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PubMed2005

Comparison of proteoglycan and collagen in articular cartilage of horses with naturally developing osteochondrosis and healing osteochondral fragments of experimentally induced fractures.

OBJECTIVE: To compare articular cartilage from horses with naturally developing osteochondrosis (OC) with normal articular cartilage and healing cartilage obtained from horses with experimentally induced osteochondral fractures. SAMPLE POPULATION: 109 specimens of articular cartilage from 78 horses. PROCEDURE: Morphologic characteristics, proteoglycan (PG), and type II collagen were analyzed in articular cartilage of OC specimens (group 1), matched healing cartilage obtained 40 days after experimentally induced osteochondral fractures (group 2), and matched normal cartilage from the same sites (group 3). RESULTS: 79 specimens of OC cartilage were obtained from horses. Ex vivo PG synthesis was significantly greater in the femoral cartilage, compared with synthesis in the tibial cartilage, and significantly greater for groups 1 and 2, compared with group 3. For groups 1 and 2, femoral fragments had significantly greater PG content, compared with PG content in tibial fragments. Keratan sulfate content was significantly less in group 3, compared with groups 1 and 2. Cartilage from the OC specimens had loss of structural architecture. The OC tissue bed stained positive for chondroitin sulfate and type II collagen, but the fracture bed did not. CONCLUSIONS AND CLINICAL RELEVANCE: Our analyses could not distinguish articular cartilage from horses with OC and a healing fracture. Both resembled an anabolic, reparative process. Immunohistochemical analysis suggested a chondromyxoid tissue in the OC bed that was morphologically similar to fibrous tissue but phenotypically resembled hyaline cartilage. Thus, tissue in the OC bed may be degenerative cartilage, whereas tissue in the fracture bed may be reparative fibrous callus.

Animals↗
PubMed2005

Correlation of local outcome after partial laryngectomy with cartilage abnormalities on CT.

BACKGROUND AND PURPOSE: The prognostic significance of laryngeal cartilage abnormalities, as seen on CT or MR imaging, in laryngeal or hypopharyngeal cancer, is unclear. The purpose is to determine whether cartilage abnormalities as seen on preoperative CT in laryngeal and pyriform sinus cancer are predictive of local outcome after partial laryngectomy. METHODS: The preoperative CT studies in a consecutive series of 16 patients who underwent extended hemilaryngectomy for squamous cell carcinoma of the glottis (n = 12), supraglottis (n = 1), or pyriform sinus (n = 3) were reviewed retrospectively. Cartilage abnormalities were defined as asymmetric cartilage sclerosis, lysis of ossified cartilage, or tumor visible on both sides of the cartilage. Tumor volume was calculated by using the summation-of-areas technique. Seven patients underwent postoperative radiation therapy. All patients had a follow-up of at least 24 months after treatment or until local recurrence. RESULTS: Eleven patients showed cartilage abnormalities. In six patients, only a single cartilage was abnormal, whereas three patients showed involvement of two cartilages and two patients of three cartilages. The overall average tumor volume was 2.7 mL; the average tumor volume was 1.5 mL in the patients without and 3.3 mL in those with cartilage involvement on CT (P > .05). Two patients suffered a local recurrence. One patient (tumor volume, 1.5 mL) did not show any cartilage abnormalities. The other patient (tumor volume, 1.9 mL) showed abnormalities in all three cartilages and also had evidence of early transcartilaginous tumor spread. CONCLUSION: In patients whose cancer is anatomically suitable for partial laryngectomy, cartilage abnormalities on CT do not preclude speech-preserving surgery.

Aged↗
PubMedDate not supplied

Cartilage cell differentiation: review.

Differentiation of cartilage cells from embryonic precursor cells is characterized by the onset of biosynthesis of at least two cartilage-specific gene products, type II collagen and cartilage-specific chondroitin sulfate proteoglycan (CSPG). Biochemical and immunological assays for these compounds now allow rapid, quantitative, and specific determination of the onset of cartilage differentiation, and present several advantages over assays that use histochemical stains or [35S]-sulfate incorporation into glycosaminoglycans. Chondrogenic differentiation also is associated with the formation of extracellular, high MW proteoglycan (CSPG) aggregates containing hyaluronic acid and the loss of fibronectin, or LETS protein, a cell surface glycoprotein found on presumptive chondroblasts, fibroblasts, and several other cell types. Comparatively little insight has been gained recently regarding the mechanism of cartilage cell differentiation. A number of factors or "inducers" of cartilage differentiation, such as chondroitin sulfate proteoglycan, notochord, spinal cord, low oxygen tension, and collagen substrates, increase the amount of glycosaminoglycan synthesis per cell, but the question remains open as to whether these factors also selectively increase the number of cells differentiating from precursor cells into chondroblasts, or whether they only increase cell viability. Other factors, such as conditioned medium from chondrocyte cultures, increase significantly the number of chondrocyte colonies arising in mass cultures of limb bud mesenchyme, but differentiation of nonchondrogenic cells is stimulated as well. Similarly, many inhibitors of cartilage differentiation, such as BrdUrd and 6-amino nicotinamide, also inhibit myogenic differentiation. It is possible that a unique and specific inducer or regulating factor of cartilage cell differentiation may not exist, for cartilage differentiation of normal embryonic mesenchyme can be triggered by a variety of environmental conditions, such as cell density, pH, potassium ion concentration, and fetal calf serum. These results imply that the temporal and spatial controls of cartilage differentiation are governed by environmental influences that are each of rather low specificity, but which together synergistically generate a morphogenetic control of high specificity. Signals which appear able to mimic those controlling normal cartilage differentiation seem to be exchanged during formation of ectopic cartilage. Muscle tissue and periosteum can be triggered to form cartilage by demineralized bone matrix. Chick limb bud epithelium induces type II collagen synthesis in embryonic mouse tooth germ, whereas homologous, oral epithelium induces the formation of dentin (type I collagen). Thus, the type of response elicited from mesenchyme cells can be determined by nearby epithelia, and that response frequently can be the formation of cartilage.

Animals↗
PubMed1997

Variations in the mechanical properties of cartilage from the canine scapulohumeral joint.

OBJECTIVE: To measure the intrinsic material properties of scapulohumeral joint cartilage in adult dogs and determine whether regional differences exist within or between the humeral and glenoid cartilages. SAMPLES: Paired shoulder joints from 7 clinically normal adult dogs. PROCEDURE: An automated indentation apparatus was used to obtain the intrinsic mechanical properties of the cartilage at 7 sites on each joint surface. RESULTS: Topographic variations in mechanical properties of the glenoid and humeral cartilages were observed. The largest aggregate modulus (HA) for the humerus was seen at the caudocentral site (0.92 MPa) and for the scapula was seen at the centrocenter site (0.84 MPa). The mean shear modulus (mu) of humeral cartilage (0.23 MPa) was significantly greater than that of the glenoid cartilage (0.19 MPa). The mean Poisson's ratio (v) of humeral cartilage (0.24) was significantly smaller than that for the glenoid cartilage (0.29). Mean humeral cartilage aggregate modulus (0.71 MPa) was larger than the value for glenoid cartilage (0.67 MPa), but these differences were not significant. There were no significant differences in the compressive stiffness of the opposing cartilage in the canine scapulohumeral joint. CONCLUSIONS: Differences in mechanical properties between opposing humeral and glenoid cartilages are not a cause of cartilage injury in the scapulohumeral joint of adult dogs. The mechanical properties of cartilage from young dogs with open physes and incomplete subchondral bone plates may be different from those of adult dogs.

Animals↗
PubMedDate not supplied

Autocrine production of IL-1 beta by human osteoarthritis-affected cartilage and differential regulation of endogenous nitric oxide, IL-6, prostaglandin E2, and IL-8.

Interleukin-1 beta (IL-1 beta) plays a central role in the pathophysiology of cartilage damage and degradation in arthritis. In noninflammatory arthropathies such as osteoarthritis (OA), the synovial-derived IL-1 beta has been implicated in the disease process. In this study, we report that human OA-affected cartilage demonstrates upregulated IL-1 beta mRNA not seen in normal cartilage. The OA-affected cartilage in ex vivo conditions spontaneously releases detectable amounts of autocrine IL-1 beta, nitric oxide (NO), and prostaglandin E2 (PGE2), known to be involved in cartilage damage and inflammation, that cannot be detected in normal cartilage. The autocrine IL-1 beta released by the OA-affected cartilage (for at least 72 hr in ex vivo conditions) is present in sufficient quantities to modulate NO and PGE2 production because addition of recombinant soluble IL-1 beta receptor (but not soluble tumor necrosis factor-alpha receptor) and cytokine-suppressive antiinflammatory drugs (CSAIDs) significantly attenuates the spontaneous release of NO and PGE2. Furthermore, OA-affected cartilage releases significant amounts of IL-6 and IL-8 in ex vivo conditions. Addition of CSAIDs to OA-affected cartilage differentially regulates IL-6 and IL-8 production by inhibiting the spontaneous release of IL-6 but not IL-8 in ex vivo conditions. These experiments demonstrate that the human OA-affected cartilage itself releases sufficient amounts of functionally active autocrine IL-1 beta that can modulate endogenous NO, PGE2, and IL-6, but not IL-8, all of which are known to be stimulated by IL-1 beta in vitro. These IL-1 beta induced pleotropic inflammatory mediators in OA-affected cartilage may be sufficient to facilitate or augment cartilage degradation and inhibit cartilage repair, and therefore lead the cartilage into an autodestructive pathway in osteoarthritis.

Anti-Inflammatory Agents↗
PubMed1999

Presence and distribution of collagen II, collagen I, fibronectin, and tenascin in rabbit normal and osteoarthritic cartilage.

OBJECTIVE: To investigate changes in the composition of articular cartilage matrix during the development of experimental osteoarthritis (OA), collagen type II, collagen type I, and the noncollagenous proteins fibronectin and tenascin were studied in normal and osteoarthritic cartilage of rabbits. METHODS: OA of the knee joint was induced by a medial meniscectomy and section of the medial collateral ligament and anterior cruciate ligament. Frozen sections of rabbit normal and OA cartilage were stained with monoclonal antibodies against collagen type II, collagen type I, fibronectin, and tenascin. RESULTS: Collagen II manifested a decreased interterritorial staining and seemed to increase territorially in the deeper zones of the OA cartilage. Collagen I was found in normal cartilage as a thin layer covering the surface and also in OA fibrillated cartilage. Fibronectin was present in normal and OA cartilage. Whereas a layer covered the normal cartilage, a thicker layer was observed in OA cartilage. In addition, changes in fibronectin distribution from the pericellular to the interterritorial matrix were observed. Tenascin was also found in normal cartilage matrix, particularly in the territorial and interterritorial matrix of the deeper zones. It showed an increased staining intensity in fibrillated cartilage, in the pericellular matrix of the upper chondrocytes, and on the surface lining in OA cartilage. CONCLUSION: Collagen type II deposition seems to increase in the deeper cartilage zones during the osteoarthritic process, as a sign of tissue repair response. Collagen type I, fibronectin, and tenascin show enhanced deposition in the upper, fibrillated osteoarthritic cartilage, suggesting a common mediator controlled pathway.

Animals↗
PubMed1983

Morphologic and biochemical changes in cartilage of foals treated with dexamethasone.

Epiphyseal and articular cartilages were examined in pony foals treated with intramuscular injections of either 0.5 mg dexamethasone per 100 kg bodyweight daily for 3, 8 or 11 months, or 5.0 mg per 100 kg for 11 months, and in horse foals treated with 5.0 mg per 100 kg for 20 weeks. The proximal femoral growth plates exhibited increased spatial separation between chondrocyte columns, narrowed zones of disorganized columnar and hypertrophic cartilage, abnormal penetration of hypertrophic cartilage by metaphyseal capillaries, retained cartilage in the spongiosa, distal terminal plate formation, transverse trabeculation, chondronecrosis and metaphyseal osteochondrosis dissecans. Destructive articular lesions were observed after 3 months of treatment with 0.5 mg per 100 kg bodyweight. Joint damage originated either at the joint surface or deep within the cartilage. Signs of surface deterioration included edema, fibrillation, enlargement of lacunae, pitting, shredding and erosions of cartilage. Inactivity of articular cartilage growth centers was common, with failure of epiphyseal capillaries to penetrate the lacunae in the calcified cartilage. Chondronecrosis adjacent to the calcification front was accompanied by cartilage ulceration and fracture. Intracartilaginous cysts and subchondral chondroid cysts were also observed. Healing responses included reparative chondrogenesis (focal cartilage hyperplasia), formation of fibrous or fibrocartilaginous "scars," subchondral osteopetrosis and epiphyseal marrow petrosis. Lactate dehydrogenase specific activities per chondrocyte, 35S uptake per cell and glycosaminoglycan contents of articular cartilages were all reduced 55% by 3 months of treatment. This inhibition of articular chondrocyte metabolism initiated cartilage degeneration. Surface destruction and osteochondrosis dissecans followed continued mechanical stress of compromised cartilage.

Animals↗
PubMed1982

Ossification of the laryngeal, tracheal and syringeal cartilages in the domestic fowl.

The process of ossification in the cartilages of the larynx, trachea and syrinx of the domestic fowl has been studied in growing and in adult Golden Comet birds. In the laryngeal cartilages, mineralisation occurred consistently in the body and wings of the cricoid cartilage, in the procricoid cartilage and in the bodies of the arytenoid cartilages. In 7 out of 12 adult birds there were small additional centres in the tips of the rostral processes of the arytenoid cartilages and in one adult bird there were small centres in the caudal processes also. When present, these additional centres were always found bilaterally. Mineralisation in the laryngeal cartilages developed from 105 days post-hatching onwards and was first seen in the bodies of the arytenoid cartilages. Some evidence of a segmental pattern was noted, both in the earliest centres and in the final stage in the caudal region of the body of the tcricoid cartilage. Mineralisation in the trachea developed from 98 days post-hatching onwards. It was first found in the caudal region and spread craniad. The rings at the caudal end of the trachea and the cranial end of the tympanum (but not the last two rings of he tympanum) were always fully involved. Rings in the cranial part of the trachea remained more lightly mineralised. In the syrinx, mineralisation regularly occurred only in the pessulus and in the base of the first bronchial syringeal cartilages. In some birds, it was also encountered more caudally in the cartilages of the primary bronchi. Histological examination showed that, in the early stages, the alizarin staining was due to the presence of mineralised cartilage. At 182 days post-hatching and in the adults, actual bony tissue was observed. The possible significance of the occurrence of ossification in these cartilages of birds in briefly considered.

Animals↗
PubMed2000

Optical and thermal properties of nasal septal cartilage.

BACKGROUNDS AND OBJECTIVES: The aim of the study was to measure the spectral dependence of optical absorption and reduced scattering coefficients and thermal conductivity and diffusivity of porcine nasal septal cartilage. Values of optical and thermal properties determined in this study may aid in determining laser dosimetry and allow selection of an optical source wavelength for noninvasive diagnostics for laser-assisted reshaping of cartilage. MATERIALS AND METHODS: The diffuse reflectance and transmittance of ex vivo porcine nasal septal cartilage were measured in the 400- to 1,400-nm spectral range by using a spectrophotometer. The reflectance and transmittance data were analyzed by using an inverse adding-doubling algorithm to obtain the absorption (mu(a)) and reduced scattering (mu(a)') coefficients. A multichannel thermal probe controller system and infrared imaging radiometer methods were applied to measure the thermal properties of cartilage. The multichannel thermal probe controller system was used as an invasive technique to measure thermal conductivity and diffusivity of cartilage at three temperatures (27, 37, 50 degrees C). An infrared imaging radiometer was used as a noninvasive method to measure the thermal diffusivity of cartilage by using a CO(2) laser source (lambda = 10.6 microm) and an infrared focal plane array (IR-FPA) camera. RESULTS: The optical absorption peaks at 980 nm and 1,180 nm in cartilage were observed and corresponded to known absorption bands of water. The determined reduced scattering coefficient gradually decreased at longer wavelengths. The thermal conductivity values of cartilage measured by using an invasive probe at 27, 37, and 50 degrees C were 4.78, 5.18, and 5.76 mW/cm degrees C, respectively. The corresponding thermal diffusivity values were 1.28, 1.31, and 1.40x 10(-3) cm(2)/sec. Because no statistically significant difference in thermal diffusivity values with increasing temperature is found, the average thermal diffusivity is 1.32 x 10(-3) cm(2)/sec. The numerical estimate for thermal diffusivity obtained from infrared radiometry measurements was 1.38 x 10(-3) cm(2)/sec. CONCLUSION: Values of the spectral dependence of the optical absorption and reduced scattering coefficients, and thermal conductivity and diffusivity of cartilage were measured. The invasive and noninvasive diffusivity measurements were consistent and concluded that the infrared imaging radiometric technique has an advantage to determine thermal properties, because damage to the cartilage sample may be avoided. The measured values of absorption and reduced scattering coefficients can be used for predicting the optical fluence distribution in cartilage and determining optical source wavelengths for the laser-assisted cartilage reshaping studies. The thermal conductivity and diffusivity values can play role in understanding thermal-dependent phenomenon in cartilage during laser irradiation and determining laser dosimetry for the laser-assisted cartilage reshaping studies.

Animals↗
PubMed2005

Shape retention in porcine and rabbit nasal septal cartilage using saline bath immersion and Nd:YAG laser irradiation.

BACKGROUND AND OBJECTIVES: The process of altering the shape of cartilage using heat has been referred to as thermoforming, and presents certain clinical benefits in reconstructive surgical procedures within the head and neck. Thermoforming allows cartilage in the upper airway and face to be reshaped without the use of classic surgical maneuvers such as carving, morselizing, or suturing. The goal of this study was to determine the dependence of cartilage shape change on both temperature and laser dosimetry using two thermoforming methods: saline bath immersion and laser irradiation. STUDY DESIGN/MATERIALS AND METHODS: Ex-vivo rabbit and porcine nasal septal cartilages were mechanically deformed and reshaped using the two thermoforming methods. With saline bath immersion using rabbit cartilage, each specimen was deformed by securing it to a small copper tube (outer diameter 8 mm) using dental bands. For porcine cartilage immersed in a saline bath, each sample was mechanically deformed between two pieces of wire mesh attached to a semicircular acrylic block. With both porcine and rabbit cartilage, the specimen and apparatus were then immersed in a hot saline bath for time intervals varying from 20 and 320 seconds and at constant temperatures between 62 and 74 degrees C. In laser reshaping, the cartilage specimens were mechanically deformed on a jig and consecutively irradiated with an Nd:YAG laser (lambda = 1.32 microm) in several spots for 6-16 seconds and irradiances of 10.2-40.7 W/cm2 per spot. After either saline bath heating or irradiation, cartilage specimens were immersed in room temperature saline for 15 minutes, then upon removal from the jig the length between the ends of each specimen was measured in order to calculate the resulting bend angle. RESULTS: The transition zone for cartilage reshaping was defined as where a significant increase in bend angle was observed between consecutive times of immersion/irradiation at the same temperature/irradiance. For the saline bath experiments, the transition zone was observed between 59-68 degrees C and 62-68 degrees C for porcine and rabbit cartilage, respectively. Similar transition zones occurred with laser irradiation below irradiances of 20.4 W/cm2 for both porcine and rabbit cartilage. In addition, the dosimetry pairs in the transition zones produce peak temperatures below the thresholds determined from the saline bath immersion studies. CONCLUSIONS: The critical transition temperature region was determined by the sharp increase in bend angle at consecutive times of immersion at the same temperature. This range was determined to be 59-68 degrees C and 62-68 degrees C for porcine and rabbit cartilage, respectively. Similar transition zones for dosimetry occurred below 20.4 W/cm2 during cartilage irradiation in both species.

Animals↗
PubMed1988

Cation movement in rat articular and non-articular cartilage and in isolated chondrocytes: calcium influx and efflux.

1. Calcium ion influx varies between different types of young adult rat cartilage. Sternal cartilage accumulates significantly less Ca2+ than other cartilage types. 2. Influxes of Ca2+ into young adult and ageing tibial cartilage display no significant differences. 3. Efflux of Ca2+ from sternal and tibial cartilage resolves into exponential phases indicative of three compartments. Tracheal cartilage displays two compartment behaviour only. 4. Efflux of Ca2+ from isolated chondrocytes has different characteristics to cartilage efflux with the third slow compartment reduced. 5. Modification of Ca2+ efflux by lanthanum and barium is suggestive of an exchange of strongly bound extracellular calcium during the slow phase of the efflux from young adult tibial cartilage. 6. The metabolic inhibitor 2,4-dinitrophenol is without effect on the efflux of Ca2+ from tibial articular cartilage. 7. The degree of calcium binding exhibited during efflux depends upon cartilage type. Non-articular sternal cartilage binds calcium more strongly than articular tibial, both binding more strongly than non-articular tracheal cartilage. 8. In articular cartilage calcium binding shows an age-related increase.

2,4-Dinitrophenol↗
PubMed2004

Articular cartilage of knee: normal patterns at MR imaging that mimic disease in healthy subjects and patients with osteoarthritis.

PURPOSE: To evaluate normal magnetic resonance (MR) imaging findings that may mimic articular cartilage diseases in healthy subjects and patients with osteoarthritis of the knee. MATERIALS AND METHODS: Sagittal fat-suppressed intermediate-weighted fast spin-echo (FSE) (repetition time msec/echo time [TE] msec, 4,000/13), sagittal T2-weighted FSE (4,000/39), and sagittal fat-suppressed three-dimensional (3D) spoiled gradient-echo (SPGR) (60/5, 40 degrees flip angle) MR images were acquired in 28 patients and four volunteers. FSE images with a TE of 13 msec were considered "short-TE images"; those with a TE of 39 msec were considered "long-TE images." Presence of normal MR imaging appearance of articular cartilage was determined by one author. Contrast between cartilage and adjacent structures (meniscus, joint capsule, synovial fluid, muscle) was calculated in posterior regions of the femoral condyle on images obtained with each sequence; Wilcoxon signed rank testing was performed. RESULTS: The following appearances were observed in patients with knee osteoarthritis (on short-TE FSE, long-TE FSE, and SPGR MR images, respectively): (a) ambiguity of surface contour in posterior region of the femoral condylar cartilage (in zero, zero, and 20 patients), (b) linear area of high signal intensity in deep zone adjacent to subchondral bone of femoral condyle (in zero, zero, and 26 patients), (c) pseudolaminar appearance in posterior region of femoral condylar cartilage (in seven, nine, and 24 patients), (d) truncation artifact in patellofemoral compartment (in seven, six, and 27 patients), (e) susceptibility artifact on cartilage surface caused by air or metal (in three, three, and 11 patients), (f) decreased signal intensity in distal part of trochlear cartilage (in 28, 28, and 28 patients), (g) cartilage thinning adjacent to the anterior horn of the lateral meniscus (in 19, 19, and 21 patients), and (h) focal cartilage flattening in posterior region of femoral condyle (in 16, 16, and nine patients). Cartilage-meniscus and cartilage-synovial fluid contrast was significantly higher on fat-suppressed FSE than on fat-suppressed 3D SPGR MR images (P <.001). CONCLUSION: Fat-suppressed FSE and 3D SPGR MR images showed nonuniform signal intensity arising from articular cartilage and cartilage thinning, both of which could mimic disease.

Adult↗
PubMed2006

Influence of hyaluronic acid on the time-dependent friction response of articular cartilage under different conditions.

Therapeutic lubricant injections of hyaluronic acid are a relatively recent treatment for osteoarthritis. Their efficacy, however, in vivo has been subject to much debate. Frictional properties of cartilage-cartilage contacts under both static and dynamic loading conditions have been investigated, using healthy cartilage and cartilage with a physically disrupted surface, with and without the addition of a therapeutic lubricant, hyaluronic acid. Most of the cartilage friction models produced typical time-dependent loading curves, with a rise in static friction with loading time. For the dynamic loading conditions the rise in friction with loading time was dependent on the spatial (and time) variation in the load on the cartilage plate. For sliding distances of 4 mm or greater, when the cartilage plate was unloaded during sliding, the dynamic friction remained low whereas, with shorter sliding distances, the dynamic friction increased with increasing loading time. Static friction was higher than dynamic friction (under the same tribological conditions). The 'damaged' cartilage models produced higher friction than healthy cartilage under equivalent tribological conditions. It was shown that hyaluronic acid was an effective boundary lubricant for articular cartilage under static conditions with both healthy and damaged cartilage surfaces. Hyaluronic acid was less effective under dynamic conditions. However, these dynamic conditions had low friction values with the control lubricant because of the effectiveness of the intrinsic biphasic lubrication of the cartilage. It was only under the tribological conditions in which the cartilage friction was higher and rising with increasing loading time because of depletion of the intrinsic biphasic lubrication, that the role of hyaluronic acid as an effective therapeutic lubricant was demonstrated.

Animals↗
PubMed2006

Immunolocalization of matrix proteins in different human cartilage subtypes.

Cartilage exerts many functions in different tissues and parts of the body. Specific requirements presumably also account for a specific biochemical composition. In this study, we investigated the presence and distribution pattern of matrix components, in particular collagen types in the major human cartilages (hyaline, fibrous, and elastic cartilage) by histochemical and immunohistochemical means. Macroscopically normal articular cartilages, menisci, disci (lumbar spine), epiglottal, and tracheal tissues were obtained from donors at autopsy. Aurical and nasal cartilages were part of routine biopsy samples from tumor resection specimens. Conventional histology and immunohistochemical stainings with collagen types I, II, III, IV, V, VI, and X and S-100 protein antibodies were performed on paraformaldehyde-fixed and paraffin-embedded specimens. The extracellular matrix is the functional component of all cartilages as indicated by the low cell densities. In particular major scaffold forming collagen types I (in fibrous cartilage) and II (in hyaline and elastic cartilages) as well as collagen type X (in the calcified layer of articular cartilages, the inner part of tracheal clips, and epiglottis cartilage) showed a specific distribution. In contrast, the "minor" collagen types III, V, and VI were found in all, collagen type IV in none of the cartilage subtypes. In this study, we present a biochemical profile of the major cartilage types of the human body which is important for understanding the physiology and the pathophysiology of cartilages.

Adult↗
PubMed2005

Time course evaluation of reparative cartilage with MR imaging after autologous chondrocyte implantation.

The aim of this study was to evaluate the qualitative change in reparative cartilage after autologous chondrocyte implantation (ACI). Ten knees of 10 patients were studied. The signal intensities of reparative and normal cartilage were evaluated by fat-suppressed three-dimensional spoiled-gradient recalled (FS 3D-SPGR) MR imaging. The signal intensity (SI) index (signal intensity of reparative cartilage divided by that of normal cartilage) was defined and the change in SI index was investigated. Histological and biochemical evaluation was done at the second look arthroscopy. The SI index was at its lowest level immediately after ACI and increased with time to 9 months thereafter. After 9-12 months, the SI index settled to almost level and was maintained at that value for at least 2-3 years postoperatively. The average of the SI indexes after 12 months to the last examination was 74.2 +/- 4.6 (range 64.2-82.8), which means signal intensity of reparative cartilage was maintained at a value lower than that of normal cartilage. The total ICRS score was 11.6 +/- 2.3 points (mean +/- SD). The GAG concentration was 107.9 +/- 17.0 microg/mg (mean +/- SD) in normal cartilage and 65.9 +/- 9.4 microg/mg in reparative cartilage. The quality of reparative cartilage as hyaline cartilage was inferior to that of normal cartilage. In the present study, the time course change in the SI index indicates that the major maturation process of implanted chondrocytes neared completion in 9-12 months. Minor changes, such as matrix remodeling with reorganization of the collagen fibers in reparative cartilage, may continue, but an almost identical condition seemed to be maintained during the first 2-3 years of follow-up. SI index does not always reflect all properties of reparative cartilage but may be a useful parameter for noninvasive evaluation.

Adolescent↗
PubMed1999

Kinetics of aggrecanase- and metalloproteinase-induced neoepitopes in various stages of cartilage destruction in murine arthritis.

OBJECTIVE: Two major cleavage sites, one mediated by metalloproteinases (MMPs) and the other by an as-yet unidentified enzyme termed aggrecanase, have been observed in aggrecan. To learn more about the relative contribution of these enzymes during cartilage degradation, this study assessed the occurrence of both specific neoepitopes in cartilage during murine arthritis and examined the correlation between neoepitope formation and different aspects of cartilage damage. METHODS: Reversible cartilage damage was induced in mice in the zymosan-induced arthritis (ZIA) model, partly irreversible cartilage damage in the antigen-induced arthritis (AIA) model, and irreversible, destructive cartilage damage in the collagen-induced arthritis (CIA) model. Immunolocalization techniques were used to detect the specific C-terminal neoepitopes VDIPEN (MMPS) and NITEGE (aggrecanase). RESULTS: In normal cartilage from young adult mice, no VDIPEN epitopes were detected, but a limited amount of NITEGE epitopes were already present. During the early phase of proteoglycan (PG) depletion, NITEGE expression was raised substantially in all arthritis models. VDIPEN epitopes were not detected in this early phase of cartilage destruction. When PG depletion progressed toward advanced cartilage damage, VDIPEN epitopes were induced. During ZIA, minimal induction of VDIPEN was observed, whereas in AIA, strong, but partly reversible, VDIPEN staining was evident, and in CIA, an extensive presence and persistence of the MMP-induced neoepitope was seen. When VDIPEN epitopes were intensely present, NITEGE epitopes were greatly reduced at that site in the cartilage. CONCLUSION: Presence of VDIPEN epitopes in cartilage correlated with severe cartilage damage, but these epitopes were not detected during early PG degradation. This suggests a limited role for VDIPEN-inducing MMPs in early PG degradation during murine arthritis. In contrast, aggrecanase epitopes were induced before the appearance of VDIPEN epitopes, but they disappeared with progression of cartilage damage.

Animals↗
PubMed2000

Modulation of collagenase 3 in human osteoarthritic cartilage by activation of extracellular transforming growth factor beta: role of furin convertase.

OBJECTIVE: Treatment of normal cartilage with transforming growth factor beta (TGFbeta) can increase the synthesis of collagenase 3 by chondrocytes and mimic the in situ distribution of this enzyme in osteoarthritic (OA) cartilage, which occurs predominantly in the deep zone. In this study, we examined the elements of the TGFbeta system that are potentially relevant to this effect. METHODS: TGFbeta1 and TGFbeta2 levels in cultured cartilage explants were determined by enzyme-linked immunosorbent assay (ELISA). OA cartilage explants were treated with small latent TGFbeta1 complex in the presence of various inhibitors, and collagenase 3 levels were determined by ELISA. The inhibitors were against serine proteases, plasmin, cathepsins, furin, and a neutralizing antibody against the mannose-6 phosphate/ insulin-like growth factor 2 receptor (M6P/IGF-2R). Small latent TGFbeta1, TGFbeta receptor types I, II, and III (TGFbetaRI, RII, and RIII), M6P/IGF-2R, and furin were immunolocalized in cartilage. RESULTS: Our data showed that latent TGFbeta1 is the major isoform that is synthesized; levels of 17.2 +/-1.7 pg/mg and 1.1 +/- 0.3 pg/mg tissue wet weight (mean +/- SEM) were found for total TGFbeta1 and TGFbeta2, respectively, in OA cartilage. A general serine protease inhibitor abrogated activation of both endogenous and exogenous small latent TGFbeta1. Plasmin and furin inhibitors and anti-M6P/IGF-2R reduced the levels of exogenous small latent TGFbeta1 complex-induced collagenase 3 by 33%, 95%, and 76%, respectively, but the cathepsin inhibitor had no effect. Immunolocalization of the small latent TGFbeta1 complex as well as of TGFbetaRI and RII revealed a statistically significant increase in the chondrocyte score in only the deep zone of OA cartilage. The M6P/IGF-2R level was significantly higher in OA cartilage in both the superficial and deep zones. Furin was found in normal cartilage exclusively in the superficial zone, whereas in OA cartilage, a level similar to that in normal cartilage was found in the superficial zone, but a significantly higher cell score (mean +/- SEM 23.6 +/- 4.7%) was registered in the deep zone. CONCLUSION: The mechanisms of TGFbeta activation/ activity with regard to collagenase 3 modulation in cartilage appear to be controlled by furin convertase with or without M6P/IGF-2R. These factors and the small latent TGFbeta complex are increased in the deep zone of OA cartilage, corresponding to the preferential site of collagenase 3 production.

Aged↗
PubMed2000

Modulation of fibroblast-mediated cartilage degradation by articular chondrocytes in rheumatoid arthritis.

OBJECTIVE: To determine the role of chondrocytes and factors released from chondrocytes in cartilage destruction by fibroblast-like synoviocytes (FLS) derived from patients with rheumatoid arthritis (RA). METHODS: RA FLS from 2 patients were implanted into SCID mice, together with fresh articular cartilage or with cartilage that had been stored for 24 hours at 4 degrees C or at 37 degrees C. The invasion of the same RA FLS into the fresh and stored cartilage was compared histologically using a semiquantitative scoring system. In addition, we investigated whether protein synthesis in chondrocytes affects the invasion of RA FLS in vitro. A 3-dimensional cartilage-like matrix formed by cultured chondrocytes was labeled with 35S. After formation of the cartilage-like matrix, protein synthesis was blocked with cycloheximide. The invasion of RA FLS from 6 patients into cycloheximide-treated and untreated matrix was assessed by measuring the released radioactivity in coculture with and without interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha). RESULTS: The SCID mouse experiments showed a significant invasion of RA FLS into the cartilage (overall mean score 3.2) but revealed significant differences when the invasion of the same RA FLS into fresh and stored cartilage was compared. RA FLS that were implanted with fresh articular cartilage showed a significantly higher invasiveness than those implanted with pieces of cartilage that had been stored for 24 hours (overall mean score 2.3). Storage at 37 degrees C and 4 degrees C resulted in the same reduction of invasion (35% and 37%, respectively). In the in vitro experiments, RA FLS rapidly destroyed the cartilage-like matrix. Blocking of chondrocyte protein biosynthesis significantly decreased the invasion of RA FLS, as shown by a decreased release of radioactivity. Addition of IL-1beta, but not TNFalpha, to the cocultures partially restored the invasiveness of RA FLS. CONCLUSION: These data underline the value of the SCID mouse in vivo model of rheumatoid cartilage destruction and demonstrate that chondrocytes contribute significantly to the degradation of cartilage by releasing factors that stimulate RA FLS. Among those, IL-1beta-mediated mechanisms might be of particular importance.

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