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.     

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

The majority of studies on cranial cruciate ligament (CrCL) disease to date have been carried out on dogs that already sustained a CrCL rupture, which is the end-stage of the disease. Investigations have recently been carried out to study humoral and cellular immunopathological mechanisms in predisposed dogs before clinical rupture of the contralateral CrCL. The cruciate ligaments are mainly composed of collagen type I, and immune responses to collagen have been suggested as a cause of CrCL degradation in dogs. None of these investigations showed evidence that anticollagen type I antibodies alone initiate CrCL damage. However, in predisposed dogs a distinct anticollagen type I antibody gradient was found towards the contralateral stifle joint that eventually sustained a CrCL rupture, suggesting that there was an inflammatory process present in these joints before detectable joint instability occurred. The importance of cellular reactivity to collagen type I in cruciate disease also remains unclear. Peripheral blood mononuclear cell proliferation to collagen type I was very diverse in dogs with cruciate disease whereas some sham operated dogs and healthy dogs tested positive as well. It is not yet determined whether cellular reactivity to collagen type I exists locally in the stifle joints nor whether this could initiate CrCL degradation. Inflammatory processes within the stifle joint can alter the composition of the cruciate ligaments. In animal models of immune-mediated synovitis, the mechanical strength of the CrCL is significantly reduced. Immunohistochemical studies on synovial tissues from dogs with rheumatoid arthritis and dogs with cruciate disease revealed that the pathologic features are similar in both joint pathologies and that the differences are mainly quantitative. Joint inflammation induced by biochemical factors such as cytokines has been implied in CrCL degeneration. In several studies, the levels of pro-inflammatory and T helper cytokines were measured in dogs that sustained a CrCL rupture, but the exact role of the various cytokines in the pathogenesis of CrCL disease remains inconclusive. More recently, the levels of the cytokines have been investigated over time in predisposed dogs before and after CrCL rupture. IL-8 expression tended to be higher in stifle joints that will rupture their CrCL during the next 6 months than in those that will not, indicating an inflammatory process in these joints before clinical rupture. This review provides a comprehensive overview of all possible implications of humoral and cell-mediated immune responses published in dogs with cruciate disease together with publications from human joint diseases. Furthermore, this review highlights recent findings on cytokines and proteinases in the accompanying joint inflammation.     

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.     

Apoptosis of ligamentous cells of the cranial cruciate ligament from stable stifle joints of dogs with partial cranial cruciate ligament rupture

OBJECTIVE: To describe the presence and amount of apoptotic ligamentous cells in different areas of partially ruptured canine cranial cruciate ligaments (prCCLs) and to compare these findings with apoptosis of ligamentous cells in totally ruptured cranial cruciate ligaments (trCCLs). ANIMALS: 20 dogs with prCCLs and 14 dogs with trCCLs. PROCEDURES: Dogs with prCCLs or trCCLs were admitted to the veterinary hospital for stifle joint treatment. Biopsy specimens of the intact area of prCCLs (group A) and the ruptured area of prCCLs (group B) as well as specimens from trCCLs (group C) were harvested during arthroscopy. Caspase-3 and poly (ADP-ribose) polymerase (PARP) detection were used to detect apoptotic ligamentous cells by immunohistochemistry. RESULTS: No difference was found in the degree of synovitis or osteophytosis between prCCLs and trCCLs. No difference was found in degenerative changes in ligaments between groups A and B. A substantial amount of apoptotic cells could be found in > 90% of all stained slides. A correlation (r(s) = 0.71) was found between the number of caspase-3-and PARP-positive cells. No significant difference was found in the amount of apoptotic cells among the 3 groups. No significant correlation could be detected between the degree of synovitis and apoptotic cells or osteophyte production and apoptotic cells. CONCLUSIONS AND CLINICAL RELEVANCE: The lack of difference between the 3 groups indicates that apoptosis could be a factor in the internal disease process leading to CCL rupture and is not primarily a consequence of the acute rupture of the ligament.     

Caudal proximal tibial deformity and cranial cruciate ligament rupture in small-breed dogs

Eight dogs presented with chronic hindlimb lameness associated with cranial cruciate ligament rupture. Seven were small terriers. A caudal deformity of the proximal tibial shaft, originating at the proximal tibial physis, and an excessive caudal slope of the tibial plateau were present bilaterally in all dogs. The deformity was thought to be responsible for the cranial cruciate ligament failure and poor response to conservative management. Tibial plateau angles were in excess of 26 degrees in all dogs. The lameness was bilateral in three dogs. There was complete cranial cruciate ligament rupture in seven stifles and partial rupture in four. There were no meniscal injuries. Surgical correction resulted in a significant improvement (P<0.0001) in all dogs, with a mean follow-up of 12 months (range three to 24 months). There were no complications.     

Nitric oxide metabolite production in the cranial cruciate ligament, synovial membrane, and articular cartilage of dogs with cranial cruciate ligament rupture

OBJECTIVE: To measure concentrations of nitric oxide metabolites (nitrite-nitrate [NOt]) in cartilage, synovial membrane, and cranial cruciate ligament (CCL) in dogs and evaluate associations with osteoarthritis in dogs with CCL rupture. ANIMALS: 46 dogs with CCL rupture and 54 control dogs without joint disease. PROCEDURE: Tissue specimens for histologic examination and explant culture were harvested during surgery in the CCL group or immediately after euthanasia in the control group; NOt concentrations were measured in supernatant of explant cultures and compared among dogs with various degrees of osteoarthritis and between dogs with and without CCL rupture. RESULTS: Osteoarthritic cartilage had significantly higher NOt concentration (1,171.6 nmol/g) than did healthy cartilage (491.0 nmol/g); NOt concentration was associated with severity of macroscopic and microscopic lesions. Synovial membrane NOt concentration did not differ between dogs with and without CCL rupture. Ruptured CCL produced less NOt than did intact ligaments. In control dogs, NOt concentrations were similar for intact ligaments (568.1 nmol/g) and articular cartilage (491.0 nmol/g). Synthesis of NOt was inhibited substantially by coincubation with inhibitors. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that NOt in canine joint tissues originates from the inducible nitric oxide synthase pathway. Nitric oxide metabolite production in cartilage was greater in dogs with osteoarthritis than in healthy dogs and was associated with lesion severity, suggesting that nitric oxide inhibitors may be considered as a treatment for osteoarthritis. The CCL produces substantial concentrations of NOt; the importance of this finding is unknown.     

Partial rupture of the cranial cruciate ligament of the stifle in dogs: 25 cases (1982-1988)

Partial rupture of the cranial cruciate ligament was diagnosed in 25 dogs. In all dogs, the primary problem at the time of physical examination was hind limb lameness. The mean time from initial onset of lameness to diagnosis at exploratory surgery was 17 weeks. A cranial drawer sign was detected in 13 of the 25 dogs; in 9, the cranial drawer sign was evident only when the stifle was positioned in flexion. Of the 25 dogs, 12 had no detectable cranial drawer sign in response to manipulation of the involved stifle. In all dogs, lateral stifle arthrotomy was performed in routine manner, and the cranial cruciate ligament was found to be incompletely torn. Lesions identified during arthrotomy were rupture of the craniomedial band (n = 20 dogs), interstitial tear (n = 4 dogs), and rupture of the caudolateral band (n = 1 dog).     

Clinical assessments of increased sensory sensitivity in dogs with cranial cruciate ligament rupture

Dogs with chronic pain have a compromised quality of life. Repeatable and accurate sensory assessments form a means by which the hypersensitivity likely to reflect chronic pain may be quantified. These assessments can be applied to individuals to identify those that may benefit from improved analgesic relief. In this study four sensory assessments were evaluated in dogs presenting with a naturally occurring chronic painful condition (cranial cruciate ligament rupture, CCLR) and were compared with healthy control animals of similar age and weight. Inter-digital von Frey filament and thermal sensitivity tests revealed that the affected hind limb of dogs with CCLR was significantly more sensitive than the opposing limb. Static weight bearing and gait parameter scores were also reduced in the affected hind limb compared to the opposing hind limb of dogs with CCLR; no such differences were found between the hind limbs of healthy (control) dogs. The quantitative sensory tests permitted the differentiation of limbs affected by CCLR from healthy limbs. Dogs presenting with CCLR demonstrate objectively quantitative sensory sensitivities, which may require additional consideration in case management.     

Pathologic changes in grossly normal menisci in dogs with rupture of the cranial cruciate ligament

OBJECTIVE: To determine whether histopathologic changes are detectable in grossly normal medial menisci from dogs with rupture of the cranial cruciate ligament (CCL). DESIGN: Case series. SAMPLE POPULATION: 40 medial menisci from dogs with rupture of the CCL and 20 medial menisci from control dogs without stifle joint disease. PROCEDURE: Data evaluated included age, duration of clinical signs, and whether rupture of the CCL was complete or incomplete. Three groups (n = 20/group) were also compared on the basis of 5 histologic criteria; group-1 menisci appeared grossly normal and were obtained from dogs with naturally occurring rupture of the CCL, group-2 menisci were grossly abnormal and were also obtained from dogs with naturally occurring CCL ruptures, and group-3 menisci were collected at postmortem from dogs without stifle joint disease that were of similar age and weight as dogs in groups 1 and 2. RESULTS: Group-2 menisci were significantly different from group-1 and -3 menisci in all histologic criteria. Group-1 menisci were significantly different from control menisci in only 1 of the 5 histologic criteria (cartilage differentiation). Dogs that were > or =3 years old had significantly more surface cellularity than did dogs that were < 3 years old. A significant difference was not detected between groups 1 and 2 with regard to completeness of rupture. CONCLUSIONS AND CLINICAL RELEVANCE: Histologic changes in meniscal cartilage correlate with gross appearance of the cartilage at time of surgery for rupture of the CCL. On the basis of minimal histologic changes, routine removal of grossly normal menisci does not appear to be warranted.     

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.     

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.     

Comparison of the tibial mechanical joint orientation angles in dogs with cranial cruciate ligament rupture

Use of the tibial mechanical joint orientation angles is now the standard of care for evaluating tibial deformities, although they have not been used to evaluate dogs with cranial cruciate ligament (CrCL) rupture. The objective of this study was to compare the tibial mechanical joint orientation angles and tibial plateau angle (TPA) between dogs with bilateral CrCL rupture (BR) and unilateral CrCL rupture with (UR-SR) and without subsequent contralateral CrCL rupture (UR-w/o-SR) as risk factors for subsequent contralateral CrCL rupture. Twenty dogs (21.7%) were classified as BR, 38 (41.3%) were classified as UR-SR, and 34 (37.0%) were classified as UR-w/o-SR. The tibial mechanical joint orientation angles and TPA, in the range studied (< 35°), were not statistically different for dogs with BR, UR-SR, and UR-w/o-SR, and were not significant risk factors for subsequent contralateral CrCL rupture.     

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.     

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.