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PubMed1989

Interaction of polymorphonuclear leucocytes with patellar cartilage of immobilised arthritic joints: a scanning electron microscopic study.

Short term immobilisation (seven days) of an antigen induced arthritic knee joint of the mouse led to attachment of polymorphonuclear leucocytes to the cartilage surface and severe cartilage damage. The events at the patellar cartilage surface were studied by scanning electron microscopy and compared with the changes found in non-immobilised arthritic joints. At day 7 the immobilised arthritic joint showed an articular cartilage which was covered by a mat of fibrinous material and cell remnants. Moreover, inflammatory cells, clearly attached to the cartilage, showed large protrusions of their membranes. The cartilage surface, furthermore, showed numerous fissures of varying size and depth. These cartilage changes were much more pronounced in immobilised arthritic joints than in non-immobilised arthritic joints, and clear cell adhesion was exclusively found in the former. These findings show that immobilisation of inflamed mouse knee joints leads to increased damage and thus although clinical immobilisation is used to relieve pain, this may also risk damage to the articular cartilage.

Animals↗
PubMed1990

Articular cartilage defects of the knee: correlation between magnetic resonance imaging and gross pathology.

Magnetic resonance imaging (MRI) of the knee articular cartilage is possible owing to the contrast provided by different signal intensities of adjacent menisci and subchondral bone. The objective of this study was to determine the accuracy of MRI in quantitatively detecting thinning and focal defects of articular cartilage in vivo. High resolution MRI was performed followed by dissection of the knee within one hour of amputations above the knee of eight patients (62-89 years) with peripheral vascular disease. Articular cartilage was examined for erosions, surface irregularities, and appearance. Mean thicknesses of femoral and tibial articular cartilage sagittal sections from MRI were statistically indistinguishable from matched gross thicknesses. In those joints in which cartilage erosions, thinning, or irregularities were detected by MRI the same defects were apparent by gross examination. Cartilage that appeared normal by MRI had a normal gross appearance by gross examination. Thus high resolution MRI can accurately predict gross articular cartilage appearance and thickness, allowing an objective, quantitative, noninvasive assessment of eroded cartilage.

Aged↗
PubMed1992

Upregulation of insulin-like growth factor I gene expression in the lesions of osteoarthritic human articular cartilage.

Expression of insulin-like growth factor I (IGF-I)mRNA and IGF-I protein was studied in human osteoarthritic and young articular cartilage by in situ hybridisation and immunohistochemistry. In situ hybridisation showed that relatively low amounts of IGF-I mRNA signal were present in anatomically normal regions of osteoarthritic and young cartilage. In fibrillated osteoarthritic cartilage, however, the signal intensity was significantly higher than in non-fibrillated cartilage. Particularly high levels of IGF-I mRNA were present in the surface cell clones of more advanced lesions, the amount of signal being about four to five times greater than in anatomically normal cartilage. The amount of message varied with cartilage depth. In young cartilage there was less IGF-I mRNA in the superficial zone than in the middle and deep zones. In fibrillated regions of osteoarthritic joints the amount of message in surface cells was greater than in deeper regions. A specific human IGF-I antibody was used to show the presence intracellularly of IGF-I protein in osteoarthritic and young cartilage. Raised levels of IGF-I message in osteoarthritic chondrocytes may represent an attempt at increased matrix repair, operating by an autocrine/paracrine mechanism.

Adolescent↗
PubMed1992

Effects of tiaprofenic acid (Surgam) on cartilage proteoglycans in the rabbit joint immobilisation model.

A well established model of arthritis induced in rabbit knee joints by immobilisation in full extension for 30 days was used to evaluate the in vivo effects of 2.5, 5.0, and 10.0 mg/kg body weight of tiaprofenic acid on articular cartilage proteoglycans. The drug was given subcutaneously every 24 hours during the entire immobilisation period. Immobilised animals not treated with drugs and normal animals were used as controls. In the non-drug treated immobilised animals articular cartilage showed evidence of surface damage accompanied by synovial hypertrophy and effusion. Proteoglycan concentrations were reduced in cartilages of these joints and the incorporation of 35SO2-4 into macromolecular proteoglycans was higher than in cartilages of non-immobilised controls. Gel filtration chromatographic studies of both resident and 35S labelled proteoglycans isolated from immobilised joint cartilage showed reduced aggregation and the presence of degraded proteoglycan subunit species. Whereas the administration of 10.0 mg/kg tiaprofenic acid every 24 hours to immobilised animals exacerbated the degradation and loss of proteoglycans from joint cartilages, 5.0 mg/kg tiaprofenic acid provided some protection of these macromolecules, as shown by the concentrations and extractability of proteoglycans from cartilages, which were comparable with those from non-immobilised controls. A high incorporation of 35S into proteoglycans was demonstrated, together with reduced catabolism of proteoglycans, indicating preservation of chondrocyte anabolic activity. At a tiaprofenic acid dose of 2.5 mg/kg, however, no beneficial effects on cartilage proteoglycans could be shown.

Animals↗
PubMed1995

Cathepsin B in osteoarthritis: zonal variation of enzyme activity in human femoral head cartilage.

OBJECTIVES: To determine the quantitative topographical distribution of cathepsin B in human femoral head cartilage by measuring the zonal variation of enzyme activity in specimens taken from various anatomical regions of normal and osteoarthritic (OA) tissues, and to correlate this parameter with the severity of the OA lesions. METHODS: OA articular cartilage was obtained at surgery for total hip replacement and control cartilage obtained at postmortem. Cylinders of full thickness cartilage with underlying bone were retrieved with a biopsy trephine. Sections of cartilage were produced by cryocutting the tissue as slices parallel to the articular surface and assayed for cathepsin B with a specific, highly sensitive fluorogenic substrate. The severity of the OA lesions was graded according to the histopathological-histochemical method of Mankin. RESULTS: Zonal cathepsin B activity of normal cartilage was uniform and low in all regions of the femoral head. In apparently intact OA cartilage and in severely degraded tissue the zonal distribution and the amounts of enzyme were similar to control values. At sites with active disease, cathepsin B activity was much greater than in controls and its irregular zonal distribution correlated with tissue degeneration, hypercellularity, or cloning of chondrocytes as determined histochemically. Particularly high enzyme levels were observed at sites with regenerating cartilage, where some zonal peaks attained 20-fold activity with respect to controls. CONCLUSION: Cathepsin B may play a role in sustaining the chronicity of OA, not as an initiator, but rather as a perpetuator of the disease and as an antagonist of regeneration.

Adult↗
PubMed1995

Magnesium whitlockite deposition in articular cartilage: a study of 80 specimens from 70 patients.

OBJECTIVE: To examine articular cartilage from a number of joint sites, using a large sample group, for the presence of magnesium whitlockite crystal deposition. METHODS: Articular cartilage specimens were taken from a total of 70 patients. The majority of specimens were taken from femoral heads, with smaller numbers from femoral condyle, tibial plateau, radius, ulna, and several small peripheral joints. Normal and osteoarthritic articular cartilage specimens were obtained from patients undergoing prosthesis replacement or amputation. Specimens were resin embedded and examined using transmission electron microscopy and x ray microanalysis. RESULTS: Magnesium whitlockite crystals were identified, on the basis of morphology, size and elemental composition, in articular cartilage from all sites sampled. The distribution of crystals was similar in all samples (restricted to the superficial zone), although the density of deposition was extremely variable, with the greatest density observed in femoral head specimens. No magnesium whitlockite crystals were observed in osteophytic or epiphysial cartilage. CONCLUSIONS: This study demonstrated the widespread extent of magnesium whitlockite deposition in human articular cartilage, albeit at much lower density than previously reported in femoral head articular cartilage. In consideration of possible roles for these crystals in articular cartilage, it is concluded that an opportunistic mode of formation, possibly influenced by mechanical stresses, would be most plausible.

Adolescent↗
PubMed1995

Chondrocyte IGF-1 receptor expression and responsiveness to IGF-1 stimulation in mouse articular cartilage during various phases of experimentally induced arthritis.

OBJECTIVE: To examine the distribution of insulin like growth factor-1 (IGF-1) receptors and the biological response to IGF-1 stimulation in articular cartilage of normal mouse knee joints and arthritic joints taken at various stages of experimentally induced arthritis. METHODS: In situ IGF-1 receptor expression and responsiveness to IGF-1 stimulation were examined in murine articular cartilage at different phases in two models of experimentally induced arthritis. IGF-1 receptor expression was visualised in joint sections with the use of anti-IGF-1 receptor antibodies and quantified by confocal laser scanning microscopy. Chondrocyte proteoglycan (PG) synthesis was measured by incorporation of 35S-sulphate. RESULTS: In control cartilage, the majority of IGF-1 receptors were found on chondrocytes localised in the middle and deeper zones of the cartilage, whereas receptor expression in surface zone chondrocytes was very low. During culture of normal articular cartilage, IGF-1 was able to maintain chondrocyte PG synthesis at the in vivo level. Concurrently with the development of arthritis, cartilage lost its capacity to react to IGF-1, but IGF-1 stimulation recovered when the inflammatory response waned. Shortly after induction of arthritis, IGF-1 receptor expression initially declined, but it had returned to normal levels by day 1 and remained increased thereafter. CONCLUSION: The distribution of IGF-1 receptor expression in the different zones of normal articular cartilage reflects IGF-1 stimulation and metabolic activity of chondrocytes in these layers. This correlation is disturbed in arthritic cartilage, suggesting inadequate or overruled signalling.

Animals↗
PubMed1998

Expression of alpha and beta subunits of the integrin superfamily in articular cartilage from macroscopically normal and osteoarthritic human femoral heads.

OBJECTIVE: The objective of this study was to detail the topographical and zonal distribution of alpha and beta subunits of the integrin superfamily in normal and osteoarthritic cartilage. METHODS: Immunohistochemistry utilising antibodies towards alpha and beta subunits was performed on cryostat sections of human articular cartilage from macroscopically normal (n = 6) and osteoarthritic (n = 6) femoral heads. Samples of articular cartilage were obtained from 12 topographically distinct sites from each femoral head. Each section was divided into zones (superficial, middle, deep) and staining scores were recorded. RESULTS: Normal cartilage stained for integrin subunits alpha 1, alpha 5, alpha V, beta 1, beta 4, and beta 5, but not for alpha 2, alpha 3, alpha 4, alpha 6, beta 2, beta 3, and beta 6. Intact and non-intact residual cartilage from osteoarthritic femoral heads stained for alpha 1, alpha 2, alpha 5, alpha V, beta 1, beta 4, and beta 5. Staining was occasionally seen for alpha 4 and beta 2, but not for alpha 3, alpha 6, beta 3, and beta 6. There was no topographical variation in the staining for any of the subunits in either normal or osteoarthritic cartilage. The only subunit that displayed a zonal variation was alpha V; staining for this subunit was most pronounced in the superficial zone compared with the middle and deep zones. CONCLUSION: Chondrocytes in normal and osteoarthritic cartilage express the integrin subunits alpha 1, alpha 5, alpha V, beta 1, beta 4, and beta 5. Chondrocytes in osteoarthritic cartilage, in addition, express the alpha 2, alpha 4, and beta 2 subunits. The alpha v subunit is expressed by more chondrocytes in the superficial zone in comparison with cells in the deeper zones. None of the subunits display topographical variation in expression.

Aged↗
PubMed1999

Destruction of articular cartilage by alpha 2 macroglobulin elastase complexes: role in rheumatoid arthritis.

OBJECTIVE: Neutrophil elastase accounts for the ability of some fresh rheumatoid synovial fluids to degrade cartilage matrix in vitro. The aim of this study was to determine if enzyme activity could result from depletion of synovial fluid inhibitors or protection of the enzyme from inhibition. METHODS: The ability of synovial fluids to inhibit porcine pancreatic elastase was investigated together with chemical pretreatments capable of inactivating alpha 1 protease inhibitor (alpha 1PI) or preventing formation of alpha 2 macroglobulin (alpha 2M) elastase complexes. Subsequently, complexes of human neutrophil elastase with alpha 2M were prepared and applied to frozen sections of cartilage. Proteoglycan loss was quantified by alcian blue staining and scanning and integrating microdensitometry. Parallel studies were carried out using a low molecular weight chromogenic elastase substrate. The effects of alpha 1PI and SF on these systems were investigated. Finally, synovial fluids were subjected to gel filtration and the fractions assayed for elastase activity. High molecular weight fractions were pooled, concentrated, and tested for their ability to degrade cartilage sections. RESULTS: All synovial fluids reduced the activity of porcine pancreatic elastase, the inhibition mainly being attributable to alpha 1PI, whereas remaining activity resulted from complexes of elastase with alpha 2M. Complexes of human neutrophil elastase with alpha 2M were shown to cause proteoglycan degradation in frozen sections of human articular cartilage. Alpha 1PI prevented alpha 2M elastase complexes from degrading cartilage but not the chromogenic substrate. The data suggested that alpha 1PI does not inhibit elastase bound to alpha 2M but sterically hinders the complex. However, only one of five synovial fluids was able to completely block the actions of alpha 2M elastase complexes against cartilage. Gel filtration of rheumatoid synovial fluids showed elastase and cartilage degrading activity to be associated with fractions that contained alpha 2M, and not with fractions expected to contain free enzyme. CONCLUSIONS: The data suggest that synovial fluid alpha 2M elastase complexes can degrade cartilage matrix in rheumatoid arthritis.

Adult↗
PubMed1997

"Aggrecanase" activity is implicated in tumour necrosis factor alpha mediated cartilage aggrecan breakdown but is not detected by an in vitro assay.

AIMS: To develop an in vitro assay for the putative glutamyl endopeptidase, "aggrecanase", which is thought to degrade cartilage aggrecan, and to examine the role of the enzyme in tumour necrosis factor stimulated aggrecan cleavage. METHODS: Aggrecan fragments released by bovine nasal cartilage explants, with and without exposure to tumour necrosis factor alpha, were purified and analysed by western blotting and N-terminal sequencing. Intact bovine aggrecan was incubated with extracts of cartilage, lysed chondrocytes, or cartilage explant conditioned culture medium under a variety of conditions. Deglycosylated aggrecan was incubated with nasal cartilage explants. Proteoglycan breakdown was assessed by metachromatic assay of fragments in culture media, and cleavage of the substrate at the aggrecanase cleavage site was detected and measured using the antibody BC3, which recognises a neoepitope produced by aggrecanase cleavage of aggrecan. RESULTS: Aggrecan fragments generated from explants treated with tumour necrosis factor had N-terminal sequences consistent with cleavage of aggrecan at a restricted number of glutamyl bonds. Aggrecanase generated fragments were found in cartilage explant culture medium and chondrocyte monolayers. However, no aggrecanase activity could be detected in extracts of cartilage, or chondrocytes from which endogenous aggrecan fragments had been removed, under a variety of assay conditions. Deglycosylated aggrecan, added to explant cultures, efficiently inhibited endogenous aggrecan breakdown. CONCLUSIONS: Aggrecanase is active in cartilage and in chondrocyte monolayers, and its action is stimulated by tumour necrosis factor alpha. However, activity due to this enzyme could not be detected in vitro under our assay conditions, although a deglycosylated version of the substrate inhibited aggrecan breakdown in explant cultures.

Aggrecans↗
PubMed2004

Patellar articular cartilage lesions: in vitro MR imaging evaluation after placement in gadopentetate dimeglumine solution.

PURPOSE: To evaluate T1-weighted magnetic resonance (MR) imaging after diffusion of gadopentetate dimeglumine for visualization of articular cartilage lesions. MATERIALS AND METHODS: MR imaging was performed in eight human cadaveric patella specimens immediately and 4 hours after placement into a vessel filled with gadopentetate dimeglumine solution (2.5 mmol/L). T1-weighted spin-echo and inversion-recovery turbo spin-echo MR sequences with nulled cartilage signal (inversion time of 300 msec) were used. In a total of 128 articular cartilage areas, MR imaging findings were compared with macroscopic and histopathologic findings. Pathologic evaluation was performed by one musculoskeletal pathologist. With knowledge of pathologic observations, MR images were analyzed by one musculoskeletal radiologist with regard to intrinsic signal intensity characteristics and surface abnormalities of articular cartilage. RESULTS: Histopathologic findings demonstrated 67 areas of normal articular cartilage and 66 cartilage lesions (grade 1, n = 19; grade 2, n = 15; grade 3, n = 26; grade 4, n = 6). All grade 3 and 4 lesions could be identified on MR images obtained immediately after submersion and after 4 hours. Ninety-four percent of grade 1 and 2 lesions were identified as areas of predominantly decreased contrast enhancement on delayed MR images obtained with both sequences. MR images obtained immediately after submersion demonstrated abnormal signal intensity in only 9% and 12% of grade 1 and 2 lesions, respectively. CONCLUSION: T1-weighted MR images obtained in vitro after gadopentetate dimeglumine diffusion allow demonstration of articular cartilage surface lesions and early stages of cartilage degradation.

Aged↗
PubMed1996

Laryngeal carcinoma after radiation therapy: correlation of abnormal MR imaging signal patterns in laryngeal cartilage with the risk of recurrence.

PURPOSE: To correlate abnormal magnetic resonance (MR) imaging signal patterns in cartilage with the effectiveness of radiation treatment. MATERIALS AND METHODS: Eighty previously untreated patients underwent MR imaging and radiation therapy with a curative intent. Cartilage was considered to have an abnormal signal pattern if it had intermediate signal intensity on T1-weighted spin-echo (SE) MR images and high signal intensity on T2-weighted SE MR images. The minimum follow-up was 2 years. RESULTS: Abnormal MR imaging signal patterns of the thyroid cartilage (P < .001; P < .04) were more ominous than those of other cartilage. Abnormal signal patterns in cartilage of patients with small tumors (< 5 cm3 and especially < 1 cm3) were less significant. Abnormal signal patterns in cartilage combined with a large tumor (> 5 cm3) worsened the prognosis significantly (P < .05). CONCLUSION: Abnormal MR imaging signal patterns in cartilage may not indicate a poor prognosis in every case. Abnormal signal intensity in the thyroid cartilage combined with a tumor volume of > 5 cm3, however, appears to indicate an adverse prognosis with regard to tumor recurrence.

Adult↗
PubMed2003

Structure-function relationships in enzymatically modified articular cartilage.

The present study is aimed at revealing structure-function relationships of bovine patellar articular cartilage. Collagenase, chondroitinase ABC and elastase were used for controlled and selective enzymatic modifications of cartilage structure, composition and functional properties. The effects of the enzymatic degradations were quantitatively evaluated using quantitative polarized light microscopy, digital densitometry of safranin O-stained sections as well as with biochemical and biomechanical techniques. The parameters related to tissue composition and structure were correlated with the indentation stiffness of cartilage. In general, tissue alterations after enzymatic digestions were restricted to the superficial cartilage. All enzymatic degradations induced superficial proteoglycan (PG) depletion. Collagenase also induced detectable superficial collagen damage, though without causing cartilage fibrillation or tissue swelling. Quantitative microscopic techniques were more sensitive than biochemical methods in detecting these changes. The Young's modulus of cartilage decreased after enzymatic treatments indicating significant softening of the tissue. The PG concentration of the superficial zone proved to be the major determinant of the Young's modulus (r(2) = 0.767, n = 72, p < 0.001). Results of the present study indicate that specific enzymatic degradations of the tissue PGs and collagen can provide reproducible experimental models to clarify the structure-function relationships of cartilage. Effects of these models mimic the changes observed in early osteoarthrosis. Biomechanical testing and quantitative microscopic techniques proved to be powerful tools for detecting the superficial structural and compositional changes while the biochemical measurements on the whole uncalcified cartilage were less sensitive.

Animals↗
PubMed2005

A morphometric study of age-related changes in adult human epiglottis using quantitative digital analysis of cartilage calcification.

The epiglottis plays an important role in deglutition in humans. The present study investigated age-related changes in the epiglottis using macroscopic and microscopic measurements. Epiglottic specimens from 281 Japanese adult cadavers (177 males, 104 females) were obtained. Specimens were divided into three groups according to age: group I: 20-39 years old (32 males, 26 females), group II: 50-69 years old (82 males, 36 females), and group III: 80-98 years old (63 males, 42 females). Width, height, and thickness were measured macroscopically. To evaluate the degree of calcium deposition, the calcium volume in digitalized von Kossa-stained sections was assessed using a quantitative analysis. An elemental analysis of the area detected with von Kossa staining was done using energy-dispersive X-ray fluorescence spectrometer (EDX). Measurements of the thickness and cell density in the superficial and deep layers of epiglottic cartilage were performed in horizontal histological sections. No significant differences in macroscopic width or height were found across the age groups in either sex. A series of three measurements in males was significantly larger than in females (p<0.05). The volume of the calcium deposit area was greater in males than in females (p<0.05) and was significantly increased in group III in males (p<0.05). The lower level of the epiglottic cartilage showed a greater calcium deposit area than the upper level. In the scanning image by line and surface analysis using EDX, the calcium deposit areas detected with von Kossa staining indicated a close association of calcium and phosphorus ions. The mean Ca/P molar ratio in the calcium deposit area was 1.32+/-0.12. Microscopic cartilage thickness increased significantly with age (p<0.05), and was greater in males than in females (p<0.05). Cartilage cell density in the superficial cartilage layer was higher than in the deep layer and was decreased in group III (p<0.05). Cartilage cell density was lower in males compared to females. Diameter of chondrocytes significantly increased in group III (p<0.05) and was larger in males than in females in group III (p<0.05). Epiglottic cartilage exhibited marked sex-related differences and progression of calcification with age. Calcification of epiglottic cartilage in elderly individuals may affect movement patterns in deglutition.

Adult↗
PubMed1977

The influence of the degree of maturation of donor tissue on the reconstruction of elastic cartilage by isolated chondrocytes.

Chondrocytes isolated from auricular cartilage of 1-, 14-, 28- and 56-day-old rabbits were injected intrasmuscularly as auto- or allogeneic transplants, and the development of the reconstructed cartilage was compared to that of intact tissue. Chondrocytes in cartilage of 1- and 14-day-old rabbits (younger group) were relatively uniform in size. During further development in situ (28 and 56 days) central cells increased considerably and many of them became binucleated. Cartilage reconstructed by chondrocytes from the younger group of animals displayed regular arrangement of cells, i.e. smaller cells at the periphery and larger in the centre. Transplantation of chondrocytes from 28 or 56-day-old rabbits (older group) led to the reconstruction of cartilage with irregular distribution of cells, i.e. some large cells were located at its periphery, while in the centre smaller and larger cells were intermingled in a haphazard manner. Elastic fibres were scanty and thin in cartilage of 1-day-old animals, but their number and size increased with time and they displayed a characteristic pattern. Formation and maturation of these fibres proceeded in cartilage reconstructed by chondrocytes from the younger gorup of animals similarly as in the intact tissue. Chondrocytes from the older group of rabbits reconstructed cartilage in which the number of elastic fibres was reduced and their arrangement appeared irregular.

Age Factors↗
PubMed1992

A comparison of the immunohistochemical localization of type I and type II collagens in craniofacial cartilages of the rat.

The immunohistochemical localization of types I and II collagen was examined in the following 4 cartilaginous tissues of the rat craniofacial region: the nasal septal cartilage and the spheno-occipital synchondrosis (primary cartilages), and the mandibular condylar cartilage and the cartilage at the intermaxillary suture (secondary cartilages). In both primary cartilages, type II collagen was present in the extracellular matrix (ECM) of the whole cartilaginous area, but type I collagen was completely absent from the ECM. In the secondary cartilages, type I collagen was present throughout the cartilaginous cell layers, and type II collagen was restricted to the ECM of the mature and hypertrophic cell layers. These observations indicate differences in the ECM components between primary and secondary craniofacial cartilages, and that these differences may contribute to their modes of chondrogenesis.

Animals↗
PubMed1970

Evidence for a role of proteinpolysaccharides in regulation of mineral phase separation in calcifying cartilage.

Our previous studies have indicated the presence of a macromolecular inhibitor of in vitro mineral growth, as well as a mineral nucleational agent in extracellular matrix fluid aspirated by micropuncture methods from epiphyseal hypertrophic cell cartilage. In this report, new miniaturized methods were used to extract proteinpolysaccharide complexes (PPC) from cartilage, to isolate a light fraction (PPL-C), and further, to separate it into R1, R2, and SR2 subfractions. These methods were applied to PPL-C complexes separated from microdissected epiphyseal cartilages and to cetylpyridinium chloride (CPC) precipitates of extracellular matrix fluid aspirated from similar cartilages. Most of all of the inhibitory action on an in vitro system of mineral growth shown by whole cartilage PPL-C and by cartilage fluid PPC obtained from noncalcifying sites was contained in the R2 fraction which represented (1/4)-[unk] of the total hexuronate. The R2 fraction was diminished or absent from calcified cartilage fluids and from whole calcified epiphyseal septa. The ratio R1 + R2: SR2 ranged from 0.37 to 0.71 in the fluids and whole tissue samples of noncalcified cartilages. The R2 fraction was distinguished from SR2 by a 2- to 3-fold higher protein: hexuronate ratio. These data are interpreted to indicate that the inhibitory R2 fraction was degraded or otherwise inactivated at the zone of provisional calcification and that this inhibitor participates in the physiological mechanism that regulates endochondral calcification.

Animals↗
PubMed1988

Kniest dysplasia is characterized by an apparent abnormal processing of the C-propeptide of type II cartilage collagen resulting in imperfect fibril assembly.

Epiphyseal and growth plate cartilages from four cases of Kniest dysplasia have been studied. In each case collagen fibril organization appeared abnormal by electron microscopy compared with age-matched normal cartilages: fibrils were much thinner, of irregular shape and did not exhibit the characteristic banding pattern. This was associated with the absence (compared with normal cartilage) of the C-propeptide of type II collagen (chondrocalcin) from the extracellular matrix of epiphyseal cartilages, although it was detected (as in normal cartilages) in the lower hypertrophic zone of the growth plate in association with calcifying cartilage. The C-propeptide was abnormally concentrated in intracellular vacuolar sites in Kniest cartilages and its total content was reduced in all cases but not in all cartilages. Moreover, it was not a part of the procollagen molecule. In contrast, type II collagen alpha-chain size was normal, indicating the formation of a triple helix. Also type II collagen content was normal and it was present in extracellular sites and only occasionally detected intracellularly. These observations suggest that the defect in Kniest dysplasia may result from the secretion of type II procollagen lacking the C-propeptide and abnormal fibril formation, and that the C-propeptide is normally required for fibril formation.

Calcium-Binding Proteins↗