Caudal cruciate ligament damage in dogs with cranial cruciate ligament rupture

Objective: To investigate the incidence of caudal cruciate ligament (CaCL) damage in dogs with cranial cruciate ligament rupture (CCLR). Study Design: Prospective clinical study. Animals: Dogs (n=24) admitted for surgical stabilization of the stifle after CCLR and 8 healthy dogs with intact cranial cruciate ligament (CCL) and CaCL studied as controls. Methods: Preoperative radiographs and stifle joint images (arthrotomy, 6; arthroscopy, 18) were collected from dogs with CCLR. Severity of arthritis, synovitis, CCL damage, and CaCL damage were assessed using numerical rating scales. The CaCL was probed to determine whether minor fraying or a full thickness defect in the ligament was present. Data collected from the study population were compared with the control population of dogs. Results: The CaCL was damaged in 21/24 (88%) of dogs with CCLR; 6/24 (25%) had a full thickness defect in the CaCL. Severity of stifle synovitis and severity of damage to the CaCL were positively correlated (P<.05). Conclusions: The CaCL is damaged in a high percentage of dogs with CCLR. A significant and positive correlation exists between the degree of synovitis present and the extent of CaCL damage. Clinical Relevance: In dogs with CCLR, cruciate ligament pathology typically involves both the CCL and CaCL. As the severity of synovitis and the extent of CaCL damage are related, this observation supports the hypothesis that stifle synovitis may contribute to CCL and CaCL degeneration and subsequent damage.     

Lateral glenohumeral ligament rupture in three dogs

Three adult large breed dogs were evaluated for chronic forelimb lameness. Clinical examination localised pain to the area of the shoulder joint. Traditional imaging methods, including radiography, arthrography and ultrasonography, were unrewarding. Arthroscopy performed via a lateral portal demonstrated complete tears of the proximal part of the lateral glenohumeral ligament in all cases. Two of the three cases responded to treatment with intra-articular methylprednisolone and rest with a resolution of the lameness, while the third failed to improve. Surgical intervention in this third case involved lateral capsulorraphy, and re-examination at five weeks postoperatively showed the dog to be without lameness. Tearing of the lateral glenohumeral ligament should be considered in the differential diagnosis of shoulder lameness. Surgical stabilisation should be considered in cases refractory to conservative treatment.     

Repair of cranial cruciate ligament rupture in an alpaca

A mature male alpaca with acute lameness of the left handlimb was diagnosed as having a rupture of the cranial cruciate ligament. Repair was achieved using a combination of surgical techniques. A patellar ligament autograft was passed under the cranial meniscal ligament, through the joint and over the femoral condyle, and anchored using a screw and washer. Two nylon sutures were passed through a hole made in the tibial crest, and secured under the screw. The alpaca was confined in a stall for 3 months. Exercise was then increased progressively for 3 months. One year after surgery the alpaca is sound and has resumed breeding activity.     

Partial rupture of the cranial cruciate ligament in dogs

Four cases of partial rupture of the craniomedial part of the cranial cruciate ligament (CCL) are presented. Clinical examination revealed only subtle signs of CCL injury. The cranial drawer sign was present in two dogs and in flexion only. As the cranial drawer sign is not always evident a tentative diagnosis of partial CCL rupture should be based on history, joint tenderness and joint effusion. Arthrotomy and careful probing of the ligament is indicated. In these cases the lesion was treated immediately after diagnosis to prevent further degeneration and possible total rupture of the ligament. A fascial graft using the ‘over the top’ reconstruction technique was performed leaving the intact portion of the ligament in situ. Follow-up examination after four to six months revealed normal limb function in three dogs whereas slight and periodic lameness persisted in one dog.     

Cruciate and collateral ligament failure in the equine stifle: seven cases (1975-1985)

Medical records of 7 adult horses with single or multiple ligament failure of the femorotibial ligaments were reviewed to evaluate signalment, history, diagnostic and treatment methods, outcome, and long-term follow-up information. Acute onset of lameness was recorded for most of the horses. Horses with multiple ligament injury had more severe clinical signs than did horses with single ligament injury. Horses with single ligament injury generally required manipulative tests to localize the lameness to the stifle. In all horses, radiography of the stifle assisted in the diagnosis. Horses either were euthanatized (n = 3) or were treated by stall rest (n = 4) after diagnosis. Of the 4 surviving horses, 2 became successful breeding animals, 1 was awaiting breeding, and 1 was used unsuccessfully as a breeding animal. Necropsy findings in 2 of the 3 horses euthanatized after diagnosis revealed early articular damage in 1 horse 1 day after injury, and degenerative joint disease in the other horse 1 year after injury.     

Feasibility of utilizing the patellar ligament angle for assessing cranial cruciate ligament rupture in dogs

The patellar ligament angle (PLA) was assessed in 105 normal stifle joints of 79 dogs and 33 stifle joints of 26 dogs with a ruptured cranial cruciate ligament (CrCL). The PLA of stifles with complete CrCL rupture was significantly lower than that of normal stifles, particularly at a flexion angle of 60~80° in both plain and stress views. If the PLA was <90.55° on the stress view with a 60~80° flexion angle, the dog was diagnosed with a complete rupture of the CrCL with a sensitivity of 83.9% and specificity of 100%. In conclusion, measuring the PLA is a quantitative method for diagnosing complete CrCL rupture in canines.     

Inheritance of rupture of the cranial cruciate ligament in Newfoundlands

OBJECTIVE: To determine prevalence, level of inbreeding, heritability, and mode of inheritance for rupture of the cranial cruciate ligament (RCCL) in Newfoundlands. DESIGN: Retrospective and recruitment study. ANIMALS: 574 client-owned Newfoundlands. PROCEDURE: Medical records from January 1, 1996, to December 31, 2002, were evaluated for prevalence of RCCL. A pedigree was constructed by use of recruited Newfoundlands with RCCL status based on results of veterinary examination; level of inbreeding, heritability, and mode of inheritance were calculated. RESULTS: Hospital prevalence for RCCL was 22%; dogs in the pedigree from the recruitment study had a mean level of inbreeding of 1.19 x 10(4), heritability of 0.27, and a possible recessive mode of inheritance with 51% penetrance for RCCL. CONCLUSIONS AND CLINICAL RELEVANCE: Identification of a genetic basis for RCCL in Newfoundlands provided evidence that investigators can now focus on developing methods to identify carriers to reduce the prevalence of RCCL.     

Angle between the patellar ligament and tibial plateau in dogs with partial rupture of the cranial cruciate ligament

OBJECTIVE: To measure the angles between the patellar ligament and the tibial plateau and between the patellar ligament and the common tangent at the tibiofemoral contact point (TFCP) in stifle joints of dogs with partial rupture of the cranial cruciate ligament (CrCL) for comparison with data obtained for stifle joints in dogs with intact CrCLs. SAMPLE POPULATION: 60 stifle joints of 54 dogs with surgically confirmed partial CrCL rupture. PROCEDURES: Mediolateral radiographic views of the stifle joints were obtained, and the angles between the patellar ligament and the conventionally defined tibial plateau (angle gamma) and between the patellar ligament and the common tangent to the TFCP (angle alpha) were measured at incidental stifle joint flexion (angle beta) by 2 independent observers. Data underwent linear regression analysis and were compared with findings in joints of dogs without degenerative joint disease. RESULTS: In stifle joints of dogs with a partial rupture of the CrCL, angles gamma and alpha were 5 degrees and 2 degrees larger than each corresponding angle in healthy canine joints. At 100 degrees of flexion, the patellar ligament was perpendicular to the conventionally defined tibial plateau. At 110 degrees of flexion, the patellar ligament was perpendicular to the common tangent at the TFCP. CONCLUSIONS AND CLINICAL RELEVANCE: In dogs, stifle joints with partially ruptured CrCLs have marginally larger angles between the patellar ligament and the tibial plateau, compared with joints with intact CrCLs; at equivalent angles of flexion, comparatively greater shear force affects the CrCLs in stifle joints with partial CrCL ruptures.     

Arthroscopic management of a lateral glenohumeral ligament rupture in two dogs.

Tears to the lateral glenohumeral ligament appear to be uncommon in dogs. Two Labrador Retrievers were arthroscopically diagnosed with lateral glenohumeral ligament tears of the shoulder. Both cases failed to respond to conservative management. Surgical stabilisation of the lateral aspect of the shoulder joint was achieved using an arthroscopically placed suture using a hanging limb technique. Lameness resolved in both cases.     

Osteochondral lesion and cranial cruciate ligament rupture in an immature dog stifle

An osteochondral flap was present on the medial femoral condyle of a stifle of a six-month-old female rottweiler in which there was also a ruptured cranial cruciate ligament. The lesion was probably osteochondritis dissecans, but the possibilities of it being secondary to joint in-stability or a subchondral fracture, as has been described in people with knee ligamentous injuries, are discussed.     

Degenerative changes of the cranial cruciate ligament harvested from dogs with cranial cruciate ligament rupture

Degenerative cranial cruciate ligament (CCL) rupture is characterized histologically by degenerating extracellular matrix (ECM) and chondroid metaplasia. Here, we describe the progression of chondroid metaplasia and the changes in the expression of ECM components in canine CCL rupture (CCLR). CCLs from 26 stifle joints with CCLR (CCLR group) and normal CCLs from 12 young beagles (control group) were examined histologically and immunohistochemically for expression of type I (COLI), type II (COLII), type III collagen (COLIII) and Sry-type HMG box 9 (SOX9). Cell density and morphology of CCLs were quantified using hematoxylin–eosin staining. The percentage of round cells was higher in the CCLR group than in controls. COLI-positive areas were seen extensively in the connecting fibers, but weakly represented in the cytoplasm of normal CCLs. In the CCLR group, there were fewer COLI-positive areas, but many COLI-positive cells. The percentages of COLII-, COLIII- and SOX9-positive cells were higher in the CCLR group than in controls. The number of spindle cells with perinuclear halo was high in the CCLR group, and most of these cells were SOX9-positive. Deposition of COLI, the main ECM component of ligaments, decreased with increased COLIII expression in degenerated CCL tissue, which shows that the deposition of the ECM is changed in CCLR. On the contrary, expression of SOX9 increased, which may contribute to the synthesis of cartilage matrix. The expression of COLII and SOX9 in ligamentocytes showed that these cells tend to differentiate into chondrocytes.     

Treatment of rupture of suspensory ligament and superficial flexor tendon in a bull

Rupture of the suspensory ligament at the insertions on the proximal sesamoid bones, and of the superficial flexor tendon of the left fore limb, occurred in an adult Angus bull as a result of fighting. There was severe hyperextension of the metacarpophalangeal (MCP) joint with the dewclaws almost touching the ground. Radiographs revealed severe hyper-extension of the MCP joint with the sesamoid bones aligned directly distal to the metacarpus. Initially, a full length fiberglass cast was applied with the limb partially flexed within the cast and the heels elevated. The cast was replaced twice. The cast was removed after 136 days and the bull was bearing full weight on the limb. Prolonged immobilisation of the limb produced new bone in the area (a normal response in cattle) to cause ankylosis of the traumatized MCP joint and partial ankylosis of the carpus. The bull was being used for pasture breeding one year after the injury.