A Fibril Reinforced Poroelastic Model of Articular Cartilage Including Depth Dependent Material Properties

1999 ◽  
Author(s):  
L. P. Li ◽  
M. D. Buschmann ◽  
A. Shirazi-Adl

Abstract Articular cartilage is a highly nonhomogeneous, anisotropic and multiphase biomaterial consisting of mainly collagen fibrils, proteoglycans and water. Noncalcified cartilage is morphologically divided into three zones along the depth, i.e. superficial, transitional and radial zones. The thickness, density and alignment of collagen fibrils vary from the superficial zone, where fibrils are oriented parallel to the articular surface, to the radial zone where fibrils are perpendicular to the boundary between bone, and cartilage. The concentration of proteoglycans increases with the depth from the cartilage surface. These regional differences have significant implications to the mechanical function of joints, which is to be explored theoretically in the present work by considering inhomogeneity along the cartilage depth. A nonlinear fibril reinforced poroelastic model is employed as per Li et al. (1999) in which the collagen fibrils were modeled as a distinct constituent whose tensile stiffness was taken to be very high and be strain dependent but whose compressive stiffness was neglected.

Author(s):  
Janice H. Lai ◽  
Marc E. Levenston

The superficial zones of articular cartilage and meniscus are structurally distinct from the rest of the tissue. In cartilage, the superficial zone is characterized by a relatively low proteoglycan content and a relatively high content of fine collagen fibrils oriented parallel to the articular surface [1], resulting in a low compressive modulus at the surface [2, 3]. In meniscus, the superficial zone is characterized by a fine mesh of randomly oriented collagen fibrils [1] while the interior of the tissue consists of bundles of circumferentially oriented collagen I fibers surrounded by a secondary network containing multiple collagen types and proteoglycans [4]. As relatively little is known about the depth-varying mechanical properties of the meniscus, this study aimed to characterize the depth-dependent response of cartilage and meniscal tissue to compression by comparing the two-dimensional strain fields of site-matched tissue pairs.


Author(s):  
Onyi N. Irrechukwu ◽  
Marc E. Levenston

As articular cartilage is avascular, diffusion at a tissue length scale is the primary mode of solute and nutrient transport to its cells. The major extracellular matrix components are water (70–80%), chondrocytes, collagen (10–20%) and proteoglycans (5–10%) bearing sulfated glycosaminoglycans (GAG) [1]. Electron microscopy studies have shown that articular cartilage can be regarded as having three separate structural zones — superficial, middle and deep. The proportions of the various matrix components vary from the surface to the deep zone in any given joint and the greatest variations in content occur in the GAG content [2]. In addition the collagen fiber alignment varies, with fibers oriented parallel to the articular surface in the superficial zone, randomly oriented in the middle zone and oriented perpendicular to the surface in the deep zone. To a large extent, it is the spatially inhomogeneous composition of articular cartilage and microstructural orientation of its extracellular matrix components that determines the tortuosity of the transport pathway [3]. We therefore hypothesized that the diffusivity profile of a solute through the cartilage depth is inversely related to the GAG content and that the ratio between the axial and lateral diffusivities within each cartilage zone is related to the degree of anisotropy within the zone.


1986 ◽  
Vol 34 (5) ◽  
pp. 619-625 ◽  
Author(s):  
A R Poole ◽  
C Webber ◽  
I Pidoux ◽  
H Choi ◽  
L C Rosenberg

A monoclonal antibody to a core-protein-related epitope of a small dermatan sulfate-rich proteoglycan (DS-PGII) isolated from adult bovine articular cartilage (22) was used to localize this molecule, or molecules containing this epitope, in bovine articular cartilages, in cartilage growth plate, and in other connective tissues. Using an indirect method employing peroxidase-labeled pig anti-mouse immunoglobulin G, DS-PGII was shown to be present mainly in the superficial zone of adult articular condylar cartilage of the metacarpal-phalangeal joint. In fetal articular and epiphyseal cartilages, the molecule was uniformly distributed throughout the matrix. By approximately 10 months of age it was confined mainly to the superficial and middle zones of articular cartilage and the inter-territorial and pericellular matrix of the deep zone. DS-PGII was not detected in the primary growth plate of the fetus except in the proliferative zone, where it was sometimes present in trace amounts. In contrast, it was present throughout the adjacent matrix of developing epiphyseal cartilage. In the trabeculae of the metaphysis, strong staining for DS-PGII was seen in decalcified osteoid and bone immediately adjacent to osteoblasts. Staining was also observed on collagen fibrils in skin, tendon, and ligament and in the adventitia of the aorta and of smaller arterial vessels in the skin. These observations indicate that DS-PGII and/or molecules containing this epitope are widely distributed in collagenous tissues, where the molecule is intimately associated with collagen fibrils; in adult cartilage this association is limited mainly to the narrow parallel arrays of fibrils which are found in the superficial zone at the articular surface. From its intimate association and other studies, this molecule may play an important role in determining the sizes and tensile properties of collagen fibrils; it may also be involved in the calcification of osteoid but not of cartilage.


2009 ◽  
Vol 7 (47) ◽  
pp. 895-903 ◽  
Author(s):  
Sang-Kuy Han ◽  
Ruth Seerattan ◽  
Walter Herzog

The aims of this study were (i) to quantify chondrocyte mechanics in fully intact articular cartilage attached to its native bone and (ii) to compare the chondrocyte mechanics for cells in healthy and early osteoarthritis (OA) tissue. We hypothesized that cells in the healthy tissue would deform less for given articular surface pressures than cells in the early OA tissue because of a loss of matrix integrity in early OA and the associated loss of structural integrity that is thought to protect chondrocytes. Chondrocyte dynamics were quantified by measuring the deformation response of the cells to controlled loading of fully intact cartilage using a custom-designed confocal indentation system. Early OA was achieved nine weeks following transection of the anterior cruciate ligament (ACL) in rabbit knees. Experiments were performed on the retropatellar cartilage of early OA rabbit knees (four joints and 48 cells), the corresponding intact contralateral control knees (four joints and 48 cells) and knees from normal control rabbits (four joints and 48 cells). Nine weeks following ACL transection, articular cartilage of the experimental joints showed substantial increases in thickness, and progression towards OA as assessed using histological grading. Local matrix strains in the superficial zone were greater for the experimental (38 ± 4%) compared with the contralateral (27 ± 5%) and normal (28 ± 4%) joints ( p = 0.04). Chondrocyte deformations in the axial and depth directions were similar during indentation loading for all experimental groups. However, cell width increased more for the experimental cartilage chondrocytes (12 ± 1%) than the contralateral (6 ± 1%) and normal control chondrocytes (6 ± 1%; p < 0.001). On average, chondrocyte volume increased with indentation loading in the early OA cartilage (8 ± 3%, p = 0.001), while it decreased for the two control groups (−8 ± 2%, p = 0.002 for contralateral and −8 ± 1%, p = 0.004 for normal controls). We conclude from these results that our hypothesis of cell deformations in the early OA tissue was only partially supported: specifically, changes in chondrocyte mechanics in early OA were direction-specific with the primary axial deformations remaining unaffected despite vastly increased average axial matrix deformations. Surprisingly, chondrocyte deformations increased in early OA in specific transverse directions which have received little attention to date but might be crucial to chondrocyte signalling in early OA.


1984 ◽  
Vol 13 (3) ◽  
pp. 153-156 ◽  
Author(s):  
D W L Hukins ◽  
R M Aspden ◽  
Y E Yarker

The gel phase of articular cartilage is reinforced by collagen fibrils. These fibrils have low flexural and torsional stiffness, but are able to provide reinforcement if deformation of the tissue increases their tensile stress. An estimate suggests that the lengths of collagen fibrils in articular cartilage are at least of the same order as their critical length so that tensile stress in the tissue will increase the stress in the fibrils rather than simply pull them out of the gel. In the surface zone the collagen fibrils are oriented so that the efficiency of reinforcement, η, is about 0.6 tangential to the surface; tension in the fibrils is thus able to withstand swelling pressure within the tissue whose condition for stability resembles that of a pressure vessel. Swelling pressure allows the tissue to support applied pressure. An intermediate zone has a roughly isotropic η value of about 0.2, while in the deep zone collagen fibrils appear to tie the cartilage to the subchondral bone; in this deep zone η has a value of about 0.6 perpendicular to the surface direction. There is also some preferred orientation of collagen fibrils in the plane of the articular surface within the surface zone; in patellar cartilage the preferred orientations can be related to the direction of stress which could be generated by movement of the joint.


1980 ◽  
Vol 28 (7) ◽  
pp. 621-635 ◽  
Author(s):  
A R Poole ◽  
I Pidoux ◽  
A Reiner ◽  
L H Tang ◽  
H Choi ◽  
...  

Using monospecific antisera and immunofluorescence microscopy, proteoglycan monomer (PG), and link proteins were demonstrated throughout the extracellular matrix of bovine articular cartilage. A narrow band of strong pericellular staining was usually observed for both molecules, indicating a pericellular concentration of proteoglycan monomer: this conclusion was supported by dye-binding studies. Whereas PG was evenly distributed throughout the remaining matrix, more link protein was detectable in interterritorial sites in middle and deep zones. Well-defined zones of weaker territorial staining for link protein stained strongest for chondroitin sulfate. Trypsin treatment of cartilage resulted in a loss of most of the PG staining, but some selective retention of link protein, particularly around chondrocytes in the superficial zone at and near the articular surface. This residual staining was largely removed if sections were fixed after chondroitinase treatment. After extraction of cartilage with 4M guanidine hydrochloride, only PG remained and this was concentrated in the superficial zone. These observations are shown to support the concept of aggregation of PG and link protein with hyaluronic acid (HA) in cartilage matrix, and the binding of PG and link protein to HA, which is attached to the chondrocyte surface. Culture of cartilage depleted of PG and link protein by trypsin demonstrated that individual chondrocytes can secrete both PG and link proteins and that the organization of cartilage matrix can be regenerated in part over a period of 4 days.


2004 ◽  
Vol 08 (04) ◽  
pp. 167-179 ◽  
Author(s):  
J. P. Wu ◽  
T. B. Kirk ◽  
M. H. Zheng

The aim of this study is to investigate the structure and the collagen matrix of the superficial zone of articular cartilage using a 3D imaging technique. The split line thought to represent the orientation of the collagen fibres in the superficial zone was found using Hultkrantz's method. A semitransparent membrane was physically peeled off from the most superficial surface of bovine articular cartilage. Using fibre optic laser scanning confocal microscopy, the collagen matrix in normal cartilage, the membrane and the cartilage with the membrane peeled off were studied. The superficial zone was found to contain a more sophisticated 3D collagenous matrix than previously reported. The collagen matrix in the membrane consists of interwoven long collagen bundles, and the collagen fibres immediately subjacent to it align spatially in a predominantly oblique direction to the articular surface. The split line does not represent the orientation of the collagen in the membrane. This study presents a 3D visualization technique for a minimal-invasive examination of the 3D architecture of the collagen fibres in the superficial zone of articular cartilage, and offers a new insight into the 3D structure of the collagen matrix in the superficial zone of native cartilage.


2016 ◽  
Vol 113 (50) ◽  
pp. 14360-14365 ◽  
Author(s):  
Haoruo Jia ◽  
Xiaoyuan Ma ◽  
Wei Tong ◽  
Basak Doyran ◽  
Zeyang Sun ◽  
...  

Osteoarthritis (OA) is the most common joint disease, characterized by progressive destruction of the articular cartilage. The surface of joint cartilage is the first defensive and affected site of OA, but our knowledge of genesis and homeostasis of this superficial zone is scarce. EGFR signaling is important for tissue homeostasis. Immunostaining revealed that its activity is mostly dominant in the superficial layer of healthy cartilage but greatly diminished when OA initiates. To evaluate the role of EGFR signaling in the articular cartilage, we studied a cartilage-specific Egfr-deficient (CKO) mouse model (Col2-Cre EgfrWa5/flox). These mice developed early cartilage degeneration at 6 mo of age. By 2 mo of age, although their gross cartilage morphology appears normal, CKO mice had a drastically reduced number of superficial chondrocytes and decreased lubricant secretion at the surface. Using superficial chondrocyte and cartilage explant cultures, we demonstrated that EGFR signaling is critical for maintaining the number and properties of superficial chondrocytes, promoting chondrogenic proteoglycan 4 (Prg4) expression, and stimulating the lubrication function of the cartilage surface. In addition, EGFR deficiency greatly disorganized collagen fibrils in articular cartilage and strikingly reduced cartilage surface modulus. After surgical induction of OA at 3 mo of age, CKO mice quickly developed the most severe OA phenotype, including a complete loss of cartilage, extremely high surface modulus, subchondral bone plate thickening, and elevated joint pain. Taken together, our studies establish EGFR signaling as an important regulator of the superficial layer during articular cartilage development and OA initiation.


2020 ◽  
Vol 64 (3) ◽  
Author(s):  
Petra Rita Basso ◽  
Elena Carava' ◽  
Marina Protasoni ◽  
Marcella Reguzzoni ◽  
Mario Raspanti

The articular cartilage has been the subject of a huge amount of research carried out with a wide array of different techniques. Most of the existing morphological and ultrastructural data on the this tissue, however, were obtained either by light microscopy or by transmission electron microscopy. Both techniques rely on thin sections and neither allows a direct, face-on visualization of the free cartilage surface (synovial surface), which is the only portion subject to frictional as well as compressive forces. In the present research, high resolution visualization by scanning electron microscopy and by atomic force microscopy revealed that the collagen fibrils of the articular surface are exclusively represented by thin, uniform, parallel fibrils evocative of the heterotypic type IX-type II fibrils reported by other authors, immersed in an abundant matrix of glycoconjugates, in part regularly arranged in phase with the D-period of collagen. Electrophoresis of fluorophore-labeled saccharides confirmed that the superficial and the deeper layers are quite different in their glycoconjugate content as well, the deeper ones containing more sulfated, more acidic small proteoglycans bound to thicker, more heterogenous collagen fibrils. The differences found between the synovial surface and the deeper layers are consistent with the different mechanical stresses they must withstand.


2021 ◽  
Vol 9 (10_suppl5) ◽  
pp. 2325967121S0032
Author(s):  
Hailey Huddleston ◽  
Theodore Wolfson ◽  
David Christian ◽  
Nozomu Inoue ◽  
Adam Yanke

Objectives: Patellar osteochondral allograft (OA) transplantation has been shown to be a successful treatment in patients with isolated patellar cartilage injury. Currently, there is minimal guidance in anatomic and sizing factors that portend similar patellar surface topography. The most commonly utilized patellar sizing criteria to match the donor and recipient is radiographic tibial width. Our hypothesis is that specific patella anatomic factors will better predict surface topography matching. To our knowledge, no prior study has investigated the topography of the patella and what intrinsic factors of the graft and the recipient affect matching of the chondral and osseous layers between the graft and defect. Methods: Computed tomography (CT) images of the specimens were acquired and three-dimensional (3D) CT models of the patella were then created and exported into point-cloud models using a 3D reconstruction software program. Circular articular cartilage and subchondral bone defect models were created in each point-cloud model of the recipient patella with a diameter of 18 mm and 22.5 mm at 3 locations: the medial, central, and lateral portions of the patellar surface. Circular articular cartilage and subchondral bone graft models were created on all possible locations on the articular cartilage surface models of the donor patellae (Figure 1). The graft models were virtually placed on the surface of the defect model. Orientation of the graft model was adjusted so that its axis matched that of the defect site. Least distances between the graft and the defect articular surface models were calculated and were defined as the shortest distance from the point in question to the corresponding point in space. A mean value of the least distances was calculated for each position of the graft model. The mean least distance of subchondral bone surface in each point was calculated simultaneously. The graft model was then rotated 360° around the axis perpendicular to the articular cartilage surface in 1° increments, and the least distance of articular cartilage surface and the resulting least distance of subchondral bone surface were calculated at each rotating angle. This procedure was repeated for all points in the articular surface model of the donor patella. Step-off was then calculated as the least mean square difference between the defect and graft along the periphery. Stepwise linear regression was used for each defect location to analyze which variables predict degree of mismatch in millimeters. Results: A total of 16 patella were utilized in analysis. Comparison of cartilage least mean square distances between locations demonstrated that the lateral location had significantly less surface incongruity compared to the other two locations (vs medial: p = .0038, vs central: p = .0046). In addition, significant differences in subchondral bone distances were observed between the locations (lateral vs medial: p = .0007, lateral vs central: p < .0001, medial vs central: p < .0001) (Table 1). The associations of six anatomic and morphologic variables with cartilage mismatch, bone mismatch, and step-off for 18 mm and 22.5 mm defects are presented in Tables 2 and Table 3. All variables were analyzed as the difference in value between the recipient and donor. For both lesion sizes, cartilage step-off was the most susceptible to variable differences. Compared to the 18 mm defect group, the 22.5 mm defects were more affected (higher coefficients) by the same differences in variables. Differences in tibial width were associated mismatch for central lesions (eg. 22.5mm defect coefficient: -0.026, p < .001), while cartilage width was associated with mismatch for lateral lesions. (eg. 22.5 mm defect coefficient: -0.034, p < .023). Conclusions: Multiple clinically relevant factors were found to affect graft and defect chondral mismatch and to a lesser extent osseous mismatch. For all three locations at both defect sizes, step-off was the most susceptible to differences in patellar morphology between the donor and recipient. In addition, differences in tibial width, a commonly used metric for patellar graft matching, did not significantly predict chondral mismatch for lateral and medial sized lesions. These findings should be considered when selecting and preparing the graft in a patella osteochondral allograft procedure.


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