The purpose of this study was to compare the clinical outcome of patients treated surgically for end stage ankle arthritis using a total ankle arthroplasty or ankle arthrodesis. This is a multicentered prospective clinical outcome study of the surgical treatment of patients with EAA using an ankle arthrodesis (n= 117) or total ankle arthroplasty (n= 210). Clinical outcome was assessed using health related quality of life (SF36v2) and joint specific (Foot Function Index, Ankle Osteoarthritis Scale, American Orthopedic Foot and Ankle Hindfoot Scale and the AAOS Foot and Ankle Baseline Questionnaire(version 2000)) outcome scores. Preoperatively, all patients had significant physical and psychological morbidity. All symptom and functional SF36 subscales were approximately two standard deviations below normal population scores. Approximately 25% of patients were three standard deviations below population values, indicating increased risk of mortality. There was no evidence that age or gender influenced the level of disability. There was a significant improvement in the health related quality of life and the joint specific clinical outcome scores at six and twelve months follow up but no consistent difference was noted between the two cohorts. This is the first multicentered prospective clinical outcome study that demonstrates equal efficacy for early follow up of patients treated for EAA with total ankle arthroplasty or ankle arthrodesis.
The purpose of this study is to assess the clinical outcome and gait analysis of a new technique for ankle arthrodesis using a Fibular Sparing Z Osteotomy (FSZO). The FSZO technique for ankle arthrodesis utilises a lateral approach where the fibula is osteotomised and reflected posteriorly on a soft tissue hinge to allow easy access to the ankle joint for an anatomic arthrodesis. Outcome assessment at six months follow up included health related quality of life (SF36) and joint specific (American Orthopedic Foot and Ankle Society Ankle-Hindfoot, Ankle Osteoarthritis Scale, Foot Function Index) clinical outcome scores. Gait Analysis was completed using the Walkabout Portable Gait Monitor® which includes a wireless gait belt housing a triaxial arrangement of accelerometers, resting behind the lumbar vertebrae, approximately at position of centre of mass to quatintfy surgery, lurch and functional limb length difference (LLD). There was a significant improvement in the health related quality of life and the joint specific clinical outcome scores at six months follow up. The six month gait study preliminary analysis showed improvement in some parameters of gait but worsening in others. The FSZO ankle arthrodesis technique provides improvement in clinical outcome scores and certain gait parameters at early follow up.
Tendon disease causes widespread morbidity ranging from mild pain to catastrophic end-stage rupture. The pathophysiology of tendon disease is not certain. An overuse exercise model was developed using rats with the aim of developing tissue with histological, biochemical and biomechanical features similar to those in human tendinosis. Results indicate that the biological response to over-exercise of the rat Achilles tendon is similar to the literature description of pathological specimens of human with disease. Biochemical and histological analysis of the rat Achilles tendons suggest that the patho-physiology is more consistent with a repair response than with a classical inflammatory response. Tendon disease causes widespread morbidity ranging from mild pain to catastrophic end-stage rupture and the pathophysiology of tendon disease is not certain. To develop an overuse exercise animal model to study the pathophysiology of Achilles tendon disease. Experimental rats were subjected to an over-exercise running regime, while control rats were maintained under normal cage activity. Achilles tendons were analyzed for histological features, glycosaminoglycan content, collagen content, collagen subtype, collagen crosslinking (hydrothermal isometric tension testing), and mechanical properties. Experimental rat Achilles tendons demonstrated: increased nuclear numbers per high-power field (527 vs. 392, p <
0.05), decreased semi-quantitative grade for collagen organization (2.9 vs. 3.7, p <
0.05) and decreased semi-quantitative grade for collagen staining (1.9 vs 3.5, p <
0.05). The total collagen content remained unchanged (84.3 vs. 89.0% p=0.38), while the glycosaminoglycan content was increased (17.5 vs. 9.0% p=0.02). Increased levels of collagen type III were not demonstrated, however. Experimental tendons were determined to have distinct differences in the collagen crosslinking patterns, with reduced total cross links and a greater population of immature, hydrolytically unstable cross links. These differences did not, however, translate into a decrease in ultimate tensile failure during mechanical testing (UTS of 77.8 vs. 88.8 N, p=0.26). The histology and biochemistry observed in the experimental rat Achilles tendons were similar to those described in the literature on human Achilles tendon disease. The rat Achilles tendon over-exercise model has demonstrated histopathology that was different from a control group and was consistent with the human literature for Achilles tendon disease. Research Grants were received from the following organizations:
Canadian Orthopaedics Foundation American Foot and Ankle Society Dalhousie University Department of Surgery Nova Scotia Capitol District Health Authority Research Fund
Tendinosis is a common problem causing wide spread morbidity ranging from mild symptoms of pain and limited mobility to catastrophic end stage rupture. The structural and mechanical properties of the rat Achilles tendon were investigated as groundwork for the development of a rat Achilles tendinosis model. This model will generate tendons afflicted with tendinosis that bear histological features identical to those observed in human tendinosis. Tissues afflicted with tendinosis derived from this model will be used in future studies to gain a better understanding of the biology of tendinosis and to evaluate various therapeutic intervention strategies. The pathology underlying tendinosis is a continuum, with mild symptoms progressing toward catastrophic rupture; still, the corresponding biochemical and biomechanical progression is poorly understood. We have developed a rat model for Achilles tendinosis, aiming to: (i) define for the first time the structural/mechanical features of the normal tendon and (ii) examine the histological changes with over-exercise. Normal rat Achilles tendons were assayed via: hydroxyproline for total collagen, SDS-PAGE electrophoresis for collagen subtypes, thermoelastic testing for immature/mature collagen crosslinking, and tensile mechanical testing. As per Soslowsky in the rat rotator cuff, the over-exercise model used 10° uphill treadmill running over twelve weeks. Light histology under H&
E staining and birefringence was assessed using a blinded, semi-quantitative scale. The normal rat Achilles is 89.6 ± 10.6% (SD) collagen with a mean UTS of 5.29 ± 1.91 MPa (SD). Only type I collagen is evident in SDS-PAGE and immature collagen crosslinking is dominant demonstrated by NaBH4-reduction required to achieve a 90°C isotherm in hydrothermal testing. The three, six and twelve-week over-exercise regimes produce increasing cell area density and decreasing collagen organization. Surprisingly, the proliferating cells do not seem to be fibroblast dominant and label with factor III antibody to human endothelial cells. The normal Achilles tendon in young (eight weeks old) but mature rats is a strong, collagen-rich tissue; however, immature crosslinking suggests remodelling. We suspect that low type III collagen in the normal Achilles may increase significantly with inflammation. However, fibroblast proliferation may not be dominant. Our rat Achilles tendon over-exercise model has demonstrated histopathology consistent with the human literature. With clear structural/mechanical characterization, future studies will focus on changes in these variables with disease tendons derived from the rat ten-dinosis model.