bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of collagen and matrix metalloproteinases in ruptured human anterior cruciate ligament: An in situ hybridization study
Authors: Spindler K. P. , Clark S. W. , Nanney L. B. , Davidson J. M. 
Published: February 2005

AbstractThe biological basis for failure of the human anterior cruciate ligament to heal after rupture is unknown. Since this failure could be influenced by abnormalities in matrix protein production or degradation, or both, several diverse matrix protein markers were utilized to survey the state of these extracellular proteins in intrinsic anterior cruciate ligament fibroblasts. Matrix gene expression was visualized by in situ hybridization 9 to 365 days after rupture using probes for type‐I collagen, collagenase, 72kDa‐gelatinase, and tissue inhibitor of metalloproteinase. Remnants of anterior cruciate ligament were biopsied arthroscopically from 20 patients at reconstruction, fixed in 4% paraformaldehyde, and processed with cDNA probes for the aforementioned mRNAs, mRNA expression of type‐I collagen was detected in all specimens, was equally distributed throughout the remnants, and remained evident even at 1 year after injury. Neither of the matrix‐degrading enzymes nor their inhibitor (tissue inhibitor of metalloproteinase) was expressed at substantial levels at any time point. Collagen expression within the anterior cruciate ligament confirmed the viability of the ligament remnants for as long as 1 year after rupture. The lack of significant expression of the two matrix‐degrading metalloproteinases by the fibroblasts is not consistent with an autodegradation of the remaining ruptured ligament tissue, and whether the lack of matrix remodelling may account, at least in part, for the poor healing response of the anterior cruciate ligament remains to be determined. This initial investigation by in situ hybridization techniques provides a descriptive profile of matrix gene expression in the damaged human anterior cruciate ligament.
Response of human osteoblasts to implant materials: Integrin‐mediated adhesion
Authors: Gronowicz G. , McCarthy M. B. 
Published: February 2005

AbstractThe initial interaction of the human osteoblast‐like cell line Saos‐2 with orthopaedic implant materials was analyzed to determine the mechanism by which these cells adhere to implant surfaces. Saos‐2 cells were allowed to attach to disks composed of the orthopaedic implant materials Tivanium (Ti6A14V) and Zimaloy (CoCrMo) and to control disks of glass and plastic. Serum had no effect on the number of cells that attached to Tivanium and Zimaloy at 4 or 24 hours but did increase the number of cells that attached to glass at 24 hours. Collagen synthesis was determined by [3H]proline incorporation into collagenase‐digestible protein and noncollagen protein. A significant increase of 19% was found for collagen synthesized in cells cultured on Zimaloy for 24 hours compared with glass, with no differences on Tivanium and plastic. However, collagenase‐digestible protein and noncollagen protein were increased the most (204 and 198%, respectively) on Tivanium compared with glass. To determine if integrins were involved in cell attachment to implant materials, the peptide GRGDSP (Gly‐Arg‐Gly‐Asp‐Ser‐Pro), which blocks integrin receptors through the Arg‐Gly‐Asp sequence, was added to the cells in serum‐free medium. This peptide inhibited cell adhesion by 28% on Tivanium and 40% on Zimaloy but had no effect on glass and plastic. The control peptide GRADSP (Gly‐Arg‐Ala‐Asp‐Ser‐Pro) had no effect on adhesion. Inhibition of protein synthesis and enzymatic removal of surface proteins did not affect the ability of Arg‐Gly‐Asp peptides to inhibit cell attachment to the implant materials. These results suggest that integrins are able to bind directly to Tivanium and Zimaloy. Western blot analysis of integrin protein demonstrated changes in many integrin subunits, depending on the substrate to which cells affached. In particular, the β1 integrin subunit was increased 3.8 to 9.5‐fold at 24 hours. To determine specifically which integrins may be involved in adhesion, antibodies to integrins were added. An antibody to the fibronectin receptor. α5β1, significantly inhibited binding of cells to Tivanium by 63% and to Zimaloy by 49% and had no effect on glass. The vitronectin receptor antibody, αvβ3/β5, did not alter cell adhesion. In conclusion, osteoblast‐like cells appear to be capable of attaching directly to implant materials through integrins. The type of substrate determines which integrins and extracellular matrix proteins are expressed by osteoblasts. These data provide information on how implant materials may affect osteoblast differentiation and bone growth.
Effect of noninvasive low intensity ultrasound on bone growth into porous‐coated implants
Authors: Tanzer M. , Harvey E. , Kay A. , Morton P. , Bobyn J. D. 
Published: February 2005

AbstractNoninvasive low intensity ultrasound has been shown to be an effective means of accelerating bone fracture healing in both animal and clinical studies. An in vivo canine study was designed to determine if noninvasive low intensity ultrasound could influence the rate and extent of bone growth into porous‐coated implants. Twenty‐two pairs of fully porous transcortical implants were inserted bilaterally into the femora of 12 dogs. In each dog, one femur served as a control and the other was subjected to daily ultrasound stimulation for 2, 3, or 4 weeks. Overall, the ultrasound‐stimulated implants demonstrated an 18% increase in bone ingrowth compared with their contralateral controls (p = 0.02). Noninvasive low intensity ultrasound had its greatest effect in the first 2–3 weeks of stimulation. At 2 and 3 weeks, the ultrasound‐stimulated implants showed 21 and 16% more ingrowth than their respective contralateral controls. Because noninvasive low intensity ultrasound had a positive effect on bone ingrowth in this experimental investigation, further research is suggested to assess the clinical potential for application to noncemented porous‐coated total joint replacements.
Recombinant human bone morphogenetic protein‐2 maintains the articular chondrocyte phenotype in long‐term culture
Authors: Sailor Laura Zenzius , Hewick Rodney M. , Morris Elisabeth A. 
Published: February 2005

AbstractBone morphogenetic proteins have been shown to increase matrix synthesis by articular chondrocytes in short‐term cultures. Members of this family of proteins have also been shown to induce endochondral ossification in vivo. The present study was performed to determine if the addition of human recombinant bone morphogenetic protein‐2 to a long‐term monolayer articular chondrocyte cell culture system affected the ability of the chondrocytes to divide in vitro, whether the cytokine altered expression of the articular chondrocyte phenotype and synthesis of matrix proteoglycans, and whether the cytokine was capable of inducing differentiation to a hypertrophic chondrocyte. Human recombinant bone morphogenetic protein‐2 did not alter cell proliferation. It caused 3.5–6.2 times more proteoglycan synthesis by articular chondrocytes during each of the time points tested after 4 days in culture. Total proteoglycan accumulation in the extracellular matrix after 28 days in culture was 6.7 times as great in the treated cultures as in the control. Treatment with human recombinant bone morphogenetic protein‐2 maintained the articular chondrocyte phenotype of cells in culture as demonstrated by Northern blot analysis: the expression of type‐I collagen genes was increased and that of type‐II collagen and aggrecan mRNA was lost in untreated chondrocyte cultures after 14–21 days in culture. In contrast, exposure to 100 ng/ml human recombinant bone morphogenetic protein‐2 maintained expression of type‐II collagen and increased expression of aggrecan compared with controls during the 28‐day culture period. Northern blot analysis of the expression of type‐X collagen and osteocalcin by chondrocytes treated with human recombinant bone morphogenetic protein‐2 showed a lack of expression of these genes, indicating no alteration in phenotype. These experiments demonstrated the ability of human recombinant bone morphogenetic protein‐2 to promote the articular chondrocyte phenotype and matrix synthesis in long‐term culture. Characteristics of cell growth were not affected, and the cytokine did not induce differentiation to a hypertrophic chondrocyte.
Significance of granulation tissue in torn supraspinatus insertions: An immunohistochemical study with antibodies against interleukin‐1β, cathepsin D, and matrix metalloprotease‐1
Authors: Gotoh Masafumi , Hamada Kazutoshi , Yamakawa Hideyuki , Tomonaga Akihito , Inoue Akio , Fukuda Hiroaki 
Published: February 2005

AbstractThe pathophysiology of rotator cuff tears can be elucidated by examining the tendinous insertion of the supraspinatus musele. As seen by light microscopy, the granulation tissue around the insertion of a torn supraspinatus tendon appears to induce osteochondral destruction by means of multinucleated giant cells and chemical mediators. The purpose of this study was to examine the contribution of certain chemical mediators to osteochondral destruction using immunohistochemical analysis of interleukin‐β, cathepsin D, and matrix metalloprotease‐1. Sixteen supraspinatus insertions with portions of the greater tuberosity, including eight complete‐thickness tears and eight incomplete‐thickness tears, were obtained during surgery. Six fresh cadaveric supraspinatus tendons without grossly evident tears served as normal controls. Strong immunoreactivity was found in all 16 torn supraspinatus insertions but not in the six insertions of apparently intact tendons. Macrophages and multinucleated giant cells, which showed immunoreactivity for all three chemical mediators, were often found at the interface between the osteochondral margin of the enthesis and the granulation tissue, suggesting that they may be involved in osteochondral destruction. We therefore concluded that, in addition to repetitive subacromial impingement, this granulation tissue may contribute to the development of rotator cuff tears by weakening the insertion.
Biomechanical changes of the wrist flexor and extensor tendons following loss of scaphoid integrity
Authors: Tang Jin Bo , Ryu Jaiyoung , Han JungSoo , Omokawa Shohei , Kish Vincent , Wearden Stanley 
Published: February 2005

AbstractLoss of integrity of the scaphoid may change the motion center of the entire carpus, and deformities from scaphoid fractures may alter the location of motor tendons of the wrist, thus altering their biomechanics. The goal of this study was to clarify biomechanical changes in these tendons following loss of scaphoid integrity. Excursions and moment arms of the principal flexor and extensor tendons of the wrist were investigated in seven cadaveric upper extremities in intact wrists after simulation of scaphoid waist fracture and after removal of the proximal scaphoid. Excursions of the flexor carpi radialis and ulnaris extensor carpi radialis longus and brevis, and extensor carpi ulnaris tendons were measured with rotary potentiometers during wrist flexion‐extension and radioulnar deviation. Simultaneously, wrist joint angulation was recorded. Moment arms of the tendons were derived from tendon excursions and joint motion. After scaphoid fracture, the moment arms of the flexor carpi radialis and extensor carpi ulnaris tendons increased significantly during wrist flexion‐extension, whereas the moment arms of the extensor carpi radialis longus and brevis tendons decreased significantly. After proximal scaphoid excision, the moment arms of the extensor carpi radialis longus and brevis tendons again decreased significantly during wrist flexion‐extension. The moment arms of the flexor carpi radialis and extensor carpi radialis brevis tendons increased significantly during radioulnar deviation, whereas those of the wrist motors on the ulnar side decreased. These findings indicate the importance of the integrity of the scaphoid in maintaining normal biomechanics of motor tendons of the wrist. An increase in the moment arm of the radial wrist flexor along with a decrease in moment arms of the radial extensors constitutes an etiology for persistent angulation of the scaphoid and the hump‐back deformity. In addition, disturbing the biomechanics of the wrist motor tendons predisposes the carpal joints to abnormal loading, potentially contributing to the development of carpal joint degeneration.
Deformation of loaded articular cartilage prepared for scanning electron microscopy with rapid freezing and freeze‐substitution fixation
Authors: Nötzli Hubert , Clark John 
Published: February 2005

AbstractTo investigate the effect of joint loading on collagen fibers in articular cartilage, 45 knees of adult rabbits were examined by scaning electron microscopy. The knees were loaded at the patella with a simulated “quadriceps force” of 0.5‐4 times body weight for 0.5 or 25 minutes, plunge‐frozen, and fixed by freezesubstitution with aldehydes. Six knees were loaded for 3 hours and then fixed conventionally. Fixed tibial plateaus were examined and then freeze‐fractured through the area of tibiofemoral contact, dried, coated, and examined by scanning electron microscopy to assess the overall deformation of the tibial articular surface and matrix collagen fibers. With tissue prepared by conventional fixation used as a standard, the quality of fixation was graded by light and transmission electron microscopy of patellar cartilage taken from half of the freeze‐fixed knees. In loaded specimens, an indentation was present where the femur contacted the tibial plateau. The diameter and apparent depth of the dent were proportional to the magnitude and duration of the load; no dent was seen in the controls. The thickness of the cartilage at the center of the indentation was reduced 15‐80%. Meniscectomy always produced larger deformations in otherwise equivalent conditions. Icecrystal damage to cells was evident by transmission electron microscopy and scanning electron microscopy, but at magnifications as high as ×30,000 the collagen fibrils prepared by freeze‐substitution and conventional aqueous methods were identical. In loaded regions, the collagen matrix of the tibial cartilage was deformed in two ways: (a) radial collagen fibers exhibited a periodic crimp, and (b) in regions where an indentation was created by the femoral condyle, the radial fibers were bent, in effect creating tangential zone where none had existed before. The radial fibers apparently are loaded axially and buckle under normal loads.
Expression of MAGE genes in osteosarcoma
Authors: Sudo Takao , Kuramoto Terukazu , Komiya Setsuro , Inoue Akio , Itoh Kyogo 
Published: February 2005

AbstractExpression of MAGE genes that encode tumor‐rejection antigens recognized by cytotoxic T lymphocytes with major histocompatibility complex class‐I antigens was investigated in human osteosarcomas (20 cell lines and eight fresh tumor tissues). MAGE‐1,2,3,4, and 6 genes were expressed at the mRNA level in 11(52.4%), 10(47.6%), 10(47.6%), one (4.8%) and 10 (47.6%) of 21 tumor cell lines, respectively, and in five (62.5%), six (75%), five (62.5%), one (12.5%) and five (62.5%) of eight fresh tumor tissues as determined by the reverse transcription‐polymerase chain reaction method. MAGE‐1 or 4 protein was detected by immunoblot analysis in eight of 11 or one of one tumor cell lines, respectively where it was expressed at the mRNA level. Major histocompatibility complex class‐I antigens were expressed 19 of 21 tumor cell lines. These results suggest that MAGE tumor‐rejection antigens are expressed in substantial numbers of osteosarcomas in a major histocompatibility class‐I‐restricted manner.
Chondrocyte biosynthesis correlates with local tissue strain in statically compressed adult articular cartilage
Authors: Wong M. , Wuethrich P. , Buschmann M. D. , Eggli P. , Hunziker E. 
Published: February 2005

AbstractIn this study, we investigated the depth‐dependent metabolic and structural responses of adult articular cartilage to large‐strain, static, unconfined compression. Changes in cell biosynthetic activity and several morphometry‐based structural parameters (cell density, cell volume fraction, cell surface‐area density, mean cell surface area, and mean cell volume) were measured at eight sites representing different depth‐zones between the articular surface and the cartilage/bone border. In addition, local axial strain in the superficial, transitional, upper radial, and lower radial zones was estimated on the basis of the change in cell density values. Static compression of articular cartilage revealed a highly heterogeneous deformation profile through the depth of the sample as well as zone‐specific changes in biosynthetic activity, as reflected by incorporation of [3H]proline. The axial strains in the top layers were greater than the applied surface‐to‐surface strain, whereas axial strains adjacent to the cartilage/bone border were significantly less than the applied strain. Zonal changes in cell density and axial strain that occurred during static compression correlated well with alterations in metabolic activity. These coordinated changes between cell biosynthesis and cartilage structure suggest that zone‐specific variations in mechanical stimuli could be responsible for spatially varied patterns of cartilage metabolic activity under load.
Contact pressure and tension in anterior cruciate ligament grafts subjected to roof impingement during passive extension
Authors: Goss Ben C. , Hull M. L. , Howell Stephen M. 
Published: February 2005

AbstractContact between an anterior cruciate ligament graft and the intercondylar roof has been termed roof impingement. Grafts with impingement sustain permanent damage, and if the injury is extensive enough, then the graft may fail, causing recurrent instability. This study evaluated two mechanical factors that could be responsible for the graft injury associated with roof impingement: an increase in graft tension or elevated pressures between the graft and the roof, or both. An anterior cruciate ligament reconstruction was performed using an Achilles tendon graft in five fresh‐frozen cadaveric knees. Using a six‐degree‐of‐freedom load application system, the anterior displacement of the knee with the native anterior cruciate ligament was restored in the reconstructed knee at a flexion angle of 30° and with an anterior force of 200 N applied. Pressure between the graft and intercondylar roof, graft tension, and flexion angle were measured during passive knee extension for three tibial tunnel placements (anterior, center, and posterior). Intercondylar roof impingement increased the contact pressure between the graft and the roof but had no significant effect on graft tension. Therefore, during passive knee extension, the contact pressure between the anterior cruciate ligament graft and the intercondylar roof is a more likely cause of graft damage than increased graft tension.
Osteoclast formation during tumor osteolysis does not require proliferating osteoclast precursor cells
Authors: Clohisy Denis R. , Ramnaraine Margaret L. R. 
Published: February 2005

AbstractThe cellular mechanism or mechanisms through which tumors induce osteoclast formation at sites of tumor osteolysis is unknown. To test the hypothesis that osteoclast formation at sites of tumor osteolysis reflects influences that tumors have on proliferating osteoclast precursor cells, a novel in vivo experimental model was developed that produced mice that were deficient in osteoclasts (op/op) and were depleted (by way of total body irradiation) of proliferating osteoclast precursor cells. The femora of irradiated op/op mice were injected with tumor cells (2472 clone) that had been previously shown to form osteolytic tumors and to induce focal osteoclastogenesis, and the influence of these tumor cells on osteoclast formation was determined in op/op mice that were depleted of proliferating osteoelast precursor cells. The results indicated that 2472 tumor cells induced osteoclast formation in op/op mice despite the absence of proliferating osteoclast precursor cells. This finding disproved the hypothesis under investigation and suggests that osteoclast formation at sites of tumor osteolysis reflects influences of tumors on postmitotic, not proliferating, osteoclast precursor cells.
Effect of radial shortening on muscle length and moment arms of the wrist flexors and extensors
Authors: Tang Jin Bo , Ryu Jaiyoung , Kish Vincent , Wearden Stanley 
Published: February 2005

AbstractThe purpose of this study was to determine the effect of distal radial shortening on muscle length and moment arm of the wrist flexors and extensors. In eight cadaveric upper extremities, distal radius fractures were simulated by an ostectomy. The distal radius was progressively shortened by 2.5, 5.0, 7.5, and 10 mm. Changes in the resting length of the flexor carpi radialis and ulnaris, extensor carpi radialis longus and brevis, and extensor carpi ulnaris muscles were measured with rotary potentiometers at neutral position, flexion, extension, and radial and ulnar deviation of the wrists. The wrists were passively moved through flexion‐extension and radioulnar deviation, and tendon excursions and wrist joint angulation were recorded simultaneously. Tendon moment arms were derived from tendon excursions and joint motion. The results showed that either muscle, length or moment arm of the principal wrist flexors and extensors was significantly affected by the radial shortening. Muscle length decreased significantly after radial shortening in all the wrist flexors and extensors except for the extensor carpi ulnaris. The moment arm of the extensor carpi ulnaris tendon decreased significantly during either wrist flexion‐extension or radioulnar deviation. The extensor carpi radialis brevis and flexor carpi ulnaris tendons also showed a significant decrease in their moment arms during radioulnar deviation of the wrist. Radial shortening of only 2.5 mm caused statistically significant changes in muscle length and moment arm of the wrist flexors and extensors. Increasing the extent of radial shortening exaggerated the biomechanical changes in the wrist motors. These results validate the importance of normal radial length for wrist kinetics and, from a biomechanical perspective, support complete correction of radial shortening after distal radius fractures.
Effects of static fingertip loading on carpal tunnel pressure
Authors: Rempel David , Keir Peter J. , Smutz W. Paul , Hargens Alan 
Published: February 2005

AbstractThe purpose of this study was to explore the relationship between carpal tunnel pressure and fingertip force during a simple pressing task. Carpal tunnel pressure was measured in 15 healthy volunteers by means of a saline‐filled catheter inserted percutaneously into the carpal tunnel of the nondominant hand. The subjects pressed on a load cell with the tip of the index finger and with 0, 6, 9, and 12 N of force. The task was repeated in 10 wrist postures: neutral; 10 and 20° of ulnar deviation; 10° of radial deviation; and 15, 30, and 45° of both flexion and extension. Fingertip loading significantly increased carpal tunnel pressure for all wrist angles (p = 0.0001). Post hoc analyses identified significant increases (p <0.05) in carpal tunnel pressure between unloaded (0 N) and all loaded conditions, as well as between the 6 and 12 N load conditions. This study demonstrates that the process whereby fingertip loading elevates carpal tunnel pressure is independent of wrist posture and that relatively small fingertip loads have a large effect on carpal tunnel pressure. It also reveals the response characteristics of carpal tunnel pressure to fingertip loading, which is one step in understanding the relationship between sustained grip and pinch activities and the aggravation or development of median neuropathy at the wrist.