The clinical association between meniscectomy and osteoarthritis has been well established; however the connection between the biomechanics and subsequent cartilage degeneration has not been thoroughly explained. The objective of this dissertation was to study how the biomechanics of meniscectomy leads to degenerative changes in articular cartilage with osteoarthritis. The sheep knee was used as a platform since meniscectomy-induced osteoarthritis is an extensively studied in vivo model of osteoarthritis in humans.
Changes in contact mechanics after meniscectomy were examined in cadaveric sheep knees. Decreased contact area and increased mean and peak contact pressures were determined. Patterns of contact pressure confirmed a loss of load peripherally and a concentration of load centrally. The biomechanical benefit of partial meniscectomy for limited, but not extensive, horizontal tears was demonstrated. The changes in contact mechanics compared well with other in vitro systems and provided a basis for validation of subsequent numerical models.
Changes in cartilage mechanics after meniscectomy were evaluated through image-based FEA of a cyclically loaded sheep knee. The tissue-level cartilage mechanics underlying observed patterns of deformation were determined. A novel modeling methodology, using a contacting indenter, was developed to reproduce the transition from a reference to a deformed configuration known from image data. Central consolidation seen in MRI corresponded to increased fluid pressure, fluid exudation, loss of fluid load support, and increased tensile strains. Decreases in peripheral consolidation corresponded to reduced contact and fluid pressure.
Articular cartilage mechanics were determined before and after meniscectomy with image-based FEA. Cartilage mechanics were correlated to patterns of biochemical and biomechanical results from a published in vivo model of meniscectomy-induced osteoarthritis. A high number of mechanical/biological correlations in intact knees indicated that articular cartilage structure and composition are finely tuned to the local mechanical environment. After meniscectomy, few correlations existed, indicating the cartilage could not remodel or adapt to a change in mechanical loading as dramatic as meniscectomy.
Finally, the properties of the meniscus important for fluid flow distribution and fluid load support in the articular cartilage were examined. We hypothesized that the low permeability of the meniscus and labrum was important for maintaining fluid pressure and minimizing fluid efflux in the knee and hip, and that changes in fluid pressure and fluid flow after removal of the meniscus and labrum are related to observed patterns of osteoarthritis development. FE models were analyzed for an idealized knee and hip. The meniscus maintained fluid pressure and flow in knee articular cartilage, and similar effects were seen with the labrum in the hip. The low permeability of fibrocartilage was found important in limiting joint consolidation.
The mechanical etiology of osteoarthritis was found in three pathways: 1) loss of cyclic fluid pressure in the joint periphery, initiating endochondral ossification, leading to cartilage thinning; 2) increased shear loading and fluid exudation centrally, leading to loss of proteoglycan content and collagen network integrity, potentially by altering chondrocyte metabolism; and 3) strains exceeding failure limits and reduced fluid load support at the location of joint contact, causing surface damage in the collagen fibril network, leading to fibrillation of the articular surface. Low permeability of the meniscus was required for cartilage load support and maintaining patterns of fluid pressurization and flow.
This understanding will benefit the engineering of cartilage constructs, meniscal repair or replacement techniques, and rehabilitation strategies.
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