Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CARTILAGE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed2003

Mechano-acoustic diagnosis of cartilage degeneration and repair.

BACKGROUND: The combined use of high-frequency ultrasound and mechanical indentation has been suggested for the evaluation of cartilage integrity. In this study, we investigated the usefulness of high-resolution B-mode ultrasound imaging and quantitative mechanical measurements for the diagnosis of cartilage degeneration and for monitoring tissue-healing after autologous chondrocyte transplantation. METHODS: In the first study, osteochondral samples (n = 32) were obtained from the lateral facet of a bovine patella, and the samples were visually classified as intact (n = 13) or degenerated (n = 19) and were graded with use of the Mankin scoring system. Samples were imaged with use of a 20-MHz ultrasound instrument, and the dynamic modulus (Edyn) of cartilage was determined in unconfined compression with use of a high-resolution materials tester. In the second study, cartilage chondrocytes were harvested from the low-weight-bearing area of six-month-old porcine knee joints and cultured. A month later, a cartilage lesion was created on the facet of the femoral trochlea and was repaired with use of the autologous chondrocyte transplantation technique (n = 10). Three months later, to estimate cartilage Edyn, the repair tissue, the adjacent cartilage, and the sham-operated contralateral joint cartilage (control) were analyzed in situ with an arthroscopic indentation instrument. Subsequently, the same sites were imaged with ultrasound. RESULTS: All visually degenerated bovine samples (mean Mankin score = 4) and five visually normal samples (Mankin score = 1) showed reduced Edyn (<2.1 MPa) as compared with histologically normal cartilage (Edyn = 13.8 +/- 3.2 MPa, Mankin score = 0). Cartilage stiffness, as shown by the indenter force, was lower (0.6 +/- 0.3 N, p < 0.05, Wilcoxon's signed-rank test) in the porcine tissue repaired with autologous chondrocyte transplantation than it was in the adjacent (1.6 +/- 0.1 N) or the control (1.9 +/- 0.4 N) tissue. The superficial and internal structure of the degenerated and repaired tissue, including the subchondral erosion at the repair site, was sensitively demonstrated by the ultrasound imaging. CONCLUSIONS: Measurement of cartilage Edyn is an objective method with which to follow changes in the mechanical integrity of cartilage. B-mode ultrasound imaging offers detailed information on the structural properties of cartilage and subchondral bone.

Animals↗
PubMed2005

Functional adaptation of articular cartilage from birth to maturity under the influence of loading: a biomechanical analysis.

REASONS FOR PERFORMING STUDY: The concept of functional adapatation of articular cartilage during maturation has emerged from earlier biochemical research. However, articular cartilage has principally a biomechanical function governed by joint loading. OBJECTIVES: To verify whether the concept of functional adaptation can be confirmed by direct measurement of biomechanical properties of cartilage. HYPOTHESIS: Fetuses have homogeneous (i.e. site-independent) cartilage with regard to biomechanical properties. During growth and development to maturity, the biomechanical characteristics adapt according to functional (loading) demands, leading to distinct, site-dependent biomechanical heterogeneity of articular cartilage. METHODS: Osteochondral plugs were drilled out of the surface at 2 differently loaded sites (Site 1: intermittent impact-loading during locomotion, Site 2: low-level constant loading during weightbearing) of the proximal articular cartilage surface of the proximal phalanx in the forelimb from stillborn foals (n = 8), horses of age 5 (n = 9) and 18 months (n = 9) and mature horses (n = 13). Cartilage thickness was measured using ultrasonic, optical and needle-probe techniques. The osteochondral samples were biomechanically tested in indentation geometry. Young's modulus at equilibrium, dynamic modulus at 1 Hz and the ratios of these moduli values between Sites 1 and 2 were calculated. Age and site effects were evaluated statistically using ANOVA tests. The level of significance was set at P<0.05. RESULTS: Fetal cartilage was significantly thicker compared to the other ages with no further age-dependent differences in cartilage thickness from age 5 months onwards. Young's modulus stayed constant at Site 1, whereas at Site 2 there was a gradual, statistically significant increase in modulus during maturation. Values of dynamic modulus at both Sites 1 and 2 were significantly higher in the fetus and decreased after birth. Values for both moduli were significantly different between Sites 1 and 2 from age 18 months onwards. The ratio of values between Sites 1 and 2 for Young's modulus and dynamic modulus showed a gradual decrease from approximately 1.0 at birth to 0.5-0.6 in the mature horse. At age 18 months, all values were comparable to those in the mature horse. CONCLUSIONS: In line with the concept of functional adaptation, the neonate is born with biomechanically 'blank' or homogeneous cartilage. Functional adaptation of biomechanical properties takes place early in life, resulting in cartilage with a distinct heterogeneity in functional characteristics. At age 18 months, functional adaptation, as assessed by the biomechanical characteristics, has progressed to a level comparable to the mature horse and, after this age, no major adaptations seem to occur. POTENTIAL RELEVANCE: Throughout life, different areas of articular cartilage are subjected to different types of loading. Differences in loading can adequately be met only when the tissue is biomechanically adapted to withstand these different loading conditions without injury. This process of functional adaptation starts immediately after birth and is completed well before maturity. This makes the factor of loading at a young age a crucial variable, and emphasises the necessity to optimise joint loading during early life in order to create an optimal biomechanical quality of articular cartilage, which may well turn out to be the best prevention for joint injury later in life.

Adaptation, Physiological↗
PubMed1985

Enhanced breakdown in vitro of bovine articular cartilage proteoglycans by conditioned synovial medium. The effect of phenylglyoxal.

Addition of conditioned medium derived from fragment cultures of synovial tissue dissected from bovine knee joints (SM) to cultures of articular cartilage derived from the same animal resulted in enhanced breakdown of cartilage proteoglycans, measured as the release of [35S]sulphate from pieces of prelabelled cartilage. Addition of conditioned medium from synovial tissue that had been cultured with 50 micrograms/ml dextran sulphate (DS-SM) to the cartilage cultures greatly enhanced cartilage degradation. Phenylglyoxal is an arginine-specific reagent which has been shown to destroy the activity of interleukin 1 (former called LAF, lymphocyte-activating factor). The addition of phenylglyoxal (0.01, 0.1 or 1.0 mM) to the cartilage cultures did not affect cartilage degradation, whereas the addition of 2.5 mM phenylglyoxal seemed to inhibit cartilage breakdown. However, the cartilage degradation induced by SM was inhibited in a dose-dependent manner by the addition of phenylglyoxal (0.1, 1.0 and 10.0 mM). Also culturing the synovial tissue with phenylglyoxal (1.0 mM) inhibited the synovial-enhanced cartilage degradation. The addition of phenylglyoxal (1.0 mM) together with DS-SM to the cartilage cultures reduced cartilage degradation to that exerted by SM. Culturing the synovial tissue with both dextran sulphate (50 micrograms/ml) and phenylglyoxal (0.1, 1.0 and 10.0 mM) also dose-dependently reduced cartilage degradation to that exerted by SM. It is therefore suggested that the cytokines produced by synovial tissue in culture may be related to interleukin 1. However, the role of other proteins, such as degradative enzymes, cannot be completely ruled out.

Aldehydes↗
PubMed1993

Thionin staining of paraffin and plastic embedded sections of cartilage.

The usefulness of thionin for staining cartilage sections embedded in glycol methacrylate (GMA) and the effect of decalcification on cartilage sections embedded in paraffin and GMA were assessed. Short decalcification periods using 5% formic acid or 10% EDTA did not influence the staining properties or the morphology of cartilage matrix and chondrocytes. The standard stain safranin O-fast green for differential staining of cartilage was used as control in these experiments. Prolonged exposure of safranin O stained sections to fast green resulted in disappearance of the safranin O stained matrix, thereby hampering the quantitative measurement of negatively charged glycosaminoglycans (GAG). Thionin stained evenly throughout all cartilage layers, independent of the staining times. In contrast to safranin O, thionin did not show metachromasia in nondehydrated cartilage sections, which made it more suitable for assessing cartilage quality in GMA embedded cartilage. To evaluate the selectivity of thionin staining in cartilage, chondroitinase ABC and trypsin digestions were carried out. Thionin staining was prevented by these enzymes in the territorial matrix, representing the interlacunar network and the chondrocyte capsule. Staining with thionin of the interterritorial matrix was only slightly reduced, possibly representing keratan sulfate and hyaluronic acid in cartilage of elderly patients. Comparison of thionin stained GMA embedded cartilage with safranin O stained paraffin embedded sections showed significant similarity in optical densitometry, indicative of the specificity of thionin bound to negatively charged GAG in cartilage. In GMA embedded cartilage morphology was relatively intact compared to paraffin embedded sections due to less shrinkage of chondrocytes and the interlacunar network.

Aged↗
PubMed1999

Immunohistological analysis of cytokine expression in human osteoarthritic and healthy cartilage.

OBJECTIVE: To investigate osteoarthritic cartilage in comparison to normal cartilage in humans for the presence of the most relevant cytokines/growth factors known to be important for degradation and formation of new cartilage. METHODS: Cartilage from knee or hip joints was obtained from 10 patients with osteoarthritis (OA) and from 7 age matched control patients with intact cartilage. Additionally, normal cartilage from 2 young patients (12 and 17 years old) was obtained after knee traumas. Immunohistological staining of cartilage sections was performed using antibodies for the following cytokines/growth factors: tumor necrosis factor alpha (TNF-alpha), interleukin 1alpha (IL-1alpha), IL-1beta, interferon-gamma, IL-6, IL-4, IL-10, transforming growth factor beta1 (TGF-beta1), insulin-like growth factor I (IGF-I), IGF-II, platelet derived growth factor AA (PDGF-AA), and PDGF-BB. RESULTS: Immunohistochemical stainings were positive for all cytokines in OA cartilage, while only a faint or no staining was found in healthy cartilage. Activated chondrocytes expressing most of the cytokines were located in the middle and partly in the lower layer of cartilage, with the exception of IGF-I, which was expressed exclusively in the upper cartilage layer close to the surface. More chondrocytes stained positive for TNF-alpha than for IL-1, and expression of the degrading cytokine TNF-alpha was inversely correlated to the expression of the regulatory cytokines IL-4, IL-10, and TGF-beta. CONCLUSION: The most relevant cytokines known to be involved in cartilage metabolism are produced by chondrocytes themselves. They are upregulated in OA cartilage, suggesting that they serve some regulatory function and could be a target for future treatment.

Adolescent↗
PubMed2000

Articular cartilage is more susceptible to blood induced damage at young than at old age.

OBJECTIVE: It has been shown that cartilage is damaged upon intraarticular hemorrhage. We investigated differences in the susceptibility of cartilage from young adult and old animals to blood induced joint damage in a canine in vivo model. METHODS: Right knees of 6 young adult beagles (aged 2.2 +/- 0.1 yrs) and 6 old beagles (7.4 +/- 0.3 yrs) were intraarticularly injected twice in 4 days with autologous blood. Dogs were killed 4 or 16 days after the first injection and cartilage matrix proteoglycan content and synthesis and collagen damage were determined. RESULTS: Shortly after blood injection (Day 4), proteoglycan synthesis was inhibited and the proteoglycan content of the cartilage was decreased in both groups. However, the degree of the inhibition of proteoglycan synthesis was significantly greater in young adult animals than in old animals. On Day 16 proteoglycan synthesis was increased in both young adult and old cartilage, but more elevated in old cartilage. The proteoglycan content remained decreased in both young adult and old cartilage, but significantly more so in young adult cartilage than in old cartilage. CONCLUSION: Results suggest that intraarticular bleeding influences cartilage metabolism and repair, and that the cartilage of young adult animals is more susceptible to these influences than cartilage of old animals. Differences in the aging of chondrocytes and age related changes in matrix integrity may be involved. Prevention and appropriate treatment of joint bleeding is indicated and this is especially relevant for young adult cartilage.

Age Factors↗
PubMed1999

Articular cartilage biomechanics: theoretical models, material properties, and biosynthetic response.

Articular cartilage has unique material properties that enable the cartilage to perform its physiological functions over a lifetime and under a wide range of loading conditions. Numerous studies have investigated the relationship between cartilage properties and composition/structure. For cartilage transplantation and regeneration, it is necessary to know how cartilage maintains its functionality and how cartilage responds to the ever-changing mechanical environment. In this review, we discuss theoretical and experimental studies on the behavior of articular cartilage to load. In the first part, the composition and structure of articular cartilage is presented. In the second part, theoretical models of the mechanical behavior of cartilage, experimental methods for the determination of cartilage properties, and material properties for normal, pathologic, and repair cartilage are summarized. In the third part, the relationship between mechanical loading of the cells and their corresponding biological responses are discussed. The goal for treating joint degeneration in the future lies in cartilage regeneration rather than prosthetic replacement. In order to achieve this goal, it has to be understood how structure and function, metabolic and biochemical properties, and biomechanical performance of articular cartilage can be restored.

Animals↗
PubMed2002

The determinants of change in patella cartilage volume in osteoarthritic knees.

OBJECTIVE: The rate of change in patella articular cartilage and factors influencing it, in subjects with osteoarthritis (OA), is unknown. We performed a cohort study to determine this. METHODS: One hundred ten subjects with OA had baseline skyline and lateral radiographs and magnetic resonance imaging (MRI) on their knee. They were followed 2 years later with a repeat MRI of the same knee. Patella and tibial cartilage volume was measured at baseline and followup. Risk factors assessed at baseline were tested for their association with change in patella cartilage volume over time. RESULTS: The annual percentage loss of patella cartilage was 4.5 +/- 4.3%. Sex, body mass index (BMI), and pain score at baseline were associated with an increase in cartilage loss. The rate of patella cartilage loss was greater in women than men, 5.3% versus 3.5% (p < 0.03), independent of age, BMI, and pain score. No association was seen between change in patellar cartilage volume and change in either medial or lateral tibial cartilage volume (r = 0.02, p = 0.86 and r = 0.08, p = 0.43, respectively). CONCLUSION: In OA, patella cartilage volume is lost at 4.5 +/- 4.3% per year. The main factors affecting this are sex, BMI, and baseline pain score. The poor correlation between patella cartilage loss and cartilage loss in the tibial compartment suggests that the pathogenetic mechanisms for OA in the patellofemoral and tibiofemoral joint may differ. Further work will be required to determine whether the rate of patella cartilage loss in OA is steady or phasic, and to determine which factors can be modified to reduce cartilage loss.

Arthrography↗
PubMed2003

Expression of the cartilage derived anti-angiogenic factor chondromodulin-I decreases in the early stage of experimental osteoarthritis.

OBJECTIVE: Chondromodulin-I (ChM-I), a cartilage derived anti-angiogenic factor, has been shown to regulate the vascular invasion during endochondral bone formation. We evaluated the expression and localization of ChM-I in articular cartilage during the progression of osteoarthritis (OA) in the rat, and correlated ChM-I expression with the increase in vascular invasion into OA articular cartilage. METHODS: Expression of ChM-I, type II collagen, basic fibroblast growth factor, vascular endothelial growth factor (VEGF), and matrix metalloproteinases MMP-9 and MMP-13 were examined in articular cartilage of intact growing and adult rats and in the surgically induced OA model using in situ hybridization, Western blot analysis, and immunohistochemistry. Co-immunostaining for ChM-I and CD-31 was performed to localize ChM-I and neovascularization in articular cartilage at advanced stage of OA. RESULTS: Abundant expression of ChM-I protein was detected in avascular regions of the developing and adult healthy articular cartilage. In early OA, ChM-I expression decreased in the superficial zone of articular cartilage, while levels of proteoglycan and type II collagen were comparable to control. In advanced OA, ChM-I expression was reduced in all zones of articular cartilage, and the number of VEGF-expressing cells was increased. Immunohistochemical studies showed that vascular invasion occurred in proximity to chondrocytes with high expression of pro-angiogenic markers, and decreased expression of ChM-I. CONCLUSION: High expression of ChM-I was detected in articular cartilage of growing and normal adult joints, implicating its role in the maintenance of avascularity of intact articular cartilage. Expression of ChM-I decreased, while expression of VEGF and other pro-angiogenic factors increased, in OA cartilage. These findings suggest the loss of ChM-I from articular cartilage might be responsible in part for promoting blood vessel invasion into the cartilage during progression of OA.

Angiogenesis Inhibitors↗
PubMed2005

[The effect of rupture and reconstruction of posterior cruciate ligament on the degeneration of articular cartilage in rabbit knee].

OBJECTIVE: To investigate the effect of rupture and reconstruction of the posterior cruciate ligament (PCL) on the degeneration of rabbit knee joint. METHODS: Thirty-three mature New Zealand white rabbits were divided into 3 groups. In experiment group I, the PCL of the right knees in 21 rabbits were resected, the contralateral joints as control group, in which only a medial arthrotomy was performed. In experiment group II, the PCL of the right knees in 12 rabbits were immediately reconstructed after PCL were resected. In experiment group I and control group the rabbits were respectively killed 6, 12 and 26 weeks after the operation. In experiment group II the rabbits were respectively killed 12, 26 weeks after the operation. The methods of ink staining, histology, immunohistochemistry and SEM were used to analyze the changes of articular cartilage of the joints. RESULTS: In experiment group I, the knee joints had obvious degeneration of articular cartilage at 26 weeks. The quantitative analysis of the results of the ink staining method showed the degeneration of knee articular cartilage was more serious at 26 weeks than that at 26 weeks in control group. Histological results demonstrated: the large area of fibrosis of cartilage could be seen in the medial condyle at 26 weeks; the fibrosis was deep into the deep layer of cartilage and the number of cells decreased; the average Mankin's score was 7.7. At 26 weeks, type I and III collagen were detected in fibrotic cartilage, while the staining of type II collagen was slight. In experiment group I, the injuries of cartilage in medial condyle could be seen at every stage through SEM, while the surface of cartilage demonstrated disorder in control group through SEM. In experiment group II, only a few specimens had mild injuries of cartilage, the degeneration of cartilage in medial condyle and trochlea were slighter at 26 weeks than that in experiment group I. CONCLUSIONS: PCL rupture can result in articular cartilage degeneration, which develops as time goes on. The degeneration of articular cartilage is more serious in medial compartment and patellofemoral joint than those in other positions. Immediate reconstruction of PCL can effectively prevent articular cartilage degeneration.

Animals↗
PubMed2006

Determinants of change in patella cartilage volume in healthy subjects.

OBJECTIVE: To examine whether the amount of patella cartilage in healthy, middle-aged subjects is stable or changes over time, and what factors may influence the changes. METHODS: Eighty-five subjects (28 men and 57 women, mean age 55.5 yrs) had magnetic resonance imaging of their dominant knee at baseline and 2 years later. Patella and tibial cartilage volume was measured at baseline and followup. Risk factors assessed at baseline were tested for their association with change in patella cartilage volume over time. RESULTS: Mean annual percentage loss of patella cartilage was 2.1 (95% confidence interval: 1.1-3.2; p < 0.001). Age, gender, body mass index, and initial cartilage volume did not affect rate of change of patellar cartilage volume. There was a weak association between change in patellar cartilage volume and change in lateral tibial cartilage volume (R = 0.23, p = 0.03) but not medial tibial cartilage volume (R = 0.09, p = 0.43). CONCLUSION: In healthy subjects, a significant amount of patella cartilage is lost annually. The poor correlation between patella and tibial cartilage loss suggests that pathogenetic mechanisms for osteoarthritis in the patellofemoral and tibiofemoral joint may differ. Further work will be required to determine whether the rate of patella cartilage loss in healthy subjects is steady or phasic, and to determine which factors can be modified to reduce cartilage loss.

Aging↗
PubMed1980

[The vascularisation of epiglottic cartilage, a histological investigation (author's transl)].

For this study 30 formaldehyde-fixed human epiglottic cartilages of both sexes from the first up to the ninth decade were used. Besides histological staining histochemical reactions for demonstration of mucopolysaccharides were performed. In the elastic cartilage of the epiglottis at the end of the first decade sporadic areas of degenerating cartilage are present, which increase and confluence with proceeding age. At first from the seventh decade large and mostly centrally situated degeneration areas are prevailing. At all aging stages the cartilaginous plate of the epiglottis is perforated with many channels. These cartilage channels were outlined everywhere with the perichondrium. There is connective tissue, adipose tissue, arteries, veins, peripheral nerves, mixed glands and excretory ducts. From the third to the sixth decade blood vessels and connective tissue penetrate from the surface of the cartilage or from the cartilage channels different far into the epiglottic cartilage. In this manner vascular channels develop, which lie both in areas with cartilage degeneration and not degenerated areas. The pericanalicular cartilage ground substance contains a lot of PAS-positive substances combined with a diminished content of acid mucopolysaccharides independent from the position of the vascular channel. The blood vessels of the channels are significant for the metabolism of the cartilage. They improve the nutrition of the epiglottic cartilage in the middle age. Therefore the relatively early beginning degenerative changes of the cartilage increase only a little in this period in order to maintain the function of the epiglottis. Only in the higher age large degeneration areas of cartilage prevail accompanied with the absence of vascular channels and worse metabolism.

Adolescent↗
PubMed1980

Biochemical studies on repair cartilage resurfacing experimental defects in the rabbit knee.

UNLABELLED: Wounds penetrating articular cartilage to bone heal with cartilage described variably as either fibrous or hyaline. In the present study, such repair cartilage was induced in the rabbit for biochemical comparison with normal articular cartilage. The main collagen in the repair tissue after three weeks was type I. By six to eight weeks, type II had become predominant and continued to be enriched up to one year; but type I still persisted as a significant constituent of the repair tissue even after a year, so the repair cartilage never fully resembled normal articular cartilage. From radiochemical analysis, type II was determined to be the major collagen synthesized by the repair tissue after three to four weeks. After six months, the repair cartilage contained more collagen and less hexosamine than control cartilage, suggesting that the fibrous texture that often developed was due to a loss of proteoglycans rather than to a change in the type of collagen. CLINICAL RELEVANCE: Procedures capable of inducing the differentiation of authentic articular cartilage to resurface degenerated human joints would be invaluable. Surgical methods, such as drilling through to subchondral bone, are often attempted. It is not known, however, whether the cartilage that forms is true articular cartilage or, for example, fibrocartilage. The present experimental study in rabbits compared the properties of such repair cartilage with those of normal articular cartilage.

Animals↗
PubMed1993

Cartilage degradation by cocultures of transformed macrophage and fibroblast cell lines. A model of metalloproteinase-mediated connective tissue degradation.

A number of human and mouse macrophage and fibroblast cell lines were examined for their ability to degrade cartilage proteoglycan in an attempt to establish a cell culture model of cartilage degradation. The mouse transformed macrophage cell line J774A.1 alone or in combination with the mouse transformed fibroblast cell line 10ME HD A.5R.1 were the only cell lines capable of extensively degradating cartilage proteoglycan. Incubation of the macrophage cell line J774A.1 on heat-killed cartilage disks resulted in the release of 36% +/- 8 (mean +/- SEM, n = 5) of the radiolabeled cartilage proteoglycan. The fibroblast cell line 10ME HD A.5R.1 alone did not degrade cartilage. However, cocultures of J774A.1 macrophages and 10ME HD A.5R.1 fibroblasts incubated on cartilage discs resulted in the release of 69% +/- 6 (mean +/- SEM, n = 5) of radiolabeled proteoglycan. There was little degradation of cartilage by macrophage/fibroblast cocultures during the first 3 days of culture. Cartilage degradation increased with each subsequent day in culture from 7% +/- 2 on day 4 to 68% +/- 3 (n = 3) by day 7. Supernatants from the macrophage/fibroblast cocultures were incubated with cartilage discs in the presence of general class-specific proteinase inhibitors. The metalloproteinase inhibitors 1,10 phenanthroline, EDTA, and recombinant tissue inhibitor of metalloproteinase were the only inhibitors that significantly blocked cartilage degradation by coculture supernatant. The cartilage degrading metalloproteinase in the macrophage/fibroblast coculture supernatant eluted as a broad peak on Sephacryl S-200HR with an estimated molecular mass between 22 and 55 kDa. These studies suggest that the macrophage/fibroblast coculture model of cartilage degradation may be a useful experimental system for the study of metalloproteinase-mediated connective tissue degradation.

Animals↗
PubMed2001

DNA cytofluorometric analysis of chondrocytes in human articular cartilages under normal aging or arthritic conditions.

OBJECTIVE: Since most chondrocytes in articular cartilage are in the resting phase (G0) of the cell cycle, it has been difficult to investigate their cell kinetics using 3H-thymidine autoradiography, or immunohistochemistry. In the present study, DNA cytofluorometry, which is useful to analyse the cell kinetics even for such inactive cell populations as in the G0 phase, was applied to human chondrocytes of the articular cartilages under normal aging and pathologic conditions such as osteoarthritis (OA), rheumatoid arthritis (RA), and aseptic necrosis (AN). DESIGN: The human articular cartilages for the study were obtained from autopsy and surgical materials. Fifty joints were used for the study of aging, 54 for the study of OA, 20 for studying RA, and 10 for AN study. The isolated chondrocytes were quickly prepared from fresh articular cartilages, using a combination method of enzymatic digestion with papain and collagenase, followed by mechanical cell separation by churning and homogenization. RESULTS: The DNA histograms obtained by cytofluorometry with propidium-iodide staining showed that most chondrocytes had diploid DNA content (2c) in all cartilages studied, suggesting that they were in the G0 phase. However, there were a few chondrocytes having tetraploid DNA content (4c) in the normally aged articular cartilages, and there were some cells having DNA content between 2c and 4c in the diseased cartilages. The former cells were considered to be G0-phase cells of the 4c chondrocytes, while the latter cells were considered to be in the DNA synthetic (S) phase or G2-phase of the 2c chondrocytes. The frequency of 4c chondrocytes in aged cartilage was significantly increased, compared to that in the young cartilage. In contrast to the normal cartilage, the frequency of S- and G2-phase cells, which was expressed as the S- G2 index, in diseased cartilages (OA, RA and AN) was significantly high (P< 0.0001). In OA cartilage, the S-G2 index was much higher in the severe or moderate stage than in the mild stage, suggesting that the chondrocytes in clusters may actively proliferate. CONCLUSION: These results showed that in normal articular cartilages most chondrocytes are in the G0 phase, while some became 4c polyploid cells, and that these G0-phase chondrocytes had a potential to proliferate under diseased conditions.

Adolescent↗
PubMed1987

Triiodothyronine stimulates cartilage growth and maturation by different mechanisms.

The mechanisms by which triiodothyronine (T3) stimulates growth and maturation of growth-plate cartilage in vitro were studied by incubating embryonic chick pelvic cartilages in serum-free medium in the presence and absence of T3 for 3 days. To determine whether T3 might stimulate production of somatomedins by the cartilage, medium from cartilage incubated with and without T3 was assayed for somatomedin C (Sm-C) by radioimmunoassay. No difference in Sm-C content was found. However, cartilage incubated with T3 and increasing amounts of human Sm-C (0.5-20 ng/ml) weighed more and had greater amounts of glycosaminoglycan than cartilage incubated in the same concentrations of Sm-C without T3, suggesting that T3 enhances the growth effect of somatomedin. We added a monoclonal antibody to Sm-C (anti-Sm-C) to the organ culture to determine whether T3's stimulatory effect on cartilage growth could be blocked. The anti-Sm-C inhibited growth of cartilage incubated in medium alone and blocked the growth response to T3. By using alkaline phosphatase as a biochemical marker to follow maturation, we found that T3 stimulated a 57% increase in alkaline phosphatase activity above cartilage incubated in medium alone and that anti-Sm-C did not inhibit T3's stimulatory effect on alkaline phosphatase activity. We propose two different mechanisms by which T3 affects growth-plate cartilage: T3 promotes cartilage growth primarily through enhancing the effect of somatomedin, and T3 stimulates cartilage maturation possibly by accelerating the normal process of cartilage differentiation from proliferative to hypertrophic chondrocytes.

Animals↗
PubMed2000

Molecular cloning, sequencing, and tissue and developmental expression of mouse cartilage oligomeric matrix protein (COMP).

Mouse cartilage oligomeric matrix protein cDNA was cloned and sequenced by a reverse transcription-polymerase chain reaction. The open reading frame encoded a product of 755 amino acids that shares a high degree of identity to and possesses all the characteristic molecular features of both rat and human cartilage oligomeric matrix protein. This suggests that cartilage oligomeric matrix protein is highly conserved during evolution. The clone was 83, 84, and 95% identical to human, bovine, and rat cartilage oligomeric matrix protein cDNA, respectively. In tissues from the adult mouse, cartilage oligomeric matrix protein was expressed not only in cartilage and tendon but in trachea, bone, skeletal muscle, eye, heart, and placenta as well, and no expression was found in other tissues. Immunohistology revealed that cartilage oligomeric matrix was deposited as early as 10 days post coitus in predifferentiated mouse embryo mesenchyme. It was detected in all cartilaginous tissues and in the skeletal muscles of the embryo at day 13. As development progressed, accumulation of cartilage oligomeric matrix protein was marked in the growth plate. At 19 days post coitus, it was prominently deposited in the hypertrophic zone of the growth plate, perichondrium, and periosteum and in the superficial layer of the articular cartilage surface but was absent in the more central areas of the epiphyseal cartilage. The restricted tissue distribution and expression of cartilage oligomeric matrix protein in developing as well as adult mouse tissues suggest the regulation of this protein at the transcriptional level. The findings reported herein are the first detailed characterization of the distribution of cartilage oligomeric matrix protein during early skeletal development of the mouse.

Animals↗
PubMed1986

Growth and growth pressure of mandibular condylar and some primary cartilages of the rat in vitro.

To compare the in vitro development of the secondary cartilage of the mandibular condyle with that of primary cartilages, several cartilaginous explants derived from 4-day-old rats were cultured in a serum-free culture system. The following cartilages were used: the mandibular condylar cartilage, the distal epiphyseal cartilage (including the growth plate) of the third metatarsal, a fragment of costal cartilage (including the osteochondral junction) of the fourth rib, the spheno-occipital synchondrosis and the chondroepiphysis of the femoral head. In addition, with a specially designed, in vitro pressure registration system, the maximal growth pressures for each of the explants, except the femoral head, were determined. The results show an independent growth potential for the primary cartilages of the epiphyseal and costal growth plates with a maximal growth pressure of 9.5 and 7.8 g/mm2, respectively. The primary cartilage of the spheno-occipital synchondrosis, on the other hand, although it possesses an independent growth potential, could exert a maximum growth pressure of only 1.5 g/mm2. The secondary cartilage of the mandibular condyle showed a limited intrinsic growth potential, as well as a low maximal growth pressure (2.6 g/mm2). If calculated per dividing and/or matrix synthesizing cell (cells mainly responsible for the cartilage growth), the cells of the condylar cartilage showed the least growth potency (0.08 mg/cell in comparison to 1.9, 1.5 and 0.3 for epiphyseal, costal, and synchondroseal cartilages, respectively.

Animals↗