bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of blood flow within the subchondral bone of the femoral head: Use of the laser speckle method at surgery for osteonecrosis
Authors: Fukuoka Shinji , Hotokebuchi Takao , Jingushi Seiya , Fujii Hitoshi , Sugioka Yoichi , Iwamoto Yukihide 
Published: February 2005

AbstractThe laser speckle method is a new form of tissue flowmetry that can analyze the interference pattern that appears when tissue is illuminated with a laser beam. During surgery for 100 cases of osteonecrosis of the femoral head, we measured the blood flow within the subchondral bone using this method. We compared the flow maps (two‐dimensional distribution of the microcirculation) obtained this way with the necrotic area estimated by the preoperative magnetic resonance images and with the collapse seen during surgery. The laser speckle method was able to distinguish between the ischemic areas and the normal areas in 92 femoral heads, including five hips for which neither the magnetic resonance images nor the collapse observed during surgery demonstrated a distinct margin surrounding the necrotic area. We concluded that the laser speckle method is useful for defining the margin around a necrotic area.
Cytokine‐induced tendinitis: A preliminary study in rabbits
Authors: Stone David , Green Colleen , Rao Uma , Aizawa Harutaka , Yamaji Toomoo , Niyibizi Christopher , Carlin Greg , Woo Savio L‐Y. 
Published: February 2005

AbstractThis study was designed to determine the effects of a single injection of a species‐specific preparation of cytokines into rabbit patellar tendons and to compare the results with a known model of tendinitis, the collagenase‐injection model. New Zealand White rabbits were divided into two groups and two time periods (4 and 16 weeks) and injected in the midsubstance of the right patellar tendon with either cytokines or collagenase under ultrasound guidance to confirm intratendinous needle placement. The left patellar tendon was injected with 0.025 ml of saline solution and served as a control. The rabbits were returned to cage activity after injection. At death, two rabbits in each group underwent histological analysis; the remaining eight animals in each time frame were evaluated biomechanically and then biochemically with use of the patella/whole patellar tendon/tibia complex. Histologic results at 4 weeks in the tendons injected with cytokines demonstrated increased cellularity, which was resolving by 16 weeks. The matrix appeared unchanged. The tendons injected with collagenase demonstrated increased angiogenesis of the matrix, hypercellularity, and fibrosis around the tendon at 4 weeks. At 16 weeks, myxoid changes, focal fibrosis, and collagen‐bundle disarray with persistent increase in cellularity were noted. Biomechanically, a significant decrease in ultimate load at 16 weeks was seen in the tendons injected with cytokines but no change was seen in cross‐sectional area. The tendons injected with collagenase demonstrated a significant increase in cross‐sectional area at 4 and 16 weeks compared with those injected with cytokines. Biochemically, there was no significant difference in collagen content between the two groups at 4 or 16 weeks but the tendons injected with collagenase demonstrated a significant increase in crosslinking at 16 weeks. Our conclusion is that the tendons injected with the cytokine preparation represent a model of mild, seemingly reversible tendon injury. The cytokine preparation produces no matrix damage or evidence of collagen degradation and is species specific.
In vivo finger flexor tendon force while tapping on a keyswitch
Authors: Dennerlein Jack Tigh , Diao Edward , Mote C. D. , Rempel David M. 
Published: February 2005

AbstractForce may be a risk factor for musculoskeletal disorders of the upper extremity associated with typing and keying. However, the internal finger flexor tendon forces and their relationship to fingertip forces during rapid tapping on a keyswitch have not yet been measured in vivo. During the open carpal tunnel release surgery of five human subjects, a tendon‐force transducer was inserted on the flexor digitorum superficialis of the long finger. During surgery, subjects tapped with the long finger on a computer keyswitch, instrumented with a keycap load cell. The average tendon maximum forces during a keystroke ranged from 8.3 to 16.6 N (mean = 12.9 N, SD = 3.3 N) for the subjects, four to seven times larger than the maximum forces observed at the fingertrip. Tendon forces estimated from an isometric tendon‐force model were only one to two times larger than tip force, significantly less than the observed tendon forces (p = 0.001). The force histories of the tendon during a keystroke were not proportional to fingertip force. First, the tendon‐force histories did not contain the high‐frequency fingertip force components observed as the tip impacts with the end of key travel. Instead, tendon tension during a keystroke continued to increase throughout the impact. Second, following the maximum keycap force, tendon tension during a keystroke decreased more slowly than fingertip force, remaining elevated approximately twice as long as the fingertip force. The prolonged elevation of tendon forces may be the result of residual eccentric muscle contraction or passive muscle forces, or both, which are additive to increasing extensor activity during the release phase of the keystroke.
Immunohistochemical analysis of type X‐collagen expression in osteoarthritis of the hip joint
Authors: Boos Norbert , Nerlich Andreas G. , Wiest Irmagard , von der Mark Klaus , Ganz Reinhold , Aebi Max 
Published: February 2005

AbstractConflicting data have been reported on the spatial distribution of type X‐collagen expression in osteoarthritis, and no concise data exist on a possible correlation between type X‐collagen expression and clinical and radiological alterations. Well defined clinical and radiological data were compared with histopathological and immunohistochemical findings to investigate the expression of type‐X collagen in osteoarthritis of the hip joint. Femoral heads were obtained in toto from 11 patients undergoing routine hip arthroplasty for femoral neck fractures (n = 3) or osteoarthritis (n = 8) and from 13 patients (age: 12 days to 69 years) without any evidence of hip‐joint pathology. Whole coronal sections from the femoral head were decalcified for routine histology and immunohistochemical analysis with use of type‐specific monoclonal antibodies to type‐X collagen. Our results demonstrate that type‐X collagen is consistently found in osteoarthritic cartilage and is absent from normal adult cartilage (including the region of calcified cartilage). Except for the occurrence of type‐X collagen in the middle zone of articular cartilage in advanced stages of osteoarthritis, there is no specific change in the staining pattern or intensity for the collagen during osteoarthritis, particularly when the staining is related to clinical and radiological parameters. Hardly more than 20% of the extracellular matrix stained for type‐X collagen; therefore, we suggest that, in most cases, this type of collagen may not play a direct biomechanical role in the weakening of osteoarthritic cartilage but rather may contribute indirectly to a disturbance of the disc biomechanics by altering matrix‐molecule interaction. However, expression of type‐X collagen may indicate a change in chondrocyte phenotype that consistently coincides with the formation of chondrocyte clusters, one of the first alterations in osteoarthritis visible on histologic examination.
Muscle regeneration and fiber‐type transformation during distraction osteogenesis
Authors: De Deyne Patrick G. , Hayatsu Kazunori , Meyer Rick , Paley Dror , Herzenberg John E. 
Published: February 2005

AbstractThe successful outcome of distraction osteogenesis depends in part on the adequate adaptation of the surrounding soft tissue. We characterized the adaptation of the tibialis anterior during distraction osteogenesis at different rates (0.7 and 1.4 mm/day) and amounts (15 and 30%) of lengthening. We documented the increased expression of neonatal and slow myosin heavy chain in the tibialis anterior of skeletally immature rabbits. There was neither expression of neonatal myosin heavy chain in the experimental soleus or in the slow muscle fibers of the tibialis anterior nor increased expression of slow myosin heavy chain in the soleus or gastrocnemius. The increased amount of neonatal myosin heavy chain was concentrated in the distal half of the muscle, whereas the increase in the number of fibers that were labeled with antibodies to slow myosin occurred to the same extent throughout the tibialis anterior. Electrophysiological methods showed that the tibialis anterior was functionally intact during and after distraction osteogenesis. We concluded that in the tibialis anterior of young, skeletally immature animals, distraction osteogenesis seems to induce a recapitulation of the developmental process without leading to functional changes. In addition, during distraction osteogenesis, a fiber‐type transformation occurs similar to that observed in models of muscle overloading.
Late‐preconditioning protection is evident in the microcirculation of denervated skeletal muscle
Authors: Wang Wei Z. , Tsai Tsu‐Min , Anderson Gary L. 
Published: February 2005

AbstractWe investigated whether ischemic preconditioning induces microvascular protection in skeletal muscle at the late phase (after 24 hours) when the same muscles are subjected to prolonged warm global ischemia. The cremaster muscle of the male Sprague‐Dawley rat underwent vascular isolation and was subjected to 4 hours of ischemia and 60 minutes of reperfusion. Early preconditioning consisted of 45 minutes of ischemia followed by 15 minutes of reperfusion before prolonged ischemia/reperfusion; late preconditioning also consisted of 45 minutes of ischemia but was done 24 hours (24‐hour period of reperfusion) before the prolonged ischemia/reperfusion. Arteriole diameters and capillary perfusion were measured with use of intravital microscopy. Four groups were compared: rats that underwent early preconditioning, their controls, rats that underwent late preconditioning, and their controls. Early and late preconditioning significantly attenuated vasospasm and capillary no‐reflow compared with the controls for each. Average arteriole diameter was significantly larger in the rats that underwent late preconditioning than in any other rats; it was also significantly larger in the controls for late preconditioning than in those for early preconditioning. We introduce a model of the rat cremaster muscle that has been isolated from its vascular supply as a useful preparation to study the effects of late preconditioning on microcirculation in skeletal muscle. Late preconditioning provided better microvascular protection than did early preconditioning. The mechanism for this preconditioning protection is being investigated because it should provide a means for therapeutic intervention.
Effect of demineralized bone matrix on polymorphonuclear leukocyte degranulation
Authors: Kale Ashay A. , Clancy Robert , Leslie Michael P. , Di Cesare Paul E. 
Published: February 2005

AbstractThe potential use of allogenic demineralized bone matrix to augment or treat bone defects or nonunios in animals and humans is currently being investigated. Demineralized bone matrix induces osteogenesis by a multistep cascade of endochondral ossification that is mediated by bone‐induction factors. The migration and activation of polymorphonuclear leukocytes appear to be critical in the initiation of the cascade of osteogenesis induced by demineralized bone matrix. This study examined the effects of demineralized bone matrix on the degranulation of polymorphonuclear leukocytes. Demineralized bone matrix stimulated the release of polymorphonuclear leukocyte‐specific, but not azurophilic, granules in a time and dose‐dependent manner. The ability of the bone matrix to induce this degranulation was independent of its size and species. The mechanism by which this degranulation occurs is not completely understood; however, it is known that it does not occur by means of a receptor that requires guanidine triphosphate‐dependent regulatory proteins as does polymorphonuclear leukocyte degranulation induced by N‐formyl peptide. The factor that stimulates degranulation is not type‐I collagen but rather appears to be a cytokine that has a heparin‐binding domain and a molar mass of 10‐70 kDa. Loss of the ability of demineralized bone matrix to induce degranulation of polymorphonuclear leukocytes correlated positively with the loss of its ability to induce bone formation.
Elastic fibers of musculoskeletal tissues in bovine marfan syndrome: A morphometric study
Authors: Gigante A. , Chillemi C. , Potter K. A. , Bertoni‐Freddari C. , Greco F. 
Published: February 2005

AbstractBovine Marfan syndrome has all the major pathognomonic, clinical, and pathological features of the human syndrome. To further explore the alterations characterizing Marfan syndrome, musculoskeletal tissues from affected and healthy cattle were subjected to histochemical and histomorphometric analysis. Our findings demonstrated reduced elastic fiber content in the periosteum, capsule, interosseous ligament, and flexor tendons of the metatarsophalangeal joint of affected cattle. The elastic properties of a tissue are supplied by elastic fibers in the extracellular matrix; therefore, their reduced content in articular tissues suggests that these fibers could be functionally incompetent to withstand normal stress, causing a predisposition to joint laxity and dislocation. Moreover, perichondrial‐periosteal membrances, which are made of collagen and elastic fibers, are known to affect the growth process of the long bones. The decrease in the number of elastic fibers in these membranes could result in reduced restraint of skeletal growth and explain some skeletal abnormalities of Marfan syndrome (i.e., dolichostenomelic habitus).
P‐glycoprotein expression in osteosarcoma: A basis for risk‐adapted adjuvant chemotherapy
Authors: Baldini N. , Scotlandi K. , Serra M. , Picci P. , Bacci G. , Sottili S. , Campanacci M. 
Published: February 2005

AbstractPrevious reports on osteosarcomas treated with multi‐agent chemotherapy have shown that P‐glycoprotein expression is a reliable prognostic indicator. The current thinking is that, of the several agents used for the treatment of osteosarcoma, only doxorubicin is involved in drug resistance mediated by P‐glycoprotein. This study examines the relationship of P‐glycoprotein expression to clinical outcome in osteosarcomas, treated only with doxorubicin in addition to surgery, to determine if the prognostic significance of P‐glycoprotein expression reflects the ability of osteosarcoma to respond to this drug. The expression of P‐glycoprotein in tumor specimens was assessed by immunohistochemistry in 37 nonmetastatic, operable osteosarcomas treated at a single institution with doxorubicin as a single adjuvant drug. The P‐glycoprotein status was analysed in relation to the length of event‐free survival. A widespread pattern of P‐glycoprotein expression in tumor cells at diagnosis was significantly associated with a higher rate of systemic relapse (p < 0.001). On comparison of this group of patients with a similar series of 92 patients, all treated with multi‐agent chemotherapy plus surgery of the primary lesion and previously analysed for P‐glycoprotein status, only P‐glycoprotein‐positive, doxorubicin‐resistant tumors consistently benefited from the addition of drugs other than doxorubicin (p < 0.001). Osteosarcomas with different abilities to respond to adjuvant chemotherapy can be identified by the expression of P‐glycoprotein in tumor cells at the clinical onset. P‐glycoprotein status may serve as a basis for risk‐adapted, individualized therapeutic regimens. Standard programs are sufficient for P‐glycoprotein‐negative osteosarcomas, whereas P‐glycoprotein‐positive tumors may benefit from the use of more intensive therapeutic approaches.
Expression of osteocalcin and its transcriptional regulators core‐binding factor alpha 1 and MSX2 in osteoid‐forming tumours
Authors: Hopyan Sevan , Gokgoz Nalan , Bell Robert Stuart , Andrulis Irene Louise , Alman Benjamin Aaron , Wunder Jay Steven 
Published: February 2005

AbstractOsteosarcoma, fibrous dysplasia, and myositis ossificans contain osteoid‐producing cells that are not necessarily morphologically typical osteoblasts. Nevertheless, these pathologic cells may share differentiation steps with osteoblasts at the molecular level. Osteocalcin, a bone‐specific extracellular matrix protein, is a marker of mature osteoblasts. Osteocalcin is upregulated by the transcription factor core‐binding factor alpha 1, which is responsible for commitment to the osteoblastic lineage, and is downregulated by MSX2, a homeobox‐containing transcription factor expressed during the early proliferative phase of osteoblast differentiation. Semiquantitative reverse transcription‐polymerase chain reaction was used to compare expression levels of osteocalcin, core‐binding factor alpha 1, and MSX2 in 34 osteosarcoma, five fibrous dysplasia, and five myositis ossificans specimens, as well as in seven normal cortical bone samples. Despite normal or elevated levels of core‐binding factor alpha‐1 expression in most specimens, osteocalcin expression was low or undetectable in most cases of osteosarcoma (25 of 34) and myositis ossificans (4 of 5). Single‐strand conformation polymorphism and sequencing did not identify and mutations in the DNA‐binding domain of core‐binding factor alpha 1. However, a high level of MSX2 expression was demonstrated in these lesions, which may inhibit osteocalcin transcription. The presence of moderate levels of osteocalcin in fibrous dysplasia may contribute to the characteristic disconnected appearance of trabeculae in that entity because osteocalcin is a negative regulator of bone formation.
Carvedilol reduces ischaemic skeletal muscle necrosis
Authors: Hvaal K. , Mathisen S. R. , Svindland A. , Kirkeby O. J. , Skjeldal S. 
Published: February 2005

AbstractCarvedilol is an alpha1 and nonselective beta‐adrenergic receptor antagonist with antioxidative properties known to protect against reperfusion injury in the heart, brain, and kidneys. The aim of this study was to test the hypothesis that carvedilol improves postischaemic reperfusion and tissue survival in skeletal muscle. Sixteen Wistar rats underwent tourniquet ischaemia of the left hindlimb for 3 hours and 15 minutes at 27°C, Single‐fiber laser Doppler probes were inserted in the left and right anterior tibial muscles, and microvascular perfusion was measured until 2 hours after removal of the tourniquet. Perfusion indices for each 15‐minute interval were calculated for the left hindlimb (tourniquet ischaemia) by dividing the postischaemic by the pre‐ischaemic laser Doppler flowmetry values, and the geometrical areas under the curves representing a plot of perfusion index relative to time, measured in arbitrary units, were compared. Laser Doppler flowmetry values for the right anterior tibial muscle were compared. Tissue damage was measured by histomorphometry of necrotic areas and no‐reflow zones in cross sections from the anterior tibial muscle 72 hours after ischaemia. Neutrophils were counted in the same sections. The treatment group received 1 mg carvedilol/kg body weight before ischaemia and 1 mg/kg immediately before removal of the tourniquets. The areas under the curves representing the plot of perfusion index relative to time were larger for the rats treated with carvedilol: 9.5 compared with 3.0 arbitrary units (p = 0.0003). Treatment did not change the laser Doppler flowmetry values for the right hindlimbs. The histomorphometric areas of necrosis in cross sections from the muscles were reduced from 88% (38‐96%) in the control animals to 41% (7‐85%) in those treated with carvedilol (p = 0.01), and the area of no‐reflow was reduced from 20% (2‐52%) to 0% (0‐7%) (p = 0.006). The number of neutrophils did not differ between groups. The study supports the hypothesis that carvedilol improves early reperfusion and protects skeletal muscle subjected to 3 hours and 15 minutes of ischaemia.
Interleukin‐4 inhibits granulocyte‐macrophage colony‐stimulating factor, interleukin‐6, and tumor necrosis factor‐alpha expression by human monocytes in response to polymethylmethacrylate particle challenge in vitro
Authors: Trindade Michael C. D. , Nakashima Yasuharu , Lind Martin , Sun Doo‐Hoon , Goodman Stuart B. , Maloney William J. , Schurman David J. , Lane Smith R. 
Published: February 2005

AbstractThe outcome of total joint arthroplasty is determined by biological events at the bone‐implant interface. Macrophages phagocytose implant or wear debris at the interface and release proinflammatory mediators such as interleukins 1 and 6, tumor necrosis factor‐alpha, and prostaglandin E2. These mediators are thought to contribute to the resorption of periprosthetic bone. Previous studies of tissues harvested from the bone‐implant interface of failed orthopaedic implants demonstrated a possible role for two other cytokines, granulocyte‐macrophage colony‐stimulating factor and interleukin‐4. The present study examined the effects of in vitro challenge with polymethylmethacrylate particles on the expression of granulocyte‐macrophage colony‐stimulating factor by primary human monocytes/macrophages and the role of interleukin‐4 in regulating this expression. The polymethylmethacrylate particles caused a dose‐dependent release of granulocyte‐macrophage colony‐stimulating factor at 48 hours. This release was accompanied by increased expression of interleukins 6 and 1beta and tumor necrosis factor‐alpha. Release of the lysosomal enzyme hexosaminidase also increased in response to the particles. Interleukin‐4 inhibited the expression of granulocyte‐macrophage colony‐stimulating factor, interleukin‐6, and tumor necrosis factor‐alpha at 48 hours in a dose‐dependent manner. The data presented in this study confirm the hypothesis that interleukin‐4 downregulates particle‐induced activation of macrophages, as demonstrated by the decreased release of proinflammatory mediators.
Reduced anterior tibial translation associated with adaptive changes in the anterior cruciate ligament‐deficient joint: Goat model
Authors: Jackson Douglas W. , Schreck Paul , Jacobson Scott , Simon Timothy M. 
Published: February 2005

AbstractAdaptive changes in the menisci and adjacent posterior capsule were documented within anterior cruciate ligament‐deficient knee (stifle) joints in the goat model. These physical changes in the menisci and capsule developed over time and were associated with reduction in the initial (time zero) abnormal anterior tibial translation following transection of the anterior cruciate ligament. At 50 N of applied force, the normal goat knee joint has a total anterior‐posterior translation of 0.6 ± 0.1 mm (± SEM) at 45° of flexion and 0.3 ± 0.1 mm at 90°. The translation immediately after transection (time zero) with 50 N of force was 8.2 ± 0.5 mm at 45° and 4.9 ± 0.9 mm at 90°. Within 8 months after transection and at 50 N of force, the treated knees had reduced translation values of 5.3 ± 0.6 mm at 45° of flexion and 2.9 ± 0.5 mm at 90°, or 35 (p < 0.001) and 40% reductions, respectively, compared with the values at time zero. Magnetic resonance images of the ligament‐deficient stifle joints, as well as gross measurements and image analysis after dissection, consistently demonstrated increases in cross‐sectional area and volume of the menisci compared with the contralateral controls. These secondary changes were most pronounced in the posterior portion of the medial menisci, and histologic evaluation demonstrated hypercellularity with the accumulation of poorly organized collagen, reduced safranin O staining (proteoglycan matrix synthesis), a thickened capsule and capsule attachment, and increased vascularity at the meniscal capsule interface.