Abstract:
This thesis presents an integrated body of research which investigates the responses of normal and
degenerate articular cartilage to compression. In the first research chapter, the first series of
experiments were performed on cartilage to measure the hydrostatic pore-pressure generated during
compressive loading, whilst the second series of experiments on cartilage-on-bone specimens were
manipulated through a combination of compressive loading followed by microscopic analysis.
The second research chapter sets out to examine how the articular surface and the matrix
interconnectivity can influence the microstructural response of normal and degenerate cartilage to
compression. The experiments performed in this work investigated how the normal intact articular
surface and the interconnectivity of the matrix can contribute towards stress redirection in normal
(surface intact), normal (surface removed) and degenerate matrices during indentation.
The final research chapter sets out to investigate how the osmotic environment can influence the
vulnerability of the matrix to surface rupture. Experiments were performed on cartilage-on-bone
samples that were soaked in varying bathing solutions (i.e. distilled water and 1.5 M saline) as it was
thought that this would be sufficient in modifying the osmotic environment within the tissues,
producing a maximum/minimum swollen state. Surface-intact, cartilage-on-bone specimens (i.e. from
normal and degenerate patellae were utilized in order to investigate the effect that both the osmotic
environment and general matrix destructuring had on surface rupture.
The investigations presented in this thesis were able to highlight the importance that the structural
integrity of the matrix has in altering the general response of cartilage to compression. Complete
removal of the articular surface, the progressive weakening/loss of an intact surface continuity, or even
the generalized destructuring of the matrix can alter the way in which cartilage responds to compressive
loading. The altered pattern of deformation can include: (i) elevated levels of peak hydrostatic pore
pressure generated in the matrix in response to compression; (ii) less of the applied load being
redirected into the wider cartilage continuum either through the articular surface or the general
interconnectivity of the matrix; (iii) elevated levels of matrix shear; and (iv) the increased vulnerability
of the intact, articular surface to rupture during compression.