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PubMed2004

Degradation of a collagen-chondroitin-6-sulfate matrix by collagenase and by chondroitinase.

Highly porous, type I collagen-chondroitin-6-sulfate (collagen-GAG) scaffolds, produced by freeze-drying techniques, have proven to be of value as implants to facilitate the regeneration of certain tissues. The objective of this project was to evaluate changes in the microstructure and mechanical properties of selected collagen-GAG scaffolds as they degrade in an in vitro model system. Environmental scanning electron microscopy and video imaging demonstrated that collagenase degradation caused strut erosion through the creation of 1-3 microm diameter micropits within a 2-h period, leading to eventual removal of strut material and strut breakage. Loss of microstructural topography may have been due to gelatinization when collagen was cleaved by collagenase. Chondroitinase degradation of GAG resulted in swelling of the struts, causing the pores to become smaller and rounder. The compressive modulus of the collagen-GAG matrix decreased when degraded by collagenase, but remained unchanged when degraded by chondroitinase. Carbodiimide-cross-linked matrices were found to have a higher cross-link density, a higher compressive stiffness and a greater resistance to collagenase and chondroitinase, compared to non-cross-linked controls and matrices that were cross-linked by the dehydrothermal process. This investigation provides information that can be used to design collagen-GAG scaffolds with desired compressive stiffness and degradation rate to collagenase and chondroitinase.

Animals↗
PubMed1995

Aging and degeneration of the human intervertebral disc.

Human intervertebral discs undergo age-related degenerative changes that contribute to some of the most common causes of impairment and disability for middle aged and older persons: spine stiffness, neck pain, and back pain. Potential causes of the age-related degeneration of intervertebral discs include declining nutrition, loss of viable cells, cell senescence, post-translational modification of matrix proteins, accumulation of degraded matrix molecules, and fatigue failure of the matrix. The most important of these mechanisms appears to be decreasing nutrition of the central disc that allows accumulation of cell waste products and degraded matrix molecules, impairs cell nutrition, and causes a fall in pH levels that further compromises cell function and may cause cell death. Although aging changes of the disc appear to be inevitable, identification of activities and agents that accelerate these changes may help decrease the rate and severity of disc degeneration; and recent work suggests that methods can be developed that will regenerate disc tissue.

Aging↗
PubMed2001

Ageing human bone: factors affecting its biomechanical properties and the role of collagen.

The incidence of fractures increases with age. This is partly due to extraosseous factors and partly to the increased fragility of the bone material itself. Ageing adversely affects the "quality" of human bone material, its elastic and ultimate properties. The hypothesis here is that these effects are caused by factors such as architectural changes, compositional changes, physicochemical changes, changes at the micromechanical level, and the degree of prior in vivo microdamage. Examination of the extent of the secondary osteonal area, the porosity level, the calcium content, the mineral/wet weight fraction, the dry density, the condition of the collagen and its content in mature x-links, the elasticity of osteonal and interstitial lamellae at the microscopic level and the numerical- and surface-density of the in vivo fatigue microcracks has been undertaken. The findings show that some factors simply affect the stiffness and the strength of bone, while others soley affect its toughness. We discuss the implications of these findings in the context of the composite nature of the ageing bone material matrix.

Aging↗
PubMed2006

Nanomechanical properties of individual chondrocytes and their developing growth factor-stimulated pericellular matrix.

The nanomechanical properties of individual cartilage cells (chondrocytes) and their aggrecan and collagen-rich pericellular matrix (PCM) were measured via atomic force microscope nanoindentation using probe tips of two length scales (nanosized and micron-sized). The properties of cells freshly isolated from cartilage tissue (devoid of PCM) were compared to cells that were cultured for selected times (up to 28 days) in 3-D alginate gels which enabled PCM assembly and accumulation. Cells were immobilized and kept viable in pyramidal wells microfabricated into an array on silicon chips. Hertzian contact mechanics and finite element analyses were employed to estimate apparent moduli from the force versus depth curves. The effects of culture conditions on the resulting PCM properties were studied by comparing 10% fetal bovine serum to medium containing a combination of insulin growth factor-1 (IGF-1)+osteogenic protein-1 (OP-1). While both systems showed increases in stiffness with time in culture between days 7 and 28, the IGF-1+OP-1 combination resulted in a higher stiffness for the cell-PCM composite by day 28 and a higher apparent modulus of the PCM which is compared to the FBS cultured cells. These studies give insight into the temporal evolution of the nanomechanical properties of the pericellar matrix relevant to the biomechanics and mechanobiology of tissue-engineered constructs for cartilage repair.

Animals↗
PubMed1986

Tensile properties of human knee joint cartilage: I. Influence of ionic conditions, weight bearing, and fibrillation on the tensile modulus.

The flow-independent (intrinsic) tensile modulus of the extracellular matrix of human knee joint cartilage has been measured for normal, fibrillated, and osteoarthritic (removed from total knee joint replacements) cartilage. The modulus was determined in our isometric tensile apparatus and measured at equilibrium. We found a linear equilibrium stress-strain behavior up to approximately 15% strain. The modulus was measured for tissues from the high and low weight-bearing areas of the joint surfaces, the medial femoral condyle and lateral patello femoral groove, and from different zones (surface, subsurface, middle, and middle-deep) within the tissue. For all specimens, the intrinsic tensile modulus was always less than 30 MPa. Tissues from low weight-bearing areas (LWA) are stiffer than those from high weight-bearing areas (HWA). The tensile modulus of the ECM correlates strongly with the collagen/proteoglycan ratio; it is higher for LWA than for HWA. Osteoarthritic cartilage from total knee replacement procedures has a tensile stiffness less than 2 MPa.

Adult↗
PubMed2002

Predictive modeling of the mechanical properties of particulate hydroxyapatite reinforced polymer composites.

The influence of particle geometry and volume fraction on the mechanical properties of a hydroxyapatite (HAp) particulate reinforced polymer (poly-L-lactide and collagen) matrix composite was investigated through finite-element (FE) analysis. For cube-shaped (near sharp and curved corners and edges) embedded particles, it was found that the maximum stress concentration factor (SCF) in the matrix decreases with an increase of the HAp particle volume fraction (PVF). The maximum stress concentration in the matrix material containing a spherical inclusion has low sensitivity to the PVF. The compressive Young's modulus was found to be slightly dependent on particle shape, but very sensitive to PVF. Calculated stiffness values from FE analysis were compared to the experimental results available in the literature and with predictions from the Halpin-Tsai model.

Biomechanical Phenomena↗
PubMed1989

Some factors affecting properties of elastin-fibrin biomaterial.

The elasticity, mechanical strength and permeability of a new biomaterial made of elastin and fibrin were investigated. It was shown that gamma-irradiation to sterilize the product, and sulphur derivatives (Merceptyl, thiourea, cystein) working as reticulating agents modified these properties. Depending on whether or not the biomaterial needs to be stiff, strong or elastic both physical processes could intervene separately or together. The good permeability of this material allows it to be used in several surgical fields as a true artificial connective matrix.

Biocompatible Materials↗
PubMed1998

Novel attributes of an androgenic steroid-mediated increase in cardiac end diastolic stiffness in rats.

Although cardiac early and mid-diastolic stiffness constants are well accepted as being modulated by alterations in myocyte active processes, increments in left ventricular end diastolic (LVED) stiffness (LVED k; g x cm(-2)) in classical pathological models of a reduced LVED k (e.g., diabetes mellitus (DM) and hypertension) are determined largely by the properties of the myocardial extracellular matrix (ECM). As such, increases in LVED k in the latter cardiac pathologies are insensitive to acute changes in cardiac load, heart rate, and contractility. We examined whether the same attributes that apply to changes in LVED k in DM and in spontaneously hypertensive rats (SHRs) also apply to an androgenic steroid (nandrolone decanoate; 5 mg x kg(-1) biweekly) induced increase in LVED k. Myocardial collagen (ECM) characteristics and the capacity of acute verapamil-mediated changes in cardiac dynamics to impact on LVED k were evaluated after 3 months of steroid treatment to rats, 4 months of DM in rats, and in 45-week-old SHRs. Chronic steroid administration increased LVED k (steroid = 42 +/- 4, control = 25 +/- 2; p < 0.01). An acute infusion of verapamil to steroid-treated rats decreased LVED k to values not different from controls (29 +/- 3; p < 0.05 as compared with LVED k at baseline). Measures of myocardial collagen concentrations, phenotype ratios, and cross-linking were unchanged following steroid administration. Verapamil failed to alter the increased LVED k that occurs in either rats with DM or in SHRs, despite similar effects on cardiac dynamics as those noted in steroid-treated rats. The increased LVED k in the former animal models was associated with alterations in the ECM. In conclusion, the unique lack of association of the androgenic steroid-induced increase in LVED k with alterations in the myocardial ECM and the novel sensitivity of the steroid-mediated increment in LVED k to acute alterations in cardiac dynamics further supports the notion that changes in LVED k should not be considered to be a reflection of ECM characteristics in all cardiac conditions.

Androgens↗
PubMed2007

Modulation of atherosclerosis, blood pressure and arterial elasticity by statins.

It is well known that dyslipidemia and hypertension frequently coexist. There is increasing recognition of a mutually facilitative interaction between dyslipidemia and renin- angiotensin system (RAS) activation in the development of atherosclerosis. Both of these systems share many of the same properties in terms of activation of pro-inflammatory, pro-oxidant and pro-atherosclerosis pathways. Statins in particular have been shown to influence the biology of endothelial cells, vascular smooth muscle cells and constituents of the interstitial matrix, particularly fibroblasts. It is no wonder that concurrent therapy of dyslipidemia with statins enhances the effects of RAS inhibitors. Although the effects of statins on the regulation of determinants of vascular stiffness are not well defined, it is quite likely that these regulatory pathways will be influenced by dyslipidemia therapy, especially statins.

Atherosclerosis↗
PubMed2005

Evolution and modulation of age-related medial elastocalcinosis: impact on large artery stiffness and isolated systolic hypertension.

Arteriosclerosis, characterized by remodeling and stiffening of large elastic arteries is the most significant manifestation of vascular aging. The increased stiffening is believed to originate from a gradual mechanical senescence of the elastic network, alterations in cross-linking of extracellular matrix components, fibrosis and calcification of elastic fibers (medial elastocalcinosis). The stiffening of large arteries reduces their capacitance and accelerates pulse wave velocity, thus contributing to a widening of pulse pressure and to the increased prevalence of isolated systolic hypertension with age. Current antihypertensive drugs were mainly designed to reduce peripheral resistance and are not adequate to alter the pathological process of vascular stiffening or even to selectively reduce systolic blood pressure in isolated systolic hypertension. This review puts forward the concept that elastocalcinosis is a valuable therapeutic target and presents evidence that this process can be prevented and reversed pharmacologically.

Aged↗
PubMed2007

Impaired angiogenesis, early callus formation, and late stage remodeling in fracture healing of osteopontin-deficient mice.

UNLABELLED: OPN is an ECM protein with diverse localization and functionality. The role of OPN during fracture healing was examined using wildtype and OPN(-/-) mice. Results showed that OPN plays an important role in regulation of angiogenesis, callus formation, and mechanical strength in early stages of healing and facilitates late stage bone remodeling and ECM organization. INTRODUCTION: Osteopontin (OPN) is an extracellular matrix (ECM) protein with diverse localization and functionality that has been reported to play a regulatory role in both angiogenesis and osteoclastic bone remodeling, two vital processes for normal bone healing. MATERIALS AND METHODS: Bone repair in wildtype and OPN(-/-) mice was studied using a femoral fracture model. microCT was used for quantitative angiographic measurements at 7 and 14 days and to assess callus size and mineralization at 7, 14, 28, and 56 days. Biomechanical testing was performed on intact bones and on fracture specimens at 14, 28, and 56 days. Histology and quantitative RT-PCR were used to evaluate cellular functions related to ECM formation and bone remodeling. RESULTS: OPN deficiency was validated in the OPN(-/-) mice, which generally displayed normal levels of related ECM proteins. Intact OPN(-/-) bones displayed increased elastic modulus but decreased strength and ductility. Fracture neovascularization was reduced at 7 but not 14 days in OPN(-/-) mice. OPN(-/-) mice exhibited smaller fracture calluses at 7 and 14 days, as well as lower maximum torque and work to failure. At 28 days, OPN(-/-) mice had normal callus size but a persistent reduction in maximum torque and work to failure. Osteoclast differentiation occurred normally, but mature osteoclasts displayed reduced functionality, decreasing late stage remodeling in OPN(-/-) mice. Thus, at 56 days, OPN(-/-) fractures possessed increased callus volume, increased mechanical stiffness, and altered collagen fiber organization. CONCLUSIONS: This study showed multiple, stage-dependent roles of OPN during fracture healing. We conclude that OPN deficiency alters the functionality of multiple cell types, resulting in delayed early vascularization, altered matrix organization and late remodeling, and reduced biomechanical properties. These findings contribute to an improved understanding of the role of OPN in vivo and provide new insight into mechanistic control of vascularization and bone regeneration during fracture repair.

Animals↗
PubMed2005

Pathomechanisms of cartilage destruction by mechanical injury.

Mechanical injury is considered to be a major inductor of articular cartilage destruction and therefore a risk factor for the development of secondary osteoarthritis. Mechanical injury induces damage to the tissue matrix directly or mediated by chondrocytes via expression of matrix-degrading enzymes and reduction of biosynthetic activity. As a consequence the mechanical properties of cartilage change. Some of the pathomechanisms of mechanical injury have already been uncovered by the use of a broad range of in vitro-models. They demonstrate that mechanical injury induces tissue swelling and decrease in both the compressive and shear stiffness of articular cartilage, probably due to disruption of the collagen network. Injurious compression induces chondrocyte death by necrosis and apoptosis and the remaining cells decrease their biosynthetic activity. The tissue content of proteoglycans also decreases with time in injured cartilage, and the tissue loses its ability to respond to physiological levels of mechanical stimulation with an increase in biosynthesis. Immature cartilage seems to be more vulnerable to injurious compression than more mature tissue. The expression of several matrix-degrading enzymes like ADAM-TS5 and matrix-metalloproteinases (MMP-1, MMP-2, MMP-3, MMP-9, MMP-13) is increased after injury and may in part be regulated by an autocrine vascular endothelial growth factor (VEGF)-dependent signalling pathway. Apoptosis seems to be mediated by caspase activity and reactive oxygen species. For that reason activation of antioxidative defense mechanisms as well as the inhibition of angiogenetic factors and MMPs might be key regulators in the mechanically induced destruction of cartilage and might be suggested as potential therapeutic interventions. This review summarizes some of the most important data from in vitro injury studies dealing with the pathomechanisms of cartilage destruction.

Biomechanical Phenomena↗
PubMed2002

Cardiac mast cell-mediated activation of gelatinase and alteration of ventricular diastolic function.

Mast cells contain proteases capable of activating matrix metalloproteinases (MMPs). However, given the relatively low density of mast cells in the myocardium (i.e., 1.5-5.3 cells/mm(2)), it is unknown whether these enzymes are present in sufficient quantities in the normal heart to mediate MMP activation. Accordingly, this study sought to determine whether chemically induced degranulation of cardiac mast cells (with compound 48/80) would have an effect in isolated, blood-perfused, functioning rat hearts. Mast cell degranulation produced a 15% increase in histamine levels present in the coronary efflux, a significant increase in myocardial water (i.e., edema) relative to normal values (80.1 +/- 3.4% vs. 77.4 +/- 1.08%, P < or = 0.03), a substantial activation of MMP-2 (126% increase relative to controls, P < or = 0.02), and a marked decrease in myocardial collagen volume fraction (0.46 +/- 0.10% vs. 0.97 +/- 0.33%, P < or = 0.001). Furthermore, although an increase in ventricular stiffness was expected due to the extent of edema resulting from mast cell degranulation, modest ventricular dilatation was observed. These findings clearly demonstrate that the number of mast cells present in normal hearts is sufficient to mediate activation of MMPs and produce extracellular matrix degradation, thereby potentially causing subsequent ventricular dilatation.

Animals↗
PubMed2006

Fabrication methods of an engineered microenvironment for analysis of cell-biomaterial interactions.

Success in tissue engineering requires an understanding of how cells integrate the signals presented from the microenvironment created by biomaterial scaffolds to alter their responses. Besides the presence of chemical stimuli, there is growing evidence that the spatial organization of cells and tissue within a 3-dimensional (3-D) extracellular matrix (ECM) context is a critical element in controlling cellular function. Therefore, in order to direct cells toward a desirable tissue structure, it is necessary to engineer biomaterials to have spatiotemporal control of the presentation of regulatory signals. Given that, micro-patterning techniques have profited by combining micro-fabrication technology with the chemical conjugation of biologically active molecules to provide new culture systems where cells can be cultured within a specific geometry. The micro-engineered environments have been developed as 2- and 3-D structures, which have proven greatly useful as versatile platforms to study cell, biomaterial, and ECM interactions on both macroscopic and microscopic levels. The main focus of this review is a brief summary of the use of micro-engineered substrates in the analysis of cell-biomaterial interactions with the aim to provide an introductory overview of practical applications available in the literature. In particular, topics regarding (1) the soft-lithography technique to prepare micro-patterned substrates for the spatial control of cell adhesion, (2) biomaterials stiffness-dependent cellular responses, and (3) the microarray techniques for analysis of cell/biomaterials interactions are discussed.

Animals↗
PubMed1990

Indentation stiffness of young canine knee articular cartilage--influence of strenuous joint loading.

The indentation stiffness of knee articular cartilage subjected to strenuous physical training (SPT: treadmill running 20 km day-1 for 15 weeks, n = 6) of young Beagles was tested and compared to that obtained from age-matched (55 weeks, n = 9) controls. The mathematical solution for the shear modulus, as determined from indentation of an elastic layer bonded to a rigid half space, was extended to small Poisson's ratios and applied to the analysis of cartilage response after a step stress (0.39 MPa) application. In these measurements with an impervious, plane-ended indenter, the equilibrium deformation was systematically greater than values predicted from the instant response by the linear biphasic theory. Therefore, the accurate determination of Poisson's ratio from the creep curves was not possible. The mean shear modulus (calculated by using the deformation at 900 s after load application and assuming a constant Poisson's ratio of 0.40 for the matrix) of canine knee articular cartilage was 0.37 MPa. While the cartilage thickness was not affected by SPT, the cartilage of the lateral tibial plateau was stiffer (13.3%, p less than 0.05) than that in controls. However, in the femoral condyles, the stiffness was at the control level or even below. Our results on cartilage structure and properties suggest that SPT, in contrast to our previous findings with moderate training, does not necessarily improve the biological properties of articular cartilage in young animals.

Animals↗
PubMed1995

Physical response of collagen gels to tensile strain.

Extra cellular matrix, which provides physical support to epithelial and endothelial cells and to fibroblasts, also affects a number of important cell biological phenomena, such as cell motility and angiogenesis. Although type I collagen has long been recognized as the primary structural component of the extra cellular matrix, little is known about the physical properties of collagen gels. In this study, we used a servo-controlled linear actuator to impose quick stretches on dilute collagen gels. An axial strain imposed on the gel within few milliseconds resulted in a rapid development of gel tension in the direction of the strain. The gel tension then decayed toward a steady-state value within several seconds. The instantaneous gel stiffness increased and the relaxed gel stiffness decreased with the extent of gel stretching. These rheological parameters were also dependent on the density of the collagen network. Taken together the results indicated that collagen gels possess nonlinear viscoelastic properties.

Biomechanical Phenomena↗
PubMed2005

Tissue engineering of articular cartilage using an allograft of cultured chondrocytes in a membrane-sealed atelocollagen honeycomb-shaped scaffold (ACHMS scaffold).

The aim of this study was to investigate with tissue engineering procedures the possibility of using atelocollagen honeycomb-shaped scaffolds sealed with a membrane (ACHMS scaffold) for the culturing of chondrocytes to repair articular cartilage defects. Chondrocytes from the articular cartilage of Japanese white rabbits were cultured in ACHMS scaffolds to allow a high-density, three-dimensional culturing for up to 21 days. Although the DNA content in the scaffold increased at a lower rate than monolayer culturing, scanning electron microscopy data showed that the scaffold was filled with grown chondrocytes and their produced extracellular matrix after 21 days. In addition, glycosaminoglycan (GAG) accumulation in the scaffold culture was at a higher level than the monolayer culture. Cultured cartilage in vitro for 14 days showed enough elasticity and stiffness to be handled in vivo. An articular cartilage defect was initiated in the patellar groove of the femur of rabbits and was subsequently filled with the chondrocyte-cultured ACHMS scaffold, ACHMS scaffold alone, or non-filled (control). Three months after the operations, histological analysis showed that only defects inserted with chondrocytes being cultured in ACHMS scaffolds were filled with reparative hyaline cartilage, and thereby highly expressing type II collagen. These results indicate that implantation of allogenic chondrocytes cultured in ACHMS scaffolds may be effective in repairing articular cartilage defects.

Animals↗
PubMed2003

The role of bone metabolism in osteoarthritis.

Bone is not structurally normal in osteoarthritis (OA). Periarticular bone in OA has increased turnover, decreased bone mineral content and stiffness, and decreased trabecular numbers. The increased turnover of collagen, in particular, may affect the biomechanical competence of bone and is driven by a number of processes, including osteoblast phenotypic expression, chondrocyte apoptosis, matrix metalloproteinases, and growth factors. This turnover is reflected in alterations in biomarkers and bone mineral density (BMD). High BMD at non-joint sites is associated with an increased risk of OA; however, low BMD and high bone turnover appears to be associated with more rapid progression. These alterations in bone turnover offer new therapeutic opportunities.

Biomarkers↗