bluuebunny/crossref_metadata_2025_split huggingface dataset:
Growth potential of loose bodies: An immunohistochemical examination of primary and secondary synovial osteochondromatosis
Authors: Saotome Koichi , Tamai Kazuya , Koguchi Yasumori , Sakai Hiroya , Yamaguchi Takehiko 
Published: February 2005

AbstractHistologic and immunohistochemical studies of growth potential were performed on 53 surgically removed loose bodies representing 10 cases of primary synovial osteochondromatosis, 37 bodies representing 12 cases of secondary synovial osteochondromatosis, and five bodies representing five cases of osteochondral fracture. Loose bodies in primary synovial osteochondromatosis were nodular, showing plump chondrocytes and irregular calcification, and all contained proliferative cell nuclear antigen‐positive chondrocytes (labeling index: 42.5%; range: 36.0–52.0%). Other markers stained less frequently. Loose bodies in secondary synovial osteochondromatosis showed uniform chondrocytes and annular calcification surrounding core tissue. Eighteen of 37 loose bodies showed proliferative cell nuclear antigen‐positive chondrocytes, mostly peripherally. Chondrocyte labeling indices were less than 5% for proliferative cell nuclear antigen and other markers, although some connective tissue cells in the outer layer were stained. Loose bodies from osteochondral fractures were composed of articular cartilage, subchondral bone, and connective tissue; cartilage was negative for markers, whereas connective tissue contained positive cells. One specimen showed cartilaginous metaplasia of connective tissue. These results suggest that loose bodies have the potential for slow growth by proliferation of chondrocytes in primary synovial osteochondromatosis and by metaplasia following proliferation of surrounding connective tissue in secondary synovial osteochondromatosis.
Immunodetection and partial cDNA sequence of the proteoglycan, superficial zone protein, synthesized by cells lining synovial joints
Authors: Schumacher Barbara L. , Hughes Clare E. , Kuettner Klaus E. , Caterson Bruce , Aydelotte Margaret B. 
Published: February 2005

AbstractWe have previously described a large proteoglycan named superficial zone protein that was isolated and purified from culture medium of superficial slices of bovine articular cartilage. Monoclonal antibodies were raised against superficial zone protein and used as probes in Western blot analyses for immunohistochemical studies both to determine precisely which cells within the joint synthesize the proteoglycan and to isolate a cDNA fragment from a bovine chondrocyte λgt11 library that encodes part of the proteoglycan. The cDNA fragment that was obtained with use of monoclonal antibody 6‐A‐1 encodes the 3′ end of the sequence for superficial zone protein. On Western blots, monoclonal antibody 3‐A‐4 recognized an epitope on native, but not reduced, superficial zone protein, whereas monoclonal antibody 6‐A‐1 reacted with both native and denatured antigen. The proteoglycan was immunolocalized with monoclonal antibody 3‐A‐4 in chondrocytes predominantly within the superficial zone of fetal and adult articular cartilage and in some cells of the synovial lining. However, the proteoglycan was not detected in chondrocytes deep in articular cartilage, in nasal septal cartilage, or in synovial stromal cells. The only matrix staining positively for superficial zone protein was at the articular surface bordering the synovial cavity in adult, but not fetal, joints. Isolated chondrocytes and synovial cells showed intracellular binding of monoclonal antibody 3‐A‐4, and flow‐cytometric analysis with the antibody gave the following percentages of immunopositive cells: 37.4, 52.5, 3.4, and 7.5 from chondrocytes from the full‐thickness, superficial, and deep zones and from synovial cells, respectively. Thus, both chondrocytes and synovial cells bordering the joint cavity synthesize superficial zone protein and substantiate its usefulness as a phenotypic marker of particular cellular species lining the articular cavity.
Mechanically modulated cartilage growth may regulate joint surface morphogenesis
Authors: Heegaard J. H. , Beaupré G. S. , Carter D. R. 
Published: February 2005

AbstractThe development of normal joints depends on mechanical function in utero. Experimental studies have shown that the normal surface topography of diarthrodial joints fails to form in paralyzed embryos. We implemented a mathematical model for joint morphogenesis that explores the hypothesis that the stress distribution created in a functional joint may modulate the growth of the cartilage anlagen and lead to the development of congruent articular surfaces. We simulated the morphogenesis of a human finger joint (proximal interphalangeal joint) between days 55 and 70 of fetal life. A baseline biological growth rate was defined to account for the intrinsic biological influences on the growth of the articulating ends of the anlagen. We assumed this rate to be proportional to the chondrocyte density in the growing tissue. Cyclic hydrostatic stress caused by joint motion was assumed to modulate the baseline biological growth, with compression slowing it and tension accelerating it. Changes in the overall shape of the joint resulted from spatial differences in growth rates throughout the developing chondroepiphyses. When only baseline biological growth was included, the two epiphyses increased in size but retained convex incongruent joint surfaces. The inclusion of mechanobiological‐based growth modulation in the chondroepiphyses led to one convex joint surface, which articulated with a locally concave surface. The articular surfaces became more congruent, and the anlagen exhibited an asymmetric sagittal profile similar to that observed in adult phalangeal bones. These results are consistent with the hypothesis that mechanobiological influences associated with normal function play an important role in the regulation of joint morphogenesis.
Size and position of a single condyle allograft influence knee kinematics
Authors: Elias John J. , DesJardins John D. , Faust Alfred F. , Lietman Steven A. , Chao Edmund Y. S. 
Published: February 2005

AbstractAn optimal match for size and shape between the donor femur and the host knee is considered a critical factor influencing the outcome of a knee allograft implantation. An in vitro allograft model was developed to determine the influence of the size and position of a lateral distal femoral condylar allograft on knee kinematics. Functional knee motion was simulated in a cadaver host knee in the intact state after removing and reimplanting the native lateral condyle of the distal femur and after serially replacing the native condyle with eight donor allografts. Each allograft was first tested in an optimal position and subsequently shifted 3 mm proximal and 3 mm distal to the joint line to quantify changes in joint kinematics due to the position of the allograft. The intact knee and the knee with the ideally implanted native allograft followed similar kinematic trends. Decreasing the width of the allograft increased the valgus knee orientation at full flexion, translated the tibia posteriorly at full extension, and externally rotated the tibia throughout knee flexion. The proximal shift in allograft position increased the valgus orientation at full extension, translated the tibia posteriorly at mid‐flexion, and externally rotated the tibia throughout flexion. The distal shift in position had the opposite effect on the kinematics of the proximal shift. These results indicate that improving techniques for preoperative size‐matching and intraoperative allograft placement may help to reduce biomechanical complications following implantation of the allograft.
Effects of isokinetic muscle activity on pressure in the supraspinatus muscle and shoulder torque
Authors: Sporrong Håkan , Styf Jorma 
Published: February 2005

AbstractWork‐related shoulder pain is an increasing problem. Work in overhead positions, which causes high pressure in the supraspinatus muscle, has been shown to increase the shoulder load. It is not known how different types of muscle activity in the shoulder affect pressure in the muscle. The aim of this study was to investigate the difference between contraction modes. This has not been done before for shoulder muscles. The results are relevant from several aspects, both clinical and experimental. Pressure in the supraspinatus muscle and torque generation in the shoulder during isokinetic concentric and eccentric activity were measured in nine healthy human subjects. Torque and arm position were measured continuously with a computerized ergonometer. The contraction velocity was 60° per second, and the range of movement was 0–120° of abduction. Electromyographic measurements were recorded with a surface electrode above the supraspinatus muscle belly. Intramuscular pressure was recorded with a microcapillary infusion technique. Peak intramuscular pressure did not differ significantly between the two modes of contraction, but the peak was reached at 115° (SD = 15°) of abduction during concentric activity and at 6° (SD = 7°) of abduction during eccentric concentric activity and 2.3 mm Hg/Nm (0.31 kPa/Nm) during eccentric activity. The peak torque occurred at 44° of abduction during concentric muscle activity and at 74° of abduction during eccentric activity. Intramuscular pressure was higher during isometric contraction than during eccentric and concentric activity, and the torque was in between the two latter contraction modes. We conclude that the supraspinatus muscle is heavily loaded not only in high arm positions during concentric contraction but also during eccentric contraction in arm positions of 0‐30° of abduction.
Interleukin‐1 beta promotes functional recovery of crushed peripheral nerve
Authors: Korompilias Anastasios V. , Chen Long‐En , Seaber Anthony V. , Urbaniak James R. 
Published: February 2005

AbstractThis study was conducted to elucidate the role of the cytokine interleukin‐1 beta on peripheral nerve recovery following crush injuries of wo different magnitudes. Eighty‐eight female rats were divided into four groups. A 5‐mm segment of the right sciatic nerve was subjected to a 100‐g crush load for 2 hours in the rats in Groups A1 and B1 or to a 15,000‐g crush load for 10 minutes in the rats in Groups A2 and B2. The rats in Groups A1 and A2 received 10 μg/100 g body weight human recombinant interleukin‐1 beta intraperitoneally 48, 24, and 1 hours before the nerve injury. The rats in Groups B1 and B2 were treated with an equal volume of normal saline solution with identical schedule guidelines. Walking‐track tests (sciatic functional index) performed at intervals until 56 days after the crush and measurements of the contractile force of the extensor digitorum longus muscle made until 28 days were used to evaluate functional recovery of the nerve. During the second week after injury, the rats treated with interleukin‐1 beta (A1) had an earlier recovery on the walking track than did those treated with saline solution (B1); this difference reached significance (p < 0.05) at day 11. Although Group A2 demonstrated a trend toward earlier recovery compared with Group B2, there was no significant difference between the two groups. After low or high‐load crush injury, tetanic contractile forces were greater in the rats treated with human recombinant interleukin‐1 beta than in those treated with saline solution. The results suggest that treatment with human recombinant interleukin‐1 beta before crush injury can promote function in the peripheral nerve after the injury. However, the mechanisms that underlie the observed beneficial effects are not completely understood and only speculations can be made.
In situ forces in the human posterior cruciate ligament in response to muscle loads: A cadaveric study
Authors: Höher Jürgen , Vogrin Tracy M. , Woo Savio L‐Y. , Carlin Gregory J. , Årøen Asbjørn , Harner Christopher D. 
Published: February 2005

AbstractThe objectives of this study were to determine the effects of hamstrings and quadriceps muscle loads on knee kinematics and in situ forces in the posterior cruciate ligament of the knee and to evaluate how the effects of these muscle loads change with knee flexion. Nine human cadaveric knees were studied with a robotic manipulator/universal force‐moment sensor testing system. The knees were subjected to an isolated hamstrings load (40 N to both the biceps and the semimembranosus), a combined hamstrings and quadriceps load (the hamstrings load and a 200‐N quadriceps load), and an isolated quadriceps load of 200 N. Each load was applied with the knee at full extension and at 30, 60, 90, and 120° of flexion. Without muscle loads, in situ forces in the posterior cruciate ligament were small, ranging from 6 ± 5 N at 30° of flexion to 15 ± 3 N at 90°. Under an isolated hamstrings load, the in situ force in the posterior cruciate ligament increased significantly throughout all angles of knee flexion, from 13 ± 6 N at full extension to 86 ± 19 N at 90°. A posterior tibial translation ranging from 1.3 ± 0.6 to 2.5 ± 0.5 mm was also observed from full extension to 30° of flexion under the hamstrings load. With a combined hamstrings and quadriceps load, tibial translation was 2.2 ± 0.7 mm posteriorly at 120° of flexion but was as high as 4.6 ± 1.7 mm anteriorly at 30°. The in situ force in the posterior cruciate ligament decreased significantly under this loading condition compared with under an isolated hamstrings load, ranging from 6 ± 7 to 58 ± 13 N from 30 to 120° of flexion. With an isolated quadriceps load of 200 N, the in situ forces in the posterior cruciate ligament ranged from 4 ± 3 N at 60° of flexion to 34 ± 12 N at 120°. Our findings support the notion that, compared with an isolated hamstrings load, combined hamstrings and quadriceps loads significantly reduce the in situ force in the posterior cruciate ligament. These data are in direct contrast to those for the anterior cruciate ligament. Furthermore, we have demonstrated that the effects of muscle loads depend significantly on the angle of knee flexion.
Effects of increased in vivo excursion on digital range of motion and tendon strength following flexor tendon repair
Authors: Silva Matthew J. , Brodt Michael D. , Boyer Martin I. , Morris Timothy S. , Dinopoulos Haralambos , Amiel David , Gelberman Richard H. 
Published: February 2005

AbstractPostoperative rehabilitation is an important factor in determining functional outcome following intrasynovial flexor tendon repair. We hypothesized that a rehabilitation protocol that produced increased in vivo excursion would lead to increased digital range of motion and tendon strength and decreased adhesion formation in a canine model. Ninety‐six flexor digitorum profundus tendons from 48 dogs were cut transversely and repaired by a multistrand suture technique. Postoperative rehabilitation was performed daily with a low excursion‐low force (1.7‐mm average excursion: < 10 N force) or a high excursion‐low force (3.6 mm excursion: < 10 N force) protocol. After death of the dogs at 10, 21, or 42 days, specimens were evaluated for digital range of motion, tensile mechanical properties, elongation of the repair site, and adhesion formation. Our data indicate that the range of motion of digits whose tendons were at low or high excursion was similar to that of controls. Increased in vivo tendon excursion due to synergistic wrist motion did not significantly affect ex vivo flexion of the distal and proximal interphalangeal joints or tendon displacement (p > 0.05). Similarly, tensile properties (ultimate load, repair site rigidity, and repair site strain at 20 N and at failure) and length of the gap at the repair site were not significantly affected by increased excursion (p > 0.05). Severity of adhesion formation was reduced slightly by increased excursion (p = 0.04). Our findings indicate that 1.7 mm of tendon excursion is sufficient to prevent adhesion formation following sharp transection of the canine flexor tendon and that additional excursion provides little added benefit.
Differences in mRNA expression patterns between patellar tendons and anterior cruciate ligaments of immature pigs
Authors: Yin C. , Wayne J. S. , Jiranek W. A. , Zuelzer W. A. 
Published: February 2005

AbstractThe patellar tendon is the most commonly used graft source in reconstruction of the anterior cruciate ligament. The performance of a patellar tendon graft in such a reconstruction is largely related to the structural and functional differences between patellar tendons and anterior cruciate ligaments. From a genetic point of view, the structural and functional differences are ultimately decided by the differential patterns of gene expression between the two tissues. In the present study, the genetic differences between normal patellar tendons and normal anterior cruciate ligaments were explored by screening a large number of mRNA species to detect the species unique to each tissue. Of the approximately 1,000 mRNAs screened, 20 differentially expressed mRNA species were detected. Eight were unique to patellar tendons, and 12 were unique to anterior cruciate ligaments. Of these 20 unique mRNA species, 12 did not match any of the known sequences in gene databases and were probably novel genes. Transcriptional control is a major step in the genetic pathway: therefore, the variations found between patellar tendons and anterior cruciate ligaments at this level of gene expression indicate that the differences between the two tissues are likely more extensive than previously thought. These differences probably influence the survival of patellar tendon autografts and should be explored further.
Histological and biochemical evaluation of perichondrial transplants in human articular cartilage defects
Authors: Bouwmeester Phianne , Kuijer Roel , Terwindt‐Rouwenhorst Els , van der Linden Ton , Bulstra Sjoerd 
Published: February 2005

AbstractFrom 1986 to 1992, 88 patients with articular defects in the knee were treated with a perichondrial arthroplasty. In this study, we report on the results for 22 biopsies of grafted tissue with a mean follow‐up of 21 months. Biopsies were obtained at routine arthroscopy after approximately 1 year or at arthroscopy or arthrotomy at a later stage when patients were operated on again because of recurrent complaints. Biopsies were taken only when a partial failure was present or when there was a clear failure resulting in fibrocartilage, a loose flap, or a loose body. The biopsies were analyzed histologically, biochemically for the amount of type‐II collagen, and immunohistochemically with antibodies for types I, II, and X collagen. The well‐being of the patients was investigated with use of the Hospital for Special Surgery knee score. The biopsies from 6 patients contained more than 50% hyaline cartilage. At arthroscopy, the mean relative amount of type‐II collagen was 56% in the biopsies classified as good. The cartilage of the grafted area was macroscopically normal for eight of the 22 biopsies. Histological and biochemical analysis of biopsies from failed transplants showed fibrocartilage with mainly type‐I collagen. These tissues were retrieved primarily from patients with additional abnormalities in the knee joint. It was concluded that adult human perichondrium is able to form hyaline‐like cartilage in an isolated cartilage defect in an otherwise healthy knee.
Compositional and metabolic changes in damaged cartilage are peak‐stress, stress‐rate, and loading‐duration dependent
Authors: Chen Chih‐Tung , Burton‐Wurster Nancy , Lust George , Bank Ruud A. , Tekoppele Johan M. 
Published: February 2005

AbstractThe first objective of this study was to determine if the cumulative effects of impact or smoothly arising compression would damage the matrix of articular cartilage. Canine cartilage explants were subjected to repeated impacts or to smoothly arising compressions of as much as 20 MPa at 0.3 Hz for as long as 120 minutes. An increase in the water content of the loaded core compared with the surrounding ring was considered indicative of matrix damage. The results showed that damage to cartilage required repeated impacts with a peak stress of at least 2.5 MPa and a stress rate of at least 30 MPa/sec for 2 minutes or longer. This suggested that impact damage is cumulative and stress‐rate dependent. The second objective was to identify biosynthetic and compositional changes in impact‐damaged cartilage over a period of time after loading. Accordingly, canine cartilage explants were subjected to repetitive impacts of 5 MPa at 0.3 Hz for 2, 20, and 120 minutes. The loaded explants were then cultured for as long as 10 days. The increase in water content (1.9‐3.8%) in the core region relative to the surrounding ring persisted during the 10‐day culture. A significant increase in fibronectin synthesis (22‐47%) was found in the core region of impact‐damaged cartilage. Proteoglycan synthesis was increased by 41‐104%. An increase in denatured collagens (11‐70%) in the loaded cores substantiated damage to the collagen network. Denatured collagens stained with COL2‐3/4m monoclonal antibody were consistent with the compositional findings and were mainly located near the articular surface and in the deep zone. These changes were consistent with early osteoarthritis and suggested the induction of the initial stages of osteoarthritis in the impact‐damaged cartilage.
Heat shock‐induced necrosis and apoptosis in osteoblasts
Authors: Li Song , Chien Shu , Brånemark Per‐Ingvar 
Published: February 2005

AbstractDamage to bone tissue due to heat shock is one of the main causes of the failure of osseointegration at the bone‐implant interface. To investigate the effect of heat shock on regeneration of bone tissue, osteoblasts were exposed to heat shock for 10 minutes at 42, 45, or 48°C or kept at 37°C as a control. After 10 minutes of heat shock, disruption of actin filaments was seen in the cells and the degree of disruption increased with the temperature. The cytoskeleton reassembled after a 12‐hour incubation at 37°C in the cells treated at 42 or 45°C, but this reversible recovery did not occur in the cells treated at 48°C. Flow cytometric analysis showed that heat shock at 48°C increased the number of necrotic cells to 15‐20% within minutes (p < 0.05 compared with 37°C). Apoptosis, evidenced by annexin V staining, DNA laddering, and caspase 3 activation, started after 6‐8 hours of incubation, reached a peak at 12 hours, and gradually declined (p < 0.05). Pretreatment with the antioxidant N‐acetyl‐L‐cysteine reduced the necrosis induced at 48°C of heat shock by one‐half (p < 0.05) but had no significant effect on caspase 3 activation induced by heat shock, suggesting that reactive oxygen species were critical in heat shock‐induced necrosis but not in apoptosis. Heat shock at 48°C induced a sustained translocation of p53 into the nucleus and a sustained activation of c‐jun N‐terminal kinase, whereas that at 42 and 45°C induced only transient p53 translocation and c‐jun N‐terminal kinase activation. These results suggest that the sustained activation of p53 and c‐jun N‐terminal kinase pathways may contribute to heat shock‐induced apoptosis. On the other hand, heat shock protein 70 increased dramatically in the cells treated at 45 or 48°C, suggesting that the protecting mechanism in the cells was also activated. Such protection was able to prevent apoptosis in cells treated at 45°C but not in those treated at 48°C.