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[Effects of periosteum, synovium and cartilage tissues on genes for joint cartilage regeneration].

OBJECTIVE: To study the effects of the periosteum,synovium and cartilage tissues on the gene expressions of proteoglycan, collagen II, and nuclear factor kappa B (NF-kappaB) and to investigate the different effects of these tissues on cartilage regeneration. METHODS: In 20 New Zealand white rabbits, 20 cartilage explants were taken from the knee joints in each rabbit, the size of which was 4 mm x 4 mm x 4 mm. All the cartilages were divided into the following 4 groups and cultured for 7 days: Group A, with 5 pieces (2 mm x 2 mm) of the synovium of the knee joints in each dish; Group B, with 5 pieces (2 mm x 2 mm) of the periosteum in each dish; Group C, with 5 pieces (2 mm x 2 mm x 2 mm) of the cartilage in each dish; and Group D, with no addition of other tissues (control group). RNA was extracted from the cells of the cartilage explants (4 mm x 4 mm x 4 mm) in all the dishes. The gene expressions of proteoglycan, collagen II and NF-kappaB were defected by a reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: In group A, the gene expression of proteoglycan was significantly decreased. The relative density of this gene expression had a significant difference when compared with that in group D (1.09 +/- 0.21 vs. 1.25 +/- 0.25, P < 0.05); the gene expressions of collagen I and NF-kappaB were also decreased, but they had no significant differences when compared with those in group D (P > 0.05). In group B, the gene expressions of proteoglycan, collagen II, and NF-kappaB were significantly increased. The relative densities of these gene expressions were 1.60 +/- 0.26, 1.57 +/- 0.24, and 4.20 +/- 2.22, respectively, which had significant differences when compared with those in group D (P < 0.05). In group C, the relative density of the gene expression of collagen II was 1.43 +/- 0.28, which had a significant difference when compared with that in group D (P < 0.05), but the relative densities of the gene expressions of proteoglycan and NF-kappaB had no significant differences when compared with those in group D (P > 0.05). CONCLUSION: The results indicate that the periosteum can up-regulate the gene expressions of proteoglycan, collagen II and NF-kappaB. The NF-kappaB is likely to be an important nuclear transcription factor related to cartilage regeneration. The results also suggest that the periosteum may be better in facilitating the cartilage repair and regeneration in clinical practice.

Animals↗

Denaturation of type II collagen in articular cartilage in experimental murine arthritis. Evidence for collagen degradation in both reversible and irreversible cartilage damage.

Degradation of type II collagen is thought to be a key step in the destruction of articular cartilage in patients with rheumatoid arthritis or osteoarthritis. The aim of this study was to investigate whether type II collagen degradation is associated with cartilage destruction. Type II collagen degradation was studied in two murine arthritis models, zymosan-induced arthritis (ZIA), which develops reversible articular cartilage damage based on proteoglycan analysis, and antigen-induced arthritis (AIA), in which there is irreversible damage to the cartilage. Type II collagen degradation was assayed immunohistochemically using the COL2-3/4m antibody which recognizes denatured type II collagen, such as is produced by collagenase cleavage. In both models, degradation of type II collagen was observed in the non-calcified articular cartilage of arthritic but not of control knees. In the patella-femoral compartment, collagen denaturation started to increase on day 3 (ZIA) and day 7 (AIA) and remained high on day 14. In contrast, in the tibia-femoral compartment, type II collagen breakdown was not increased before 14 days in either model. By 28 days, collagen denaturation was strongly reduced in the patella-femoral compartment in the ZIA model, but persisted in the tibia-femoral compartment in both models. In conclusion, increased type II collagen degradation was found in articular cartilage of both ZIA and AIA animals. Since ZIA does not develop irreversible cartilage destruction, this indicates that cartilage may have the ability to withstand a limited degree of type II collagen degradation without developing irreversible damage.

Animals↗

Immature articular cartilage is more susceptible to blood-induced damage than mature articular cartilage: an in vivo animal study.

OBJECTIVE: Cartilage of young but skeletally mature dogs is more susceptible to blood-induced damage than that of old dogs. The aim of the present study was to investigate whether cartilage of skeletally immature individuals is even more adversely affected by exposure to blood than that of mature individuals, as suggested by clinical practice experience with humans. METHODS: Right knees of 3 groups of 6 beagle dogs (skeletally immature, young mature, and old animals) were injected with autologous blood on days 0 and 2. On day 4, cartilage matrix proteoglycan turnover (content, synthesis, and release), synovial inflammation, and cartilage-destructive properties of the synovial tissue were determined and compared with those of the left uninjected control knees. RESULTS: Subsequent to intraarticular bleeding, cartilage proteoglycan content decreased in an age-dependent manner, with the largest decrease occurring in cartilage of immature animals. Proteoglycan synthesis per cell also decreased in an age-dependent manner, with the largest decrease occurring in the immature animals. Cartilage proteoglycan release increased in all 3 groups, but the decrease was not age dependent. Interestingly, immature animals showed a large increase in cartilage DNA content upon exposure to blood, whereas mature animals did not. Histologic analysis showed a mild synovitis in animals of all ages, but catabolic inflammatory activity was found only in immature animals. CONCLUSION: Joints of skeletally immature dogs appeared to be more susceptible than joints of mature dogs to the adverse effects of a joint hemorrhage. These data suggest that for humans, specifically young children are at risk for joint damage after a joint hemorrhage.

Age Factors↗

Exposure of human cartilage tissue to low concentrations of blood for a short period of time leads to prolonged cartilage damage: an in vitro study.

OBJECTIVE: Joint bleeding, or hemarthrosis, leads in time to severe joint damage. This study was carried out to test the in vitro thresholds of exposure time and concentration that lead to irreversible joint damage, to add to the discussion on the usefulness of aspiration of the joint after a hemorrhage. METHODS: Explants of healthy human articular cartilage tissue were cultured in the presence or absence of 50% (volume/volume) blood for 1, 2, 3, or 4 days or in the presence of 0%, 5%, 10%, 20%, 30%, or 50% (v/v) blood for 4 days, followed by a 12-day period of recovery after withdrawal of blood. The effect of blood exposure on cartilage was determined by measuring the rate of proteoglycan synthesis as well as the release and content of cartilage matrix proteoglycans and the activity of matrix metalloproteinases. RESULTS: Exposure of cartilage to 50% (v/v) blood led to adverse changes that were largely independent of the exposure time. The adverse effects persisted after an initial exposure of up to or exceeding 2 days. Exposure of cartilage to increasing concentrations of blood for 4 days led to concentration-dependent adverse changes. These effects persisted when the concentration equaled or exceeded 10% (v/v) blood. Moreover, after 2 days of exposure to a blood load of 10% (v/v), the adverse effects on cartilage were not reversible. CONCLUSION: A 2-day exposure of cartilage in vitro to 10% (v/v) blood leads to prolonged impairment of joint cartilage. This suggests that aspiration of blood from the joint within 2 days after hemarthrosis should be considered to prevent blood-induced joint damage in the long term.

Blood↗

Minced cartilage without cell culture serves as an effective intraoperative cell source for cartilage repair.

Traumatic articular cartilage injuries heal poorly and may predispose patients to the early onset of osteoarthritis. One current treatment relies on surgical delivery of autologous chondrocytes that are prepared, prior to implantation, through ex vivo cell expansion of cartilage biopsy cells. The requirement for cell expansion, however, is both complex and expensive and has proven to be a major hurdle in achieving a widespread adoption of the treatment. This study presents evidence that autologous chondrocyte implantation can be delivered without requiring ex vivo cell expansion. The proposed improvement relies on mechanical fragmentation of cartilage tissue sufficient to mobilize embedded chondrocytes via increased tissue surface area. Our outgrowth study, which was used to demonstrate chondrocyte migration and growth, indicated that fragmented cartilage tissue is a rich source for chondrocyte redistribution. The chondrocytes outgrown into 3-D scaffolds also formed cartilage-like tissue when implanted in SCID mice. Direct treatment of full-thickness chondral defects in goats using cartilage fragments on a resorbable scaffold produced hyaline-like repair tissue at 6 months. Thus, delivery of chondrocytes in the form of cartilage tissue fragments in conjunction with appropriate polymeric scaffolds provides a novel intraoperative approach for cell-based cartilage repair.

Animals↗

Cartilage degradation by stimulated human neutrophils: elastase is mainly responsible for cartilage damage.

Although neutrophilic granulocytes are assumed to contribute to cartilage degradation during rheumatic diseases, there is still a discussion whether reactive oxygen species (ROS) or proteolytic enzymes that are both released by the neutrophils are most relevant to cartilage degradation. To gain further insight into these processes, an in vitro approach to study the interaction between the products of stimulated neutrophilic granulocytes and cartilage was used: Neutrophils from the blood of healthy volunteers were treated with different stimulators (e.g., Ca(2+) ionophores) in order to induce degranulation. Supernatants of neutrophils were afterward incubated with thin slices of pig articular cartilage. Some experiments were also performed in the presence of selected enzyme inhibitors. Supernatants of cartilage were subsequently assayed by one- and two-dimensional high-resolution proton NMR spectroscopy, and the content of soluble carbohydrates in the supernatant was additionally determined by biochemical methods. The selective inhibition of elastase decreased most significantly the extent of cartilage degradation, whereas all other inhibitors had much smaller effects. These results were additionally confirmed by measuring the effect of isolated elastase on articular cartilage in the absence and presence of different inhibitors. It is concluded that elastase released [EC 3.4.21.37] by neutrophils is the most relevant enzyme for cartilage degradation.

Animals↗

Measurement of articular cartilage volumes in the normal knee by magnetic resonance imaging: can cartilage volumes be estimated from physical characteristics?

In recent times several studies have been performed on magnetic resonance imaging (MRI) sequences for imaging cartilage. A fat-suppressed three-dimensional sequence is one such noteworthy example. More recent studies have reported that the total volume of cartilage in a knee joint can be elucidated using this sequence. Based on these studies, we hypothesized that the total volume of cartilage in the knee joint may reflect certain other physical characteristics. The purpose of the current study was to clarify the articular cartilage volumes of the patella and femur in the human knee joints of healthy adults using MRI and to analyze the correlation of these volumes with other physical characteristics. The material comprised 68 knees of 68 Japanese healthy volunteers, aged from their twenties to their forties (37 men and 31 women) who had no past history of joint disease or trauma in the legs. The knees were imaged by MRI with a fat-suppressed three-dimensional sequence, and the cartilage volumes were calculated by computer processing. The factors analyzed were age, body weight, height, leg length, foot size, circumferences of the thigh and lower leg, the distance between medial and lateral femoral condyles, the diameter of the tibial head, body mass index, general joint laxity, quadriceps angle, and leg-heel alignment. The mean cartilage volume was 7.6 +/- 1.6 cm(3) (8.3 +/- 1.6 cm(3) in men, 6.7 +/- 0.9 cm(3) in women). It was significantly larger in men than in women. However, the volume positively correlated with body weight, height, leg length, and foot size, without distinction of gender or age. Based on these data, a multiple regression analysis was developed: cartilage volume = 0.113 x height - 11.053. We concluded that the cartilage volume depends on physical size regardless of gender, and it can be estimated from factors of physical size.

Adult↗

Expression of mouse HtrA1 serine protease in normal bone and cartilage and its upregulation in joint cartilage damaged by experimental arthritis.

Levels of HtrA1 protein in cartilage have been reported to elevate in joints of human osteoarthritis patients. To understand roles of HtrA1 in normal osteogenesis as well as in pathogenesis of arthritis, we examine HtrA1 expression pattern during bone and cartilage development and in articular cartilage affected by experimental arthritis. HtrA1 is not expressed in mesenchymal or cartilage condensations before initiation of ossification. When ossification begins in the condensations, the expression of HtrA1 starts in chondrocytes undergoing hypertrophic differentiation near the ossification center. Hypertrophic chondrocytes found in adult articular cartilage and epiphyseal growth plates also express HtrA1. When arthritis is induced by injection of anti-collagen antibodies and lipopolysaccharide, resting chondrocytes proceed to terminal hypertrophic differentiation and start expressing HtrA1. These data suggest that hypertrophic change induces HtrA1 expression in chondrocytes both in normal and pathological conditions. HtrA1 has been reported to inhibit TGF-beta signaling. We show that HtrA1 digests major components of cartilage, such as aggrecan, decorin, fibromodulin, and soluble type II collagen. HtrA1 may, therefore, promote degeneration of cartilage by inducing terminal hypertrophic chondrocyte differentiation and by digesting cartilage matrix though its TGF-beta inhibitory activity and protease activity, respectively. In bone, active cuboidal osteoblasts barely express HtrA1, but osteoblasts which flatten and adhere to the bone matrix and osteocytes embedded in bone are strongly positive for HtrA1 production. The bone matrix shows a high level of HtrA1 protein deposition akin to that of TGF-beta, suggesting a close functional interaction between TGF-beta and HtrA1.

Aging↗

Delayed gadolinium-enhanced magnetic resonance imaging (dGEMRIC) of hip joint cartilage: better cartilage delineation after intra-articular than intravenous gadolinium injection.

PURPOSE: To investigate and compare delayed gadolinium (Gd-DTPA)-enhanced magnetic resonance imaging (MRI) of cartilage (dGEMRIC) in the hip joint using intravenous (i.v.) or ultrasound-guided intra-articular (i.a.) Gd-DTPA injection. MATERIAL AND METHODS: In 10 patients (50% males, mean age 58 years) with clinical and radiographic hip osteoarthritis (OA; Kellgren score II-III), MRI of the hip was performed twice on a clinical 1.5T MR scanner: On day 1, before and 90-180 min after 0.3 mmol/kg body weight i.v. Gd-DTPA and, on day 8, 90-180 min after ultrasound-guided i.a. injection of a 4 mmol/l Gd-DTPA solution. Coronal STIR, coronal T1 fat-saturated spin-echo, and a cartilage-sensitive gradient-echo sequence (3D T1 SPGR) in the sagittal plane were applied. RESULTS Both the post-i.v. and post-i.a. Gd-DTPA images showed significantly higher signal-to-noise (SNR) and contrast-to-noise (CNR) in the joint cartilage compared to the non-enhanced images (P < 0.002). I.a. Gd-DTPA provided significantly higher SNR and CNR compared to i.v. Gd-DTPA (P < 0.01). Furthermore, a better delineation of the cartilage in the synovial/cartilage zone and of the chondral/subchondral border was observed. CONCLUSION: The dGEMRIC MRI method markedly improved delineation of hip joint cartilage compared to non-enhanced MRI. The i.a. Gd-DTPA provided the best cartilage delineation. dGEMRIC is a clinically applicable MRI method that may improve identification of early subtle cartilage damage and the accuracy of volume measurements of hip joint cartilage.

Adult↗

Comparison of diced cartilage graft wrapped in surgicell and diced cartilage graft wrapped in fascia: an experimental study.

HYPOTHESIS: This study was conducted to compare diced cartilage grafts wrapped in fascia and diced cartilage grafts wrapped in surgicell with respect to their resorption. STUDY DESIGN: Experimental study. METHODS: Eight male Wistar Albino rats were used. After general anesthesia, two different subcutaneous pockets (upper and lower pocket) were prepared in the rat's abdomen. Surgicell-wrapped homograft that was taken from the ear was placed into the upper subcutaneous pocket. Fascia-wrapped homograft which was taken from the ear was placed into the lower subcutaneous pocket. All the rats were killed at the end of 2 months, and the samples were collected to be examined histopathologically. Cartilage mass, foreign body reaction, fibrosis, chronic inflammation, and vascularization were researched. RESULTS: Diced cartilage wrapped surgicell stained negative for glial fibrillary acidic protein (GFAP). Diced cartilage wrapped in fascia stained positive for GFAP. There was a significant difference between two groups with respect to fibrosis, chronic inflammation, and cartilage mass. There was no significant difference between the two groups regarding vascularization. CONCLUSIONS: This study suggests that diced cartilage graft wrapped in surgicell was absorbed, whereas diced cartilage graft wrapped in fascia was not.

Absorption↗

Toward an MRI-based method to measure non-uniform cartilage deformation: an MRI-cyclic loading apparatus system and steady-state cyclic displacement of articular cartilage under compressive loading.

Recent magnetic resonance imaging (MRI) techniques have shown potential for measuring non-uniform deformations throughout the volume (i.e. three-dimensional (3D) deformations) in small orthopedic tissues such as articular cartilage. However, to analyze cartilage deformation using MRI techniques, a system is required which can construct images from multiple acquisitions of MRI signals from the cartilage in both the underformed and deformed states. The objectives of the work reported in this article were to 1) design an apparatus that could apply highly repeatable cyclic compressive loads of 400 N and operate in the bore of an MRI scanner, 2) demonstrate that the apparatus and MRI scanner can be successfully integrated to observe 3D deformations in a phantom material, 3) use the apparatus to determine the load cycle necessary to achieve a steady-state deformation response in normal bovine articular cartilage samples using a flat-surfaced and nonporous indentor in unconfined compression. Composed of electronic and pneumatic components, the apparatus regulated pressure to a double-acting pneumatic cylinder so that (1) load-controlled compression cycles were applied to cartilage samples immersed in a saline bath, (2) loading and recovery periods within a cycle varied in time duration, and (3) load magnitude varied so that the stress applied to cartilage samples was within typical physiological ranges. In addition the apparatus allowed gating for MR image acquisition, and operation within the bore of an MRI scanner without creating image artifacts. The apparatus demonstrated high repeatability in load application with a standard deviation of 1.8% of the mean 400 N load applied. When the apparatus was integrated with an MRI scanner programmed with appropriate pulse sequences, images of a phantom material in both the underformed and deformed states were constructed by assembling data acquired through multiple signal acquisitions. Additionally, the number of cycles to reach a steady-state response in normal bovine articular cartilage was 49 for a total cycle duration of 5 seconds, but decreased to 33 and 27 for increasing total cycle durations of 10 and 15 seconds, respectively. Once the steady-state response was achieved, 95% of all displacements were within +/- 7.42 microns of the mean displacement, indicating that the displacement response to the cyclic loads was highly repeatable. With this performance, the MRI-loading apparatus system meets the requirements to create images of articular cartilage from which 3D deformation can be determined.

Adaptation, Physiological↗

Inactivation of one allele of the type II collagen gene alters the collagen network in murine articular cartilage and makes cartilage softer.

OBJECTIVE: To evaluate the influence of inactivation of one allele ("heterozygous knockout" or "heterozygous inactivation") of the type II procollagen gene (Col2a1) on the biomechanical properties and structure of the articular cartilage and subchondral bone in 15 month old mice. METHODS: Indentation stiffness of the humerus head articular cartilage was measured by a microindentation method. Cartilage and subchondral bone were prepared for digital densitometry of proteoglycans (PGs), polarised light microscopy (PLM) of collagen, and osteoarthrosis (OA) grading. RESULTS: Heterozygous inactivation of the Col2a1 gene softened articular cartilage (p=0.002) as measured by indentation stiffness ((mean (SEM) 0.50 (0.07) MPa v 0.94 (0.13) MPa in controls). Fibrillar collagen network exhibited lower birefringence in the intermediate (p=0.04) and deep zones (p=0.01) of cartilage by PLM, indicating either decreased collagen content or a lower degree of fibril parallelism in the knockout mice. The total and zonal thicknesses of articular cartilage were unchanged. Zonal PG contents did not differ significantly. In knockout mice, the prevalence of superficial fibrillation-that is, a sign of OA, was higher than in controls (73% v 21%, p=0.002). The collagen induced birefringence of the superficial zone was not reduced. The subchondral bone volume fraction was lower in knockout mice than in controls, 31% v 43% (p=0.01), and optical retardation values in PLM of bone collagen were slightly but significantly lower (p=0.01). CONCLUSION: Heterozygous inactivation of the Col2a1 gene made articular cartilage softer, altered the collagenous network, reduced subchondral bone volume, and altered its microstructure. Changes in the cartilage collagen network probably contributed to increased susceptibility to OA.

Animals↗

Regeneration of cartilage tissue by autologous chondrocytes transplantation for cartilage defects in a experimental bovine model.

To evaluate the effects of chondrocytes transplantation on the regeneration of cartilage by intraarticular injection or injection into blood clots at cartilage defects, eight full-thickness cartilage defects were created surgically on the articular surface of each femoral trochlea of two calves. Autologous chondrocytes were isolated individually from the cartilage pieces collected at the creation of defects. And isolated cells were cultured in monolayers for proliferation. Cells were injected into synovial fluid (Group 2, n=11) or into the blood clots at the cartilage defects (Group 3, n=5) of the left femoropatellar joint on weeks 2 and 3, respectively after the operation. The defects (Group 1, n=16) of right femoropatellar joint were left untreated in the control group. After 14 weeks, repaired tissues were evaluated based on gross and histological examinations. In Group 3, more repaired tissues and a better interface between the repaired tissue and host cartilage were observed compared with the results for Groups 1 and 2. Moreover, cartilaginous tissue were observed more in defects of Group 3 than in defects of other groups. In conclusion, the present study suggests that the injection of cells into the blood clot at a cartilage defect might be applicable for the regeneration of damaged cartilage.

Animals↗

Inhibition of sulphate incorporation by chondrocytes in intact cartilage by hyaluronate from foetal cartilage.

A number of regulators are available in cartilage to effect the local control of matrix production by chondrocytes. A cartilage slice assay has been used in this study to investigate the influence of such regulators (extracted from foetal cartilage) on intact cartilage. A net inhibition of sulphation was found, rather than stimulation as reported for extracts rich in the somatomedin-like, cartilage derived factor (CDF). Inhibition was due, to a high molecular weight component identified as hyaluronic acid (based on enzyme sensitivity, chromatographic behaviour and temperature stability). Its inhibition of sulphation in intact cartilage was more profound than that produced by commercially available umbilical cord hyaluronate. We conclude that foetal cartilage hyaluronate is a far more potent inhibitor of sulphation than hyaluronate from other sources, suppressing sulphation even in the presence of a somatomedin-like activator and in intact cartilage, which responds poorly to commercial hyaluronate.

Animals↗

Active matrix metalloproteinases are present in cartilage during immune complex-mediated arthritis: a pivotal role for stromelysin-1 in cartilage destruction.

The involvement of immune complexes during experimental arthritis in induction of metalloproteinases (MMP)-induced neoepitopes in aggrecan in cartilage, as well as the role of stromelysin-1 (SLN-1) in the induction of this neoepitope, was investigated. Passive immune complex arthritis was induced, and generation of the MMP-specific cleavage product (VDIPEN) was studied by immunolocalization. The role of SLN-1 was studied with use of SLN-1-deficient (SLN-1KO) mice. VDIPEN expression was studied in vitro by exposing the cartilage to IL-1 and subsequent activation of latent MMPs. Immune complex arthritis was characterized by an acute inflammation, with influx of mainly polymorphonuclear cells into the joint cavity. Expression of VDIPEN neoepitopes was consistently found in areas extensively depleted from proteoglycans. SLN-1KO mice did not show expression of the VDIPEN neoepitope, although inflammation and proteoglycan depletion was comparable to wild-type mice. In addition, erosions of cartilage were absent in SLN-1KO mice, but were present in wild-type mice, suggesting an important role for SLN-1 in cartilage destruction. In vitro studies showed that SLN-1 is also pivotally involved in IL-1-induced MMP activity. Stimulated polymorphonuclear neutrophils were able to activate latent MMPs present in the cartilage. Neutrophil elastase was also capable of activating IL-1-induced latent MMPs, which identifies elastase as a possible activator for latent VDIPEN-inducing MMPs. This study suggests that IC are important in the activation of latent MMPs in cartilage, possibly through polymorphonuclear neutrophil activation on the cartilage edge. SLN-1 is a pivotal enzyme in overall MMP-activity in cartilage during immune complex-mediated arthritis.

Animals↗

Articular cartilage preservation and storage. III. Quantitative zonal analysis of cytoplasmic components of stored versus in vivo articular cartilage chondrocytes.

The cytoplasmic components of chondrocytes in the various zones of articular cartilage of the medial femoral condyle of six-week-old male New Zealand white rabbits stored in tissue culture medium at 37 degrees in 5% CO2 and air were quantitated from electron micrographs, and the results were compared statistically with the cytoplasmic components of chondrocytes in the corresponding zones of in vivo articular cartilage. The major changes that occurred during storage were: (1) an increase in the amount of lipid bodies in chondrocytes in the tangential, transitional, and calcified zones; (2) a decrease in the number of holes in the cytoplasm of chondrocytes in the radial and calcified zones; (3) a decrease in the amount of endoplasmic reticulum in the radial and calcified zones; and (4) an increase in cell size and cytosol area in the tangential and transitional zones but a significant decrease in cell size and cytosol area in the calcified zone. Stored articular cartilage chondrocytes demonstrated cellular changes associated with aging, whereas in vivo articular cartilage chondrocytes demonstrated changes associated with degeneration. The matrix of stored articular cartilage in the tangential, transitional, and upper part of the radial zones showed a decrease in opacity due to a decrease in the number of collagen fibers per unit area of matrix, a condition termed "chondroporosis." This study demonstrates that articular cartilage stored in standard tissue culture medium under ideal physiological conditions is morphologically abnormal. Based on these findings, one would not expect such stored cartilage to remain functionally intact when transplanted to replace articular cartilage loss.

Animals↗

The development of hyaline-cell cartilage in the head of the black molly, Poecilia sphenops. Evidence for secondary cartilage in a teleost.

The development of hyaline-cell cartilage attached to membrane (dentary, maxilla, nasal, lacrimal and cleithrum) and cartilage (basioccipital) bones has been studied in the viviparous black molly, Poecilia sphenops. Intramembranous ossification commences before the first appearance of hyaline cells. As hyaline-cell cartilage is densely cellular and as that attached to the dentary, maxilla and cleithrum develops from the periosteum of these membrane bones, it must be regarded as secondary cartilage according to current concepts. It is also argued that the hyaline-cell cartilage attached to the perichondral bone of the basioccipital (a cartilage bone), could also be viewed as secondary. The status of the cartilage on the nasal and lacrimal bones is less clear, for it develops, at least in part, from mucochondroid (mucous connective) tissue. This is the first definitive report of secondary cartilage in any lower vertebrate. The tissue is therefore not restricted to birds and mammals as hitherto believed, and a multipotential periosteum must have arisen early in vertebrate evolution.

Animals↗

Influence of polydioxanone foil on growing septal cartilage after surgery in an animal model: new aspects of cartilage healing and regeneration (preliminary results).

OBJECTIVE: To determine whether late complications after septoplasty in growing septal cartilage in children can be prevented by the use of a resorbable polydioxanone (PDS) foil in combination with the cartilage. DESIGN: Animal study with 45 young rabbits, operated on at the nasal septum. Four typical septoplasty procedures were carried out, including elevation of the mucoperichondrium, cartilage excision, and reimplantation of crushed and noncrushed cartilage; for each of the procedures, resorbable PDS foil was used in half of the animals. Observation time ranged from 2 weeks to 5 months, to observe the healing process until complete outgrowth of the septum and complete resorption of the foil were achieved. SETTING: Ear, Nose, and Throat Department at University of Pécs, Pécs, Hungary. MAIN OUTCOME MEASURE: Histomorphologic findings on specimens of septum stained with hematoxylin-eosin and periodic acid-Schiff stains. RESULTS: Depending on the surgical procedure, there were various degrees of differences between the groups with and without PDS. After elevation of the mucoperichondrium, there were almost no differences between the 2 groups. After cartilage resection, reimplantation, and crushing, however, there was a remarkable difference between groups. In the group without PDS, septal deviations and poorly regenerated cartilage were observed, but in the group with PDS no significant deviation after complete regeneration of septal cartilage was observed. CONCLUSIONS: The resorbable PDS foil prevented a secondary deviation in the surgically treated growing septal cartilage in young rabbits. Use of this foil could reduce late complications such as septal deviations and possibly prevent growth inhibition in the growing nasal septum after septoplasty.

Animals↗