The influence of the acetabular labrum on hip joint cartilage consolidation: a poroelastic finite element model
Introduction
The causes of osteoarthrosis (OA) in the hip are not fully understood, but it has been proposed that contributory factors are changes in the mechanical environment of the joint and changes to the mechanical properties of the articular cartilage (Mankin (1974a), Mankin (1974b); Mow et al., 1995; Poole, 1995). As any discussion of the nature and origin of OA should consider, among other factors, the function of the accessory structures of the joint (Gardner, 1983), one may speculate that an abnormal acetabular labrum may be implicated in the aetiology of joint degeneration. The acetabular labrum is a fibrocartilaginous lip with a tissue structure similar to the meniscus of the knee. The majority of the labrum is composed of thick, Type I collagen fibre bundles principally arranged parallel to the acetabular rim, with some fibres scattered throughout this layer running obliquely to the predominant fibre orientation (Shibutani, 1988). It is attached to the osseus margin of the acetabulum, deepening the acetabular socket and extending the coverage of the femoral head (Fig. 1). Several studies have shown that labrum excision or pathology of the intact labrum is associated with joint changes consistent with early OA (Gibson and Benson, 1982; Dorrell and Catterall, 1986; Altenberg, 1977; Harris et al., 1979; McCarthy and Busconi, 1995). Cartilage fibrillation has been observed directly adjacent to labrum defects in post-mortem hip joint specimens (Rushfeldt et al., 1981; Byers et al., 1970). While these simultaneous observations do not resolve the issue of cause and effect, Ikeda et al. (1988) postulated that tears in the labrum compromised the load-bearing and stability-enhancing function of the labrum.
The mechanical role of the labrum in normal hip function is not well understood. Several experimental studies have shown that the labrum can provide a seal against fluid flow in and out of the intra-articular space (Weber and Weber, 1837; Takechi et al., 1982; Terayama et al., 1980). Besides improving the stability of the joint through a vacuum effect, this possible sealing function of the labrum could enhance lubrication mechanisms in the hip joint. The ability of the labrum to contain a pressurised fluid layer within the hip joint under simple loading conditions was the focus of a previous study (Ferguson et al., 1999). This analysis demonstrated that the labrum could seal a fluid layer within the joint for a period of several minutes. This pressurised fluid layer prevented direct contact of the joint surfaces and distributed the applied load more evenly across the cartilage surfaces.
The labrum may play another role in normal hip joint function independent of its ability to seal the intra-articular space of the joint. With a relatively low permeability, the labrum may limit the rate of fluid expression from the cartilage layers during loading. McCutchen (1975) demonstrated, in an analytical model of joint contact, the ability of cartilage to carry loads through fluid pressurisation for extremely long periods of time, due to its mixed solid/fluid composition and the high resistance to flow of interstitial fluid out of the tissue. By slowing fluid expression from the cartilage layers, loads applied to the joint are carried by fluid pressure within the cartilage, limiting the magnitude of stresses within the collagenous solid matrix of the cartilage (Ateshian and Wang, 1995; Soltz and Ateshian, 1998). Fluid pressurisation in cartilage is not limited to short duration loading; interstitial fluid pressures in congruent joints could theoretically persist for hours. Using finite element models, others have demonstrated the importance of this fluid pressurisation mechanism in cartilage (Macirowski et al., 1994; van der Voet et al., 1993; Donzelli et al., 1997). Fluid pressurisation limits the magnitude of contact solid-on-solid stresses (i.e. the stress between contacting asperities of the mesh-like collagenous solid matrix), lessening friction at the cartilage surfaces (Macirowski et al., 1994; McCutchen, 1962; Wang et al., 1997). Failure of this mechanism could lead to increased friction and higher loading in the solid matrix of the cartilage surfaces, and eventually to the degenerative changes associated with OA.
Our hypothesis is that the labrum adds an important resistance in the flow path of fluid expressed from the cartilage layers, enhancing this protective mechanism for the tissue. The goal of this study was to develop a computer model to study the influence of the labrum on hip joint cartilage deformation, fluid pressures and solid stresses during extended loading periods.
Section snippets
Method
For this study, the commercial finite element software ABAQUS was chosen for its ability to simultaneously model contact mechanics and poroelastic (i.e. fluid-saturated porous elastic) materials (ABAQUS (1997a), ABAQUS (1997b)). A two-dimensional, plane-strain finite element model was developed. The model represents a coronal slice through the hip joint (Fig. 2). Representative hip joint geometry was based on average measurements from several clinical MRI data sets of non-symptomatic hip joints
Results
The results from this finite element analysis demonstrated the influence of the labrum on hip joint load transfer over an extended loading period. The changes which resulted from parametric variation of mechanial properties were small compared to the differences observed in the presence or absence of the labrum. Therefore, only the results of the model with a labrum and with baseline material properties were compared to those of the model without a labrum.
After imposition of the load, the femur
Discussion
The model predicted that the presence of the labrum limited the level of cartilage deformation and stress through a sealing mechanism. The labrum added an additional resistance in the flow path of fluid being expressed from the cartilage layers of the hip joint, enhancing the retention of interstitial fluid within the tissue. Since cartilage layers deform predominantly through changes in the tissue volume, and this occurs through fluid expression due to the assumed incompressible nature of its
Acknowledgements
This work was supported by a grant from the AO Foundation (Switzerland) and from the Natural Sciences and Engineering Research Council (Canada)
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