Hamstring graft technique for stabilization of canine cranial cruciate ligament deficient stifles

OBJECTIVE: To investigate the harvest and application of hamstring grafts for canine cranial cruciate ligament (CrCL) reconstruction. STUDY DESIGN: Experimental study. ANIMALS: Four adult female hounds, weighing 26.3 +/- 1.6 kg (mean +/- SEM). METHODS-One stifle in each dog was randomly chosen for hamstring graft CrCL reconstruction after native CrCL transection. Arthroscopy was performed to evaluate graft integrity at 12 weeks. Gait analysis and stifle radiographs were performed preoperatively and up to 52 weeks after graft placement. Dogs were killed 12 (n = 2) or 52 weeks (n = 2) after CrCL reconstruction. Tissues were evaluated grossly and with light and confocal laser microscopy. RESULTS: Hamstring grafts were intact in all stifles at 12 weeks (n = 4) and 52 weeks (n = 2). Grossly, there was no osteoarthritis in stifles at 12 weeks and only chondrophytes along the trochlear ridges at 52 weeks. Minimal radiographic evidence of osteoarthritis developed in stifles with grafts during the study. Lameness in limbs with grafts resolved by 52 weeks. Graft tissue was highly vascular, ligamentized, and undergoing active remodeling at 12 weeks. Fifty-two weeks after graft placement, intraarticular graft tissue was well vascularized, mature, and encapsulated by synovium, and graft-bone interfaces were characterized by Sharpey's fiber insertions. There was no evidence of graft necrosis using confocal laser microscopy at either time point. CONCLUSIONS: The hamstring graft technique may be a viable method of canine CrCL reconstruction. CLINICAL RELEVANCE: Hamstring grafts may be an alternative technique for canine CrCL reconstruction. Further study is needed before clinical application.     

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.     

Relationship of tibial plateau slope to limb function in dogs treated with a lateral suture technique for stabilization of cranial cruciate ligament deficient stifles

OBJECTIVE: To evaluate the effect of a lateral suture technique (LST) on tibial plateau angle (TPA) measurement and to compare TPA with functional outcome in dogs treated for cranial cruciate ligament (CrCL) rupture with LST. STUDY DESIGN: Prospective clinical study. SAMPLE POPULATION: Dogs (n=34) with unilateral CrCL instability. METHODS: All dogs had lameness examination, survey stifle radiographs, and force plate analysis before and at 6, 12, 24, and 48 weeks after surgery. Radiographic osteoarthritis (OA) scores and lameness scores were assigned using previously reported methods. Preoperative radiographs were performed in all dogs, and postoperative serial radiographs were performed in 6 dogs for measurement of TPA. Differences in TPA measurements were evaluated with a random effects repeated measures model. The significance of LST on TPA measurement was established in 6 dogs and the effect of TPA on vertical impulse, peak vertical force, progression of radiographic scores, and lameness score were analyzed by general linear models in all dogs. Differences were considered significant if P<.05. RESULTS: Significant differences were not noted between pre- and serial postoperative measurements of TPA. A significant correlation was not established between TPA and postoperative vertical impulse, peak vertical force, lameness score, or radiographic OA scores. CONCLUSIONS: TPA values were unchanged after LST and TPA does not affect outcome measures in dogs treated with LST. CLINICAL RELEVANCE: TPA has no predictive value on clinical outcome in dogs treated with LST for stabilization of CrCL deficient stifles.     

Long-term outcome of surgery for dogs with cranial cruciate ligament deficiency

Fifty-eight dogs with cranial cruciate ligament deficiency were assessed and treated surgically. At an average of 50 months postoperatively, the functional outcome was assessed by means of an owner-based clinical assessment and a clinical examination. Client-based data were available for 26 dogs and 20 dogs were reassessed after 50 months. The results were compared with the initial values and with data from an assessment 13 months postoperatively. The level of disability at 50 months was judged to be significantly less than initially. However, there were no differences between the initial assessments and those made after 50 months for the perceived 'effect of cold weather' and the dogs' 'ability to jump', despite both measures having improved after 13 months. Age and meniscal injury were identified as poor prognostic indicators for the long-term outcome. The equivalent joint on the contralateral limb deteriorated significantly during the study.     

Bone and lean tissue changes following cranial cruciate ligament transection and stifle stabilization

Following cranial cruciate ligament transection and extracapsular stabilization, dual-energy X-ray absorptiometry was used to analyze bone mineral content and lean tissue mass in the surgical and nonsurgical legs (n=14) at 0, 2, 4, and 8 weeks, and to evaluate bone mineral content and bone mineral density (BMD) of the proximal, mid-, and distal tibia of both the surgical and nonsurgical legs (n=15) at 0, 5, and 10 weeks. There was significant loss of bone mineral content and lean tissue in the surgical leg compared to the nonsurgical leg. Significant loss in bone mineral content and BMD was detected in the tibia of the surgical leg and was most pronounced in the metaphyseal region.     

Tibial osteotomies for cranial cruciate ligament insufficiency in dogs

Objective— To review the biomechanical considerations, experimental investigations, and clinical data pertaining to tibial osteotomy procedures for treatment of cranial cruciate ligament (CrCL) insufficiency in dogs.
Study Design— Literature review.
Methods— Literature search through Pub Med, Veterinary Information Network, Commonwealth Agricultural Bureau Abstracts, and conference proceedings abstracts (November 1977 to March 2007).
Results— Reported tibial osteotomy procedures attempt to eliminate sagittal instability (cranial tibial thrust) in CrCL-deficient stifles by altering the conformation of the proximal tibia. Functional stability can be achieved by decreasing the tibial plateau slope (cranial tibial closing wedge osteotomy [CTWO], tibial plateau leveling osteotomy [TPLO], combined TPLO and CTWO, proximal intraarticular osteotomy, chevron wedge osteotomy), altering the alignment of the patellar tendon (tibial tuberosity advancement), or both (triple tibial osteotomy). Clinical reports assessing the efficacy of these procedures frequently use subjective outcome measures, and the periods of follow-up evaluation are highly variable. Satisfactory results have been reported in most (>75%) dogs irrespective of the type of tibial osteotomy procedure.
Conclusions— Currently available data does not allow accurate comparisons between different tibial osteotomy procedures, or with traditional methods of stabilizing the CrCL-deficient stifle. Carefully designed long-term clinical studies and further biomechanical analyses are required to determine the optimal osteotomy technique, and whether these procedures are superior to other stabilization methods.
Clinical Relevance— Limb function in dogs with CrCL insufficiency can be improved using the currently described tibial osteotomy techniques.     

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.     

Evaluation of ligament fibroblast viability in ruptured cranial cruciate ligament of dogs

OBJECTIVE: To determine fibroblast viability, assess development of apoptosis, and evaluate tissue hypoxia via histochemical, in-situ hybridization, or immunohistochemical staining in ruptured and intact cranial cruciate ligaments (CCLs) of dogs. ANIMALS: 32 dogs with ruptured CCLs, and 8 aged and 19 young dogs with intact CCLs. PROCEDURE: Markers of cell viability (lactate dehydrogenase [LDH]), apoptosis (terminal deoxynucleatidyl transferase-mediated deoxyuridine triphosphate-nick end labeling [TUNEL] method), and hypoxia (hypoxia-inducible factor-1alpha [HIF-1alpha] monoclonal antibody) were applied to CCL specimens; positive cells were assessed objectively (LDH) and subjectively (TUNEL and HIF-1alpha) in the main axial tissue component (core) and synovial intima and subintima (epiligamentous tissue). RESULTS: Viable fibroblasts were seen in all intact and ruptured CCLs. More nonviable cells were found in the core regions of ruptured CCLs and intact CCLs of young dogs than in the epiligamentous regions. Number of nonviable cells in the core region of ruptured CCLs was greater than that in intact CCLs of young and aged dogs, whereas the number in the epiligamentous region was similar in all specimens. The TUNEL and HIF-1alpha staining was only found in the epiligamentous region of ruptured CCLs. CONCLUSIONS AND CLINICAL RELEVANCE: Ruptured CCLs contained a high number of nonviable cells but not a great number of apoptotic cells. Repair processes in the epiligamentous region of the CCL include a metabolic response to hypoxia, suggesting that necrosis of ligament fibroblasts and transformation of surviving cells to a spheroid phenotype may be a response to hypoxia cause by microinjury or inadequate blood flow.     

Force plate analyses before and after stabilization of canine stifles for cruciate injury

Ground reaction forces were measured from the hind limbs of 9 dogs before and after stabilization of unilateral cranial cruciate ligament rupture. Before surgery, peak vertical force, associated impulses, and weight distribution were significantly less (multivariate analysis P less than 0.02) in the affected limb, compared with the clinically normal limb. Craniocaudal peak forces and impulses, divided into braking and propulsion, also were significantly less in the affected limb. At a minimum of 7 months after retinacular imbrication, all vertical and craniocaudal measurements in the affected limb were increased significantly. Significant changes were not found in the normal limb. Furthermore, at the postoperative evaluation, there was no significant difference in any measurement between the affected and normal hind limbs. The results indicated restoration of function in the cruciate-deficient limb when compared with the clinically normal hind limb at a walking gait during the study time period.     

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.     

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.     

The effect of cranial cruciate ligament insufficiency on caudal cruciate ligament morphology: An experimental study in dogs

OBJECTIVES: To investigate the effect of cranial cruciate ligament (CrCL) insufficiency on morphology of the canine caudal cruciate ligament (CdCL). STUDY DESIGN: In vivo experimental study. ANIMALS: Five adult foxhounds. METHODS: Two years after CrCL transection, the histologic appearance of CdCLs from CrCL-deficient and unoperated contralateral control (CrCL-intact) stifle joints were evaluated using light and transmission electron microscopy. RESULTS: CdCLs from CrCL-deficient joints had extracellular matrix changes, characterized by chondroid metaplasia and disruption of cell architecture. Percent of small-diameter fibrils in CdCLs from CrCL-deficient joints was significantly greater (P <.05) than that in CdCLs from CrCL-intact joints. Collagen fibril density in CdCLs from CrCL-deficient joints (41.09 +/- 5.39%) tended to be less than that in CdCLs from CrCL-intact joints (52.96 +/- 6.92%); however, this difference was not significant (P =.056). Mean eccentricity (ratio of minor to major diameters) of collagen fibrils was significantly (P <.0001) lower for CdCLs from CrCL-deficient joints (0.85 +/- 0.016) when compared with that for CdCLs from CrCL-intact joints (0.87 +/- 0.015). CONCLUSIONS: Significant alterations were found in the morphology of CdCLs from CrCL-deficient joints. These changes may be associated with repetitive microtrauma to the CdCL secondary to instability or enzymatic degradation in the hostile synovial environment of an unstable joint. CLINICAL RELEVANCE: Regardless of the cause, the switch to a predominantly small-diameter collagen fibril profile may reflect compromised material properties of the CdCL. This should be taken into account when considering surgical techniques that rely on the CdCL to stabilize CrCL-deficient stifles.     

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.     

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.     

Correlative biomechanical and histologic study of the cranial cruciate ligament in dogs

The mechanical properties of the cranial cruciate ligament were determined, using unilateral bone-ligament-bone preparations from 65 dogs of various ages and body sizes. Tensile loading of the cranial cruciate ligament from 1 of each pair of stifle joints demonstrated a decrease in material properties (modulus, maximum stress, strain energy) with aging. The decreases in maximum stress and strain energy with age were significantly less (P less than 0.05 and P less than 0.05, respectively) in the cranial cruciate ligament from dogs weighing less than 15 kg, compared with those weighing 15 kg or more. The cranial cruciate ligament and remaining femorotibial ligaments were collected from the opposite stifle joints and examined microscopically. By 5 years of age, the cranial cruciate ligaments of dogs weighing greater than 15 kg consistently had microscopic evidence of degenerative disease (loss of ligamentocytes, metaplasia of surviving ligamentocytes to chondrocytes, and failure to maintain collagen fibers and primary collagen bundles) which progressed in severity with age. The caudal cruciate ligaments were similarly affected, although the degenerative changes were rarely as severe as in the cranial cruciate ligament. The collateral ligaments underwent minimal degeneration. Sex differences had no bearing on degeneration. The cranial cruciate ligaments in dogs weighing less than 15 kg generally had less severe alterations than those in heavier dogs, and the onset of the degenerative process was delayed by several years. Cranial cruciate ligaments removed from dogs after ligament failure not only had degenerative disease, but also had undergone unsuccessful attempts at repair. In contrast, fibrous repair was rarely present in intact ligaments of asymptomatic dogs with degenerative disease of the cranial cruciate ligament.     

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.     

Incidence of meniscal injury in cats with cranial cruciate ligament ruptures

This retrospective study evaluated the incidence of meniscal injury in cats with cranial cruciate ligament (CCL) ruptures. Medical records for cats diagnosed with CCL ruptures treated by a lateral fabellotibial suture (LFS) were reviewed for signalment, history, physical examination and surgical findings. Ninety-five cats (98 stifles) met the inclusion criteria. The incidence of meniscal injuries in feline CCL deficient stifles was 67%. Isolated medial meniscal injuries were found in 55 stifles (56%), isolated lateral meniscal injuries were found in 5 stifles (5%), and lateral and medial meniscal injuries were found in 6 stifles (6%). There was no correlation between the presence of a meniscal injury and age, breed, sex, weight, duration of lameness, presence of concurrent medial patellar luxation, degree of degenerative joint disease, or presenting side of lameness. Given the high rate of meniscal pathology in cats with CCL ruptures, exploratory surgery for meniscal assessment and concurrent stifle stabilization should be considered in feline patients.