Role of cartilage collagen fibrils networks in knee joint biomechanics under compression

Collagen fibrils networks in knee cartilage and menisci change in content and structure from a region to another. While resisting tension, they influence global joint response as well as local strains particularly at short-term periods. To investigate the role of fibrils networks in knee joint mechanics and in particular cartilage response, a novel model of the knee joint is developed that incorporates the cartilage and meniscus fibrils networks as well as depth-dependent properties in cartilage. The joint response under up to 2000 N compression is investigated for conditions simulating the absence in cartilage of deep fibrils normal to subchondral bone or superficial fibrils parallel to surface as well as localized split of cartilage at subchondral junction or localized damage to superficial fibrils at loaded areas. Deep vertical fibrils network in cartilage play a crucial role in stiffening (by 10%) global response and protecting cartilage by reducing large strains (from maximum of 102% to 38%), in particular at subchondral junction. Superficial horizontal fibrils protect the tissue mainly from excessive strains at superficial layers (from 27% to 8%). Local cartilage split at base disrupts the normal function of vertical fibrils at the affected areas resulting in higher strains.Deep fibrils, and to a lesser extent superficial fibrils, play dominant mechanical roles in cartilage response under transient compression. Any treatment modality attempting to repair or regenerate cartilage defects involving partial or full thickness osteochondral grafts should account for the crucial role of collagen fibrils networks and the demanding mechanical environment of the tissue.     

Effect of superficial collagen patterns and fibrillation of femoral articular cartilage on knee joint mechanics-a 3D finite element analysis

Collagen fibrils of articular cartilage have specific depth-dependent orientations and the fibrils bend in the cartilage surface to exhibit split-lines. Fibrillation of superficial collagen takes place in osteoarthritis. We aimed to investigate the effect of superficial collagen fibril patterns and collagen fibrillation of cartilage on stresses and strains within a knee joint. A 3D finite element model of a knee joint with cartilage and menisci was constructed based on magnetic resonance imaging. The fibril-reinforced poroviscoelastic material properties with depth-dependent collagen orientations and split-line patterns were included in the model. The effects of joint loading on stresses and strains in cartilage with various split-line patterns and medial collagen fibrillation were simulated under axial impact loading of 1000 N. In the model, the collagen fibrils resisted strains along the split-line directions. This increased also stresses along the split-lines. On the contrary, contact and pore pressures were not affected by split-line patterns. Simulated medial osteoarthritis increased tissue strains in both medial and lateral femoral condyles, and contact and pore pressures in the lateral femoral condyle. This study highlights the importance of the collagen fibril organization, especially that indicated by split-line patterns, for the weight-bearing properties of articular cartilage. Osteoarthritic changes of cartilage in the medial femoral condyle created a possible failure point in the lateral femoral condyle. This study provides further evidence on the importance of the collagen fibril organization for the optimal function of articular cartilage.     

Chondrocyte damage and contact pressures following impact on the rabbit tibiofemoral joint

Epidemiological studies show that tibial plateau fractures comprise about 10% of all below-knee injuries in car crashes. Studies from this laboratory document that impacts to the tibiofemoral (TF) joint at 50% of the energy producing gross fracture can generate cartilage damage and microcracks at the interface between calcified cartilage and underlying subchondral bone in the tibial plateau. These injuries are suggestive of the initiation for a long term chronic disease, such as osteoarthritis. The disease process may be further encouraged by acute damage to chondrocytes in the cartilage overlying areas of occult microcracking. The hypothesis of the current study was that significant damage to chondrocytes in tibial plateau cartilage could be generated in areas of high contact pressure by a single impact delivered to the rabbit TF joint, without a gross fracture of bone. Three rabbits received a single, 13 J of energy blunt insult to the TF joint, while another three animals were used as controls. Cell viability analyses compared chondrocyte damage in impacted versus control cartilage. Two additional rabbits were impacted to document contact pressures generated in the TF joint. The study showed high contact pressures in uncovered areas of the plateau, with a trend for higher pressures in the lateral versus medial facets. A significantly higher percentage of damaged chondrocytes existed in impacted versus the opposite, nonimpacted limbs. Additionally, more chondrocyte damage was documented in the superficial zone (top 20% of cartilage thickness) of the cartilage compared to middle (middle 50% of thickness) and deep (bottom 30% of thickness) zones. This study showed that a single blunt insult to the in situ rabbit TF joint, generating large areas of contact pressure exceeding 20 MPa, produces significant chondrocyte damage in the tibial articular cartilage, especially in the superficial zone, without gross fracture of bone. Future studies will be needed to investigate the long term, chronic outcome of this blunt force joint trauma.     

Regional differences of tibial and femoral cartilage in the chondrocyte gene expression,immunhistochemistry and composite in different stages of osteoarthritis

The function of articular cartilage as an avascular tissue is mainly served by collagen type II and proteoglycan molecules. Within this matrix homeostasis between production and breakdown of the matrix is exceptionally sensitive.The current study was conducted to identify regional differences in specific alterations in cartilage composition during the osteoarthritic process of the human knee joint. Therefor the changes in the expression of the key molecules of the extracellular matrix were measured in dependence of the anatomical side (femoral vs tibial) and associated with immunohistochemistry and quantitative measurement.60 serial osteochondral femoral condyle and the tibial plateau samples of patients undergoing implantation of total knee endoprosthesis of areas showing mild (Group A, macroscopically ICRS grade 1b) respectively advanced (Group B, macroscopically ICRS grade 3a/3b) (30 each) osteoarthritis according to the histological-histochemical grading system (HHGS) were compared with 20 healthy biopsies with immunohistochemistry and histology. We quantified our results on the gene expression of collagen type I and II and aggrecan with the help of real-time (RT)-PCR. Proteoglycan content was measured colorometrically.In group A slightly increased colour intensity was found for collagen II in deeper layers, suggesting a persisting but initially still intact repair process. But especially on the medial tibia plateau the initial Col II increase in gene expression is followed by a decrease leading to the lowest over all Col II expression on the medial plateau, here especially in the central part. There in late stage diseases the collagen type I expression was also more pronounced. Markedly decreased safranin O staining intensity was observed in the radial zone and less reduced intensity in the transitional zone with loss of zonal anatomy in 40% of the specimens in group A and all specimens in group B. Correlation between colorometrically analysed proteoglycan GAG content and aggrecan Real Time PCR is mainly weak.Tibial and femoral cartilage in contrast to patellar cartilage both are preferential exposed to compressive stresses, but presence of menisci affects the load distribution at the tibial side, which creates varying conditions for the different cartilage surfaces in the knee.As directly measured Poissońs ratio in tibial cartilage is higher but Youn?s modulus is lower than in femoral cartilage, different resulting feedback amplification loops interact with proceeding cartilage damage. The initial loss of aggrecan may support Matrix metalloproteinases (Mmps) in the access to the collagen network and the considerably differing mechanical properties at both joint surfaces result in varying increased synthesis and release of matrix degrading enzymes.The present study has identified a selection of events which reflect the response of cartilage structure and composite, chondrocytes itself and their productivity to changes in mechanical stress depending on the anatomical site.     

Tibiofemoral joint contact force in deep knee flexion and its consideration in knee osteoarthritis and joint replacement

The aim of the study was to estimate the tibiofemoral joint force in deep flexion to consider how the mechanical load affects the knee. We hypothesize that the joint force should not become sufficiently large to damage the joint under normal contact area, but should become deleterious to the joint under the limited contact area. Sixteen healthy knees were analyzed using a motion capture system, a force plate, a surface electromyography, and a knee model, and then tibiofemoral joint contact forces were calculated. Also, a contact stress simulation using the contact areas from the literature was performed. The peak joint contact forces (M +/- SD) were 4566 +/- 1932 N at 140 degrees in rising from full squat and 4479 +/- 1478 N at 90 degrees in rising from kneeling. Under normal contact area, the tibiofemoral contact stresses in deep flexion were less than 5 MPa and did not exceed the stress to damage the cartilage. The contact stress simulation suggests that knee prosthesis having the contact area smaller than 200 mm2 may be problematic since the contact stress in deep flexion would become larger than 21 MPa, and it would lead damage or wear of the polyethylene.     

Pathways of load-induced cartilage damage causing cartilage degeneration in the knee after meniscectomy

Results of both clinical and animal studies show that meniscectomy often leads to osteoarthritic degenerative changes in articular cartilage. It is generally assumed that this process of cartilage degeneration is due to changes in mechanical loading after meniscectomy. It is, however, not known why and where this cartilage degeneration starts. Load induced cartilage damage is characterized as either type (1)--damage without disruption of the underlying bone or calcified cartilage layer--or type (2), subchondral fracture with or without damage to the overlying cartilage. We asked the question whether cartilage degeneration after meniscectomy is likely to be initiated by type (1) and/or type (2) cartilage damage. To investigate that we applied an axisymmetric biphasic finite element analysis model of the knee joint. In this model the articular cartilage layers of the tibial and the femoral condyles, the meniscus and the bone underlying the articular cartilage of the tibia plateau were included. The model was validated with data from clinical studies, in which the effects of meniscectomy on contact areas and pressures were measured. It was found that both the maximal values and the distributions of the shear stress in the articular cartilage changed after meniscectomy, and that these changes could lead to both type (1) and type (2) cartilage damage. Hence it likely that the cartilage degeneration seen after meniscectomy is initiated by both type (1) and type (2) cartilage damage.     

Three dimensional patient-specific collagen architecture modulates cartilage responses in the knee joint during gait

Site-specific variation of collagen fibril orientations can affect cartilage stresses in knee joints. However, this has not been confirmed by 3-D analyses. Therefore, we present a novel method for evaluation of the effect of patient-specific collagen architecture on time-dependent mechanical responses of knee joint cartilage during gait. 3-D finite element (FE) models of a human knee joint were created with the collagen architectures obtained from T₂ mapped MRI (patient-specific model) and from literature (literature model). The effect of accuracy of the implementation of collagen fibril architecture into the model was examined by using a submodel with denser FE mesh. Compared to the literature model, fibril strains and maximum principal stresses were reduced especially in the superficial/middle regions of medial tibial cartilage in the patient-specific model after the loading response of gait (up to ?413 and ?26%, respectively). Compared to the more coarsely meshed joint model, the patient-specific submodel demonstrated similar strain and stress distributions but increased values particularly in the superficial cartilage regions (especially stresses increased >60%). The results demonstrate that implementation of subject-specific collagen architecture of cartilage in 3-D modulates location- and time-dependent mechanical responses of human knee joint cartilage. Submodeling with more accurate implementation of collagen fibril architecture alters cartilage stresses particularly in the superficial/middle tissue.     

A dynamic finite element analysis of impulsive loading of the extension-splinted rabbit knee

A dynamic nonlinear finite element model was developed to study juxtarticular stresses in the splinted rabbit knee, an established laboratory model for creating osteoarthrosis due to impulsive loading. Plane strain finite element results were validated by comparison with corresponding experimental data. Parametric effects studied included the input tibial displacement speed, the local bone density distribution, and the modulus of cartilage and subchondral bone. While the computed resultant contact force magnitude was sensitive to a number of model parameters, the stress patterns, when normalized to a given resultant force magnitude, were not. Despite comparable force peaks, the finite element results showed approximately six-fold higher effective strain rate levels for a severely impulsive loading protocol known to induce rapid osteoarthrosis, versus those for a mildly impulsive loading protocol not usually associated with cartilage damage. A propensity for elevated shear in the deep cartilage layer near the contact periphery, observed in nearly all computed stress distributions, is consistent with previous experimental findings of fissuring at that level in the impulsively loaded rabbit knee.     

Effects of joint unloading and reloading on human cartilage morphology and function, muscle cross-sectional areas, and bone density - a quantitative case report

Recent studies have shown that thinning of human cartilage occurs with unloading, but no data are available on the effect of remobilization (after immobilization) on knee joint cartilage status in humans. We examined a 36-year-old patient after 6 weeks of unilateral immobilization. Knee joint cartilage morphology (patella and tibia), patellar cartilage deformation, and thigh muscle cross-sectional areas were assessed with quantitative MR imaging and bone density with peripheral quantitative computed tomography (pQCT) during 24 months of remobilization. The immobilized limb displayed lower muscle cross-sectional areas (MCSA) of the knee extensors (-36%), lower bone density of the femur and tibia (-12/-6%), lower patellar cartilage thickness (-14%), but no side differences of tibial cartilage thickness. During remobilization, side differences decreased to -4% for knee extensor MCSAs, to -6%/-3% for femoral and tibial BMD, and to -8% for patellar cartilage thickness. No change was observed in tibial cartilage. Patellar deformation decreased from 9% to 4% after 15 months. In conclusion, we observed substantial changes of thigh MCSAs, but little (patella) to no (tibia) change in cartilage thickness during remobilization. These preliminary results indicate that human cartilage macro-morphology may be less adaptive to variations of the mechanical loading than muscle and bone.     

Stress distribution and consolidation in cartilage constituents is influenced by cyclic loading and osteoarthritic degeneration

The understanding of load support mechanisms in cartilage has evolved with computational models that better mimic the tissue ultrastructure. Fibril-reinforced poroelastic models can reproduce cartilage behaviour in a variety of test conditions and can be used to model tissue anisotropy as well as assess stress and pressure partitioning to the tissue constituents. The goal of this study was to examine the stress distribution in the fibrillar and non-fibrillar solid phase and pressure in the fluid phase of cartilage in axisymmetric models of a healthy and osteoarthritic hip joint. Material properties, based on values from the literature, were assigned to the fibrillar and poroelastic components of cartilage and cancellous and subchondral compact bone regions. A cyclic load representing walking was applied for 25 cycles. Contact stresses in the fibrillar and non-fibrillar solid phase supported less than 1% of the contact force and increased only minimally with load cycles. Simulated proteoglycan depletion increased stresses in the radial and tangential collagen fibrils, whereas fibrillation of the tangential fibrils resulted in increased compressive stress in the non-fibrillar component and tensile stress in the radial fibrils. However neither had an effect on fluid pressure. Subchondral sclerosis was found to have the largest effect, resulting in increased fluid pressure, non-fibrillar compressive stress, tangential fibril stress and greater cartilage consolidation. Subchondral bone stiffening may play an important role in the degenerative cascade and may adversely affect tissue repair and regeneration treatments.     

Articular cartilage in the knee joint of the African elephant, Loxodonta africana, Blumenbach 1797

Knee joints of one adult and three juvenile African elephants were dissected. The specific features of the articular cartilage with particular reference to matrix components were studied by light and electron microscopy and immunohistochemistry. The elephant knee joint cartilage contains an unusually low concentration of proteoglycans resulting in rather eosinophilic staining properties of the matrix. The very thick collagen fibers of the cartilage possibly represent collagen I. Except for the different thickness of cartilage at the weight-bearing surfaces of femur (approximately 6.7 mm) and tibia (approximately 11.2 mm) in juvenile elephants, light and electron microscopy did not reveal distinct topographical differences in cartilage structure, perhaps because of the high congruency of the articulating surfaces and resulting uniform load distribution in the knee. The number of cell profiles per section area of both femoral (approximately 950 cell profiles/mm(2)) and tibial cartilage (approximately 898 cell profiles/mm(2)) was low, indicating excessive matrix production by the chondrocytes during cartilage development. These unique properties could be a result of the enormous compressive load resting on the elephant knee. Maintenance of the equilibrium between biological function and resistance to compression seems to be crucial in the elephant knee joint cartilage. Any disturbance that interferes with this equilibrium appears to lead to arthrotic alterations, as particularly seen in captive elephants.     

Chronic changes in the rabbit tibial plateau following blunt trauma to the tibiofemoral joint

The knee is often a site of injury that can often lead to a chronic disease known as osteoarthritis (OA). The disease may be initiated, in part, by acute injuries to joint cartilage and its cells. In a recent study by this laboratory, using Flemish Giant rabbits, an impact compressive load on the tibial femoral joint was shown to cause significant levels of acute damage to chondrocytes in cartilage of the medial and lateral tibial plateaus. In the current study, using the same model, histological and mechanical data from the plateaus were documented at 6 and 12 months post impact, and compared to the unimpacted control limbs and a limb from unimpacted, control animals. The mechanical properties of cartilage were measured with indentation relaxation tests on the medial and lateral plateaus in regions covered and uncovered by the meniscus. The histological studies on impacted limbs showed surface lesions on both plateaus, thickening of the underlying subchondral bone at 12 months and numerous occult microcracks at the calcified cartilage–subchondral bone interface at 6 and 12 months, without significant changes in cartilage thickness or its mechanical properties versus controls. Yet, there was an increase in both the matrix and fiber moduli and a decrease in the permeability of uncovered, medial plateau cartilage in both limbs of impacted animals between 6 and 12 months post impact that was not documented in control animals.     

Depth-dependent analysis of the role of collagen fibrils, fixed charges and fluid in the pericellular matrix of articular cartilage on chondrocyte mechanics

The pericellular matrix of articular cartilage has been shown to regulate the mechanical environment of chondrocytes. However, little is known about the mechanical role of collagen fibrils in the pericellular matrix, and how fibrils might help modulate strains acting on chondrocytes when cartilage is loaded. The primary objective was to clarify the effect of pericellular collagen fibrils on cell volume changes and strains during cartilage loading. Secondary objectives were to investigate the effects of pericellular fixed charges and fluid on cell responses. A microstructural model of articular cartilage, in which chondrocytes and pericellular matrices were represented with depth-dependent structural and morphological properties, was created. The extracellular matrix and pericellular matrices were modeled as fibril-reinforced, biphasic materials with swelling capabilities, while chondrocytes were assumed to be isotropic and biphasic with swelling properties. Collagen fibrils in the extracellular matrix were represented with an arcade-like architecture, whereas pericellular fibrils were assumed to run tangential to the cell surface. In the early stages of a stress-relaxation test, pericellular fibrils were found to sensitively affect cell volume changes, even producing a reversal from increasing to decreasing cell volume with increasing fibril stiffness in the superficial zone. Consequently, steady-state volume of the superficial zone cell decreased with increasing pericellular fibril stiffness. Volume changes in the middle and deep zone chondrocytes were smaller and opposite to those observed in the superficial zone chondrocyte. An increase in the pericellular fixed charge density reduced cell volumes substantially in every zone. The sensitivity of cell volume changes to pericellular fibril stiffness suggests that pericellular fibrils play an important, and as of yet largely neglected, role in regulating the mechanical environment of chondrocytes, possibly affecting matrix synthesis during cartilage development and degeneration, and affecting biosynthetic responses associated with articular cartilage loading.     

Rapid prototyping of anatomically shaped, tissue-engineered implants for restoring congruent articulating surfaces in small joints

Background:  Preliminary studies investigated advanced scaffold design and tissue engineering approaches towards restoring congruent articulating surfaces in small joints.
Materials and methods:  Anatomical femoral and tibial cartilage constructs, fabricated by three-dimensional fibre deposition (3DF) or compression moulding/particulate leaching (CM), were evaluated in vitro and in vivo in an autologous rabbit model. Effects of scaffold pore architecture on rabbit chondrocyte differentiation and mechanical properties were evaluated following in vitro culture and subcutaneous implantation in nude mice. After femoral and tibial osteotomy and autologous implantation of tissue-engineered constructs in rabbit knee joints, implant fixation and joint articulation were evaluated.
Results:  Rapid prototyping of 3DF architectures with 100% interconnecting pores promoted homogeneous distribution of viable cells, glycosaminoglycan (GAG) and collagen type II; significantly greater GAG content and differentiation capacity (GAG/DNA) in vitro compared to CM architectures; and higher mechanical equilibrium modulus and dynamic stiffness (at 0.1 Hz). Six weeks after implantation, femoral and tibial constructs had integrated with rabbit bone and knee flexion/extension and partial load bearing were regained. Histology demonstrated articulating surfaces between femoral and tibial constructs for CM and 3DF architectures; however, repair tissue appeared fibrocartilage-like and did not resemble implanted cartilage.
Conclusions:  Anatomically shaped, tissue-engineered constructs with designed mechanical properties and internal pore architectures may offer alternatives for reconstruction or restoration of congruent articulating surfaces in small joints.     

How the stiffness of meniscal attachments and meniscal material properties affect tibio-femoral contact pressure computed using a validated finite element model of the human knee joint

In an effort to prevent degeneration of articular cartilage associated with meniscectomies, both meniscal allografts and synthetic replacements are subjects of current interest and investigation. The objectives of the current study were to (1) determine whether a transversely isotropic, linearly elastic, homogeneous material model of the meniscal tissue is necessary to achieve a normal contact pressure distribution on the tibial plateau, (2) determine which material and boundary condition (attachments) parameters affect the contact pressure distribution most strongly, and (3) set tolerances on these parameters to restore the contact pressure distribution to within a specified error. To satisfy these objectives, a finite element model of the tibio-femoral joint of a human cadaveric knee (including both menisci) was used to study the contact pressure distribution on the tibial plateau. To validate the model, the contact pressure distribution on the tibial plateau was measured experimentally in the same knee used to create the model. Within physiologically reasonable bounds on five material parameters and four attachment parameters associated with a meniscal replacement, an optimization was performed under 1200 N of compressive load on the set of nine parameters to minimize the difference between the experimental and model results. The error between the experimental and model contact variables was minimized to 5.4%. The contact pressure distribution of the tibial plateau was sensitive to the circumferential modulus, axial/radial modulus, and horn stiffness, but relatively insensitive to the remaining six parameters. Consequently, both the circumferential and axial/radial moduli are important determinants of the contact pressure distribution, and hence should be matched in the design and/or selection of meniscal replacements. In addition, during surgical implantation of a meniscal replacement, the horns should be attached with high stiffness bone plugs, and the attachments of the transverse ligament and deep medial collateral ligament should be restored to minimize changes in the contact pressure distribution, and thereby possibly prevent the degradation of articular cartilage.     

Altered trabecular bone structure and delayed cartilage degeneration in the knees of collagen VI null mice

Mutation or loss of collagen VI has been linked to a variety of musculoskeletal abnormalities, particularly muscular dystrophies, tissue ossification and/or fibrosis, and hip osteoarthritis. However, the role of collagen VI in bone and cartilage structure and function in the knee is unknown. In this study, we examined the role of collagen VI in the morphology and physical properties of bone and cartilage in the knee joint of Col6a1(-/-) mice by micro-computed tomography (microCT), histology, atomic force microscopy (AFM), and scanning microphotolysis (SCAMP). Col6a1(-/-) mice showed significant differences in trabecular bone structure, with lower bone volume, connectivity density, trabecular number, and trabecular thickness but higher structure model index and trabecular separation compared to Col6a1(+/+) mice. Subchondral bone thickness and mineral content increased significantly with age in Col6a1(+/+) mice, but not in Col6a1(-/-) mice. Col6a1(-/-) mice had lower cartilage degradation scores, but developed early, severe osteophytes compared to Col6a1(+/+) mice. In both groups, cartilage roughness increased with age, but neither the frictional coefficient nor compressive modulus of the cartilage changed with age or genotype, as measured by AFM. Cartilage diffusivity, measured via SCAMP, varied minimally with age or genotype. The absence of type VI collagen has profound effects on knee joint structure and morphometry, yet minimal influences on the physical properties of the cartilage. Together with previous studies showing accelerated hip osteoarthritis in Col6a1(-/-) mice, these findings suggest different roles for collagen VI at different sites in the body, consistent with clinical data.     

Stresses in the local collagen network of articular cartilage: a poroviscoelastic fibril-reinforced finite element study

Osteoarthritis (OA) is a multifactorial disease, resulting in diarthrodial joint wear and eventually destruction. Swelling of cartilage, which is proportional to the amount of collagen damage, is an initial event of cartilage degeneration, so damage to the collagen fibril network is likely to be one of the earliest signs of OA cartilage degeneration. We propose that the local stresses and strains in the collagen fibrils, which cause the damage, cannot be determined dependably without taking the local arcade-like collagen-fibril structure into account. We investigate this using a poroviscoelastic fibril-reinforced FEA model. The constitutive fibril properties were determined by fitting numerical data to experimental results of unconfined compression and indentation tests on samples of bovine patellar articular cartilage. It was demonstrated that with this model the stresses and strains in the collagen fibrils can be calculated. It was also exhibited that fibrils with different orientations at the same location can be loaded differently, depending on the local architecture of the collagen network. To the best of our knowledge, the present model is the first that can account for these features. We conclude that the local stresses and strains in the articular cartilage are highly influenced by the local morphology of the collagen-fibril network.     

Analysis of bone–prosthesis interface micromotion for cementless tibial prosthesis fixation and the influence of loading conditions

A lack of initial stability of the fixation is associated with aseptic loosening of the tibial components of cementless knee prostheses. With sufficient stability after surgery, minimal relative motion between the prosthesis and bone interfaces allows osseointegation to occur thereby providing a strong prosthesis-to-bone biological attachment. Finite element modelling was used to investigate the bone–prosthesis interface micromotion and the relative risk of aseptic loosening. It was anticipated that by prescribing different joint loads representing gait and other activities, and the consideration of varying tibial–femoral contact points during knee flexion, it would influence the computational prediction of the interface micromotion. In this study, three-dimensional finite element models were set up with applied loads representing walking and stair climbing, and the relative micromotions were predicted. These results were correlated to in-vitro measurements and to the results of prior retrieval studies. Two load conditions, (i) a generic vertical joint load of 3×body weight with 70%/30% M/L load share and antero-posterior/medial-lateral shear forces, acted at the centres of the medial and lateral compartments of the tibial tray, and (ii) a peak vertical joint load at 25% of the stair climbing cycle with corresponding antero-posterior shear force applied at the tibial–femoral contact points of the specific knee flexion angle, were found to generate interface micromotion responses which corresponded to in-vivo observations. The study also found that different loads altered the interface micromotion predicted, so caution is needed when comparing the fixation performance of various reported cementless tibial prosthetic designs if each design was evaluated with a different loading condition.     

Dynamic contact mechanics on the tibial plateau of the human knee during activities of daily living

Despite significant advances in scaffold design, manufacture, and development, it remains unclear what forces these scaffolds must withstand when implanted into the heavily loaded environment of the knee joint. The objective of this study was to fully quantify the dynamic contact mechanics across the tibial plateau of the human knee joint during gait and stair climbing. Our model consisted of a modified Stanmore knee simulator (to apply multi-directional dynamic forces), a two-camera motion capture system (to record joint kinematics), an electronic sensor (to record contact stresses on the tibial plateau), and a suite of post-processing algorithms. During gait, peak contact stresses on the medial plateau occurred in areas of cartilage–cartilage contact; while during stair climb, peak contact stresses were located in the posterior aspect of the plateau, under the meniscus. On the lateral plateau, during gait and in early stair-climb, peak contact stresses occurred under the meniscus, while in late stair-climb, peak contact stresses were experienced in the zone of cartilage–cartilage contact. At 45% of the gait cycle, and 20% and 48% of the stair-climb cycle, peak stresses were simultaneously experienced on both the medial and lateral compartment, suggesting that these phases of loading warrant particular consideration in any simulation intended to evaluate scaffold performance. Our study suggests that in order to design a scaffold capable of restoring ‘normal’ contact mechanics to the injured knees, the mechanics of the intended site of implantation should be taken into account in any pre-clinical testing regime.     

Genetic mechanisms of knee osteoarthritis: a population-based longitudinal study

To describe the differences in knee structure and non-knee structural factors between offspring having at least one parent with a total knee replacement for severe primary knee osteoarthritis and age- and sex-matched controls with no family history of knee osteoarthritis, a population-based longitudinal study of 163 matched pairs (mean age 45 years, range 26 to 61) was performed at baseline and about 2 years later. Knee cartilage defect score (0 to 4), cartilage volume and bone size were determined with T1-weighted fat saturation magnetic resonance imaging. Body mass index (BMI), lower-limb muscle strength, knee pain, physical work capacity at 170 beats/minute (PWC170) and radiographic osteoarthritis were measured by standard protocols. In comparison with controls, offspring had higher annual knee cartilage loss (-3.1% versus -2.0% at medial tibial site, -1.9% versus -1.1% at lateral tibial site and -4.7% versus -3.7% at patellar site, all P < 0.05), a greater increase in medial cartilage defect score (+0.15 versus -0.01, P < 0.05) and a greater decline in PWC170 (-0.7 watts/kg versus -0.4 watts/kg, P < 0.01). There were no significant differences in change in BMI, lower-limb muscle strength, knee pain or tibial bone area between these two groups; however, the differences in knee cartilage loss and cartilage defect change decreased in magnitude and became non-significant after adjustment for baseline cartilage volume, tibial bone area, BMI and knee pain. This longitudinal study suggests that knee cartilage loss, change in cartilage defects and decrease in physical fitness all have roles in the development of knee osteoarthritis, which is most probably polygenic but may reflect a shared environment. Importantly, the cartilage changes are largely dependent on baseline differences in cartilage volume, tibial bone area, BMI and knee pain, suggesting that these factors might have a role in their initiation.