The effects of focal articular defects on intra-tissue strains in the surrounding and opposing cartilage.

Focal damage to articular cartilage is commonly found in symptomatic knees and may contribute to patient discomfort and progressive cartilage degeneration. The objective of this study was to quantify changes in cartilage intra-tissue strain and sliding occurring near a focal defect. Pairs of human osteochondral blocks were compressed by 20% of the total cartilage thicknesses, and tissue deformation was recorded by video microscopy. Then, a single, full-thickness defect was created in one block from each pair, blocks were allowed to re-swell, and the pairs were retested. Stained nuclei, acting as fiducial markers, were tracked by digital image correlation and used to calculate cartilage strains and surface displacement. With intact samples, axial strain decreased with depth, as is typical of cartilage, and relatively little sliding occurred between surfaces. With defect samples, axial compression of cartilage at the defect rim rose by approximately 30%, shear in the opposing tissue increased 10-fold to approximately 0.15, and local sliding was elevated to > 50 microm. In vivo, tissue near a defect likely experiences increased overall compression, magnifying these observed in vitro effects. Excessive strains may contribute to cell death, matrix damage, or accelerated wear, and repair efficacy may depend on the ability to alleviate adverse mechanical conditions.

Depth-varying density and organization of chondrocytes in immature and mature bovine articular cartilage assessed by 3d imaging and analysis.

Articular cartilage is a heterogeneous tissue, with cell density and organization varying with depth from the surface. The objectives of the present study were to establish a method for localizing individual cells in three-dimensional (3D) images of cartilage and quantifying depth-associated variation in cellularity and cell organization at different stages of growth. Accuracy of nucleus localization was high, with 99% sensitivity relative to manual localization. Cellularity (million cells per cm3) decreased from 290, 310, and 150 near the articular surface in fetal, calf, and adult samples, respectively, to 120, 110, and 50 at a depth of 1.0 mm. The distance/angle to the nearest neighboring cell was 7.9 microm/31 degrees , 7.1 microm/31 degrees , and 9.1 microm/31 degrees for cells at the articular surface of fetal, calf, and adult samples, respectively, and increased/decreased to 11.6 microm/31 degrees , 12.0 microm/30 degrees , and 19.2 microm/25 degrees at a depth of 0.7 mm. The methodologies described here may be useful for analyzing the 3D cellular organization of cartilage during growth, maturation, aging, degeneration, and regeneration.

Effect of a focal articular defect on cartilage deformation during patello-femoral articulation.

The objective of this study was to determine cartilage strains near, and in apposition to, a focal defect during patello-femoral articulation. Bovine osteochondral blocks from the trochlea (TRO) and patella (PAT) were apposed, compressed 12%, and subjected to sliding under video microscopy. Samples, lubricated with synovial fluid, were tested intact and then with a full-thickness defect in PAT cartilage. Shear (E(xz)), axial (E(zz)), and lateral (E(xx)) strains were determined locally for TRO and PAT cartilage. For articulation with a focal defect, the strain amplitudes of PAT cartilage near the surface were ∼2-8× lower in E(xz) and ∼1.4× higher in -E(zz) than intact PAT cartilage. At 20% depth, E(xz) and E(xx) for PAT cartilage with a focal defect were ∼2× and ∼10-25× higher than intact PAT, respectively. For TRO articulating against a focal defect, E(xz) and -E(zz) near the surface and at 20% depth were ∼2-4× lower than that for articulation against intact cartilage. The results elucidate dramatic region-specific changes in strain due to lateral motion. In these regions, such altered cartilage mechanics during knee movement may cause focal defects to extend by induction of damaging levels of strain to bordering regions of cartilage.

Mechanical asymmetry during articulation of tibial and femoral cartilages: local and overall compressive and shear deformation and properties.

During knee movement, femoral cartilage articulates against cartilage from the tibial plateau, and the resulting mechanical behavior is yet to be fully characterized. The objectives of this study were to determine (1) the overall and depth-varying axial and shear strains and (2) the associated moduli, of femoral and tibial cartilages during the compression and shearing of apposing tibial and femoral samples. Osteochondral blocks from human femoral condyles (FCs) characterized as normal and donor-matched lateral tibial plateau (TP) were apposed, compressed 13%, and subjected to relative lateral motion. When surfaces began to slide, axial (-E(zz)) and shear (E(xz)) strains and compressive (E) and shear (G) moduli, overall and as a function of depth, were determined for femoral and tibial cartilages. Tibial -E(zz) was approximately 2-fold greater than FC -E(zz) near the surface (0.38 versus 0.22) and overall (0.16 versus 0.07). Near the surface, E(xz) of TP was 8-fold higher than that of FC (0.41 versus 0.05), while overall E(xz) was 4-fold higher (0.09 versus 0.02). For TP and FC, -E(zz) and E(xz) were greatest near the surface and decreased monotonically with depth. E for FC was 1.7-fold greater than TP, both near the surface (0.40 versus 0.24MPa) and overall (0.76 versus 0.47MPa). Similarly, G was 7-fold greater for FC (0.22MPa) than TP near the surface (0.03MPa) and 3-fold higher for FC (0.38MPa) than TP (0.13MPa) overall. These results indicate that tibial cartilage deforms and strains more axially and in shear than the apposing femoral cartilage during tibial-femoral articulation, reflecting their respective moduli.

Macroscopic assessment of cartilage shear: effects of counter-surface roughness, synovial fluid lubricant, and compression offset.

During joint articulation, cartilage is subjected to compression, shear, and sliding, mechanical factors that regulate and affect cartilage metabolism. The objective of this study was to use an in vitro material-on-cartilage shear test to elucidate the effects of counter-surface roughness (Polished, Mildly rough, and Rough), lubricants (phosphate buffered saline (PBS) and bovine synovial fluid (bSF)), and compression offset on the shearing and sliding of normal human talar cartilage under dynamic lateral displacement. Peak shear stress (sigma(xz,m)) and strain (E(xz,m)) increased with increasing platen roughness and compression offset, and were 30% higher with PBS than with bSF. Compared to PBS, bSF was more effective as a lubricant for P than for M and R platens as indicated by the higher reduction in kinetic friction coefficient (-60% vs. -20% and -19%, respectively), sigma(xz,m) (-50% vs. -14% and -17%) and E(xz,m) (-54% vs. -19% and -17%). Cartilage shear and sliding were evident for all counter-surfaces either at low compression offset (10%) or with high lateral displacement (70%), regardless of lubricant. An increase in tissue shear occurred with either increased compression offset or increased surface roughness. This material and biomechanical test system allow control of cartilage sigma(xz,m) and E(xz,m), and hence, sliding magnitude, for an imposed lateral displacement. It therefore can facilitate study of cartilage mechanobiological responses to distinct regimes of cartilage loading and articulation, such as shear with variable amounts of sliding.

The effects of focal articular defects on cartilage contact mechanics.

Focal damage to articular cartilage is common in arthroscopy patients, and may contribute to progressive tissue degeneration by altering the local mechanical environment. The effects of a focal defect, which may be oriented at various orientations relative to the subchondral bone, on the dynamics of cartilage contact and deformation are unclear. The objective of this study was to elucidate the effect of experimental full thickness focal defects, oriented at 80 degrees or 100 degrees relative to the subchondral bone, on intratissue strain and surface sliding of opposing cartilage surfaces during compression and stress relaxation. Pairs of intact bovine osteochondral blocks were compressed uniaxially by 20%, and allowed to stress relax. Tissue deformation was recorded by video microscopy. A full-thickness defect (with either 80 degrees or 100 degrees edges) was created in one block from each pair. Blocks were allowed to reswell and retested. Defect edges were then recut with the opposite orientation, allowed to reswell, and retested again. Stained nuclei were tracked by digital image correlation and used to quantify cartilage strains and surface sliding. The results indicated that loading of intact samples caused axial strain magnitudes that decreased with depth and relatively little sliding. With loading of samples containing defects, strain magnitudes were elevated in cartilage adjacent to, and opposing, defects. For samples with edge orientations of 100 degrees, sliding magnitudes were increased over surfaces adjacent to defects. These local mechanical changes due to full-thickness articular cartilage defects may contribute to altered chondrocyte metabolism, tissue damage, or accelerated wear.

Shear deformation kinematics during cartilage articulation: effect of lubrication, degeneration, and stress relaxation.

During joint articulation, the biomechanical behavior of cartilage not only facilitates load-bearing and low-friction, but also provides regulatory cues to chondrocytes. Elucidation of cartilage kinematics under combined compression and shearing conditions clarifies these cues in health and disease. The objectives of this study were to elucidate the effects of lubricant, tissue degeneration, and stress relaxation duration on cartilage shear kinematics during articulation. Human osteochondral cores with normal and mildly degenerate surface structures were isolated. Paired blocks from each core were apposed, compressed, allowed to stress relax for 5 or 60 min, and shear tested with a micro-scale video microscopy system using phosphate-buffered saline (PBS) or synovial fluid as lubricant. During applied lateral motion, local and overall shear strain (Exz) of articular cartilage were determined. The applied lateral displacement at which Exz reached 50% of the peak (Deltax(1/2)) was also determined. Quantitatively, surface Exz increased at the onset of lateral motion and peaked just as surfaces detached and slid. With continued lateral motion, surface Exz was maintained. After short stress relaxation, effects of lubrication on Exz and Deltax(1/2) were not apparent. With prolonged stress relaxation, Exz and Deltax(1/2) near the articular surface increased markedly when PBS was used as lubricant. Similar patterns were observed for overall Exz and Deltax(1/2). With degeneration, surface Exz was consistently higher for all cases after the onset of lateral motion. Thus, cartilage shear kinematics is markedly affected by lubricant, cartilage degeneration, and loading duration. Changes in these factors may be involved in the pathogenesis of osteoarthritis.

Biomechanics of cartilage articulation: effects of lubrication and degeneration on shear deformation.

OBJECTIVE: To characterize cartilage shear strain during articulation, and the effects of lubrication and degeneration. METHODS: Human osteochondral cores from lateral femoral condyles, characterized as normal or mildly degenerated based on surface structure, were selected. Under video microscopy, pairs of osteochondral blocks from each core were apposed, compressed 15%, and subjected to relative lateral motion with synovial fluid (SF) or phosphate buffered saline (PBS) as lubricant. When cartilage surfaces began to slide steadily, shear strain (Exz) and modulus (G) overall in the full tissue thickness and also as a function of depth from the surface were determined. RESULTS: In normal tissue with SF as lubricant, Exz was highest (0.056) near the articular surface and diminished monotonically with depth, with an overall average Exz of 0.028. In degenerated cartilage with SF as lubricant, Exz near the surface (0.28) was 5-fold that of normal cartilage and localized there, with an overall E(xz) of 0.041. With PBS as lubricant, Exz values near the articular surface were approximately 50% higher than those observed with SF, and overall Exz was 0.045 and 0.062 in normal and degenerated tissue, respectively. Near the articular surface, G was lower with degeneration (0.06 MPa, versus 0.18 MPa in normal cartilage). In both normal and degenerated cartilage, G increased with tissue depth to 3-4 MPa, with an overall G of 0.26-0.32 MPa. CONCLUSION: During articulation, peak cartilage shear is highest near the articular surface and decreases markedly with depth. With degeneration and diminished lubrication, the markedly increased cartilage shear near the articular surface may contribute to progressive cartilage deterioration and osteoarthritis.