Veterinary Science Collected Works - Theses
Permanent URI for this collection
Search Results
1 - 2 of 2
-
ItemBiomechanical and microstructural properties of subchondral bone from three metacarpophalangeal joint sites in Thoroughbred racehorses( 2022)Reasons for performing the study: Fatigue induced subchondral bone (SCB) injury is common in racehorses. Understanding how subchondral microstructure and microdamage influence mechanical properties is important for developing injury prevention strategies. Mechanical properties of the disto palmar third metacarpal condyle (MCIII) correlate poorly with microstructure, and it is unknown whether the properties of other sites within the metacarpophalangeal (fetlock) joint are similarly complex. Objectives: We aimed to investigate the mechanical and structural properties of equine SCB from three sites within the metacarpophalangeal joint: the disto-palmar MCIII, disto-dorsal MCIII and proximal sesamoid bone. Two regions of SCB within each specimen were compared, a 2 mm superficial and underlying 2 mm deep layer. Methods: Cartilage-bone specimens were analysed with micro-computed tomography to determine bone volume fraction (BVTV) and bone mineral density (BMD), then loaded in cyclic compression for 100 cycles at 2 Hz. Disto-dorsal MCIII specimens were loaded to 30 MPa (n = 10), while disto-palmar MCIII (n = 10) and proximal sesamoid (n = 10) specimens were loaded to 40 MPa. Digital image correlation was performed on the first nine cycles to determine local strains. Specimens were stained with lead-uranyl acetate for volumetric microdamage quantification. Results: The dorsal MCIII SCB had lower BVTV, BMD, and stiffness compared to the palmar MCIII and sesamoid bone (P < 0.05). Superficial SCB had higher BVTV and lower BMD than deeper SCB (P < 0.05), except at the palmar MCIII site where there was no difference in BVTV between depths (P = 0.419). At all sites the deep bone was stiffer (P < 0.001), although the superficial to deep gradient was smaller in the dorsal MCIII. Hysteresis (energy loss) was greater superficially in palmar MCIII and sesamoid (P < 0.001), but not dorsal MCIII specimens (P = 0.118). Stiffness increased with cyclic loading in total cartilage-bone specimens (P < 0.001), but not in superficial and deep layers of the bone, whereas hysteresis decreased with cycle for all sites and layers (P < 0.001). Main limitations: Small sections of bone from each site were examined. Surface staining complicated volumetric microdamage quantification. Unconfined compression and end artefacts may have contributed to initial changes in stiffness and hysteresis. Conclusions: Superficial equine SCB is uniformly less stiff than deeper bone despite non uniform differences in bone density and damage levels. The more compliant superficial layer has an important role in energy dissipation, but whether this is a specific adaptation or a result of microdamage accumulation is not clear.
-
ItemResponse of subchondral bone and articular cartilage to joint surface incongruity: an equine osteochondral defect model( 2019)Many diseases and injuries of synovial joints result in a focal loss of articular surface congruity. These conditions are known to lead to degenerative changes within the affected joint and subsequent osteoarthritis (OA). Incongruity due to loss of articular cartilage is also a feature of OA itself. However there is little work specifically investigating how the tissues of a synovial joint respond to loss of congruity. The aim of this study was to observe how articular cartilage and subchondral bone (SCB) respond to a focal loss of surface congruity using an equine model. It was hypothesised that the degree of remodelling and bone volume of SCB is dependent on local loading of the overlying joint surface and that intact cartilage would respond to changes in local surface pressure in a way that attempts to restore congruity. An osteochondral defect was created in one surface of the midcarpal joint of six adult horses. Two weeks post-operatively the animals began an eight-week treadmill training program. Following this, osteochondral samples were collected from the site of the defect and immediately adjacent to it in the radial carpal bone (Cr), and from the unloaded site directly opposing the defect and a loaded site immediately adjacent to this in the third carpal bone (C3). Control samples were collected from equivalent sites in the sham-operated contralateral limb and from un-operated, untrained control animals. Undemineralised samples were imaged with microCT and backscattered scanning electron microscopy (BSEM) and stained with Masson’s Goldner trichrome to measure cartilage thickness and osteoid. Decalcified cryosections were stained for TRAP to identify osteoclasts. Cartilage was examined with routine histology and differential interference contrast microscopy. In SCB immediately below the Cr lesion in treated joints bone volume fraction (BV/TV) was 32% lower and bone formation and erosion were markedly increased, whereas in the deeper bone formation was increased, erosion activity became less prominent and BV/TV did not change. In the unloaded region of C3 opposing the defect in treated joints the hyaline cartilage (HC) was 50% thicker, while SCB displayed a mild increase in remodelling activity with a net decrease in BV/TV of 5.3%. In the loaded region adjacent to the lesion in Cr HC was 30% thinner in treated joints while there was no change in SCB parameters. At the loaded site of C3 the HC thickness was unchanged while the calcified cartilage in treated joints was 40% thicker than in controls. In the underlying SCB in treated joints there was a mild reduction in remodelling activity and unchanged BV/TV. In this equine osteochondral defect model the articular cartilage and SCB of adult synovial joints responded in a focal manner to changes in joint surface congruity. Local unloading due to a loss of surface contact resulted in thickened HC and, in the underlying SCB, increased remodelling activity and loss of bone volume. Focally increased loading resulted in thickened calcified cartilage and decreased SCB bone remodelling activity. These focal responses may play a role in normal joint homeostasis and in the pathogenesis of OA.