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PubMed1994

Collagen network of the myocardium: function, structural remodeling and regulatory mechanisms.

A collagen network, composed largely of type I and III fibrillar collagens, is found in the extracellular space of the myocardium. This network has multiple functions which includes a preservation of tissue architecture and chamber geometry. Given its tensile strength, collagen is a major determinant of tissue stiffness. Its disproportionate accumulation, in the form of either a reactive or a reparative fibrosis, further increases stiffness. A degradation of collagen tethers, on the other hand, is an anatomic requisite for a distortion in tissue architecture and a reduction in stiffness that can lead to chamber dilatation, wall thinning, and even rupture of the myocardium. Collagen turnover in the myocardium is dynamic. When synthesis exceeds degradation, an adverse accumulation of collagen appears to distort tissue structure. This is true for either the hypertrophied and/or nonhypertrophied ventricle. Factors that contribute to the appearance of myocardial fibrosis are largely different from those that promote cardiac myocyte growth. Included amongst these fibrogenic factors are effector hormones of the reinin-angiotensin-aldosterone system (RAAS). Studies conducted both in intact animals (relative to dietary sodium intake) and in cultured adult cardiac fibroblasts have pointed toward the association between collagen accumulation and chronic elevations in circulating angiotensin II and aldosterone. A tissue hormonal system involving angiotensin II, endothelins and bradykinin, may likewise regulate fibrogenesis. In this regard, angiotensin converting enzyme is found in connective tissue of the normal heart, including the matrix of heart valves and the adventitia of the intramural coronary arteries, and fibrous tissue that forms following infarction or with chronic RAAS activation. The importance of ACE in the regulation of local angiotensin II and bradykinin levels and their contribution to collagen turnover is a fruitful area of research with important clinical implications. The myocardium also contains a proteolytic system, including collagenase. The characteristics and regulation of matrix metalloproteinases and their tissue inhibitors in various cardiovascular disease states requires further investigation.

Angiotensin II↗
PubMed2006

The efficacy of cylindrical titanium mesh cage for the reconstruction of a critical-size canine segmental femoral diaphyseal defect.

The authors developed a novel technique for the reconstruction of large segmental long bone defects using a cylindrical titanium mesh cage (CTMC). Although the initial clinical reports have been favorable, the CTMC technique has yet to be validated in a clinically relevant large animal model, which is the purpose of this study. Under general anesthesia, a unilateral, 3-cm mid-diaphyseal segmental defect was created in the femur of an adult canine. The defect reconstruction technique consisted of a CTMC that was packed and surrounded with a standard volume of morselized canine cancellous allograft and canine demineralized bone matrix. The limb was stabilized with a reamed titanium intramedullary nail. Animals were distributed into four experimental groups: in Groups A, B, and C (six dogs each), defects were CTMC reconstructed, and the animals euthanized at 6, 12, and 18 weeks, respectively; in Group D (three dogs), the same defect reconstruction was performed but without a CTMC, and the animals were euthanized at 18 weeks. The femurs were harvested and analyzed by gross inspection, plain radiography, computed tomography (CT), and single photon emission computed tomography (SPECT). The femurs were mechanically tested in axial torsion to failure; two randomly selected defect femurs from each group were analyzed histologically. Groups A, B, and C specimens gross inspection, plain radiography, and CT, demonstrated bony restoration of the defect, and SPECT confirmed sustained biological activity throughout the CTMC. Compared to the contralateral femur, the 6-, 12-, and 18-week mean defect torsional stiffness was 44.4, 45.7, and 72.5%, respectively; the mean torsional strength was 51.0, 73.6, and 83.4%, respectively. Histology documented new bone formation spanning the defect. Conversely, Group D specimens (without CTMC) demonstrated no meaningful bone formation, biologic activity, or mechanical integrity at 18 weeks. The CTMC technique facilitated healing of a canine femur segmental defect model, while the same technique without a cage did not. The CTMC technique may be a viable alternative for the treatment of segmental long bone defects.

Animals↗
PubMed2002

Effects of collagen unwinding and cleavage on the mechanical integrity of the collagen network in bone.

The objective of this study was to investigate how molecular level changes in the collagen network affect its mechanical integrity. Our hypothesis is that the cleavage and unwinding of triple helices of collagen molecules significantly reduce the mechanical integrity of the collagen network in bone, whereas collagen crosslinks play a major role in sustaining the structural integrity of the collagen network. To test this hypothesis, the collagen molecular structure was altered in demineralized human cadaveric bone samples in the following two ways: heat induced unwinding and pancreas elastase induced cleavage of collagen molecules. Along with control specimens, the treated specimens were mechanically tested in tension to determine their strength, elastic modulus, toughness, and strain to failure. Also, the percentage of denatured collagen molecules and amounts of two major collagen crosslinks (hydroxylysylpyridinoline and lysylpyridinoline) were determined using high-performance liquid chromatography techniques. It was found that unwinding of collagen molecules may cause more reduction in stiffness (E) but less strain to failure (ef) than cleavage. Both collagen denaturation types cause similar changes in the strength (ss) and work to fracture (Wf) of the collagen network with no significant changes in hydroxylysylpyridinoline and lysylpyridinoline crosslinks. The results of this study indicate that the integrity of collagen molecules significantly affect the mechanical properties of the collagen network in bone, and that collagen crosslinks may play an important role in maintaining the mechanical integrity of the collagen network after collagen denaturation occurs.

Adult↗
PubMed2003

A novel bioreactor for the dynamic flexural stimulation of tissue engineered heart valve biomaterials.

Dynamic flexure is a major mode of deformation in the native heart valve cusp, and may effect the mechanical and biological development of tissue engineered heart valves (TEHV). To explore this hypothesis, a novel bioreactor was developed to study the effect of dynamic flexural stimulation on TEHV biomaterials. It was implemented in a study to compare the effect of uni-directional cyclic flexure on the effective stiffness of two candidate TEHV scaffolds: a non-woven mesh of polyglycolic acid (PGA) fibers, and a non-woven mesh of PGA and poly L-lactic acid (PLLA) fibers, both coated with poly 4-hydroxybutyrate (P4HB). The bioreactor has the capacity to dynamically flex 12 rectangular samples (25 x 7.5 x 2mm) under sterile conditions in a cell culture incubator. Sterility was maintained in the bioreactor for at least 5 weeks of incubation. Flexure tests to measure the effective stiffness in the "with-flexure" (WF) and opposing "against-flexure" (AF) directions indicated that dynamically flexed PGA/PLLA/P4HB scaffolds were approximately 72% (3 weeks) and 76% (5 weeks) less stiff than static controls (p<0.01), and that they developed directional anisotropy by 3 weeks of incubation (stiffer AF, p<0.01). In contrast, both dynamically flexed and static PGA/P4HB scaffolds exhibited a trend of decreased stiffness with incubation, with no development of directional anisotropy. Dynamically flexed PGA/P4HB scaffolds were significantly less stiff than static controls at 3 weeks (p<0.05). Scanning electron microscopy revealed signs of heterogeneous P4HB coating and fiber disruption, suggesting possible explanations for the observed mechanical properties. These results indicate that dynamic flexure can produce quantitative and qualitative changes in the mechanical properties of TEHV scaffolds, and suggest that these differences need to be accounted for when comparing the effects of mechanical stimulation on the development of cell-seeded TEHV constructs.

Absorbable Implants↗
PubMed2003

Long-term cyclic distention enhances the mechanical properties of collagen-based media-equivalents.

In this study, we sought to identify the key parameters involved in long-term cyclic distension (CD) as they pertain to the development of collagen-based media-equivalents (MEs). By using only highly compacted, cross-linked constructs, we avoided the complicating issues of irrecoverable creep and transient alignment, and isolated the effects of cyclic mechanical loading on ME development. Our system allowed us to study this development over a wide range of parameters including strain amplitude, pulse frequency, pulse shape, and culture time. We found that in most cases involving cyclic distension, MEs were both stronger and stiffer than constructs that were grown under static conditions. The mechanical properties were not significantly different from static controls after two weeks of CD, however, five weeks of CD was sufficient to note significant increases in both stiffness and strength. The strain, stretch time, and relaxation time were all important variables in determining ME mechanical properties. While we were unable to detect a significant net change in the amount of total collagen, we observed significant deposition of insoluble elastin in our CDMEs, something that has never been previously reported using adult smooth muscle cells. Finally, these changes in ME development did not depend on the age of the MEs prior to the initiation of CD.

Adaptation, Physiological↗
PubMed2001

Influence of calcium ions on the mechanical properties of a model biofilm of mucoid Pseudomonas aeruginosa.

The mechanical properties of biofilms and in particular their mechanical strength is of great importance for both biofilm reactors and for the removal of undesired biofilms as in cases of biofouling and biocorrosion. By uniaxial compression measurements, it is possible to determine the apparent elastic or Young's modulus and the yield stress as parameters for mechanical stability. This was performed with a recently developed device, using model biofilms of mucoid strain Pseudomonas aeruginosa SG81. The biofilms were grown on membrane filters placed on nutrient agar medium with different concentrations of calcium ions. The compressive stress-strain behaviour up to failure was recorded at a compression speed of 1 micron s-1. The apparent Young's modulus, representing the stiffness of the biofilm, and the yield stress obtained from the stress--strain diagram were used for the description of mechanical properties of biofilms. A certain critical concentration of calcium ions was found where the Young's modulus of the P. aeruginosa biofilms increases strongly and subsequently remains constant for higher calcium concentrations. This behaviour is explained by the presence of calcium ions crosslinking alginate, which is the major component of the extracellular polymeric substances produced by the mucoid P. aeruginosa strain used in this investigation.

Biofilms↗
PubMed2005

Compliance of abdominal aortic aneurysms evaluated by tissue Doppler imaging: correlation with aneurysm size.

OBJECTIVES: Several studies have shown that an increase in abdominal aortic aneurysm (AAA) growth rate occurs when the diameter reaches 40 to 50 mm. AAA expansion is related to remodeling of the parietal extracellular matrix. The parietal mechanisms involved in this critical phase of sudden increase remain unexplained. Analysis of AAA wall movements and determination of AAA compliance may provide information about the constitution of the arterial wall. If a change in parietal wall motion somewhere between 40 and 50 mm could be shown, this would contribute to the understanding of the growth of AAA. Furthermore, it would provide a valuable additional parameter for AAA monitoring. This study had two aims: first, to evaluate the relationship between AAA compliance and maximum diameter using the tissue Doppler imaging system; and second, to test the hypothesis of a change in AAA behavior at around 45 mm in diameter. METHODS: Fifty-six patients with AAA (mean diameter, 39 mm) were prospectively investigated using the tissue Doppler imaging system, which provides information concerning arterial wall motion. Maximum mean segmental dilation (MMSD), segmental compliance, pressure strain elastic modulus (Ep), and stiffness were determined and related to the maximum diameter of AAA. Results After natural log transformation of all variables, there was a significant positive linear relationship between maximum diameter and both MMSD (P < .001) and segmental compliance (P < .001) but not with Ep or stiffness (P = .37 and .22, respectively). MMSD and segmental compliance were significantly higher in AAA > or = 45 mm than in AAA < 45 mm (P < .0002 and <. 004, respectively). Ep and stiffness tended to decrease in larger AAAs, but this was not statistically significant (P < .43 and .24, respectively). Dispersion of Ep and stiffness values seemed to be wider among AAA < 45 mm compared with those > or = 45 mm. CONCLUSION: Compliance parameters can easily be measured during routine AAA ultrasound monitoring using the tissue Doppler imaging system. The study showed an increase in MMSD and segmental compliance as well as a nonsignificant trend toward increased distensibility (decreased Ep and stiffness) with increased AAA diameter. A change in dispersion of AAA distensibility may appear around 45 mm in diameter, but a larger study will be needed to clarify this.

Abdominal Wall↗
PubMed2004

Do changes in the mechanical properties of articular cartilage promote catabolic destruction of cartilage and osteoarthritis?

Osteoarthritis (OA) is a joint disease characterized by cartilage degeneration, a thickening of subchondral bone, and formation of marginal osteophytes. Previous mechanical characterization of cartilage in our laboratory suggests that energy storage and dissipation is reduced in osteoarthritis as the extent of fibrillation and fissure formation increases. It is not clear whether the loss of energy storage and dissipation characteristics is a result of biochemical and/or biophysical changes that occur to hyaline cartilage in joints. The purpose of this study is to present data, on the strain rate dependence of the elastic and viscous behaviors of cartilage, in order to further characterize changes that occur in the mechanical properties that are associated with OA. We have previously hypothesized that the changes seen in the mechanical properties of cartilage may be due to altered mechanochemical transduction by chondrocytes. Results of incremental tensile stress-strain tests at strain rates between 100%/min and 10,000%/min conducted on OA cartilage indicate that the slope of the elastic stress-strain curve increases with increasing strain rate, unlike the reported behavior of skin and self-assembled collagen fibers. It is suggested that the strain-rate dependence of the elastic stress-strain curve is due to the presence of large quantities of proteoglycans (PGs), which protect articular cartilage by increasing the apparent stiffness. The increased apparent stiffness of articular cartilage at high strain rates may limit the stresses borne and prolong the onset of OA. It is further hypothesized that increased compressive loading of chondrocytes in the intermediate zone of articular cartilage occurs as a result of normal wear to the superficial zone or from excessive impact loading. Once the superficial zone of articular cartilage is worn away, the tension is decreased throughout all cartilage zones leading to increased chondrocyte compressive loading and up-regulation of mechanochemical transduction processes that elaborate catabolic enzymes.

Aged↗
PubMed2003

Molecular weight, tertiary structure, water binding and colon behaviour of ispaghula husk fibre.

Molecular variables, using aqueous and alkaline extracts, of the polysaccharide from ispaghula husk (IH) were examined using gel-permeation chromatography linked to multi-angle laser light scattering. Progressive extraction can yield a component with a molecular weight (MW)value up to about 7 x 106 Da, and gels, which accompany the extraction, have MW ranging from 10-20 x 106 Da. To mimic the polysaccharide degradation, particularly in the colon, the solid IH was degraded progressively using ionising radiation. A chain break occurs every 7.5 kGy in NaOH and every 15 kGy in water. The solid-state matrix is opened by the radiation to yield increased visco-elasticity of the aqueous extracts at critical radiation doses, before further degradation occurs after about 12 kGy. Differential scanning calorimetry is used to study the mechanism of interaction of water with IH. The first water to be taken up is non-freezing water and represents about twelve water molecules/disaccharide unit of the polysaccharide. As the water content is increased, the water becomes bound to the polysaccharide and freezes and melts at a temperature different from free water. This water is thermodynamically distinguishable from free water. It forms amorphous ice on cooling which crystallises exothermically and subsequently melts endothermically. Saturation occurs at a water content of 2-3 g water/g polymer, showing that about 60% of the water in the system is 'bound'. The most surprising conclusion is that despite the fact that the IH swells in water to form a solid and stiff gel, the greater part of that water in the gel is still free and behaves like liquid water.

Chromatography, Gel↗
PubMed2005

Cartilage degeneration in different human joints.

Variations among joints in the initiation and progression of degeneration may be explained, in part, by metabolic, biochemical and biomechanical differences. Compared to the cartilage in the knee joint, ankle cartilage has a higher content of proteoglycans and water, as well as an increased rate of proteoglycan turnover and synthesis, all of which are responsible for its increased stiffness and reduced permeability. Chondrocytes within ankle cartilage have a decreased response to catabolic factors such as interleukin-1 and fibronectin fragments, compared to the chondrocytes of knee cartilage. Moreover, in response to damage, ankle chondrocytes synthesize proteoglycans at a higher rate than that found in knee cartilage chondrocytes, which suggests a greater capacity for repair. In addition to the cartilages of the two joints, the underlying bones also respond differently to degenerative changes. Taken together, these metabolic, biochemical and biomechanical differences may provide protection to the ankle.

Adult↗
PubMed1998

Compression-induced degeneration of the intervertebral disc: an in vivo mouse model and finite-element study.

STUDY DESIGN: An in vivo study of the biologic and biomechanical consequences of static compressive loading on the mouse tail intervertebral disc. OBJECTIVES: To determine whether static compression in vivo alters the biologic activity of the disc and leads to diminished biomechanical performance. SUMMARY OF BACKGROUND DATA: Static compressive stress that exceeds the disc's swelling pressure is known to change hydration and the intradiscal stress distribution. Alterations in hydration and stress have been associated with changes in disc cell activity in vitro and in other collagenous tissues in vivo. METHODS: Mouse tail discs were loaded in vivo with an external compression device. After 1 week at one of three different stress levels, the discs were analyzed for their biomechanical performance, morphology, cell activity, and cell viability. A second group of mice were allowed to recuperate for 1 month after the 1-week loading protocol to assess the disc's ability to recover. As an aid to interpreting the histologic and biologic data, finite-element analysis was used to predict region-specific changes in tissue stress caused by the static loading regimen. RESULTS: With increasing compressive stress, the inner and middle anulus became progressively more disorganized, and the percentage of cells undergoing apoptosis increased. The expression of Type II collagen was suppressed at all levels of stress, whereas the expression of aggrecan decreased at the highest stress levels in apparent proportion to the decreased nuclear cellularity. Compression for 1 week did not affect the disc bending stiffness or strength but did increase the neutral zone by 33%. As suggested by the finite-element model, during sustained compression, tension is maintained in the outer anulus and lost in the inner and middle regions where the hydrostatic stress was predicted to increased nearly 10-fold. Discs loaded at the lowest stress recovered anular architecture but not cellularity after 1 month of recuperation. Discs loaded at the highest stress did not recover anular architecture, displaying islands of cartilage cells in the middle anulus at sites previously populated by fibroblasts. CONCLUSIONS: The results of the current project demonstrate that static compressive loading initiates a number of harmful responses in a dose-dependent way: disorganization of the anulus fibrosus; an increase in apoptosis and associated loss of cellularity; and down regulation of collagen II and aggrecan gene expression. The finite element model used in this study predicts loss of collagen fiber tension and increased matrix hydrostatic stress in those anular regions observed to undergo programmed cell death after 1 week of loading and ultimately become populated by chondrocytes after one month of recuperation. This correspondence conforms with the suggestions of others that the cellular phenotype in collagenous tissues is sensitive to the dominant type of tissue stress. Although the specific mechanisms by which alterations in tissue stress lead to apoptosis and variation in cell phenotype remain to be identified, our results suggest that maintenance of appropriate stress within the disc may be an important basis for strategies to mitigate disc degeneration and initiate disc repair.

Aggrecans↗
PubMed1997

Vinculin promotes cell spreading by mechanically coupling integrins to the cytoskeleton.

Mouse F9 embryonic carcinoma 5.51 cells that lack the cytoskeletal protein vinculin spread poorly on extracellular matrix compared with wild-type F9 cells or two vinculin-transfected clones (5.51Vin3 and Vin4; Samuels et al., 1993, J. Cell Biol. 121, 909-921). In the present study, we used this model system to determine how the presence of vinculin promotes cytoskeletal alterations and associated changes in cell shape. Microscopic analysis of cell spreading at early times, revealed that 5.51 cells retained the ability to form filopodia; however, they could not form lamellipodia, assemble stress fibers, or efficiently spread over the culture substrate. Detergent (Triton X-100) studies revealed that these major differences in cell morphology and cytoskeletal organization did not result from differences in levels of total polymerized or cross-linked actin. Biochemical studies showed that 5.51 cells, in addition to lacking vinculin, exhibited slightly reduced levels of alpha-actinin and paxillin in their detergent-insoluble cytoskeleton. The absence of vinculin correlated with a decrease in the mechanical stiffness of the integrin-cytoskeleton linkage, as measured using cell magnetometry. Furthermore, when vinculin was replaced by transfection in 5.51Vin3 and 5.51Vin4 cells, the levels of cytoskeletal-associated alpha-actinin and paxillin, the efficiency of transmembrane mechanical coupling, and the formation of actin stress fibers were all restored to near wild-type levels. These findings suggest that vinculin may promote cell spreading by stabilizing focal adhesions and transferring mechanical stresses that drive cytoskeletal remodeling, rather than by altering the total level of actin polymerization or cross-linking.

Actinin↗
PubMed2003

Beta-catenin accumulates in intercalated disks of hypertrophic cardiomyopathic hearts.

OBJECTIVE: To evaluate whether cardiomyocyte membrane structure and cell/extracellular matrix adhesion alterations perturb the cadherin/catenin complex in the hypertrophic cardiomyopathy (HCM). METHODS: Hypertrophic cardiomyopathic hamster (UM-X7.1 strain) and human hearts were studied by light and electron microscopy, Northern and Western blot analyses and immunohistochemistry. RESULTS: Intercalated disks are disorganized in both hamster and human cardiomyopathic hearts; beta-catenin is increased and accumulated in intercalated disks depriving cardiomyocyte nuclei of fundamental signals. The accumulation of beta-catenin is post-translationally regulated by an increased Wnt expression, a simultaneous decrease in glycogen synthase kinase 3beta (GSK3beta) expression and a different expression pattern of adenomatous polyposis coli (APC) isoforms. CONCLUSION: The reorganization of cell/cell adhesion in cardiomyopathic hearts is mainly contributed by the cadherin/catenin system, which is differently regulated to sustain cell structural rather than signalling needs causing considerable consequences in the determination of cardiomyocyte phenotype and clinical outcome. The accumulation of beta-catenin in intercalated disks could concur to increase myocardial wall stiffness and left ventricular end-diastolic pressure (LVEDP) in hypertrophic cardiomyopathic hamster and human hearts.

Animals↗
PubMed2004

The relationship between cell and tissue strain in three-dimensional bio-artificial tissues.

Continuum constitutive laws are needed to ensure that bio-artificial tissue constructs replicate the mechanical response of the tissues they replace, and to understand how the constituents of these constructs contribute to their overall mechanical response. One model designed to achieve both of these aims is the Zahalak model, which was modified by Marquez and co-workers to incorporate inhomogeneous strain fields within very thin tissues. When applied to reinterpret previous measurements, the modified Zahalak model predicted higher values of the continuum stiffness of fibroblasts than earlier estimates. In this work, we further modify the Zahalak model to account for inhomogeneous strain fields in constructs whose cell orientations have a significant out-of-plane component. When applied to reinterpret results from the literature, the new model shows that estimates of continuum cell stiffness might need to be revised upward. As in this article's companion, we updated the average cell strain by defining a correction factor ("strain factor"), based upon the elastic response. Three different cell orientation distributions were studied. We derived an approximate scaling model for the strain factor, and validated it against exact and self-consistent (mean-field) solutions from the literature for dilute cell concentrations, and Monte Carlo simulations involving three-dimensional finite element analyses for high cell concentrations.

Animals↗
PubMed1998

Is osteoporosis a matter of over-adaptation?

The stiffness and strength of cancellous bone depends on the amount of bone mineral (BMD) and on the three-dimensional distribution of the mineral (architecture). The relationship between mechanical properties and architecture, excluding confounding effects due to BMD can be studied using computer models of cancellous bone. It was shown that adaptation to mechanical deformation energy leads to an architecture which is an optimal or semi-optimal configuration with respect to maximal stiffness and minimal mass. Thus, the stiffness of the cancellous bone relative to the amount of bone (the bone density) can be considered as an optimality criterion. Based on these findings we assumed that the status of osteoporosis - or better fracture risk - could be related to how close this optimality criterion was met. In other words, we assumed that a higher fracture risk is simply related to a less optimal structure. This was tested for cancellous bone samples taken from post mortem vertebral bodies from two groups of subjects: one group with high fracture incidence during their lives and one group of "healthy" controls. It was found that the specimen from the high fracture incidence group had an architecture leading to a slightly stiffer structure relative to the BMD value. The conclusion is therefore that vertebral bone specimen from subjects with high fracture incidence are better optimized which was contradictory to what we expected. This finding indicates that bone specimen from the "healthy" control subjects had bone matrix at locations which are relatively unloaded. This tissue can be considered as not mechanically efficient or functional. A possible explanation of the present findings is that bone from subjects with increased fracture incidence is better adapted to mechanical stress, because it needs all bone material to carry the load. This stronger adaptation might be related to a compromised safety factor against bone loss, or diminished intrinsic matrix properties (e.g., microdamage).

Adaptation, Physiological↗
PubMed2004

Strain-rate sensitive mechanical properties of tendon fascicles from mice with genetically engineered alterations in collagen and decorin.

Tendons have complex mechanical behaviors that are nonlinear and time dependent. It is widely held that these behaviors are provided by the tissue composition and structure. It is generally thought that type I collagen provides the primary elastic strength to tendon while proteoglycans, such as decorin, play a role in failure and viscoelastic properties. This study sought to quantify such structure-function relationships by comparing tendon mechanical properties between normal mice and mice genetically engineered for altered type I collagen content and absence of decorin. Uniaxial tensile ramp to failure experiments were performed on tail tendon fascicles at two strain rates, 0.5%/s and 50%/s. Mutations in type I collagen led to reduced failure load and stiffness with no changes in failure stress, modulus or strain rate sensitivity. Fascicles without decorin had similar elastic properties to normal fascicles, but reduced strain rate sensitivity. Fascicles from immature mice, with increased decorin content compared to adult fascicles, had inferior elastic properties but higher strain rate sensitivity. These results showed that tendon viscoelasticity is affected by decorin content but not by collagen alterations. This study provides quantitative evidence for structure-function relationships in tendon, including the role of proteoglycan in viscoelasticity.

Animals↗
PubMed1996

Exposure to low-intensity ultrasound increases aggrecan gene expression in a rat femur fracture model.

The effects of ultrasound stimulation on various parameters of bone repair after diaphyseal injury were assessed in a standard rat femur fracture model. Bilateral closed femoral fractures were made in 79 skeletally mature male Long-Evans rats. An ultrasound signal consisting of a 200 microsecond burst sine wave of 0.5 MHz repeating at 1 kHz, with an intensity of 50 or 100 mW/cm2 spatial and temporal average, was applied to one fracture in each animal. The contralateral fracture was not exposed to ultrasound and served as a control. Mechanical testing of the healing fracture was performed 3 weeks after injury. In fractures treated with a 50 mW/cm2 ultrasound signal, the average maximum torque (223.5 +/- 50.5 Nmm compared with 172.6 +/- 54.9 Nmm, p = 0.022, paired t test) and average torsional stiffness (13.0 +/- 3.4 Nmm/degree compared with 9.5 +/- 2.9 Nmm/degree, p = 0.017) were significantly greater in treated than in control fractures. In animals treated with a 100 mW/cm2 ultrasound signal, the average maximum torque and torsional stiffness were greater in treated than in control fractures, but this trend did not reach statistical significance. Biochemical analysis of callus in ultrasound-treated and control fractures failed to demonstrate significant differences in cell number, collagen content, or calcium content. Evaluation of gene expression in fractures treated with 50 mW/cm2 ultrasound demonstrated a shift in the expression of genes associated with cartilage formation; aggrecan gene expression was significantly higher on day 7 after fracture and significantly lower on day 21 (p = 0.033 and 0.035, respectively). alpha 1(II) procollagen gene expression was similarly modified, but this trend did not reach statistical significance. Expression of genes coding for bone-related proteins, including alpha 1(I) procollagen, bone gamma-carboxyglutamic acid protein, alkaline phosphatase, and transforming growth factor-beta 1, did not differ between ultrasound-treated and control fractures. These data suggest that ultrasound stimulation increased the mechanical properties of the healing fracture callus by stimulating earlier synthesis of extracellular matrix proteins in cartilage, possibly altering chondrocyte maturation and endochondral bone formation.

Aggrecans↗
PubMed2004

Consolidation responses of delipidized articular cartilage.

OBJECTIVE: To determine the role of articular cartilage lipids in its load-bearing function. DESIGN: Normal and delipidised, bovine articular cartilage specimens were statically loaded and both the hydrostatic excess pore pressure and creep strain were measured. From this the compression stiffness of the skeletal structures of both types of matrices was determined. BACKGROUND: It has been hypothesized that surfactant injection could relief osteoarthritis, but there is no study in the literature relating to the influence of lipids, the main ingredients of such products, on cartilage load-carriage. METHODS: Articular cartilage specimens were obtained from the patellar grooves of 2-3 year old bovine animals. When required specimen delipidization was carried out using chloroform/methanol rinsing. Both normal and delipidised samples were loaded in the consolidometer and the hydrostatic excess pore pressure and strain were measured. RESULTS: The transient patterns of the hydrostatic excess pore pressure were similar for both types of tissue, with a relatively insignificant increase of 2% in the maximum hydrostatic excess pore pressure of the delipidized samples relative to the normal intact specimens. The maximum creep strain of the delipidised specimens decreased by 10% on average relative to their normal intact counterparts, thereby indicating that delipidization causes stiffening of the cartilage matrix. CONCLUSION: The delipidized fluid-saturated articular cartilage is stiffer than its intact counterpart with consequence for cartilage compliance during function. RELEVANCE: Because osteoarthritis can be accompanied by lipid loss in cartilage, this study contributes to the further understanding of the disease with potential benefit for treatment.

Adaptation, Physiological↗