Sprains and strains result from collagen fibre overextension. This study investigated changes in the molecular state of collagen due to overextension damage, thereby gaining insight into tissue degeneration and cellular detection of damage. Overextension results in intermolecular and intrafibrillar sliding, detected with x-ray diffraction. Tendon rupture results in increased susceptibility to proteolytic enzymes. These observations and contemporary theory concerning collagen fibre stability lead to the hypothesis that sub-rupture overextension should result in reduced thermal stability of fibrous collagen. Tendons were harvested from steer tails. Each provided a specimen for control and for overextension. Sub-rupture overextension at 1%/s strain rate was accomplished on a mechanical testing system, under the control of custom software, until the slope of the force-deformation curve was approximately zero (before complete failure). Two loading treatments were tested: one-cycle and five-cycles. Two specimen types were tested: native tendons ± NaBH4 crosslink stabilization. Tendons in each of the four groups (2x2) were paired by originating tail. Thermal stability was assessed in terms of denaturation temperature (Td) using hydrothermal isometric tension testing. Specimens were held at constant length and heated from ambient temperature to 90degC. Td was defined as the temperature where load suddenly increased due to molecular unraveling and attempted shrinkage. Overextension of native specimens reduced the thermal stability of the collagen (p<
0.0001) and five-cycles had a still greater effect (p=0.03). Td of controls was 64.5±1.0degC (mean±SD). After one-cycle, Td dropped to 63.2±1.0degC and, after five-cycles, Td dropped to 61.8±2.0degC. For stabilised tendons, the effect of multiple cycles was lost (p=0.08) but overstretching decreased Td by ~2degC (p<
0.0001). This study confirms that the molecular state of collagen is altered by overextension damage, reducing Td by up to 10% of the expected range (37–65degC) in our experiments. This is thought to occur due to intermolecular sliding that liberates specific domains on the molecules, lowering the activation energy for uncoiling. These domains may also be key targets in degeneration and cell-collagen signaling.
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.
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
We present the clinical and radiological results of percutaneous vertebroplasty in the treatment of 58 vertebral compression fractures in 51 patients at a minimum follow-up of two years. Group 1 consisted of 39 patients, in whom there was no associated intravertebral cleft, whilst group 2 comprised 12 patients with an intravertebral cleft. The Oswestry disability index (ODI) and visual analogue scale (VAS) scores were recorded prospectively. The radiological evidence of kyphotic deformity, vertebral height, leakage of cement and bone resorption around the cement were studied restrospectively, both before and after operation and at the final follow-up. The ODI and VAS scores in both groups decreased after treatment, but the mean score in group 2 was higher than that in group 1 (p = 0.02 (ODI), p = 0.02 (VAS)). There was a greater initial correction of the kyphosis in group 2 than in group 1, although the difference was not statistically significant. However, loss of correction was greater in group 2. Leakage of cement was seen in 24 (41.4%) of 58 vertebrae (group 1, 32.6% (15 of 46); group 2, 75% (9 of 12)), mainly of type B through the basal vertebral vein in group 1 and of type C through the cortical defect in group 2. Resorption of bone around the cement was seen in three vertebrae in group 2 and in one in group 1. There were seven adjacent vertebral fractures in group 1 and one in group 2. Percutaneous vertebroplasty is an effective treatment for osteoporotic compression fractures with or without an intravertebral cleft. Nonetheless, higher rates of complications related to the cement must be recognised in patients in the presence of an intravertebral cleft.
Extensor Pollicis Longus (EPL) rupture occurs in 0.2 – 3% of fractures of the distal radius. The underlying mechanism is unknown. This study prospectively evaluates EPL and surrounding structures using high-resolution ultrasound (US) in patients with distal radius fracture 6 weeks after injury and correlates the findings with initial radiographic measurements. US can assess tendon size, echogenicity and peak velocity, haematoma depth and thickness of the extensor retinaculum and tendon sheath. The normal wrist was examined as a control.
Radiographic measurements – AO classification: A-32, B-12 and C-14. 76% were undisplaced fractures with dorsal tilt less than 10. Statistical analysis revealed that EPL tendon peak velocity is significantly slower on the fractured side (p=0.001). The extensor retinaculum thickness is greater (p=0.003) and the synovial sheath thickness is greater (p less than 0.001) on the fractured side. Synovial sheath thickness was also found to be significantly greater in the intra-articular fractures (p=0.03) and the undisplaced fractures (p=0.03).
As expected, the peak tendon velocity is reduced following fracture, but this is still significant at 6 weeks. This could be associated with impaired diffusion of nutrients within the synovial sheath. There is also persistent soft tissue swelling with significantly increased extensor retinaculum and synovial sheath thickness. This is a protective response to trauma, but we propose that this could interfere with the already tenuous blood supply of the EPL tendon. It could also reduce diffusion of nutrients within the tendon sheath, particularly in undisplaced fractures, where the extensor retinaculum is not torn and any increased pressure may not be dispersed. The study is ongoing with the aim to be able to identify patients at risk for EPL rupture and potentially be able to prevent it by early surgical decompression.
SEM analysis of the surfaces of the metals revealed large deep scratches of the CoCr implants which were aligned in the A-P sliding direction. Barium sulphate particles were seen embedded in the surface of the femoral component. Voids were seen in the surface of the cobalt chrome and particles of silicate polishing powder were seen in these voids. There was also evidence of scratches originating at these voids. By contrast oxidised zirconium, showed small amounts of superficial scratching with an intact surface and no evidence of third body particles.
In clinical studies of cemented total hip arthroplasty (THA), polished stems produce less slippage at the bone-cement interface than roughened stems. Our objective is to assess the effect of stem-cement debonding on the bone-cement interface shear behaviour of hip implants using simplified axisymmetric stem-cement-aluminum models. We emulated the femoral stems using stainless steel tapered plugs with either a rough (i.e. bonded) or smooth (i.e. unbonded) surface finish. Three different taper angles (5°, 7.5°, 10°) were used for the unbonded constructs. Non-tapered and tapered (7.5°) aluminum shells were used to emulate the diaphyseal and metaphyseal segments of the femur. In all cases, the cement-aluminum interface was designed to have the same shear strength as has been reported for bone-cement interfaces (~8 MPa). The test involved applying axial compressive loading at a rate of 0.02 mm/s until failure. Six specimens were tested for each combination of the parameters. The unbonded stems sustained about twice as much load as the bonded stem, regardless of taper angle, and the metaphyseal model carried 35-50% greater loads than the diaphyseal models before shear failure or slippage. The unbonded constructs reached peak load with excessive displacement due to creep of the cement mantle while the bonded constructs failed in shear at the cement-aluminum interface. This result supports the hypothesis that the wedging forces created in the unbonded construct increase the compression forces across the aluminum-cement interface, thereby increasing its shear resistance. A finite element analysis predicted that the cement could withstand the hoop stress under these loading circumstances and this prediction was confirmed by visual inspection of the cement after each test. Our results suggest that smooth or unbonded stems should sustain less slippage and shear damage at the bone-cement interface than roughened or bonded stems due to the wedge-induced compressive stress; this increased load capacity will be particularly valuable when the condition of the bone-cement interface is suboptimal.
The outcomes were assessed by stress radiographs, maximal manual test with KT-2000 arthrometer, IKDC grading and OAK knee score.
Average OAK score improved from 64.3 to 86.4
We reviewed retrospectively the role of monitoring of somatosensory spinal evoked potentials (SSEP) in 99 patients with neuromuscular scoliosis who had had operative correction with Luque-Galveston rods and sublaminar wiring. Our findings showed that SSEP monitoring was useful and that a 50% decrease in the amplitude of the trace optimised both sensitivity and specificity. The detection of true-positive results was higher than in cases of idiopathic scoliosis, but the method was less sensitive and specific and there were more false-negative results. In contrast with the findings in idiopathic scoliosis, recovery of the trace was associated with a 50% to 60% risk of neurological impairment. Only one permanent injury occurred during the use of this technique, and any temporary impairment resolved within two months.
Reports of differing failure rates of total hip prostheses made of various metals prompted us to measure the size of metallic and polyethylene particulate debris around failed cemented arthroplasties. We used an isolation method, in which metallic debris was extracted from the tissues, and a non-isolation method of routine preparation for light and electron microscopy. Specimens were taken from 30 cases in which the femoral component was of titanium alloy (10), cobalt-chrome alloy (10), or stainless steel (10). The mean size of metallic particles with the isolation method was 0.8 to 1.0 microns by 1.5 to 1.8 microns. The non-isolation method gave a significantly smaller mean size of 0.3 to 0.4 microns by 0.6 to 0.7 microns. For each technique the particle sizes of the three metals were similar. The mean size of polyethylene particles was 2 to 4 microns by 8 to 13 microns. They were larger in tissue retrieved from failed titanium-alloy implants than from cobalt-chrome and stainless-steel implants. Our results suggest that factors other than the size of the metal particles, such as the constituents of the alloy, and the amount and speed of generation of debris, may be more important in the failure of hip replacements.
We studied the healing and torsional strength of non-vascularised (28) and vascularised (28) sections of tibial diaphyses in 56 cats. Both types of graft achieved fracture union in the same period of time, and at 12 and 16 weeks the non-vascularised grafts were as strong as the vascularised grafts.