Tendinitis and Bursitis

Tendinitis

Lower intensity trauma can result in tendon sprains or tendinitis rather than complete rupture. Such injuries are more commonly diagnosed in horses; however, they are recognized in canine athletes and are probably under-diagnosed in active dogs. Tendinitis refers to inflammation of the tendon with a few or many tendon fibers being torn; however, total discontinuity of the tendon is not produced. Hypoxic tendon injury can result in fibrocartilaginous metaplasia, which can interfere with tendon function and be a source of pain. Repeated microstrains and mechanical overload with hyperthermia, free-radical production, and hypoxia are pathophysiologic mechanisms important in the development of tendinitis. Goals of treatment of tendinitis are to increase the number of fibroblasts, increase matrix production, increase the proportion of type I collagen versus type III collagen, and increase the organization of collagen fibers. This will allow an increase in tensile strength, a decreased incidence of reinjury, and a decreased rehabilitation time. Restoration of structurally normal tendinous tissue with normal tensile strength and elasticity is the goal of tendon repair rather than promoting a connective tissue scar.

Mineralization of the Tendon of Insertion of the Supraspinatus Muscle

Mineralization of the tendon of insertion of the supraspinatus muscle or calcifying tendinopathy of the supraspinatus tendon can result in a chronic, intermittent, or progressive weight-bearing lameness that worsens after exercise. Pain is elicited on shoulder extension. Mineralization of soft tissues to the level of the greater tubercle of the humerus cranial to the scapulohumeral joint on a cranioproximal-craniodistal radiographic view is suggestive of the disease. A poor correlation between the size of the lesion and lameness has been identified [1]. Hypoxia of the tendon is considered the primary initiating factor in the deposition of calcium. The tendon undergoes fibrocartilaginous transformation; calcium crystals are then deposited in the matrix and coalesce to form deposits. The location of the injury may be related to a hypovascular area of the tendon adjacent to the major tubercle that may be predisposed to hypoxic injury. Treatment options include rest, nonsteroidal anti-inflammatory therapy, intralesional steroid injections, surgical excision, and extracorporeal shock-wave therapy. The mineral deposits commonly reform; however this is poorly correlated to a recurrence of lameness [1].

Bicipital Tenosynovitis

Biceps tendon injury is a common cause of forelimb lameness and shoulder pain in dogs. Biceps tears commonly occur within the glenohumeral joint, outside the bicipital groove and adjacent to the supraglenoid tubercle, as this is a relatively avascular zone [2]. Inflammation of the biceps tendon can occur as a primary lesion or secondary to intra-articular disease such as glenohumeral instability. The cause of primary bicipital tenosynovitis is unknown and may include overuse or chronic repetitive trauma resulting in an inflammatory response. Gross pathologic changes include hyperemia of the bursa, leading to joint effusion; chronic synovitis, causing synovial hyperplasia of the bursa; chondromalacia of the intertubercular groove with osteophyte formation at its margins; and metastatic calcification of the biceps tendon. Adhesions between the tendon and the tendon sheath may develop. Hypoxia of the tendon as a result of damaged blood supply promotes chondroid metaplasia and calcification, with the normal synovial space and smooth gliding surface of the intertubercular groove typically being replaced by proliferative synovium and fibrotic adhesions. Fibrocartilaginous metaplasia, however, can be seen in normal dogs [3] and the relationship between histopathologic findings and clinical findings is inconsistent [4]. Diagnosis of bicipital tenosynovitis can be made via an orthopedic examination, by eliciting a positive "biceps test" (pain on palpation of the biceps tendon with the shoulder in a flexed position), and with plain radiographs including a skyline view of the bicipital groove, contrast arthrography, ultrasonography, or MRI. Treatment includes rest and nonsteroidal anti-inflammatory treatment, intraarticular or intralesional steroid injections, open tenodesis, arthroscopic tenodesis, and arthroscopic biceps tenotomy. Results of tenodesis are excellent [5,6], however, arthroscopic tenotomy offers a less demanding approach with apparently good results [7]. The indications and long-term results for tenodesis versus tenotomy in dogs has not been established [6].

Calcaneal Tendinitis

Inflammation of the area of the insertion of the calcaneal tendon onto the calcaneus may progress to avulsion and failure of the Achilles mechanism. It is recommended that evaluation of the opposite calcaneal tendon be performed in cases of a unilateral injury to ensure that calcaneal tendinitis is not present in the contralateral limb. Ultrasonography has been shown to be a useful tool for imaging lesions of the Achilles tendon [8].

Stenosing Tenosynovitis of the Abductor Pollicis Longus Muscle

The abductor pollicis longus muscle abducts the first digit. Injury of this tendon can result in forelimb lameness, a swelling on the medial aspect of the carpus, and pain on carpal flexion [9]. Connective tissue proliferation leads to stenosis of the synovial sheath and pain associated with constriction of the tendon within the tendon sheath. Radiographically, proliferative bone reactions at the distal radius in the area of the fibro-osseus canal of the abductor pollicis longus can be found in advanced cases of the disease [9]. Conservative treatment involves injection of corticosteroids in the area of the synovial sheath; however, nonresponding cases benefit from surgical release of the tendon rather than tenotomy [9].

Tendinitis of the Insertion of the Flexor Carpi Ulnaris

This injury commonly occurs in the tendon of insertion of the flexor carpi ulnaris muscle to the accessory carpal bone in racing greyhounds. Chronic inflammation with repeated bouts of lameness is common [10].

Bursitis

Bursae are connective tissue sacs that are lined by a synovial epithelium and contain synovial fluid. A bursa serves to reduce friction between moving parts such as tendons, ligaments, or muscles or to cushion the effects of excess pressure between these movable structures and bony prominences. True bursae are normal anatomic structures and can be described as subtendinous, submuscular, subfascial, or interligamentous. Bursae are abundantly supplied with vessels and nerves and tendon injuries involving a bursa, therefore, are extremely painful. False bursae are acquired structures secondary to repeated trauma over pressure points and consist of a nonepithelial-lined sac full of fluid, also known as a hygroma.

Many anatomic bursae have been described in the dog [11]. In the forelimb are located bursae associated with the infraspinatus muscle and the caudal part of the greater tubercle of the humerus, where the tendon of the triceps brachii muscle crosses the proximal end of the olecranon (bursa subtendinea olecrani), under the tendon of the extensor carpi radialis tendon at the carpus, under the tendon of origin of the extensor carpi ulnaris muscle, and also between its tendon of insertion and the distal ulna and where the abductor pollicis longus passes over the extensor carpi radialis muscle. A bursa also exists between the tendon of origin of the superficial digital flexor muscle and the underlying medial epicondyle of the humerus and beneath the tendon of origin of the deep digital flexor muscle. In the hindlimb, bursae are located under the tendon of origin of the rectus femoris muscle, between the distal third of the rectus femoris muscle and the femur, under the insertion of the vastus lateralis and medialis muscles, under the superficial digital flexor tendon as it passes over the tuber calcanei, between the internal obturator muscle and the ischial ramus, and at the insertion of the internal obturator muscle in the trochanteric fossa. Many dogs also have bursae beneath the deep and superficial gluteal muscles at the insertion on the greater trochanter of the femur. Projections of joint capsules can also function in a similar manner as bursae, some examples include the projection of the glenohumeral joint capsule beneath the tendon of origin of the biceps brachii muscle, the projection of the elbow joint capsule beneath the origin of the flexor carpi radialis muscle, the projection of the patellar joint capsule under the tendon of the quadriceps muscle, the projection of the stifle joint capsule under the origin of the long digital extensor muscle, and a communication between the joint capsule between the third and fourth tarsal bones and the bursa of the tendon of insertion of the peroneus longus muscle.

Acquired bursae occur as a result of trauma to the skin and subcutaneous tissue over bony prominences. The pressure on bony prominences is transmitted from the surface to the underlying dense bone, compressing all intervening tissues, and this in turn, can obstruct blood flow, leading to cell death. A spectrum of injury exists from a pressure sore, which is a dilatation of blood vessels, inflammatory edema in the skin and subcutaneous tissue over bone, to a false bursa where a hematoma has formed in the subcutaneous tissues and has become enclosed in a well delineated sac. The progression to a false bursa is dependent on the persistence of the underlying trauma and failure of a protective skin callus to protect the underlying tissues.

Specific Injuries of Anatomic Bursae

Bursitis of the Bursa Associated with the Extensor Carpi Radialis

This injury occurs in racing greyhounds and causes lameness after racing and a palpable fluid swelling [12].

Bicipital Tenosynovitis (Bursitis)

This condition is described above under specific tendon sprains.

Chronic Calcification of the Bursa over the Greater Trochanter of the Femur

This is commonly seen as an incidental finding on radiographs, and lameness is not evident.

Specific Injuries of Acquired Bursae

Acquired bursa have been described over the olecranon (elbow hygroma) and other pressure points including the acromion of the scapula, tuber ischii, tuber coxa, greater trochanter of the femur, lateral malleolus of the tibia, tuber calcanei, and over the fifth digits and the sternum. Acquired bursae are generally sterile unless organisms are introduced via centesis or corticosteroid injection [13]. Treatment of hygromas involves removal of the inciting trauma by providing soft bedding and protective padding. Drainage followed by protective padding is considered for persistent swelling or when the bursa has become infected.