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PubMed1976

Cartilage sulfation and serum somatomedin in rats during and after cortisone-induced growth arrest.

The uptake of sulfate by rib cartilage in vitro and in vivo and the serum somatomedin activity by bioassay were determined in male rats during and after cortisone-induced growth arrest. Experimental treatment consisted of subcutaneous injections of cortisone acetate in a dose of 2.5 mg/rat/day for 4 days, beginning at 29 to 30 days of age in Buffalo rats, or 5 mg/rat/day for 4 or 5 days, beginning at 39 to 41 days of age in Long-Evans rats. Groups of hypophysectomized rats were studied in parallel in one experiment. The sulfate uptake in the controls declined linearly with increasing age in both the in vitro and the in vivo studies. Hypophysectomy resulted in a constant low level of sulfate uptake in vitro. At the end of cortisone treatment, the in vitro sulfate uptake was approximately midway between that of the hypophysectomized rats and that of controls; at 7 days recovery, it was at the control level; at 14 days it showed an additional rise above the control value; from 14 days to 35 days it declined parallel with but above the sulfate uptake of controls. The in vivo sulfate uptake was depressed by cortisone treatment. During recovery it approximately control values at recovery day 21. In succeeding recovery periods in vivo sulfate uptake remained at control levels. Serum somatomedin activity was significantly reduced during cortisone treatment; it returned to the control level by 21 days of recovery. The incubation of the cartilage of controls and cortisone-treated rats at 14 days of recovery with and without the presence of normal rat serum, cortisone recovery serum, or hypophysectomy serum resulted in significantly higher sulfate uptake in the cortisone-treated rat cartilage in each medium. These sera did not differ significantly in their stimulation of sulfate uptake in either cortisone recovery cartilage or control cartilage. Both treated and control cartilage had greater sulfate uptake with larger doses of serum added to the medium. The dose-response curves were parallel during treatment and early recovery; but the slopes of the dose-response curves of the cartilage of cortisone-treated rats were greater than those of the controls during late recovery. It is concluded that the increased in vitro sulfation after 14 days of recovery in cortisone-treated rats signifies a persistent alteration in cartilage metabolism. Normal in vivo sulfate uptake during that time may be the result of humoral controls. A mechanism other than the impairment of somatomedin production is probably involved in the failure of catch-up growth after glucocorticoid treatment in the rat.

Animals↗
PubMed1996

Jaw and branchial arch mutants in zebrafish II: anterior arches and cartilage differentiation.

In a large scale screen for mutants that affect the early development of the zebrafish, 109 mutants were found that cause defects in the formation of the jaw and the more posterior pharyngeal arches. Here we present the phenotypic description and results of the complementation analysis of mutants belonging to two major classes: (1) mutants with defects in the mandibular and hyoid arches and (2) mutants with defects in cartilage differentiation and growth in all arches. Mutations in four of the genes identified during the screen show specific defects in the first two arches and leave the more posterior pharyngeal arches largely unaffected (schmerle, sucker, hoover and sturgeon). In these mutants ventral components of the mandibular and hyoid arches are reduced (Meckel's cartilage and ceratohyal cartilage) whereas dorsal structures (palatoquadrate and hyosymplectic cartilages) are of normal size or enlarged. Thus, mutations in single genes cause defects in the formation of first and second arch structures but also differentially affect development of the dorsal and ventral structures within one arch. In 27 mutants that define at least 8 genes, the differentiation of cartilage and growth is affected. In hammerhead mutants particularly the mesodermally derived cartilages are reduced, whereas jellyfish mutant larvae are characterized by a severe reduction of all cartilaginous elements, leaving only two pieces in the position of the ceratohyal cartilages. In all other mutant larvae all skeletal elements are present, but consist of smaller and disorganized chondrocytes. These mutants also exhibit shortened heads and reduced pectoral fins. In homozygous knorrig embryos, tumor-like outgrowths of chondrocytes occur along the edges of all cartilaginous elements. The mutants presented here may be valuable tools for elucidating the genetic mechanisms that underlie the development of the mandibular and the hyoid arches, as well as the process of cartilage differentiation.

Animals↗
PubMed2002

A zebrafish sox9 gene required for cartilage morphogenesis.

The molecular genetic mechanisms of cartilage construction are incompletely understood. Zebrafish embryos homozygous for jellyfish (jef) mutations show craniofacial defects and lack cartilage elements of the neurocranium, pharyngeal arches, and pectoral girdle similar to humans with campomelic dysplasia. We show that two alleles of jef contain mutations in sox9a, one of two zebrafish orthologs of the human transcription factor SOX9. A mutation induced by ethyl nitrosourea changed a conserved nucleotide at a splice junction and severely reduced splicing of sox9a transcript. A retrovirus insertion into sox9a disrupted its DNA-binding domain. Inhibiting splicing of the sox9a transcript in wild-type embryos with splice site-directed morpholino antisense oligonucleotides produced a phenotype like jef mutant larvae, and caused sox9a transcript to accumulate in the nucleus; this accumulation can serve as an assay for the efficacy of a morpholino independent of phenotype. RNase-protection assays showed that in morpholino-injected animals, the percent of splicing inhibition decreased from 80% at 28 hours post fertilization to 45% by 4 days. Homozygous mutant embryos had greatly reduced quantities of col2a1 message, the major collagen of cartilage. Analysis of dlx2 expression showed that neural crest specification and migration was normal in jef (sox9a) embryos. Confocal images of living embryos stained with BODIPY-ceramide revealed at single-cell resolution the formation of precartilage condensations in mutant embryos. Besides the lack of overt cartilage differentiation, pharyngeal arch condensations in jef (sox9a) mutants lacked three specific morphogenetic behaviors: the stacking of chondrocytes into orderly arrays, the individuation of pharyngeal cartilage organs and the proper shaping of individual cartilages. Despite the severe reduction of cartilages, analysis of titin expression showed normal muscle patterning in jef (sox9a) mutants. Likewise, calcein labeling revealed that early bone formation was largely unaffected in jef (sox9a) mutants. These studies show that jef (sox9a) is essential for both morphogenesis of condensations and overt cartilage differentiation.

Alleles↗
PubMed2003

Macroscopic cartilage formation with embryonic stem-cell-derived mesodermal progenitor cells.

The totipotent embryonic stem cell generates various mesodermal cells when stimulated with BMP4. Among the resulting cells, those expressing flk-1 and/or PDGFRalpha displayed chondrogenic activity in the presence of TGFbeta3 and expressed cartilage-specific genes in 7 to 16 day pellet cultures. Depositions of cartilage matrix and type II collagen were detected by day 14. TGFbeta-stimulated chondrogenesis was synergistically enhanced by PDGF-BB, resulting in a larger cartilage particle filled with a cartilaginous area containing type II collagen, with a surface cell layer expressing type I collagen. In contrast, noggin inhibited both the TGFbeta- and TGFbeta+PDGF-stimulated cartilage formation, suggesting that a BMP-dependent pathway is involved. In fact, replacement of TGFbeta3 with BMP4 on days 10 to 12 markedly elevated the cartilage matrix deposition during the following 7 to 8 days. Moreover, culture with TGFbeta3 and PDGF-BB, followed by the incubation with BMP4 alone, resulted in a cartilage particle lacking type I collagen in the matrix and the surface layer, which suggests hyaline cartilage formation. Furthermore, such hyaline cartilage particles were mineralized. These studies indicate that the PDGFRalpha+ and/or flk-1+ cells derived from embryonic stem cells possess the full developmental potential toward chondrocytes, in common with embryonic mesenchymal cells.

Animals↗
PubMed1998

The compressive strength of articular cartilage.

Articular cartilage provides the smooth bearing surfaces in freely moving (synovial) joints. Its mechanical properties are important because structural failure of cartilage is closely associated with joint disorders, including osteoarthritis. Some mechanical properties of cartilage are well characterized, but little is known about its compressive strength. A technique for measuring cartilage compressive strength is evaluated, and an overview of experiments which relate strength to stiffness and tissue hydration is given. Specimens of bovine articular cartilage-on-bone, approximately 15 mm square, were loaded on a hydraulic materials testing machine using flat impermeable indentors. Linear-ramp loading/unloading cycles of 1 s duration, and of increasing severity, were applied until failure was evident on force-displacement graphs. Some specimens were tested following a 30 min period of creep loading. Inkstaining and histology were used to locate the site of initial damage to each specimen. Specimen failure occurred first in the cartilage surface layer at a nominal applied stress of 14-59 MPa (mean 35.7 MPa). Mechanical properties were little affected by specimen or indentor size, provided both remained within defined limits, and compressive strength could be measured to an accuracy of approximately +/- 5 per cent. Compressive stiffness was a significant predictor of strength, but only if it was measured at high levels of stress. Strength increased following creep-induced water loss, and initial mechanical damage could propagate under moderate cyclic loading. This technique for measuring cartilage compressive strength has potential for investigating the causes of cartilage failure in vivo.

Animals↗
PubMed2001

Demonstration of inhibitory effect of oral shark cartilage on basic fibroblast growth factor-induced angiogenesis in the rabbit cornea.

Several angiogenic inhibitors have been obtained from shark cartilage, some of these are currently in clinical trials for assessment of safety and therapeutic efficacy in humans. Still, shark cartilage taken orally is commonly used in alternative and complimentary medicine for various ailments including serious diseases such as cancer. However, only few studies of oral shark cartilage have demonstrated pharmacological effects in experimental animals or patients, to indicate safe doses with sufficient bioavailability. In the present study we demonstrated the antiangiogenic properties of oral shark cartilage in the rabbit cornea model. Slow-release, polymethylmetacrylate pellets containing basic fibroblast growth factor (bFGF) were surgically implanted in the rabbit cornea to stimulate neovascularization scored by stereo microscopy. Powdered shark cartilage (PSC; commercial product) was tested orally along with a water-soluble fraction (WSF) of this cartilage product which was tested by local application. Animals were treated with oral dosages of 100 mg/kg PSC or 200 mg/kg thalidomide as positive control. Pellets containing WSF (50, 100 or 200 microg/pellet) or bFGF-inhibitor pentosan polysulfate were implanted adjacent to the bFGF pellet. Oral shark cartilage inhibited bFGF-induced angiogenesis, as did oral thalidomide, in this in vivo model. WSF and pentosan polysulfate was shown to block neovascularization in the cornea when applied locally. This study demonstrates that in the rabbit, oral shark cartilage appears to produce systemic levels of angiogenesis inhibitors that can exert their effect at the cornea.

Administration, Oral↗
PubMed1983

Alterations of glycosaminoglycans synthesized by chick embryo cartilage treated with 6-amino-nicotinamide.

Treatment of day-4 chick embryos with 6-aminonicotinamide (6-AN) impairs limb chondrogenesis and produces micromelia. However, treatment of day-10 chick embryos with 6-AN does not produce micromelia. In the present study, the glycosaminoglycan (GAG) biosynthesis in the cartilage isolated from the day-10 chick embryos treated with 6-AN in vitro and in the cartilage from the day-11 chick embryos treated with 6-AN in ovo at day-10 was examined. In the epiphyseal cartilage treated in vitro, the radioactivity incorporated into the GAG fraction was significantly decreased and the 35S/3H ratio in the GAG fraction and the molecular size of GAG chain were also decreased. However, the percent distribution of delta Di-0S was almost unchanged. In the epiphyseal and diaphyseal cartilage treated in ovo at day-10, the alteration in GAG biosynthesis was not observed except the reduction of the molecular size of GAG in epiphyseal cartilage. Furthermore, the biosynthetic activity of GAG in the process of recovery/repair was also examined using the micromelial cartilage isolated from day 11-chick embryos given 6-AN in ovo at day-4. In the diaphyseal cartilage, the radioactivity incorporated into the GAG fraction and the 35S/3H ratio were increased, whereas the percent distribution of delta Di-0S was almost unchanged. These results indicate that treatment of day-4 chick embryos with 6-AN produces the rebound phenomena in the diaphyseal cartilage isolated at day-11.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Aminonicotinamide↗
PubMed1993

[Influence of epiphyseal cartilages on bone resorption of fetal rat femora].

We developed a facile method for studying bone resorption using fetal rat femur by labelling the bone with 45Ca in vitro. We found that cartilages stimulated the bone resorption of a shaft which was obtained by cutting off both distal and proximal cartilages from the femur. When the shaft was co-cultured with the cartilages isolated by a 0.4-microns microporous membrane in the same Transwell, the bone resorption of the shaft was increased. This finding suggests that the stimulation of bone resorption by the cartilages is not a result of recruitment of osteoclasts or the precursor cells from the cartilages. Indomethacin (10(-6) M) failed to influence the bone resorbing activity of the cartilages. The bone resorbing activity in the supernatant obtained from the cartilage-culture was decreased by heating. The bone resorbing activity of the supernatant did not remain in the lipid-extract or the pronase-digested supernatant, but was present in a fraction whose molecular weight was greater than 50,000. These results collectively suggest that the cartilages produce a bone resorption-stimulating factor(s) which is water-soluble, is a non-prostanoid material, contains protein and has a molecular weight greater than 50,000.

Animals↗
PubMed1992

Subluxation of the patella: evaluation of patellar articular cartilage with MR imaging.

In patients with subluxation of the patella, injury of the patellar articular cartilage is frequently observed, and correct evaluation of this cartilage injury is extremely important for the management of these patients. Magnetic Resonance (MR) studies were performed on 102 patellofemoral (PF) joints of 51 patients with subluxation of the patella and 20 PF joints of 10 healthy volunteers. In 77 of the 102 PF joints with subluxation, arthroscopy and/or operation were performed. MR images were obtained with spin-echo and FLASH sequences, and para-axial images were obtained. We retrospectively analysed the MR findings of the 77 joints with special attention to the surface and thickness of the cartilage, and classified them into four grades. These MR grades were compared with the grades on arthroscopy, and the following results were obtained: MR grade 0, normal cartilage (n = 27, sensitivity 90.9%, specificity 74.2%); MR grade 1, thickening of the cartilage (n = 24, sensitivity 50%, specificity 89.1%); MR grade 2, surface irregularity of the cartilage (n = 20, sensitivity 85%, specificity 94.7%); MR grade 3, loss of the cartilage (n = 6, sensitivity 100%, specificity 100%). Although the early changes observed by arthroscopy were underestimated from the MR images, MR imaging proved to be extremely useful for evaluating moderately or advanced patellar cartilage injury.

Adolescent↗
PubMed2000

Boron neutron capture therapy of the rat 9L gliosarcoma: evaluation of the effects of shark cartilage.

A number of anti-angiogenic substances are now under evaluation, both experimentally and clinically, as potential agents for the treatment of cancer. It has recently been demonstrated that anti-angiogenic agents can increase the therapeutic potential of photon irradiation in a range of tumour models. In the present communication a preliminary assessment is made of the effects of shark cartilage on the response of the rat 9L gliosarcoma to boron neutron capture therapy (BNCT). Shark cartilage was administered orally as an aqueous suspension at a daily dose of approximately 2000 mg kg-1 body weight. The mean survival time of rats receiving no treatment was 20.7 +/- 0.5 days post intracranial tumour implantation. Administration of shark cartilage alone extended the survival time. Two of the rats treated with shark cartilage were healthy and fully active at the end of the evaluation period (43 days post implantation). At autopsy the brain tumours of these animals were a factor of approximately 4 smaller than controls. In a repeat study with shark cartilage alone the survival time was extended by approximately 30%. After boronophenylalanine-mediated BNCT, with or without shark cartilage, the survival time of rats that eventually became moribund was increased by a factor of approximately 2 relative to controls. In both treatment groups approximately 20% of rats were healthy at 1 year after BNCT. There was no evidence of residual tumour at post-mortem. It was concluded that shark cartilage, when given alone, significantly increased the survival time of tumour-bearing rats, presumably owing to an anti-angiogenic effect. However, the survival data suggested that boronophenylalanine-mediated BNCT did not appear to be enhanced by the administration of shark cartilage.

Angiogenesis Inhibitors↗
PubMed2002

Bone morphogenetic protein signals are required for cartilage formation and differently regulate joint development during skeletogenesis.

The bone morphogenetic protein (BMP) family consists of a large number of members and has diverse biological activities during development. Various tissues express pleural BMP family members, which seem to cooperatively regulate developmental events. Here, multiple BMP signals were inactivated in chondrocytes to clarify the function of BMPs during skeletogenesis. To obtain tissue-specific inactivation, Noggin gene (Nog) was overexpressed in cartilage under the control of a2(XI) collagen gene (Collla2) promoter/enhancer sequences. The resultant transgenic mice lacked most of their cartilaginous components, suggesting that cartilage does not develop without BMP signals. These effects seem to be mediated through down-regulation of Sox9 expression. Conversely, specific BMP signals were activated in the skeleton by targeted expression of Bmp4 in cartilage and the resultant phenotype was compared with that of transgenic mice expressing growth and differentiation factor-5 (GDF-5), another BMP family member. Overactivity of Bmp4 in the skeleton caused an increase of cartilage production and enhanced chondrocyte differentiation, as GDF5 expression did, but it did not disturb joint formation as GDF5 did. During skeletogenesis, unique roles of each BMP may reside in the regulation of joint development. Together with the common effect on the cartilage overproduction by Bmp4 and GDF5 overactivation, loss of cartilage by inactivation of multiple BMPs in Noggin transgenic mice indicates that signals for cartilage production are reinforced by multiple BMPs exclusively. These conclusions may account for the reason why multiple BMPs are coexpressed in cartilage.

Animals↗
PubMed2002

Development of gene-based therapies for cartilage repair.

Articular cartilage is particularly vulnerable to injury and degenerative conditions, and has a limited capacity for self-repair. Although current clinical procedures cannot restore a normal articular surface, there are a growing number of proteins that may be used to augment a repair process, or protect cartilage from degeneration. Because proteins are often difficult to administer effectively, gene therapy approaches are being developed to provide their sustained synthesis at sites of injury or disease. To promote cartilage repair, cDNAs can be targeted to synovium, or cartilage. Gene transfer to the synovium is generally considered more suitable for chondroprotective therapies that rely on expression of large amounts of anti-inflammatory mediators. The delivery of genes to cartilage defects to promote enhanced repair can be performed by either direct administration of gene delivery vectors, or by implantation of genetically modified chondrogenic cells. Variations of these methods have been used to demonstrate that exogenous cDNAs encoding growth factors can be delivered locally to sites of cartilage damage where they are expressed at physiologically relevant levels. Data is beginning to emerge that suggests that delivery and expression of these genescan influence a repair response toward the synthesis of normal articular cartilage in vivo. This article reviews the current status of gene delivery for cartilage healing and presents some of the remaining challenges.

Animals↗
PubMed2006

Synovial stem cells are regionally specified according to local microenvironments after implantation for cartilage regeneration.

We previously demonstrated that synovium-derived MSCs had greater in vitro chondrogenic ability than other mesenchymal tissues, suggesting a superior cell source for cartilage regeneration. Here, we transplanted undifferentiated synovium-derived MSCs into a full-thickness articular cartilage defect of adult rabbits and defined the cellular events to elucidate the mechanisms that govern multilineage differentiation of MSCs. Full-thickness osteochondral defects were created in the knee; the defects were filled with 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate-labeled MSCs and covered with periosteum. After 4 weeks, although the cell density decreased, transplanted MSCs produced a great amount of cartilage matrix extensively. The periosteum became thinner, and chondroprogenitors in the periosteum produced a small amount of cartilage matrix. In the deeper zone, transplanted MSCs progressed to the hypertrophic chondrocyte-like cells. In the deep zone, some transplanted cells differentiated into bone cells and were replaced with host cells thereafter. In the next phase, the border between bone and cartilage moved upwards. In addition, integrations between native cartilage and regenerated tissue were improved. Chondrocyte-like cells derived from the transplanted MSCs still remained at least after 24 weeks. Histological scores of the MSC group improved continuously and were always better than those of two other control groups. Immunohistological analyses and transmission electron microscopy confirmed that the MSCs produced abundant cartilage matrix. We demonstrated that transplanted synovium-derived MSCs were altered over a time course according to the microenvironments. Our results will advance MSC-based therapeutic strategies for cartilage injury and provide the clues for the mechanisms that govern multilineage differentiation of MSCs.

Animals↗
PubMed2001

Histopathologic changes in growth-plate cartilage following ischemic necrosis of the capital femoral epiphysis. An experimental investigation in immature pigs.

BACKGROUND: The developing capital femoral epiphysis consists of a secondary center of ossification surrounded by epiphyseal cartilage. Between the epiphyseal cartilage and the secondary center of ossification is a growth plate, which contributes to the circumferential increase in size of the secondary center of ossification during development. The main objective of this study was to describe the histopathologic changes that occur in the growth plate surrounding the secondary center of ossification during the early and reparative phases following the induction of ischemic necrosis of the capital femoral epiphysis in immature pigs. METHODS: Ischemic necrosis of the capital femoral epiphysis was induced in eighteen piglets by placing a nonabsorbable suture ligature around the femoral neck following a capsulotomy and transection of the ligamentum teres. The animals were killed three days to eight weeks following the induction of ischemia, and visual, radiographic, and histologic assessments were performed. RESULTS: Two to four weeks after the induction of ischemic necrosis, the growth plate surrounding the secondary center of ossification became necrotic. The observed histopathologic changes included chondrocyte death, loss of safranin-O staining of the matrix of the necrotic growth-plate cartilage, an absence of vascular invasion of terminal hypertrophic chondrocytes, and a decrease in the amount of primary spongiosa, indicating cessation of endochondral ossification. In the reparative phase, at four to eight weeks postoperatively, chondrocyte clusters and intense safranin-O staining were observed in the epiphyseal cartilage around the necrotic growth-plate cartilage. In the peripheral region of the femoral head, necrotic growth-plate cartilage surrounding the secondary center of ossification was resorbed by a fibrovascular tissue from the marrow space. By six weeks, new accessory centers of ossification with restored endochondral ossification were observed in the peripheral epiphyseal cartilage. New ossification centers contributed to the fragmented radiographic appearance of the secondary center of ossification. The physis appeared essentially normal in most animals, although five of the eighteen piglets showed mild or moderate histopathologic changes. CONCLUSIONS: In this model, ischemic necrosis of the capital femoral epiphysis resulted in necrosis of the growth plate surrounding the secondary center of ossification. Small new ectopic centers of ossification appeared in the epiphyseal cartilage, explaining in part the fragmented radiographic appearance of the secondary center of ossification.

Animals↗
PubMed2005

Articular cartilage degeneration in post-collapse osteonecrosis of the femoral head. Radiographic staging, macroscopic grading, and histologic changes.

BACKGROUND: Osteonecrosis of the femoral head is a debilitating condition characterized by progressive degeneration of bone that eventually leads to collapse of the femoral head in the majority of patients. Femoral head-sparing procedures have been more successful in pre-collapse stages of osteonecrosis than in post-collapse stages, although some patients with early post-collapse disease have had no additional progression of the disorder. Nevertheless, the effects of collapse on the articular cartilage are not well understood, and radiographic staging of femoral head collapse does not address the condition of the articular cartilage. METHODS: In the current study, we investigated the relationship between the mechanical properties of post-collapse articular cartilage and the histologic findings and macroscopic grades of the articular cartilage from hips with stage-IV osteonecrosis, those with stage-V osteonecrosis, and those without osteonecrosis. RESULTS: The cartilage from both stage-IV and stage-V hips showed significant degeneration compared with the normal control cartilage, but there was no significant difference between the two stages. There was significant variability in the histologic and mechanical properties of these samples that correlated strongly with the gross appearance of the cartilage surface but not with the lesion size. CONCLUSIONS: These results suggest that articular cartilage that appears macroscopically normal may remain mechanically functional even in patients with large osteonecrotic lesions or a late radiographic stage of the disease.

Biomechanical Phenomena↗
PubMed1988

Effects of interleukin-1 and anti-inflammatory drugs on the degradation of human articular cartilage.

It has been suggested that metalloproteases produced by chondrocytes play an important role in cartilage breakdown in joint diseases. The aim of this study was to investigate changes in enzyme activities in human rheumatoid and osteoarthritic articular cartilage. Cartilage fragments were incubated with various drugs for 48 hours. The concentrated culture media were used as enzyme solutions. Collagenase was assayed using FITC-collagen as the substrate. Proteoglycanase (PGase) was measured either by the release of 35S-labelled proteoglycans from cartilage into the medium, or by enzyme assay using proteoglycan monomer bound to fluorescein-conjugated hyaluronic acid as the substrate. Collagenase and proteoglycanase were found only in trace amounts in the concentrated media of healthy cartilage. Interleukin-1 (IL-1) enhanced the enzyme activities significantly. Marked increases of enzyme activities were observed in the concentrated media of rheumatoid (RA) and osteoarthritic (OA) cartilage. The sensitivity to interleukin-1 was also higher in OA and RA cartilage compared with healthy cartilage. Dexamethasone (10(-6) mol/L) markedly depressed enzyme activity. Tiaprofenic acid (4 x 10(-5) mol/L) also decreased enzyme activity, whereas indomethacin (4 x 10(-6) mol/L) and naproxen (3 x 10(-4) mol/L) had no effect.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

Assessment of articular cartilage thickness of the humeral head: MR-anatomic correlation in cadavers.

OBJECTIVE: The purpose of our study was to evaluate several commonly used MR sequences to determine how accurately each demonstrates the thickness of the articular cartilage of the humeral head. MATERIALS AND METHODS: Ten cadaveric shoulders (age at death, 58-92 years; mean, 79 years) were imaged with fat-suppressed transaxial T1-weighted spin-echo three-dimensional gradient-recalled sequences, both before and after injection of 12 ml of diluted gadopentetate dimeglumine. Articular cartilage was measured to the nearest 10th of a millimeter on the MR images and corresponding anatomic sections. RESULTS: Cartilage could not be differentiated from surrounding structures in 14 of 112 locations (13%) on the spin-echo images obtained without contrast material, in 4 of 112 locations (4%) on the spin-echo images obtained with contrast material, in 4 of 112 locations (4%) on the gradient-echo images obtained without contrast material, and in 6 of 112 locations (5%) on the gradient-echo images obtained with contrast material. Mean true cartilage thickness was 1.23 mm (SD, 0.52 mm). The mean MR-anatomic differences (absolute values) were 0.38 mm for the spin-echo images obtained without contrast material, 0.42 mm for the spin-echo images obtained with contrast material, 0.49 mm for the gradient-echo images obtained without contrast material, and 0.37 mm for the gradient-echo images obtained with contrast material. There was a tendency to overestimate thin cartilage and to underestimate thick cartilage. CONCLUSION: Several of the routinely used MR sequences, with and without intraarticular contrast medium, may cause errors in the assessment of the articular cartilage of the humeral head. Some of these errors result from either insufficient contrast between cartilage and surrounding structures or inadequately concentrated contrast medium.

Aged↗
PubMed2005

Imaging of patellar cartilage with a 2D multiple-echo data image combination sequence.

OBJECTIVE: We sought to evaluate the diagnostic value of a 2D multiple-echo data image combination (MEDIC) MRI sequence in the detection of patellar cartilage defects. MATERIALS AND METHODS: Our study included 52 consecutive patients who had knee surgery within 4 months of undergoing an MRI examination including an axial 2D MEDIC (TR/TE, 884/26; flip angle, 30 degrees ) sequence. Cartilage was surgically graded on a 5-point scale: 0, normal; 1, softening or swelling; 2, partial thickness defect; 3, fissuring to the level of the subchondral bone; or 4, exposed subchondral bone. Cartilage was graded on MRI according to a scale that was almost identical to the surgical scale except that grade 1 lesions were defined as signal alteration or swelling of cartilage. Two blinded reviewers independently analyzed patellar cartilage. Sensitivity, specificity, accuracy, and weighted kappa values for interobserver variability were calculated. RESULTS: Low-grade cartilage lesions predominated in our study group. When grade 2 or higher was considered the threshold for relevance, the sensitivity, specificity, and accuracy for the MEDIC sequence was as high as 79%, 82%, and 81%, respectively. Increasing the threshold of relevance to grade 3 increased the sensitivity, specificity, and accuracy to as high as 83%, 91%, and 90%, respectively. Interobserver agreement for the MEDIC sequence was good (weighted kappa = 0.68). CONCLUSION: The 2D MEDIC sequence performs comparably to previously described sequences optimized for cartilage imaging such as the 3D double-echo steady-state or 3D spoiled gradient-recalled sequences with good interobserver agreement, high sensitivity, and excellent specificity for revealing low- to intermediate-degree cartilage defects.

Adult↗