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PubMed1998

Articular cartilage repair. Rabbit experiments with a collagen gel-biomatrix and chondrocytes cultured in it.

To repair a full-thickness articular cartilage defect in rabbit knees, we developed a technique of using a collagen gel hardened by cultured allogeneic chondrocytes in it. The gel-chondrocyte composite accumulated an intense metachromatic matrix, and had elasticity and stiffness enough to be shaped easily after 2 weeks' culture in vitro. It was implanted into full-thickness articular cartilage defects. Histologic evaluation was performed up to 6 months after surgery, using a histologic grading scale composed of 5 categories. In the gel-chondrocyte composite implanted group, good repair was observed from as early as 1 day up to 6 months. On the other hand, in the empty control group, no repair was observed 1 day to 2 weeks after the defects were made. At 4 weeks, some repair occurred, but even at 6 months the repair was not good.

Animals↗
PubMed2001

Composition and structure of articular cartilage: a template for tissue repair.

The authors review the structure and composition of articular cartilage. This tissue is composed of an extensive extracellular matrix synthesized by chondrocytes. It contains different zones with respect to depth from the articular surface and has a regional organization around the chondrocytes. Its composition varies regionally and zonally in its collagen and proteoglycan contents and those of other matrix molecules. There is a macrofibrillar collagen network and a microfilamentous network about which other noncollagenous molecules are organized. Its structure and composition are reflective of its special mechanical properties that primarily reflect its tensile strength (collagens) and compressive stiffness (proteoglycan aggrecan) and cell-matrix interactions (noncollagenous proteins).

Cartilage, Articular↗
PubMed2003

Role of pericellular matrix in development of a mechanically functional neocartilage.

The role of the chondrocyte pericellular matrix (PCM) was examined in a three-dimensional chondrocyte culture system to determine whether retention of the native pericellular matrix could stimulate collagen and proteoglycan accumulation and also promote the formation of a mechanically functional hyaline-like neocartilage. Porcine chondrocytes and chondrons, consisting of the chondrocyte with its intact pericellular matrix, were maintained in pellet culture for up to 12 weeks. Sulfated glycosaminoclycans and type II collagen were measured biochemically. Immunocytochemistry was used to examine collagen localization as well as cell distribution within the pellets. In addition, the equilibrium compressive moduli of developing pellets were measured to determine whether matrix deposition contributed to the mechanical stiffness of the cartilage constructs. Pellets increased in size and weight over a 6-week period without apparent cell proliferation. Although chondrocytes quickly rebuilt a PCM rich in type VI collagen, chondron pellets accumulated significantly more proteoglycan and type II collagen than did chondrocyte pellets, indicating a greater positive effect of the native PCM. After 5 weeks in chondron pellets, matrix remodeling was evident by microscopy. Cells that had been uniformly distributed throughout the pellets began to cluster between large areas of interterritorial matrix rich in type II collagen. After 12 weeks, clusters were stacked in columns. A rapid increase in compressive strength was observed between 1 and 3 weeks in culture for both chondron and chondrocyte pellets and, by 6 weeks, both had achieved 25% of the equilibrium compressive stiffness of cartilage explants. Retention of the in vivo PCM during chondrocyte isolation promotes the formation of a mechanically functional neocartilage construct, suitable for modeling the responses of articular cartilage to chemical stimuli or mechanical compression.

Animals↗
PubMed1990

Mechanical properties of biodegradable polymers and composites proposed for internal fixation of bone.

The mechanical properties of biodegradable polymers and composites proposed for use in internal fixation (in place of stainless steel) are crucial to the performance of devices made from them for support of healing bone. To assess the reported range of properties and degradation rates, we searched and reviewed papers and abstracts published in English from 1980 through 1988. Mechanical property data were found for poly(lactic acid), poly(glycolic acid), poly(epsilon-caprolactone), polydioxanone, poly(ortho ester), poly(ethylene oxide), and/or their copolymers. Reports of composites based on several of these materials, reinforced with nondegradable and degradable fibers, were also found. The largest group of studies involved poly(lactic acid). Mechanical test methods varied widely, and studies of the degradation of mechanical properties were performed under a variety of conditions, mostly in vitro rather than in vivo. Compared to annealed stainless steel, unreinforced biodegradable polymers were initially up to 36% as strong in tension and 54% in bending, but only about 3% as stiff in either test mode. With fiber reinforcement, reported highest initial strengths exceeded that of stainless steel. Stiffness reached 62% of stainless steel with nondegradable carbon fibers, 15% with degradable inorganic fibers, but only 5% with degradable polymeric fibers. The slowest-degrading unreinforced biodegradable polymers were poly(L-lactic acid) and poly(ortho ester). Biodegradable composites with carbon or inorganic fibers generally lost strength rapidly, with a slower loss of stiffness, suggesting the difficulty of fiber-matrix coupling in these systems. The strength of composites reinforced with (lower modulus) degradable polymeric fibers decreased more slowly. Low implant stiffness might be expected to allow too much bone motion for satisfactory healing. However, unreinforced or degradable polymeric fiber reinforced materials have been used successfully clinically. The key has been careful selection of applications, plus use of designs and fixation methods distinctly different from those appropriate for stainless steel devices.

Biocompatible Materials↗
PubMed1991

A triphasic theory for the swelling and deformation behaviors of articular cartilage.

Swelling of articular cartilage depends on its fixed charge density and distribution, the stiffness of its collagen-proteoglycan matrix, and the ion concentrations in the interstitium. A theory for a tertiary mixture has been developed, including the two fluid-solid phases (biphasic), and an ion phase, representing cation and anion of a single salt, to describe the deformation and stress fields for cartilage under chemical and/or mechanical loads. This triphasic theory combines the physico-chemical theory for ionic and polyionic (proteoglycan) solutions with the biphasic theory for cartilage. The present model assumes the fixed charge groups to remain unchanged, and that the counter-ions are the cations of a single-salt of the bathing solution. The momentum equation for the neutral salt and for the intersitial water are expressed in terms of their chemical potentials whose gradients are the driving forces for their movements. These chemical potentials depend on fluid pressure p, salt concentration c, solid matrix dilatation e and fixed charge density cF. For a uni-uni valent salt such as NaCl, they are given by mu i = mu io + (RT/Mi)ln[gamma 2 +/- c(c + cF)] and mu w = mu wo + [p-RT phi (2c + cF) + Bwe]/pwT, where R, T, Mi, gamma +/-, phi, pwT and Bw are universal gas constant, absolute temperature, molecular weight, mean activity coefficient of salt, osmotic coefficient, true density of water, and a coupling material coefficient, respectively. For infinitesimal strains and material isotropy, the stress-strain relationship for the total mixture stress is sigma = - pI-TcI + lambda s(trE)I + 2 musE, where E is the strain tensor and (lambda s, mu s) are the Lamé constants of the elastic solid matrix. The chemical-expansion stress (-Tc) derives from the charge-to-charge repulsive forces within the solid matrix. This theory can be applied to both equilibrium and non-equilibrium problems. For equilibrium free swelling problems, the theory yields the well known Donnan equilibrium ion distribution and osmotic pressure equations, along with an analytical expression for the "pre-stress" in the solid matrix. For the confined-compression swelling problem, it predicts that the applied compressive stress is shared by three load support mechanisms: 1) the Donnan osmotic pressure; 2) the chemical-expansion stress; and 3) the solid matrix elastic stress. Numerical calculations have been made, based on a set of equilibrium free-swelling and confined-compression data, to assess the relative contribution of each mechanism to load support. Our results show that all three mechanisms are important in determining the overall compressive stiffness of cartilage.

Biomechanical Phenomena↗
PubMed2004

Heterogeneous nanostructural and nanoelastic properties of pericellular and interterritorial matrices of chondrocytes by atomic force microscopy.

Hyaline cartilage consists of sparse chondrocytes and abundant extracellular matrix. There is a paucity of experimental data in support of the notion of conceivable regional differences in the mechanical properties of chondral matrices. Upon visual differentiation of the pericellular and interterritorial matrices in each of 19 fresh growth plate samples with toluidine blue and alizarin red labels, nanoindentation was applied separately to the pericellular matrix and interterritorial matrix to using fluid-phase atomic force microscopy and real-time imaging. The interterritorial matrix demonstrated elongated parallel ridges, whereas the pericellular matrix showed irregular, short-range elevations with characteristic pores and canals. Analysis of surface contours at 600nm(2) scan size revealed that the interterritorial matrix had significantly greater surface roughness (71+/-18nm; mean+/-SE) than the pericellular matrix (24+/-4nm) ( P< 0.001). The average Young's modulus of the interterritorial matrix was 636+/-123 (kPa), significantly greater than the pericellular matrix (265+/-53kPa) (P< 0.001 ). Thus, the interterritorial matrix appears to possess not only distinct microtopographic contours in comparison with the pericellular matrix, but also significantly greater mechanical stiffness. These distinctive nanostructural and nanomechanical properties may have implications in nutrient diffusion and fluid dynamics, both of which are of vital importance for cartilage health and function.

Animals↗
PubMed2004

Matrix metalloproteinase-9 (MMP-9), MMP-2, and serum elastase activity are associated with systolic hypertension and arterial stiffness.

BACKGROUND: Arterial stiffness is an independent determinant of cardiovascular risk, and arterial stiffening is the predominant abnormality in systolic hypertension. Elastin is the main elastic component of the arterial wall and can be degraded by a number of enzymes, including matrix metalloproteinase-9 (MMP-9) and MMP-2. We hypothesized that elastase activity would be related to arterial stiffness and tested this using isolated systolic hypertension (ISH) as a model of stiffening and separately in a large cohort of healthy individuals. METHODS AND RESULTS: A total of 116 subjects with ISH and 114 matched controls, as well as 447 individuals free from cardiovascular disease were studied. Aortic and brachial pulse wave velocity (PWV) and augmentation index were determined. Blood pressure, lipids, C-reactive protein, MMP-9, MMP-2, serum elastase activity (SEA), and tissue-specific inhibitor 2 of metalloproteinases were measured. Aortic and brachial PWV, MMP-9, MMP-2, and SEA levels were increased in ISH subjects compared with controls (P=0.001). MMP-9 levels correlated linearly and significantly with aortic (r=0.45; P=0.001) and brachial PWV (r=0.22; P=0.002), even after adjustments for confounding variables. In the younger, healthy subjects, MMP-9 and SEA were also independently associated with aortic PWV. CONCLUSIONS: Aortic stiffness is related to MMP-9 levels and SEA, not only in ISH, but also in younger, apparently healthy individuals. This suggests that elastases including MMP-9 may be involved in the process of arterial stiffening and development of ISH. The relationship between arterial stiffness and elastase activity was examined in isolated systolic hypertension (ISH), and separately in a large cohort of healthy individuals. Aortic stiffness is related to MMP-9, not only in ISH, but also in healthy individuals, suggesting elastases may be involved in the process of arterial stiffening and the development of ISH.

Aged↗
PubMed1997

[Spironolactone: renaissance of anti-aldosterone therapy in heart failure?].

Mortality of patients with severe congestive heart failure (CHF) is still high despite combined treatment with angiotensin-converting enzyme (ACE) inhibitors, diuretics, and digitalis. Further therapeutic regimens are needed which include reversal of adverse myocardial remodeling and subsequent ventricular dysfunction. One third of all patients with CHF have diastolic left ventricular (LV) dysfunction with preserved systolic function. In these patients myocardial collagen matrix is the major determinant of myocardial stiffness and therefore diastolic function. Cardiac fibroblasts, expressing mRNA for types I and III collagens which are the major fibrillar proteins of the myocardial collagen network and for matrix metalloproteinase (MMP) 1 which is the key enzyme for interstitial collagen degradation, are controlled by the renin-angiotensin-aldosterone (RAAS) system irrespective of hemodynamics and cardiac myocyte growth. In the rat with primary or secondary hyperaldosteronism, myocardial fibrosis occurs in the pressure overloaded, hypertrophied left and in the normotensive, nonhypertrophic right ventricle. In contrast, no fibrosis is found in either ventricle of rats with infrarenal aortic banding, when the RAAS is not activated, despite comparable systemic hypertension and LV hypertrophy. In cultured cardiac fibroblasts, either effector hormone of the RAAS, angiotensin (Ang) II and aldosterone (Aldo) stimulate collagen synthesis measured by 3H-proline incorporation under serum-free conditions. Aldo is able to stimulate collagen synthesis normalized per total protein synthesis in a dose-dependent manner and at concentrations (10(-9) M) which are comparable to stimulated states in vivo (e.g., CHF). While Aldo does not affect collagen degradation AngII significantly inhibits, MMP 1 activity that would lead to further accumulation of collagen in the myocardium. Specific AngII type I or Aldo receptor antagonists are able to abolish the AngII or Aldo-mediated increase in collagen synthesis, respectively. In vivo in rats with primary or secondary hyperaldosteronism, the Aldo antagonist spironolactone has been shown to prevent myocardial fibrosis in both ventricles irrespective of the development of LV hypertrophy and hypertension. Thus, in vivo and in vitro evidence could be provided that the mineralocorticoid. Aldo, plays a pivotal role in promoting myocardial fibrosis and can be antagonized by its competitive receptor blocker, spironolactone. This may be of particular clinical relevance in treating patients with CHF where the RAAS is activated leading to myocardial fibrosis with subsequent deterioration of myocardial function. Clinical trials are needed to confirm these experimental data. If the ongoing RALES mortality study will prove that survival and/or morbidity of patients with CHF are improved by combined ACE inhibitor/spironolactone treatment a renaissance of anti-aldosterone therapy in patients with CHF would occur.

Animals↗
PubMed2000

Outside-in signalling of fibronectin stimulates cardiomyocyte hypertrophy in cultured neonatal rat ventricular myocytes.

Cardiac hypertrophy involves the accumulation of extracellular matrix proteins, such as fibronectin, leading to increasing myocardial stiffness, ventricular dysfunction and heart failure. To better understand the possible role of extracellular matrix-evoked intracellular signalling in ventricular myocytes, we investigated the effect of fibronectin on myocyte hypertrophic responses using cell culture models. Cell size in myocytes cultured on fibronectin-coated dishes was three times larger than that grown on non-coated dishes. However, the number of cells on fibronectin-coated dishes was not changed throughout the experiment. Protein synthesis was significantly increased by fibronectin, as were synthesis of atrial and brain natriuretic peptides. Fibronectin also elicited actin reorganization, co-localization of beta 1 integrin and vinculin, formation of focal adhesions and tyrosine phosphorylation of focal adhesion kinase in myocytes. These fibronectin-mediated effects were inhibited in a dose-dependent manner by GRGDSP, a competitive antagonist of the fibronectin receptors; GRGDSP had no effect on cell number or viability. Blocking antibody for beta 1 and beta 3 integrin significantly suppressed fibronectin-induced secretion of natriuretic peptides. Myocyte hypertrophy was observed in myocyte-nonmyocyte co-culture that reflects more closely the myocyte environment in vivo. GRGDSP may also suppress the myocyte hypertrophic response in the co-culture. These findings demonstrate that the interaction of fibronectin and RGD-dependent integrins is involved in the hypertrophic responses of myocyte in vitro, and suggest that extracellular matrix proteins such as fibronectin are not merely passive adhesive molecules but are active participants in processes leading to myocyte hypertrophy.

Animals↗
PubMed2004

The local matrix distribution and the functional development of tissue engineered cartilage, a finite element study.

Assessment of the functionality of tissue engineered cartilage constructs is hampered by the lack of correlation between global measurements of extra cellular matrix constituents and the global mechanical properties. Based on patterns of matrix deposition around individual cells, it has been hypothesized previously, that mechanical functionality arises when contact occurs between zones of matrix associated with individual cells. The objective of this study is to determine whether the local distribution of newly synthesized extracellular matrix components contributes to the evolution of the mechanical properties of tissue engineered cartilage constructs. A computational homogenization approach was adopted, based on the concept of a periodic representative volume element. Local transport and immobilization of newly synthesized matrix components were described. Mechanical properties were taken dependent on the local matrix concentration and subsequently the global aggregate modulus and hydraulic permeability were derived. The transport parameters were varied to assess the effect of the evolving matrix distribution during culture. The results indicate that the overall stiffness and permeability are to a large extent insensitive to differences in local matrix distribution. This emphasizes the need for caution in the visual interpretation of tissue functionality from histology and underlines the importance of complementary measurements of the matrix's intrinsic molecular organization.

Biomechanical Phenomena↗
PubMed1990

Collagen and the myocardium: fibrillar structure, biosynthesis and degradation in relation to hypertrophy and its regression.

The extracellular matrix of the myocardium contains an elaborate structural matrix composed mainly of fibrillar types I and III collagen. This matrix is responsible for the support and alignment of myocytes and capillaries. Because of its alignment, location, configuration and tensile strength, relative to cardiac myocytes, the collagen matrix represents a major determinant of myocardial stiffness. Cardiac fibroblasts, not myocytes, contain the mRNA for these fibrillar collagens. In the hypertrophic remodeling of the myocardium that accompanies arterial hypertension, a progressive structural and biochemical remodeling of the matrix follows enhanced collagen gene expression. The resultant significant accumulation of collagen in the interstitium and around intramyocardial coronary arteries, or interstitial and perivascular fibrosis, represents a pathologic remodeling of the myocardium that compromises this normally efficient pump. This report reviews the structural nature, biosynthesis and degradation of collagen in the normal and hypertrophied myocardium. It suggests that interstitial heart disease, or the disproportionate growth of the extracellular matrix relative to myocyte hypertrophy, is an entity that merits greater understanding, particularly the factors regulating types I and III collagen gene expression and their degradation.

Animals↗
PubMed2005

[New concepts in reconstruction of arm and hand function in tetraplegia--basic research and clinical application].

Reconstructive hand surgery improves the ability to meet the needs of daily life and the independence of patients who have lost their upper extremity function due to cervical spinal cord injury. Tendon transfer procedures provide the potential to restore key functions, such as elbow and wrist extension or hand grip control, ameliorate joint balance, reduce pain in spasticity and prevent joint contractures. The choice of the optimal donor muscle should be based on a thorough understanding of the biomechanical principles of the muscle-tendon unit. Intraoperative sarcomere length measurements allow to predict and set the optimal muscle-tendon unit length during reconstructive upper extremity surgery in order to prevent overstretch which may lead to insufficient active force generation. Macro-proteins and the extracellular matrix are in charge of the muscle ultrastructure, elasticity and thus passive muscle tension. Spastic muscles are characterized by greater stiffness, a shorter sarcomere length and an extracellular matrix with inferior mechanical properties. Basic science research and clinical studies in cooperation with international centers are of great importance to promote the development of refined techniques of surgical reconstruction and postoperative rehabilitation of upper extremity function in tetraplegic patients.

Arm↗
PubMed2000

Relationships between plantar flexor muscle stiffness, strength, and range of motion in subjects with diabetes-peripheral neuropathy compared to age-matched controls.

STUDY DESIGN: Descriptive study to compare relationships between muscle performance measures in 2 subject groups. OBJECTIVES: To determine the relationships between plantar flexor (PF) muscle stiffness, strength (concentric peak torque), and dorsiflexion (DF) range of motion (ROM) in subjects with diabetes who have peripheral neuropathy (n = 17, 10 men, 7 women; age = 58 +/- 11 years) and age-matched controls (n = 17, 10 men, 7 women; age = 62 +/- 6 years). BACKGROUND: The relationships between muscle stiffness, strength, and joint ROM have not been clearly established. Furthermore, the effect of neuromuscular pathology on these relationships is unknown. METHODS AND MEASURES: PF stiffness and strength measurements were obtained with an isokinetic dynamometer. DF ROM was measured with a goniometer. A Pearson correlation matrix was constructed for each subject group using stiffness, strength, and ROM variables. The percent contribution of passive torque to total torque was computed at 2 joint angles. RESULTS: In subjects with diabetes and peripheral neuropathy (DM-PN) peak concentric PF torque was positively correlated with passive torque at 5 degrees DF (r = 0.77), Stiffness #1 (r = 0.58), and Stiffness #2 (r = 0.50). The percentage of passive PF torque at 5 degrees DF was greater in subjects with DM-PN, compared to control subjects (29.3 +/- 9.4% versus 12.6 +/- 5.9%). CONCLUSIONS: The positive correlation between PF stiffness and strength, and the greater percentage of passive PF torque in subjects with DM-PN suggest that patients with decreased strength may use passive torque to maximize total torque. Therefore, treatment methods designed to decrease stiffness should be used cautiously.

Aged↗
PubMed1998

Articular cartilage: tissue design and chondrocyte-matrix interactions.

The unique biologic and mechanical properties of articular cartilage depend on the design of the tissue and the interactions between the chondrocytes and the matrix that maintain the tissue. Chondrocytes form the macromolecular framework of the tissue matrix from three classes of molecules: collagens, proteoglycans, and noncollagenous proteins. Type II, IX, and XI collagens form a fibrillar meshwork that gives the tissue as form and tensile stiffness and strength. Type VI collagen forms part of the matrix immediately surrounding the chondrocytes and may help the chondrocytes to attach to the macromolecular framework of the matrix. Large aggregating proteoglycans (aggrecans) give the tissue its stiffness to compression and its resilience and contribute to its durability. Small proteoglycans, including decorin, biglycan, and fibromodulin, bind to other matrix macromolecules and thereby help to stabilize the matrix. They may also influence the function of the chondrocytes and bind growth factors. Anchorin CII, a noncollagenous protein, appears to help to anchor chondrocytes to the matrix. Cartilage oligomeric protein may have value as a marker of turnover and degeneration of cartilage, and other noncollagenous proteins, including tenascin and fibronectin, can influence interactions between the chondrocytes and the matrix. The matrix protects the cells from injury due to normal use of the joint, determines the types and concentrations of molecules that reach the tells and helps to maintain the chondrocyte phenotype. Throughout life, the tissue undergoes continual internal remodeling as the cells replace matrix macromolecules lost through degradation. The available evidence indicates that normal matrix turnover depends on the ability of chondrocytes to detect alterations in the macromolecular composition and organization of the matrix, including the presence of degraded molecules, and to respond by synthesizing appropriate types and amounts of new molecules. In addition, the matrix acts as a signal transducer for the cells. Loading of the tissue due to use of the joint creates mechanical, electrical, and physicochemical signals that help to direct the synthetic and degradative activity of chondrocytes. A prolonged severe decrease in the use of the joint leads to alterations in the composition of the matrix and eventually to loss of tissue structure and mechanical properties, whereas use of the joint stimulates the synthetic activity of chondrocytes and possibly the internal tissue remodeling Aging leads to alterations in the composition of the matrix and the activity of the chondrocytes, including the ability of the cells to respond to a variety of stimuli such as growth factors. These alterations may increase the probability of degeneration of the cartilage.

Animals↗
PubMed2003

Material properties of subchondral bone from patients with osteoporosis or osteoarthritis by microindentation testing and electron probe microanalysis.

Cancellous bone from patients with osteoarthritis (OA) has a reduced material density and appears to be undermineralized. It is hypothesized that this will result in a reduction in the mechanical stiffness and strength of the bone matrix. In this study, bone was obtained from superior and inferior sites, subjected to relatively high and low loads, respectively, from human femoral heads retrieved after surgery for osteoporotic hip fracture (OP), or for hip arthroplasty due to OA. Microindentation testing was used to measure the hardness of cancellous bone at various depths from the subchondral bone plate. The elemental composition from immediately adjacent microscopic sites was determined using electron probe microanalysis (EPMA). Overall, OA bone was found to have hardness values that were 7% lower than those from OP bone. Bone from the inferior site was harder than that from the superior in both diseases except in female OP patients. There was no variation with depth below the subchondral plate and no difference between sexes. No difference was found in the composition of the bone from the different disease groups and no correlation was found between hardness and any of the composition measurements. Though only an indirect measurement of stiffness, the reduction in hardness values supports the hypothesis that OA bone has a reduced elastic modulus.

Aged↗
PubMed1990

Extracellular matrix disruption and pain after eccentric muscle action.

Pain, stiffness, and indicators of muscle damage occur at different times after eccentric muscle action. After a single bout of maximal resisted lengthening of the elbow flexors, elbow position, pain perception, and indicators of cellular damage were measured. Immediately postexercise, a significant decrease in resting muscle length was observed that continued to 48 h. At this time, an increase in perceived muscle soreness was noted (P less than 0.05), and a biopsy of the biceps brachii revealed mast cell degranulation, separations of the extracellular matrix from myofibers, and increased plasma constituents in the extracellular space. It is proposed that myofiber disruption allows intracellular proteins to escape and extracellular proteins and ions to enter, causing swelling, whereas the disrupted extracellular matrix initiates the inflammatory response, which includes the release of mast cell granules seen at 48 h postexercise. Thus the delayed sensation of pain (soreness) after repeated eccentric muscle actions probably results from inflammation in response to extracellular matrix disruption.

Adult↗
PubMed2006

Cooperative deformation of mineral and collagen in bone at the nanoscale.

In biomineralized tissues such as bone, the recurring structural motif at the supramolecular level is an anisotropic stiff inorganic component reinforcing the soft organic matrix. The high toughness and defect tolerance of natural biomineralized composites is believed to arise from these nanometer scale structural motifs. Specifically, load transfer in bone has been proposed to occur by a transfer of tensile strains between the stiff inorganic (mineral apatite) particles via shearing in the intervening soft organic (collagen) layers. This raises the question as to how and to what extent do the mineral particles and fibrils deform concurrently in response to tissue deformation. Here we show that both mineral nanoparticles and the enclosing mineralized fibril deform initially elastically, but to different degrees. Using in situ tensile testing with combined high brilliance synchrotron X-ray diffraction and scattering on the same sample, we show that tissue, fibrils, and mineral particles take up successively lower levels of strain, in a ratio of 12:5:2. The maximum strain seen in mineral nanoparticles (approximately 0.15-0.20%) can reach up to twice the fracture strain calculated for bulk apatite. The results are consistent with a staggered model of load transfer in bone matrix, exemplifying the hierarchical nature of bone deformation. We believe this process results in a mechanism of fibril-matrix decoupling for protecting the brittle mineral phase in bone, while effectively redistributing the strain energy within the bone tissue.

Animals↗
PubMed2001

In situ compressive stiffness, biochemical composition, and structural integrity of articular cartilage of the human knee joint.

OBJECTIVE: Reduction of compressive stiffness of articular cartilage has been reported as one of the first signs of cartilage degeneration. For the measurement of in situ compressive stiffness, a hand-held indentation probe has recently been developed and baseline data for macroscopically normal knee joint cartilage were provided. However, the histological stage of degeneration of the measured cartilage was not known. The purpose of this study was to investigate whether there is a relationship between the in situ measured compressive stiffness, the histological stage of degeneration, and the biochemical composition of articular cartilage. DESIGN: Instantaneous compressive stiffness was measured for the articular cartilage of 24 human cadaver knees. Additionally, biochemical composition (total proteoglycan and collagen content) and histological appearance (according to the Mankin score) were assessed for each measurement location. RESULTS: Despite visually normal surfaces, various histological signs of degeneration were present. A high correlation between Mankin score and cartilage stiffness was observed for the lateral patellar groove (R(2)=0.81), the medial (R(2)=0.83) and the lateral femoral condyle (R(2)=0.71), whereas a moderate correlation was found for the medial patellar groove (R(2)=0.44). No correlation was observed between biochemical composition and cartilage compressive stiffness. CONCLUSIONS: Our results are in agreement with others and show that the instantaneous compressive stiffness is primarily dependent on the integrity of the extracellular matrix, and not on the content of the major cartilage constituents. The high correlation between stiffness and Mankin score in mild osteoarthrosis suggests that the stage of cartilage degeneration can be assessed quantitatively with the hand-held indentation probe. Moderate and severe case of osteoarthrosis remains to be investigated.

Adult↗