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PubMed1999

Mechanical characteristics of human skin subjected to static versus cyclic normal pressures.

Several hypotheses exist for the etiology of decubitus ulcers, with external pressures exceeding internal capillary pressures over bony prominences claimed to be the major factor. This investigation evaluated the mechanical changes that occurred in human skin as a result of its exposure to static versus cyclic normal pressures of the magnitudes earlier recorded for the heels of human subjects on various support surfaces. The skin was characterized through uniaxial tensile testing. Static pressure alone altered the tissue's mechanical properties more than dynamic pressure cycles. Tissue subjected to pressure prior to uniaxial tensile testing always was less stiff than control tissue. Damage to the initially randomly oriented tissue collagen fiber bundles in the fibrous matrix, which may occur as a result of sustained compression, may be the cause of a decrease in stiffness of tissue subjected to prior pressure loading. This is the first report of compressive-pre-load-induced strain softening (Mullins effect) of a biological material.

Humans↗
PubMed1989

Collagen and proteoglycan in a sea urchin ligament with mutable mechanical properties.

The "problematic ligament" of sea urchins is a connective tissue which crosses the ball-and-socket joint between spine and body wall. The problem of this ligament is that it is composed of parallel collagen fibrils, yet normally undergoes rapid and dramatic alterations in mechanical properties and in length. Previous work has suggested that the collagen fibrils of the ligament are able to slide past one another during length changes but are inhibited from sliding when the ligament is in "catch". In this model of the ligament both the collagen fibrils and the interfibrillar matrix are mechanically important. We have found that the collagen fibrils of the spine ligament of the pencil urchin Eucidaris tribuloides are discontinuous and end by tapering within the body of the ligament. Intact fibrils that have been isolated from the ligament vary by more than an order of magnitude in length and in radius but have a constant length/radius (aspect) ratio of about 5,300. This is the first determination of the aspect ratio of collagen fibrils from any source. The constant aspect ratio of the fibrils is consistent with their functioning as the discontinuous fiber phase in a fiber-reinforced composite material, while the high value of the aspect ratio indicates that the nonfibrillar matrix, which must act to transfer stress between fibrils, can produce a stiff and strong ligament even if it is several orders of magnitude weaker and more compliant than the fibrils. Moreover, the tensile properties of the ligament may be determined by the properties of the matrix. A prominent component of the interfibrillar matrix is a proteoglycan which associates with specific bands at the surface of the collagen fibrils through noncovalent binding of its core protein. The glycosaminoglycan moiety of this proteoglycan is partly comprised of chondroitin sulfate/dermatan sulfate polymers. These results are consistent with the "sliding fibril" hypothesis and suggest that the proteoglycan may be an important component of the stress-transfer matrix.

Animals↗
PubMed2004

Vascular stiffening and arterial compliance. Implications for systolic blood pressure.

Hypertension in older persons is characterized by increased systolic blood pressure, and isolated systolic hypertension (ISH) is the most common type of hypertension in this population. It is thought that ISH results from age-associated vascular stiffening and reduced compliance that can be revealed and quantified by analysis of arterial pressure waveforms. Evaluation of pulse wave velocity and other related measures has shown that arterial stiffness increases with advancing age and other cardiovascular (CV) risk factors including hypertension, the metabolic syndrome, diabetes, obesity, hypercholesterolemia, and elevated C-reactive protein. Many of these relationships have been demonstrated in patients without clinical CV disease and are independent of patient age. Arterial stiffness is significantly and independently associated with both target organ damage and increased risk for CV morbidity and mortality. The mechanisms underlying age- and disease-related arterial stiffening are not fully understood. However, assessment of changes in gene expression associated with increased arterial stiffness and gene polymorphisms that increase the risk for vascular stiffening suggests that components of the renin-angiotensin system, matrix metalloproteinases, intracellular signaling, and extracellular matrix components may all be involved in this process. Interventions aimed at these targets may reduce vascular stiffness, lower systolic blood pressure, decrease the prevalence of ISH, and improve outcomes for patients (particularly older patients) with hypertension or other CV conditions.

Aging↗
PubMed1999

Effect of porosity and environment on the mechanical behavior of acrylic bone cement modified with acrylonitrile-butadiene-styrene particles: I. Fracture toughness.

The elastomeric copolymer acrylonitrile-butadiene-styrene (ABS) was added to a conventional acrylic bone cement matrix. The results obtained show that although strength and stiffness decreased with an increasing second phase volume fraction, ductility and toughness both increased. The crack propagation became stable for specimens containing over a 5% volume fraction of the second phase. The fracture toughness increased up to 60% when the amount of ABS reached 20% (v/v). For larger amounts linear elastic fracture mechanics techniques could not be used properly. The effects of porosity and environmental conditions on the mechanical behavior were also studied. The mechanisms that control the fracture process were investigated by means of scanning electron microscopy.

Acrylic Resins↗
PubMed2005

Long-term in vivo stability of rabbit nasal septal cartilage following laser cartilage reshaping: a pilot investigation.

BACKGROUND AND OBJECTIVES: To evaluate the long-term effect of laser cartilage reshaping on rabbit nasal septal cartilage viability and mechanical integrity in an in vivo model. STUDY DESIGN/MATERIALS AND METHODS: In vivo animal investigation. Rabbit septal cartilage specimens were laser (Nd:YAG, lambda = 1.32 mum, spot size 5.4-mm diameter, 10 W, 10 seconds, 50 Hz PPR) reshaped and subsequently reimplanted into an interscapular subcutaneous pocket. Specimens were harvested at 8 and 12 months and evaluated using photography, flow cytometry, and histology. RESULTS: Grossly, specimens showed alteration in the physical integrity with varying degrees of tissue resorption. The non-irradiated control specimens demonstrated significantly increased stiffness. Histologically, there was marked depletion of the extracellular matrix and an overall reduction in tissue mass in laser irradiated tissues. However, flow cytometry data identified viable chondrocytes in laser-irradiated specimens that were identical to those observed in controls. CONCLUSIONS: Study results demonstrate that the rabbit nasal septal cartilage model can be effectively used to study laser reshaping, however alternative recipient sites with perichondrial lining, such as the pinna, may provide a more realistic physiologic environment for reshaped graft tissue. The dosimetry used in this pilot study likely led to significant thermal injury. Study results underscore the importance of elucidating the optimal laser dosimetry required to initiate permanent shape change while minimizing thermal damage.

Animals↗
PubMed1988

Effects of chronic beta-aminoproprionitrile treatment on rat carotid artery.

The effects of chronic treatment of young rats (initially 8 weeks old) with the collagen cross-linking inhibitor, beta-aminoproprionitrile (BAPN), on arterial wall properties were studied. BAPN was added to the drinking water for 8 weeks to produce intakes of 0, 100, 200 and 400 mg/kg/day. Systolic pressure of treated animals did not increase with age as rapidly as that of untreated controls. Weight gain of treated animals was inhibited at the highest (BAPN) treatment level. Passive stiffness of isolated, cylindrical segments of carotid arteries was decreased in BAPN-treated animals in a dose-dependent manner. BAPN treatment had no significant effect on the total collagen or elastin content (hydroxyproline) of carotid arteries. Values of maximum active force development to 10 microM norepinephrine plus 75 mM K+ were decreased by BAPN treatment in a dose-dependent manner. There was no significant effect of BAPN treatment on total water content or its cellular and extracellular components in the carotid artery. The relative cell volume of carotid arteries was not altered by BAPN treatment, suggesting that the decreased force development was a characteristic of individual cells. These results suggest that BAPN treatment may decrease stiffness by altering secondary characteristics of the connective tissue matrix without affecting connective tissue content. The decreased maximum smooth muscle force development may be responsible for the blood pressure-lowering effects of BAPN.

Administration, Oral↗
PubMed2005

The modulus of elasticity of fibrillin-containing elastic fibres in the mesoglea of the hydromedusa Polyorchis penicillatus.

Hydromedusan jellyfish swim by rhythmic pulsation of their mesogleal bells. A single swimming muscle contracts to create thrust by ejecting water from the subumbrellar cavity. At the end of the contraction, energy stored in the deformation of the mesogleal bell powers the refilling stage, during which water is sucked back into the subumbrellar cavity. The mesoglea is a mucopolysaccharide gel reinforced with radially oriented fibres made primarily of a protein homologous to mammalian fibrillin. Most of the energy required to power the refill stroke is thought to be stored by stretching these fibres. The elastic modulus of similar fibrillin-rich fibres has been measured in other systems and found to be in the range of 0.2 to 1.1 MPa. In this paper, we measured the diameters of the fibres, their density throughout the bell, and the mechanical behaviour of the mesoglea, both in isolated samples and in an intact bell preparation. Using this information, we calculated the stiffness of the fibres of the hydromedusa Polyorchis penicillatus, which we found to be approximately 0.9 MPa, similar in magnitude to other species. This value is two orders of magnitude more compliant than the stiffness of the component fibrillin microfibrils previously reported. We show that the structure of the radial fibres can be modelled as a parallel fibre-reinforced composite and reconcile the stiffness difference by reinterpreting the previously reported data. We separate the contributions to the bell elasticity of the fibres and mesogleal matrix and calculate the energy storage capacity of the fibres using the calculated value of their stiffness and measured densities and diameters. We conclude that there is enough energy potential in the fibres alone to account for the energy required to refill the subumbrellar cavity.

Animals↗
PubMed2005

Ramipril reduces large-artery stiffness in peripheral arterial disease and promotes elastogenic remodeling in cell culture.

Ramipril improves cardiovascular outcome in patients with peripheral arterial disease; however, the precise mechanisms of benefit remain to be elucidated. The effect of ramipril on large-artery stiffness in patients with peripheral arterial disease was examined. In addition, we determined the effect of ramiprilat on extracellular matrix from human aortic smooth muscle cell culture. Forty patients with peripheral arterial disease were randomized to receive ramipril, 10 mg once daily or placebo for 24 weeks. Arterial stiffness was assessed globally via systemic arterial compliance and augmentation index (carotid tonometry and Doppler velocimetry), and regionally via carotid-femoral pulse wave velocity. Angiotensin-converting enzyme inhibition increased arterial compliance by 0.10+/-0.02 mL/mm Hg, (P<0.001, all probability values relative to placebo) and reduced pulse wave velocity by 1.7+/-0.2 m/s (P<0.001), augmentation index by 4.1+/-0.3% (P<0.001), and systolic blood pressure by 5+/-1 mm Hg (P<0.001). Ramipril did not reduce mean arterial pressure significantly compared with placebo (P=0.59). In cell culture, ramiprilat decreased collagen deposition by >50% and increased elastin and fibrillin-1 deposition by >3- and 4-fold respectively (histochemistry and immunohistochemistry). Fibrillin-1 gene expression was increased 5-fold (real-time reverse-transcriptase polymerase chain reaction). Ramiprilat also reduced gene and protein (Western) expression of both matrix metalloproteinase (MMP)-2 and MMP-3. In conclusion, ramipril promoted an elastogenic matrix profile that may contribute to the observed clinical reduction in large-artery stiffness and carotid pressure augmentation, which occurred independently of mean arterial blood pressure reduction in patients with peripheral arterial disease.

Aged↗
PubMed2003

Advanced glycation endproducts and osteoarthritis.

Non-enzymatic glycation of proteins, such as collagen, results in the formation of advanced glycation endproducts (AGE). Advanced glycation endproducts result in pathologic stiffening of cartilage and extracellular matrix and accumulate with age. Pentosidine, an AGE, is present in serum, synovial fluid, and articular cartilage from patients with osteoarthritis (OA). However, AGE levels are not always increased, and may be decreased locally, in association with osteoarthritic pathology. The finding of pentosidine in articular cartilage of individuals with OA may not be specific for that disease, independent of chronologic age. Advanced glycation endproduct modification of normal articular cartilage increases its stiffness, increases chondrocyte-mediated proteoglycan degradation, reduces its susceptibility to matrix metalloproteinase-mediated degradation, and decreases proteoglycan synthesis by chondrocytes. These observations parallel findings in osteoarthritic cartilage, which suggests that AGE modification could contribute to the pathogenesis of OA. However, a causative link between AGEs and OA has not yet been established.

Aging↗
PubMed1995

Evidence that calcium-dependent cellular processes are involved in the stiffening response of holothurian dermis and that dermal cells contain an organic stiffening factor

Although previous investigations have shown that experimental increases and decreases of the concentration of extracellular Ca2+ produce correlated changes in the stiffness of holothurian dermis, they have failed to determine whether the Ca2+-correlated changes were due to Ca2+-dependent cellular events or to direct effects of Ca2+ on the viscosity of the extracellular matrix. We have addressed this question by testing two explicit predictions of the latter hypothesis: that dermal stiffness should be correlated with the Ca2+ concentration in the absence of viable cells; and that, in the presence of a normal extracellular Ca2+ concentration, drugs that inhibit cellular pathways dependent on Ca2+ should not affect dermal stiffness. Our results are inconsistent with the hypothesis and support the alternative hypothesis that Ca2+ is important only in the cellular regulation of dermal stiffness. In addition, we have extracted from dermal cells an organic factor that stiffens the extracellular matrix.

Journal Article↗
PubMed2001

The stiffness of bone marrow cell-knit composites is increased during mechanical load.

A novel device for mechanical stimulation of primary adult rat bone marrow cells cultured on three-dimensional knitted textiles has been prototyped. A method has been developed ensuring a well-defined, high-density, and reproducible cell seeding on the knitted fabric. After culturing for 18-52 days the cell-knit composites were subjected to uniaxial 2% stretching and relaxation. The frequency was altered between 0.1 Hz (196 min, loading phase) and 0.01 Hz (360 min, resting phase). Identically treated knits without cells exhibited a slight stiffness reduction, whereas the stiffness of knits with cells increased from cycle to cycle. The stiffness increase was found to depend on the duration of the culture period before mechanical loading. Our data suggest that the extracellular matrix deposited by the cells on the knit and intact microtubuli of living cells cause the observed stiffness increase. In comparison to the unstrained static cell-knit composites cell proliferation and bone cell differentiation were reduced by the mechanical load.

Animals↗
PubMed2002

Molecular basis for differences between human joints.

The molecular program of a cell determines responses including induction or inhibition of genes for function and activity, and this is true of the cells within articular cartilage, a major functional component of the joint. While our studies have previously focussed on differences in the molecular programs of the cells within the superficial and deep zones, we have recently begun to focus on relative differences between joints, such as the knee and ankle. In the human, these joints vary greatly in their susceptibility to joint diseases, such as osteoarthritis (OA). We have predicted that there would be a molecular basis for differences between joints that could lead to differences in susceptibility to OA, if inherent pathways locked into the resident cells induce differences in their response to their environment. We have been able to show that there are differences between the matrix components and water content; these properties correspond to a higher equilibrium modulus and dynamic stiffness but lower hydraulic permeability and serve to make the ankle cartilage stiffer, slowing movement of molecules through the cartilage. In addition to these biochemical differences in the cartilage matrix, we have also identified relative differences in the strength of the response to stimulation of chondrocytes from knee and ankle. The stronger response of the knee chondrocytes includes factors that increase damage to the cartilage matrix, such as a depression of matrix synthesis and increased enzyme activity. This response by the knee chondrocytes results in enzyme damage to the matrix that the cells may not be able to repair, while the weaker response of the ankle chondrocytes may allow the cells to repair their matrix damage.

Alginates↗
PubMed2005

Impact of myocardial structure and function postinfarction on diastolic strain measurements: implications for assessment of myocardial viability.

We sought to assess the role of regional diastolic function by Doppler echocardiography in predicting myocardial viability. Sixteen dogs underwent left anterior descending coronary artery (n = 8) or circumflex (n = 8) occlusion. All animals were imaged at baseline and 1-8 wk postinfarction (post-MI). In 10 dogs, invasive hemodynamic monitoring with a conductance catheter placed in the left ventricle (LV) was performed at the above time points. Dobutamine was infused at 1-8 wk post-MI to determine LV contractile reserve. Histomorphological analysis was performed to determine the presence of viable myocardium and changes in interstitial matrix. Post-MI, diastolic strain rate measurements (in radial and longitudinal planes) decreased significantly in the distribution of the diseased artery (P < 0.01) and on multiple regression analysis were determined by time constant of LV relaxation, end-diastolic pressure, regional stiffness, and the ratio of cellular infiltration to collagen deposition in the interstitial matrix. Among several indexes, diastolic strain rate during dobutamine infusion readily identified segments with >20% transmural infarction and related best to the extent of interstitial fibrosis (r = -0.86, P < 0.01). In an animal model of healing canine infarcts, diastolic strain rate by Doppler echocardiography appears to be a promising novel index of myocardial viability.

Animals↗
PubMed2006

Optical coherence elastography of engineered and developing tissue.

Biomechanical elastic properties are among the many variables used to characterize in vivo and in vitro tissues. Since these properties depend largely on the micro- and macroscopic structural organization tissue, it is crucial to understand the mechanical properties and the alterations that occur tissues respond to external forces or to disease processes. Using a novel technique called coherence elastography (OCE), we mapped the spatially distributed mechanical displacements strains in a representative model of a developing, engineered tissue as cells began to proliferate attach within a three-dimensional collagen matrix. OCE was also performed in the complex tissue of the Xenopus laevis (African frog) tadpole. Displacements were quantified a cross-correlation algorithm on pre- and postcompression images, which were acquired using coherence tomography (OCT). The images of the engineered tissue were acquired over a 10-development period to observe the relative strain differences in various regions. OCE was able differentiate changes in strain over time, which corresponded with cell proliferation and matrix as confirmed with histological observations. By anatomically mapping the regional variation stiffness with micron resolution, it may be possible to provide new insight into the complex by which engineered and natural tissues develop complex structures.

Animals↗
PubMed2004

Strain-rate dependence of cartilage stiffness in unconfined compression: the role of fibril reinforcement versus tissue volume change in fluid pressurization.

The strain and strain-rate-dependent response of articular cartilage in unconfined compression was studied theoretically. The transient stress and stiffness of cartilage were determined for strain rates ranging from zero to infinity. It is shown, for a given compressive strain, that the axial stress initially increases quickly as a function of strain rate, and then increases progressively more slowly towards the stress corresponding to the instantaneous response. The volume change of the tissue does not give its transient stiffness uniquely, because of the strong strain-rate dependence. The variation of tissue stiffness is primarily determined by the transient stiffness of the radial fibrils. Load sharing between the solid matrix and fluid pressurization also depends on the strain rate. At 15% axial compression, the matrix bears more than 80% of the applied load at a strain rate of 0.005%/s, while the fluid pressurization contributes more than 80% of the load at a strain rate of 0.15%/s. These results show the interplay between fibril reinforcement and fluid pressurization in articular cartilage: the fluid drives fibril stiffening which in turn produces high pore pressure at high strain rates. As a secondary objective of the present work, a fibrillar continuum element was formulated to replace the fibrillar spring element used previously in fibril-reinforced modeling, in order to eliminate the deformation incompatibility between the spring system and the nonfibrillar matrix. The results obtained using the two fibrillar elements were compared with the closed-form solutions for the static and instantaneous responses for the case of large deformation. It was found for unconfined compression that using the spring elements did not generally result in greater numerical errors than using the fibrillar continuum elements.

Animals↗
PubMed1991

Pathologic fibrosis and matrix connective tissue in the subaortic myocardium of patients with hypertrophic cardiomyopathy.

To evaluate scar-type and matrix connective tissue and to assess their role in the diastolic dysfunction of hypertrophic cardiomyopathy, surgically resected subaortic myectomy specimens and several autopsy hearts from patients with hypertrophic cardiomyopathy were studied. Eighteen specimens were differentially stained by a newly developed method that precisely determines relative collagen content; these tissues were compared with postmortem hypertrophied and normal control subaortic specimens. Quantitation revealed a 72% higher level (36.5 vs. 22.1 micrograms collagen/mg protein) of stainable collagen in the hearts with hypertrophic cardiomyopathy than in hypertrophied control hearts. The endocardial plaque was quantitated morphometrically, and it constituted only 4.6 +/- 1.7% of the total increased collagen content in the cardiomyopathy specimens. For the matrix studies, the cardiomyopathy specimens were stained by a silver impregnation technique that identifies connective tissue elements not normally visible with routine histologic methods. There was a marked increase in content of all matrix components, both in areas of pathologic scarring and in "normal" zones. Whorls of matrix connective tissue were noted in regions of myocyte whorls, as well as independent of them. Thus, these studies revealed a striking increase of both scar-type and matrix connective tissue in hypertrophic cardiomyopathy. The extensive scarring and the pronounced interstitial and intercellular matrix connective tissue may contribute to the increased ventricular chamber stiffness and impaired relaxation in this disease.

Cardiomyopathy, Hypertrophic↗
PubMed2005

Rigidity sensing at the leading edge through alphavbeta3 integrins and RPTPalpha.

Cells require optimal substrate stiffness for normal function and differentiation. The mechanisms for sensing matrix rigidity and durotaxis, however, are not clear. Here we showed that control, Shp2-/-, integrin beta1-/-, and talin1-/- cell lines all spread to a threefold greater area on fibronectin (FN)-coated rigid polyacrylamide surfaces than soft. In contrast, RPTPalpha-/- cells spread to the same area irrespective of rigidity on FN surfaces but spread 3x greater on rigid collagen IV-coated surfaces than soft. RPTPalpha and alphavbeta3 integrins were shown previously to be colocalized at leading edges and antibodies to alphavbeta3 blocked FN rigidity sensing. When FN beads were held with a rigid laser trap at the leading edge, stronger bonds to the cytoskeleton formed than when held with a soft trap; whereas back from the leading edge and in RPTPalpha-/- cells, weaker bonds were formed with both rigid and soft laser traps. From the rigidity of the trap, we calculate that a force of 10 pN generated in 1 s is sufficient to activate the rigidity response. We suggest that RPTPalpha and alphavbeta3 at the leading edge are critical elements for sensing FN matrix rigidity possibly through SFK activation at the edge and downstream signaling.

Animals↗
PubMed2005

Mechanical unloading during left ventricular assist device support increases left ventricular collagen cross-linking and myocardial stiffness.

BACKGROUND: Left ventricular assist devices (LVADs) induce reverse remodeling of the failing heart except for the extracellular matrix, which exhibits additional pathophysiological changes, although their mechanisms and functional consequences are unknown. METHODS AND RESULTS: Hearts were obtained at transplant from patients with idiopathic dilated cardiomyopathy (DCM) not requiring LVAD support (n=30), patients requiring LVAD support (n=16; LVAD duration, 145+/-33 days), and 5 nonfailing hearts. Left (LV) and right ventricular (RV) ex vivo pressure-volume relationships were measured, and chamber and myocardial stiffness constants were determined. Myocardial tissue content of total and cross-linked collagen, collagen types I and III, MMP-1, MMP-9, TIMP-1, and angiotensin (Ang) I and II were measured. LV size, mass, and myocyte diameter decreased after LVAD compared with DCM without LVAD (P<0.05). Total and cross-linked collagen and ratio of type I to III collagen increased in DCM compared with nonfailing hearts and increased further after LVAD (P<0.05 versus DCM and nonfailing). Concomitantly, chamber and myocardial stiffness increased with LVAD. The ratio of MMP-1 to TIMP-1 increased in DCM and almost normalized after LVAD, favoring decreased collagen degradation. Tissue Ang I and II also increased during LVAD. There was no significant change in the RV of LVAD-supported heart compared with DCM. CONCLUSIONS: LVAD support increases LV collagen cross-linking and the ratio of collagen type I to III, which is associated with increased myocardial stiffness. Decreased tissue MMP-1-to-TIMP-1 ratio (decreased degradation) and increased Ang levels (stimulants of synthesis) are likely mechanisms for these changes. Lack of significant effects on the RV suggest that hemodynamic unloading of the LV (not provided to the RV) might be the primary factor that regulates these extracellular matrix changes.

Adult↗