tion, with mechanical properties varying according to thedistance of the layer from the joint surface. The homeostasisbetween chondrocytes, water, collagen, ultrastructural archi-tecture, and proteoglycans dictates the tensile stiffness andstrengths of each zone. From the superficial to deep zones,sheer stress increases while tensile stiffness decreases. Thesuperficial zone contains chondrocytes that synthesize amatrix that has a high concentration of collagen and a lowconcentration of proteoglycan. The parallel arrangement of the collagen fibrils in this zone provides greater tensile stiff-ness and strength than in the deeper zones, and this may helpresist shear forces generated during use of the joint. The mid-dle (transition) zone has a morphologic and matrix compo-sition in between that of the superficial and deep zones andcomprises the largest part (40% to 60%) of the articular car-tilage. The deep (radial) zone has the largest-diameter colla-gen fibrils, the highest concentration of proteoglycans, andthe lowest concentration of water. The collagen fibrils passinto the tidemark, a thin basophilic line seen on lightmicroscopy sections of decalcified articular cartilage thatroughly corresponds to the boundary between calcified anduncalcified cartilage. Shear stresses are greatest at the tide-mark. A zone of calcified cartilage separates the radial zonefrom the subchondral bone. The cells of this zone have a verysmall volume and appear to be surrounded completely bycalcified cartilage. Recent work suggests that they may have arole in the development and progression of osteoarthrosis.
Biomechanics and Physiology
Articular cartilage exhibits a time-dependent behavior (vis-coelastic) when subjected to a constant load or constantdeformation. When a constant compressive stress (load/area)is applied to the tissue, its deformation will increase withtime, that is, it will creep until an equilibrium value isreached. Similarly, when the tissue is deformed and held at aconstant strain, the stress will rise to a peak, followed by aslow stress-relaxation process until an equilibrium value isreached. Two mechanisms are responsible for viscoelasticity:a flow-independent and a flow-dependent mechanism.During walking or running, articular cartilage is subjectedto compressive forces that rise to several times body weightwithin a very short period of time. Under this dynamic load-ing environment, interstitial fluid trapped within the carti-lage matrix enables the tissue to resist these high compressiveforces without mechanical damage. The instantaneousincreased hydrostatic pressure will be sustained within thetissue matrix for an extended period of time. When the inter-stitial fluid flows through the dense matrix, a frictional inter-action between the fluid and the matrix is created, providinga mechanism for energy dissipation. This phenomenon, theflow-dependent biphasic viscoelasticity of articular cartilage,provides additional protection of the tissue matrix frommechanical damage. Independent of the interstitial fluidflow, the proteoglycan molecules and the collagen fibersthemselves have shown significant viscoelastic characteris-tics. Thus, the cartilage matrix constitutes the intrinsic vis-coelasticity in shear deformation. This second phenomenonis called flow-independent intrinsic viscoelasticity, and hasbeen shown to significantly govern the short-term behaviorof articular cartilage immediately after a mechanical load isapplied to the tissue, such as in running or walking.Joint loading and motion are required to maintain normaladult articular cartilage. Immobilization of a joint will causea rapid loss of proteoglycans from the cartilage matrix.Proteoglycan content is affected to a greater extent than col-lagen composition. Because proteoglycan is lost, fluid fluxand deformation in response to compression will increase.Tensile properties, which depend primarily on collagen, aremaintained. These biochemical and biomechanical changesare, at least in part, reversible with the restoration of motion.The extent of recovery decreases with increasing periods of immobilization.Increased joint loading, either through excessive use orincreased magnitudes of loading, will also affect articular car-tilage. Disruption of the intra-articular structures, such asmenisci or ligaments, will alter forces acting on the articularsurface. In experimental animal models, responses to tran-section of the anterior cruciate ligament (ACL) or meniscec-tomy have included fibrillation of the cartilage surface,increased hydration, and changes in proteoglycan content.Significant and progressive decreases in the tensile and shearmodulus have been observed in response to transection of the ACL.While the overall metabolic activity of articular cartilage islow, the activity surrounding each individual chondrocyteand surrounding ECM is quite dynamic. This activity isdetermined by a cellular response to soluble mediators(nutrients, growth factors, cytokines), mechanical loads,matrix composition, hydrostatic pressure changes, and elec-tric fields. Growth factors, such as insulin-like growth factor-I and transforming growth factor-
), may stimulatematrix synthesis and cell proliferation. Chondrocytes synthe-size and release these growth factors, which further enhancethe metabolic activity of chondrocytes and matrix produc-tion. Matrix catabolism is mediated by enzymes, includingstromelysin, aggrecanase, and collagenase, which are regulat-ed in a complex manner by local factors such as interleukin-1 (IL-1), prostaglandins, TFG-
, tumor necrosis factor, andother molecules.The ECM is known to act as a signal transducer for the
4General KnowledgeAmerican Academy of Orthopaedic Surgeons
Orthopaedic Knowledge Update