial osteochondromatosis have been described.
The paucity of reports in the veterinary literature doesn't allow to indicate clear age, breed, or sex predilection. The few reported animals were of big breeds, age ranging from 1 to 11 years. Beside the shoulder joint, synovial osteochondromatosis has also been described in the tarsal, stiffle, elbow and carpal joint. The dog is presented with a chronic and progressive lameness of several months' duration. The joint cavity and proximal bicipital tendon area may be distended by synovial fluid. Manipulation of the shoulder joint elicits pain. Parameters of the joint fluid may be normal or consistent with osteoarhrosis. The nodules may stay adherent to the synovium, or break free and form a «joint mouse», both beeing a source of cartilage trauma, or bicipital tenosynivitis if the joint mice migrate in bicipital groove. On the Xrays, multiple intra-articular nodular lesions, with different radiodensity types, are seen within the joint capsule and its recesses. Lesions of degenerative joint disease are frequently observed. Anti-inflammatory agents may offer symptomatic improvement, but surgical exploration of the affected joint with removal of the nodular lesions and synovectomy is the recommended method of treatment. A significant improvement of joint function is generally obtained, but recurence is considered as almost certain. Arthrodesis should be considered for the intractably painful joint.
SHOULDER DYSPLASIA
Depending on the authors, shoulder dysplasia is described as a different pathologic situation. For some authors (Butterworth), shoulder dysplasia is a condition similar to hip dysplasia that is an excessive joint laxity, with or without modification of bony joint components (shallow glenoid and flatttened humeral head, as seen in Basset-Hounds). Sometimes a forelimb lameness is observed, but all other likely diagnoses must be ruled out before attributing the lameness to the observed hyperlaxity.
Others (Bonath & Prieur) regard as shoulder dysplasia all the congenital shoulder luxations encountered in the small-size breeds.
The last group of authors (Morgan, Wind, Davidson, and the present lecturer), take the word «dysplasia» under its definition: «faulty development." They consider shoulder dysplasia to be a faulty development of the caudal portion of the ossification center of the humeral head.
In some dogs, the caudal portion of the humeral head ossification center fails to form. Very soon, there is a collapse of the caudal portion of the humeral head, which leads to a concave zone opened caudally. The glenoid cavity, because of the lack of support by a convex humeral head, fails to form too, and develops into a convex surface, badly congruent with the shallow humerus.
Due to scant reports, the condition is quite rare and the related clinical situation is not clear. Nethertheless, as this abnormal situation is sometimes fortuitously discovered in adult sound dogs, we may think that, like for some congenital shoulder luxation, a rather surprisingly big possibility of functional compensation is possible.
References
Shoulder Osteochondrosis
1. Butterworth (S.) The Shoulder in Houlton (J.E.F) & Collinson (R.W) Manual of small animal arthrology BSAVA 1994, 149-174
2. Fayolle (P.) les ostéochondroses canines. le Point Vétérinaire 1992, 24, 148, 17-24. KINCAID (S.A.), Rudd (R.G.) & coll. Lipids of normal and osteochondritic cartilage of the immature canine humeral head Am. J. Vet. Res. 1985, 46, 5, 1060-1065
3. May (C.) Osteochondrosis in the dog: a review . Vet.Annual, 1989, 29, 207-216
4. Morgan (J.P), Wind (A.), Davidson (A.P) Hereditary bone and joint diseases in the dog. SCHLUTERSCHE Ed. 2000, 314 pp
5. Nap (R.C.), Hazewinkel (H.A.W.) & al. The influence of the dietary protein content on growth in giant breed dogs. V.C.O.T. 1993, 6, 1-8
Shoulder Synovial Osteochondromatosis
1. Dice (J.) Neoplastic and neoplastic-like conditions of joints in HOULTON (J.E.F) & COLLINSON (R.W) Manual of small animal arthrology BSAVA 1994, 135-146
2. Flo (G.L), Rus (L.S), Dunstan (R.W) Synovial chondrometaplasia in five dogs J.A.V.M.A . 1987, 191, 11, 1417-1422
3. Gregory (S.P), Pearson (G.R) Synovial osteochondromatosis in a labrador retriever bitch JSAP, 1990, 31, 580-583
4. Pool (R.R) Osteochondromatosis in BOJRAB (M.J) Disease mechanisms in small animal surgery, Lea & Febiger 1993, 820-833
Shoulder Dysplasia
1. Butterworth (S.) The Shoulder In HOULTON (J.E.F) & COLLINSON (R.W) Manual of small animal arthrology BSAVA 1994, 149-174
2. Schawalder (P), Prieur (W.D), Koch (H) Dysplasien und Wachstumsstörungen in BONATH (K.H) & PRIEUR (W.D) Kleintierkrankheiten Band 3: Orthopädische Chirurgie und Traumatologie, ULMER 1998, 356-413
3. Morgan (J.P), Wind (A.), Davidson (A.P) Hereditary bone and joint diseases in the dog. SCHLUTERSCHE Ed. 2000, 21-40