bluuebunny/crossref_metadata_2025_split huggingface dataset:
Migration and healing of ligament cells under inflammatory conditions
Authors: Witkowski Jeanine , Yang Li , Wood Douglas J. , Sung K‐L. Paul 
Published: February 2005

AbstractIt is well documented that the adult human medial collateral ligament has a functional healing response, whereas the anterior cruciate ligament does not. The differential healing responses of the medial collateral and anterior cruciate ligaments could be due to factors caused by different biological conditions and locations in vivo. In addition, different intrinsic properties of the constituent cells of these ligaments may contribute to their different healing abilities. Ligament healing follows an orderly process of hemorrhage, inflammation, proliferation, and remodeling. At the cellular level, healing involves a cell's detachment from and attachment to the matrix adjacent to the wound area, migration, and proliferation. This study sought to investigate whether, during migration, the responses of the medial collateral and anterior cruciate ligament fibroblasts are intrinsically different under the same inflammatory conditions. Human medial collateral arid anterior cruciate ligament fibroblast cells were cultured, and in vitro wounds were simulated by streaking the cells with an inoculating loop, creating a cell‐free area. The migration of the cells into this gap, thus filling the cell‐free area, was observed. Two sets of experiments were conducted; one varied the wound width and the, other added the inflammatory factors tumor necrosis factor‐a, complement C5a, and lipopolysaccharide the width of the wound increased, the rate of recovery decreased for both types of ligament cells (slope: anterior cruciate ligament, 0.13 hour/μm and medial collateral ligament, 0.10 hour/μm). Also, the three inflammatory factors used all inhibited the recovery rates of both ligaments to ones that were 1.4–2.3 times slower than controls. However, in both sets of experiments, the anterior cruciate ligament fibroblasts were more sensitive to inflammatory factors, and the medial collateral ligament fibroblasts had faster recovery rates (anterior cruciate ligament, 1.2–3.4 times slower than rates for medial collateral ligament fibroblasts, excluding those under lipopolysaccharide treatment). The results showed that medial collateral and anterior cruciate ligament fibroblasts responded differently under the same inflammatory conditions. This may suggest that these differences in intrinsic properties contribute to their different healing responses and abilities.
In situ forces in the anterior cruciate ligament and its bundles in response to anterior tibial loads
Authors: Sakane Masataka , Fox Ross J. , Glen Savio L‐Y. Woo , Livesay A. , Li Guoan , Fu Freddie H. 
Published: February 2005

AbstractThe anterior cruciate ligament has a complex fiber anatomy and is not considered to be a uniform structure. Current anterior cruciate ligament reconstructions succeed in stabilizing the knee, but they neither fully restore normal knee kinematics nor reproduce normal ligament, function. To improve the outcome of the reconstruction, it may be necessary to reproduce the complex function of the intact anterior cruciate ligament in the replacement graft. We examined the in situ forces in nine human anterior cruciate ligaments as well as the force distribution between the anteromedial and posterolateral bundles of the ligament in response to applied anterioi tibial loads ranging from 22 to 110 N at knee flexion angles of 0–90°. The analysis was performed using a robotic manipulator in conjunction with a universal force‐moment sensor. The in situ forces were determined with no device attached to the ligament, while the knee was permitted to move freely in response to the applied loads. We found that the in situ forces in the anterior cruciate ligament ranged from 12.8 ± 7.3 N under 22 N of anterior tibial load applied at 90° of knee flexion to 110.6 ± 14.8 N under 110 N of applied load at 15° of flexion. The magnitude of the in situ force in the posterolateral bundle was larger than that in the anteromedial bundle at knee flexion angles between 0 and 45°, reaching a maximum of 75.2 ± 18.3 N at 15° of knee flexion under an anterior tibial load of 110 N. The magnitude of the in situ force in the posterolateral bundle was significantly affected by knee flexion angle and anterior tibial load in a fashion remarkably similar to that seen in the anterior cruciate ligament. The magnitude of the in situ force in the anteromedial bundle, in contrast, remained relatively constant, not changing with flexion angle. Significant differences in the direction of the in situ force between the anteromedial bundle and the posterolateral bundle were found only at flexion angles of 0 and 60° and only under applied anterior tibial loads greater than 66 N. We have demonstrated the nonuniformity of the anterior cruciate ligament under unconstrained anterior tibial loads. Our data further suggest that in order for the anterior cruciate ligament replacement graft to reproduce the in situ forces of the normal anterior cruciate ligament, reconstruction techniques should take into account the role of the posterolateral bundle in addition to that of the anteromedial bundle.
Changes in the flexibility characteristics of the ankle complex due to damage to the lateral collateral ligaments: An in vitro and in vivo study
Authors: Lapointe Stephan J. , Siegler Sorin , Hillstrom Howard , Nobilini Robert R. , Mlodzienski Alan , Techner Lee 
Published: February 2005

AbstractThis study was part of a long‐term effort to develop a reliable diagnostic procedure for ankle ligament injuries. Earlier efforts led to the development and validation of a six‐degrees‐of‐freedom instrumented linkage capable of measuring the flexibility characteristics of the ankle complex in vitro and in vivo. The major goal of the present study was to determine if these flexibility measurements are sufficiently sensitive to detect the presence of damage to the lateral collateral ligaments of the ankle joint both in vitro and in vivo. The in vitro testing was conducted on the legs from six fresh cadavers before and after serial sectioning of the anterior talofibular ligament and the calcaneofibular ligament. The flexibility in inversion‐eversion, anterior drawer, and internal‐external rotation was measured before and after resection of the ligaments. The in vivo testing was conducted on five patients with unilateral injuries to the ankle ligament. The flexibility evaluation used for in vitro specimens was also performed on both the injured and the intact ankles. For the in vitro testing, the data analysis was based on comparison of flexibility values before and after resection of the ligaments, whereas the data analysis for the in vivo testing was based on comparison of the flexibility of the injured joint with that of the intact contralateral joint. The results of the in vitro study indicated that both an isolated rupture of the anterior talofibular ligament and combined damage of the anterior talofibular and calcaneofibular ligaments produce statistically significant changes in flexibility. Furthermore, the most sensitive parameters to the presence of ligament injuries were found to be early flexibility in anterior drawer, early flexibility in inversion, and the amount of coupling between internal rotation and inversion. These parameters provided a basis for differentiating between an isolated injury to the anterior talofibular ligament and a combined anterior talofibular and calcaneofibular ligament injury. For an isolated anterior talofibular ligament injury, a significant increase in flexibility in anterior drawer was present, whereas the increase in inversion flexibility or in the amount of coupling was insignificant. However, the increases in inversion flexibility and the amount of coupling became significant when both ligaments were involved. The results of the in vivo study indicated that significant changes in flexibility can be detected in patients with lateral ankle injuries. Finally, both the in vitro and in vivo results suggest that development of a reliable diagnostic test for ankle ligament injury based on changes in passive flexibility may be possible.
Effects of continuous distraction on cartilage in a moving joint: An investigation on adult rabbits
Authors: Hung Shih‐Chieh , Nakamura Kozo , Shiro Ryoji , Tanaka Kiyokazu , Kawahara Hazime , Kurokawa Takahide 
Published: February 2005

AbstractAn animal model, using distraction force on adult rabbits, was developed to study the effects of nonweight‐bearing on articular cartilage in a moving joint. Histologic evaluation was used to compare the morphology of chondrocytes, safranin O intensity, cartilage thickness, and structural changes between the test and contralateral joints. At 3 and 6 weeks, the chondrocytes in superficial and intermediate zones were round, with an increase in cellular volume density and mean cell volume and with less metachromasia; the safranin O intensity and cartilage thickness were the same as in the controls. In cartilage of the 9‐week group, mean cell volume decreased with cell cloning in the superficial zone, while numerical density increased and mean matrix volume per cell decreased in the superficial and intermediate zones. The cartilage, with a 34% reduction in thickness and a 53–72% decrease in safranin O intensity from the superficial to the deep zone, had superficial fibrotic proliferation, suface erosion or depression, ard tidemark irregularity. Continuous distraction in a moving joint caused morphological changes in chondrocytes prior to degeneration of cartilage. These results support the hypothesis that the forces perceived by cells may dictate their shape and then stimulate alterations in cellular biochemistry and matrix metabolism.
Comparison of the tissue response to absorbable self‐reinforced polylactide screws and metallic screws in the fixation of cancellous bone osteotomies: An experimental study on the rabbit distal femur
Authors: Viljanen Janne T. , Pihlajamäki Harri K. , Törmälä Pertti O. , Rokkanen Pentti U. 
Published: February 2005

AbstractThe availability of absorbable fracture‐fixation devices for clinical use calls for better knowledge of the reaction of bone tissue to absorbable polyester implants as compared with similar metallic devices. To examine and compare the tissue response to biodegradable and metallic screws within cancellous bone, a transverse transcondylar osteotomy of the distal femur was fixed with absorbable self‐reinforced polylevolactide screws in 35 rabbits and with stainless‐steel screws in 35 rabbits. New bone formation and consolidation of the osteotomy were examined histologically, histomorphometrically, and microradiographically within standardized sample fields 1,3,6,12,24,36, and 48 weeks postoperatively. The intact contralateral femur served as the control. A vigorous osteoconductive response to the polylevolactide screws was observed at 3 weeks postoperatively, and the osteoid surface fraction was significantly higher in all follow‐ups than in the contralateral femora. In the femora with metallic screws, new bone formation was seen 3,6, and 12 weeks postoperatively, but at 24,36, and 48 weeks the osteoid surface fraction did not differ significantly from that of the intact control femora. The total bone area was significantly larger in the femora with self‐reinforced polylevolactide screws than in the control bone 6‐48 weeks postoperatively; in the femora with metallic screws, this was found only at 6 and 12 weeks. After 48 weeks, the femora fixed with metallic screws had statistically smaller total bone area than the intact control femora. Solid bone union was seen in 84% of the osteotomies in the self‐reinforced polylevolactide group and in 76% of those in the metallic group after 3 weeks or more. No signs, of degradation of the self‐reinforced polylevolactide implant and only a mild foreign‐body reaction with no accumulations of inflammatory cells to either self‐reinforced polylevolactide or metallic screws were observed during the follow‐up period. Both types of screws seemed to induce an osteostimulatory response around their threads. This phenomenon was transient for metallic screws but lasted for at least 48 weeks for self‐reinforced polylevolactide screws. The polylevolactide screw does not seem to cause osteopenia at the implantation site. The fixation properties of both self‐reinforced polylevolactide screws and metallic screws appear to be sufficient for the fixation of small fragments of cancellous bone.
Subfracture insult to a knee joint causes alterations in the bone and in the functional stiffness of overlying cartilage
Authors: Newberry William N. , Zukosky Derek K. , Haut Roger C. 
Published: February 2005

AbstractThe current criteria used by the automotive industry for predicting joint injury are based on fracture of bone, but clinical studies suggest that chronic diseases such as osteoarthrosis can occur from a single blunt insult without bone fracture. In the current study, blunt insults were delivered to the patellofemoral joints of rabbits without producing bone fractures. Biomechanical and histological studies were performed on joint tissues at various times after insult. The functional integrity of the retropatellar cartilage on the lateral facet was measured with mechanical indentation experiments, and the thickness of the subchondral bone was measured from histological sections. Impacts produced surface lesions on the retropatellar cartilage. The thickness of the subchondral bone in representative animals tended to increase with time after insult, and the bone exhibited significant thickening at 12 months. The overlying cartilage showed signs of degeneration. However, the mechanical stiffness of the cartilage did not change until 12 months after the insult.
Extracellular collagen modulates the regulation of chondrocytes by transforming growth factor‐β1
Authors: Qi Wen‐Ning , Scully Sean P. 
Published: February 2005

AbstractThis article describes the modulation, by extracellular collagen, of DNA and proteoglycan synthesis in articular chondrocytes stimulated with transforming growth factor‐β1, Type‐I and type‐II collagen, heat denatured type‐II collagen, and bovine serum albumin were each incorporated into alginate in increasing concentrations. Bovine articular chondrocytes were isolated and were resuspended in the alginate, yielding alginate beads with final extracellular protein concentrations of 0‐1.5% (wt/vol) for the collagens and 0‐2.5% (wt/vol) for bovine serum albumin. Cultures of beads were maintained for 7 days in basal Dulbecco's modified Eagle medium or in medium supplemented with 10 ng/ml transforming growth factor‐β1. Subsequently, the synthesis of DNA and proteoglycan was measured by radiolabel‐incorporation methods with [35S]sulfate and [3H]thymidine, and the values were normalized to the DNA content. Transforming growth factor‐β1 stimulated the synthesis of both DNA and proteoglycan in a bimodal fashion. The presence of extracellular type‐II collagen increased the rate of DNA and proteoglycan synthesis in a dose‐dependent fashion in cultures stimulated by transforming growth factor‐β1, whereas heat‐inactivated type‐II collagen abrogated the effects observed with type‐II collagen for synthesis of both DNA and proteoglycan. In contrast, the presence of extracellular type‐I collagen caused a dose‐dependent inhibition of synthesis of both DNA and proteoglycan in cultures stimulated with transforming growth factor‐β1. Extracellular bovine serum albumin brought about a limited increase in synthesis rates, presumably by blocking nonspecific cytokine binding. These results suggest that type‐II collagen has a specific role in chondrocyte regulation and serves to mediate the response of chondrocytes to transforming growth factor‐β1.
Forearm muscle oxygenation decreases with low levels of voluntary contraction
Authors: Murthy Gita , Kahan Norman J. , Hargens Alan R. , Rempel David M. 
Published: February 2005

AbstractThe purpose of our investigation was to determine if the near infrared spectroscopy technique was sensitive to changes in tissue oxygenation at low levels of isometric contraction in the extensor carpi radialis brevis muscle. Nine subjects were seated with the right arm abducted to 45°, elbow flexed to 85°, forearm pronated 45°, and wrist and forearm supported on an armrest throughout the protocol. Altered tissue oxygenation was measured noninvasively with near infrared spectroscopy. The near infrared spectroscopy probe was placed over the extensor carpi radialis brevis of the subject's right forearm and secured with an elastic wrap. After 1 minute of baseline measurements taken with the muscle relaxed, four different loads were applied just proximal to the metacarpophalangeal joint such that the subjects isometrically contracted the extensor carpi radialis brevis at 5, 10, 15, and 50% of the maximum voluntary contraction for 1 minute each. A 3‐minute recovery period followed each level of contraction. At the end of the protocol, with the probe still in place, a value for ischemic tissue oxygenation was obtained for each subject. This value was considered the physiological zero and hence 0% tissue oxygenation. Mean tissue oxygenation (±SE) decreased from resting baseline (100% tissue oxygenation) to 89 ± 4, 81 ± 8, 78 ± 8, and 47 ± 8% at 5, 10, 15, and 50% of the maximum voluntary contraction, respectively. Tissue oxygenation levels at 10, 15, and 50% of the maximum voluntary contraction were significantly lower (p < 0.05) than the baseline value. Our results indicate that tissue oxygenation significantly decreases during brief, low levels of static muscle contraction and that near infrared spectroscopy is a sensitive technique for detecting deoxygenation noninvasively at low levels of forearm muscle contraction. Our findings have important implications in occupational medicine because oxygen depletion induced by low levels of muscle contraction may be directly linked to muscle fatigue.
Effect of low dietary calcium on bone metabolism in the SENCAR mouse
Authors: Murray Elsa J. Brochmann , Murray Samuel S. , Grisanti Mario , Duarte Maria Eugenia L. , Urist Marshall R. 
Published: February 2005

AbstractThe SENCAR (sensitive to carcinogenesis) mouse is a unique tool for investigating the interaction between a specific defect in intracellular signaling, dietary calcium, and metabolic bone disease. The SENCAR mouse was developed by selective breeding for enhanced sensitivity to two‐stage carcinogenesis. Its major genetic defect, which renders it exquisitely sensitive to stimulation with diacylglycerol or phorbol esters, is in the regulatory domain of protein kinase C, one of the primary intracellular mediators of hormonal effects. At sexual maturity, SENCAR mice are large and have big bones, but our previous pharmacokinetic studies showed that they accumulate lesscalcium under normal conditions and lose more calcium under adverse conditions than do other, standard strains of mice. To histologically define the effect of low dietary calcium on bone metabolism, we performed histomorphometric analysis of tetracycline‐labeled sections of femoral bone from male SENCAR mice maintained on calcium‐sufficient and calcium‐deficient diets during the critical period from 10 to 14 weeks of age. The bone volume, absolute osteoid volume, and mineral apposition rate were lower at 14 than at 10 weeks of age in SENCAR mice fed 0.02 or 0.6% calcium diets. Calcium deficiency increased the architectural disarray and the probability of observing focal discontinuities in the growth plate. Thus, characteristic features of impaired bone metabolism (low bone volume and apposition rate) develop early in SENCAR mice and are exacerbated by low dietary calcium. Detailed examinations of the histology and biochemistry of SENCAR mouse bone will provide insights into the mechanisms by which specific defects in the signal transduction of protein kinase C contribute to impaired bone metabolism.
Surface remodeling of trabecular bone using a tissue level model
Authors: Smith Tait S. , Martin R. Bruce , Hubbard Mont , Bay Brian K. 
Published: February 2005

AbstractWe propose a two‐dimensional mathematical model of trabecular bone remodeling that simulates the surface‐based addition and removal of material in the actual physiological process. The model is based on a finite element representation of individual trabecular struts in which the material properties of the subtrabecular elements are constant. The remodeling stimulus is strain energy density, sensed and communicated through the osteocytic network as proposed by Mullender et al. We propose a modified osteocyte communication scheme that incorporates bone‐lining cells and examines the implications of set point locations in one or the other of these two cell types. This model produces trabecular struts that align with its general loading direction. Placing the set point in the bone‐lining cells rather than in the osteocytes makes the model more sensitive to changes in the other biological parameters. Introduction of a dead zone causes the model to reach a less oscillatory equilibrium in fewer iterations and produces better in‐filling of trabecular strut intersections. The model gravitates to equilibrium states in which the average strain energy density is inversely proportional to the bone volume fraction to the 3.2 power.
Bone maintenance and remodeling: A control system based on fatigue damage
Authors: Taylor David 
Published: February 2005

AbstractThis paper explores the relationship between damage, repair, and remodeling in compact bone. A model of microcrack growth is developed that takes account of recent findings on the behaviour of small fatigue cracks in other materials. This is combined with a simple model of a repair process, envisaged as a constant rate of decrease in crack length. The system that results is capable of achieving a stable and precise control of crack length without the need to measure it. This is very useful because it implies that bone does not require the complexities of crack‐measuring, transducers or active decision‐making processes. A simple explanation is suggested for the presence of a “lazy zone” of remodeling equilibrium strains, and the limits of this zone are quantified. The model is developed through a necessarily simplified geometry and loading scheme but can be extended to provide a general solution applicable to in vivo conditions.
Model of flexural fatigue damage accumulation for cortical bone
Authors: Griffin L. V. , Gibeling J. C. , Martin R. B. , Gibson V. A. , Stover S. M. 
Published: February 2005

AbstractAnalytical models that predict modulus degradation in cortical bone subjected to uniaxial fatigue loading in tension and compression are presented. On the basis of experimental observations, damage was modeled as self‐limiting for tension but not for compression. These mechanistic uniaxial damage models were then developed into a model for flexural fatigue of cortical bone based on laminated beam theory. The unknown coefficients in the uniaxial damage models were obtained by successfully fitting the resulting equations to uniaxial fatigue data from the literature on human cortical bone in tension and compression. Then, the predictions of the flexural model for the behavior of human cortical bone were compared with experimental results from a small but independent set of specimens tested at three different ranges of load in our laboratory. The behavior of the modulus degradation curves and the flexural fatigue lives of the specimens were in excellent agreement with the predictions of the model.