The effects of a subchondral bone perforation on the load support mechanism within articular cartilage

Abstract

Impact loading of diarthrodial joints of skeletally mature animals can crack the zone of calcified cartilage and subchondral bone (ZCC-SB), often without immediate disruption to the joint surface. A common sequelae to transarticular impact is the development of osteoarthritis (OA) in the traumatized joint. An understanding of how and why damage to cartilage occurs and progresses in deep regions of cartilage would therefore increase our understanding of the etiology of this type of traumatic OA. In this study, a 2D linear biphasic finite element analysis was performed to determine articular cartilage deformations, and interstitial fluid flow and pressurization, under both uniform and non-uniform hydrodynamic pressure distributions. The crack in the ZCC-SB was modelled by a “moderate-size” perforation at which there is no load support or fluid pressurization (i.e. a free surface under a free-draining condition). The effects of such a defect on the cartilage solid matrix stresses and strains, and interstitial fluid flows and pressures have been calculated. Results show that in normal cartilage, consistent with our previous contact analysis (G.A. Ateshian, W.M. Lai, W.B. Zhu and V.C. Mow, A biphasic model for contact in diarthrodial joints, Adv. Bioeng., ASME, 22 (1992) 191–194), interstitial fluid pressurization plays a dominant role in providing support when cartilage is loaded. Hence, normally, the solid matrix of cartilage is shielded from the high stresses of joint loading. In cartilage with a perforation in the ZCC-SB, however, the solid matrix stresses and strains are significantly increased as a consequence of a diminished fluid pressurization in the region of the defect. Thus, to maintain local equilibrium, there is a transfer of internal load support from interstitial fluid pressure to solid matrix stress defeating the normal stress-shielding effect. This stress transfer suggests a mechanism for progressive solid matrix damage, thus increasing the likelihood of cartilage failure following a single episode of impact.