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PubMedDate not supplied

A compositional analysis of human nasal septal cartilage.

BACKGROUND: Nasal septal cartilage is well established as an autograft material. Tissue engineering methods are now being developed to synthesize cartilage constructs with the properties of this type of cartilage. However, important baseline data on the composition of native septal cartilage is sparse. OBJECTIVES: To characterize quantitatively the major biochemical constituents of native adult human septal cartilage and determine age- or sex-related variation in composition. METHODS: Cartilage was harvested from the inferior region of the nasal septum in 33 patients (mean +/- SD age, 47.0 +/- 13.5 years; range, 24-80 years) during routine septoplasty or septorhinoplasty. Biochemical assays were used to determine the quantities, relative to wet weight, of the major constituents of cartilage: water, collagen (from hydroxyproline), sulfated glycosaminoglycan (sGAG), and chondrocytes (from DNA). RESULTS: On average, each gram of wet cartilage contained 77.7% water, 7.7% collagen, 2.9% sGAG, and 24.9 million cells. Hydration and collagen content showed no significant age variation. Advancing age was associated with a reduction in sGAG content (7.7% per decade, P =.02) and cellularity (7.4% per decade, P =.05). No significant sex differences were found in any of these cartilage constituents. CONCLUSIONS: This study represents the first biochemical characterization of the composition of native human septal cartilage. The data serve as a baseline for future comparison of the properties of tissue-engineered neocartilage constructs. Furthermore, the age-associated variations in cartilage composition have implications for patient selection for reconstructive procedures.

Adult↗
PubMed2000

[Degree of differentiation of chondrocytes and their pretreatment with platelet-derived-growth factor. Regulating induction of cartilage formation in resorbable tissue carriers in vivo].

Current methods for articular cartilage repair are unpredictable with respect to clinical success. In the present study, we investigated the ability of cells from articular cartilage, perichondrium, and costochondral resting zone to form new cartilage when loaded onto biodegradable scaffolds and implanted into calf muscle pouches of nu/nu mice. Prior in vitro studies showed that platelet derived growth factor-BB (PDGF-BB), but not transforming growth factor beta-1 (TGF-beta 1), basic fibroblast growth factor, or bone morphogenetic protein-2 promoted proliferation and extracellular matrix sulfation of resting zone chondrocytes without causing the cells to exhibit a hypertrophic chondrocyte phenotype. TGF-beta 1 has also been shown to stimulate chondrogenesis by multipotent chondroprogenitor cells like those in the perichondrium. In addition, PDGF-BB has been shown to modulate chondrogensis by resting zone cells implanted in poly(D,L-lactide-co-glycolide) (PLG) scaffolds. In the present study we examined whether the cartilage formation is dependent on state of chondrocyte maturation and whether the pretreatment of chondrocytes with growth factors has an influence on the cartilage formation. Scaffolds were manufactured from 80% PLG with a 75:25 lactide:glycolide ratio and 20% modified PLG with a 50:50 lactide:glycolide ratio (PLG-H scaffolds). For each experimental group, four nude mice received two identical implants, one in each calf muscle resulting in an N = 8 implants: PLG-H scaffolds alone; PLG-H scaffolds with cells derived from either the femoral articular cartilage, costochondral periochondrium, or costochondral resting zone cartilage of 125 g male Sprague-Dawley rats; PLG-H scaffolds with either articular chondrocytes or resting zone chondrocytes that were pretreated with 37.5 ng/ml rhPDGF-BB for 4 h or 24 h before implantation, or with perichondrial cells treated with PDGF-BB plus 0.22 ng/ml rhTGF beta-1 for 4 h and 24 h. At 4 or 8 weeks after implantation, samples were harvested and analyzed histomorphometrically for new cartilage formed, area of residual implant and area of fibrous connective tissue. Only resting zone cells showed the ability to form new cartilage at a heterotopic site in this study. There was no neocartilage found in nude mice with implants loaded with either articular chondrocytes or perichondrial cells. Pretreatment of resting zone chondrocytes for 4 h prior to implantation significantly increased the amount of newly formed cartilage after 8 weeks and suppressed chondrocyte hypertrophy. The amount of fibrous connective tissue around implants containing either articular chondrocytes or perichondrial cells decreased with time, whereas the amount of fibrous connective tissue around implants containing resting zone chondrocytes pretreated with PDGF-BB was increased. The results showed that resting zone cells can be successfully incorporated into biodegradable porous PLG scaffolds and can induce new cartilage formation in a nonweight-bearing site. Articular chondrocytes as well as perichondrial cells did not have the capacity for neochondrogenesis when implanted heterotopically in this model.

Animals↗
PubMed1998

Mechanical properties of the normal human tibial cartilage-bone complex in relation to age.

OBJECTIVE: This study investigates the age-related variations in the mechanical properties of the normal human tibial cartilage-bone complex and the relationships between cartilage and bone. DESIGN: A novel technique was applied to assess the mechanical properties of the cartilage and bone by means of testing the cartilage-bone complex. BACKGROUND: Up to now, mechanical testing of cartilage and bone has been reported separately, and little is known about the mechanical behaviour of both tissues when examined as a unit. METHODS: Cylindrical human proximal tibial cartilage-bone complex specimens from 31 normal donors aged 16-83 years were tested in compression. The deformation was measured simultaneously in bone and cartilage to obtain the mechanical properties of both tissues. RESULTS: The stiffnesses and elastic energies of both cartilage and bone showed an initial increase, with maxima at 40 years, followed by a steady decline. The viscoelastic energy was maximal at younger ages (16-29 years), followed by a steady decline. The energy absorption capacity did not vary with age. Stiffnesses and elastic energies were correlated significantly between cartilage and bone. CONCLUSIONS: The present study demonstrates that similar age-related trends were seen in cartilage and bone, as if they behaved as a single mechanical unit. RELEVANCE: The basic information presented here on the mechanical properties of cartilage and bone and the correlations between them reveals the unit function of both tissues that are of importance for the understanding of the etiology and pathogenesis of degenerative joint diseases, such as arthrosis.

Journal Article↗
PubMed1998

Osteoarthritic cartilage fibrillation is associated with a decrease in chondrocyte adhesion to fibronectin.

OBJECTIVE: Cartilage destruction in osteoarthritis (OA) is generally accepted as a failed repair process. Cell adhesion is implicated in tissue repair. Therefore, adhesion of OA chondrocytes to extracellular matrix proteins was investigated. DESIGN: Using chondrocytes from human OA femoral head cartilage, adhesion to fibronectin and type II collagen of cells from distinct areas showing an intact cartilage surface or a fibrillated cartilage surface was studied. Modulation of chondrocyte adhesion by both protein kinase C (PKC) inhibitors and glucosamine sulfate (GS) was also investigated. RESULTS: A significant (P < 0.05) decrease in adhesion to fibronectin of chondrocytes from fibrillated cartilage, relative to those from grossly normal OA cartilage, was demonstrated. Adhesion to type II collagen was not modified by the chondrocyte origins (either from normal or fibrillated OA cartilage). Adhesion to fibronectin of cells from grossly intact cartilage was decreased by the addition of PKC and calmodulin-dependent kinase inhibitors, W7 and sphingosine, to the cell culture. Adhesion to fibronectin of chondrocytes from fibrillated cartilage was significantly (P < 0.05) increased after glucosamine sulfate treatment. CONCLUSION: Fibrillation of cartilage from OA femoral head is associated with a defective adhesion of chondrocytes to fibronectin. The process is suggested to be dependent of PKC and/or calmodulin-dependent kinases and potentially reversible. Conceivably, it could play a role in OA cartilage destruction.

Aged↗
PubMed1989

Effect of thyroid hormone and growth hormone on recovery from hypothyroidism of epiphyseal growth plate cartilage and its adjacent bone.

Hypothyroidism was induced in young female Sprague-Dawley rats by the addition of methimazole (0.67 mg/ml) to drinking water for a period of 7 weeks (7-14 weeks of age). The responses of the articular cartilage, epiphyseal growth plate cartilage, epiphyseal trabecular bone, and metaphyseal trabecular bone in the proximal tibia were assessed by structural parameters. In addition, replacement therapies were introduced for the last 2 weeks of the experimental period. These included 0.7 U/kg BW human GH (hGH), 15 micrograms/kg BW L-T4 (T4), and a combination of hGH and T4 at the same doses. In the hypothyroid rats, the width of epiphyseal growth plate cartilage decreased by 27%, that of articular cartilage by 35%, epiphyseal trabecular bone volume by 30%, and metaphyseal trabecular bone volume by 66% relative to those in age-matched control tissues. T4 treatment led to a full restoration of the epiphyseal trabecular bone and surpassed by 40% the control value. The magnitude of the articular cartilage and the epiphyseal trabecular bone volume returned to control values, while that of metaphyseal trabecular bone was 68% of control values. Treatment with hGH did not improve the epiphyseal growth plate cartilage or articular cartilage. It did restore epiphyseal trabecular bone to almost normal values, but metaphyseal trabecular bone improved to only a small though significant level (45% of control value). The combination of T4 and hGH resulted in an additional enlargement in the width of the epiphyseal growth plate cartilage and an increase in metaphyseal trabecular bone volume compared to those in the T4 group. Qualitative examinations indicated that it was only in the T4 and T4 plus hGH groups that the lowest chondrocytes in the epiphyseal growth plate cartilage resumed their normal hypertrophied size. These results suggest that the change in the hypothyroid state do not rely solely on the lack of pituitary GH synthesis and secretion, as replacement by exogenous GH did not restore normal epiphyseal growth plate cartilage morphology or its remodeling into metaphyseal trabecular bone. Treatment with T4 (which restored endogenous pituitary GH to 30% of control levels) results in full recovery of the epiphyseal growth plate cartilage morphology along with its associated metaphyseal trabecular bone. In addition, it can also be concluded that the decrease in epiphyseal trabecular bone volume observed in the hypothyroid animals was due solely to the GH-deficient state that accompanied hypothyroidism.

Animals↗
PubMed2001

The occurrence of autoantibodies to matrilin 1 reflects a tissue-specific response to cartilage of the respiratory tract in patients with relapsing polychondritis.

OBJECTIVE: Relapsing polychondritis (RP) is an inflammatory disease that mainly affects cartilage tissue in the auricle, nose, and lower respiratory tract. When tracheolaryngeal cartilage is involved, the disease is occasionally fatal. Matrilin 1 is a cartilage-specific protein most prominently expressed in tracheal cartilage, but not in joint cartilage. Immunization with the protein in rats and mice induces respiratory distress and nasal destruction, as seen in RP. We investigated the response to matrilin 1 and other cartilage proteins in sera from patients with RP, 4 additional groups of patients with other major connective tissue diseases, and healthy control subjects. METHODS: Sera were analyzed by enzyme-linked immunosorbent assay (ELISA) for antibody responses to matrilin 1, types II, IX, and XI collagen, and cartilage oligomeric matrix protein (COMP). Titers above the mean + 3SD of controls were considered positive. Specificity of matrilin 1 recognition was further investigated by the capacity of high-titer sera to block the binding of a matrilin 1-specific monoclonal antibody in inhibition ELISAs. In vivo reactivity and specificity were tested by injecting sera into neonatal mice, and antibody binding was detected by immunohistochemical staining. RESULTS: Serum antibodies from RP patients bound tracheolaryngeal and nasal cartilage in vivo and inhibited the binding of anti-matrilin 1-specific monoclonal antibodies. Thirteen of the 97 RP patients had increased titers of matrilin 1 antibody. Positive titers correlated with respiratory symptoms in 69% of the cases. Significant responses to type II collagen and COMP were also detected. CONCLUSION: Antibodies to matrilin 1 bind tracheolaryngeal cartilage in vivo and are correlated with an inflammatory attack on tracheolaryngeal cartilage that is often seen in RP.

Adult↗
PubMed2005

Induction of cartilage damage by overexpression of T cell interleukin-17A in experimental arthritis in mice deficient in interleukin-1.

OBJECTIVE: To examine the capacity of T cell interleukin-17A (IL-17A; referred to hereinafter as IL-17) to induce cartilage damage during experimental arthritis in the absence of IL-1. METHODS: Local IL-17 gene transfer was performed in the knee joint of IL-1-deficient mice and wild-type controls during streptococcal cell wall (SCW)-induced arthritis. Knee joints were isolated at various time points for histologic analysis of cartilage proteoglycan (PG) depletion. Expression of messenger RNA for inducible nitric oxide synthase, matrix metalloproteinases (MMPs) 3, 9, and 13, and ADAMTS-4 was determined by quantitative polymerase chain reaction analysis. VDIPEN staining was analyzed to study MMP-mediated cartilage damage. In addition, systemic anti-IL-1alpha/beta antibody treatment was performed in mice immunized with type II collagen and injected locally with an adenoviral vector expressing IL-17 or with control adenovirus. Knee joints were isolated and analyzed for cartilage PG depletion, chondrocyte death, and cartilage surface erosion. RESULTS: During SCW-induced arthritis, local T cell IL-17 gene transfer turned this acute, macrophage-driven joint inflammation into a severe, chronic arthritis accompanied by aggravated cartilage damage. Of high interest, the IL-1 dependency of cartilage PG depletion was fully abrogated when IL-17 was locally overexpressed in the joint. Moreover, local IL-17 gene transfer increased MMP expression without the need for IL-1, although IL-1 remained essential for part of the cartilage VDIPEN expression. Furthermore, when IL-17 was overexpressed in the knee joints of mice with collagen-induced arthritis, anti-IL-1 treatment did not reduce the degree of chondrocyte death or cartilage surface erosion. CONCLUSION: These data show the capacity of IL-17 to replace the catabolic function of IL-1 in cartilage damage during experimental arthritis.

Animals↗
PubMed1996

Age-related changes in the localization of glycosaminoglycans in condylar cartilage of the mandible in rats.

There is little information available regarding the morphological and biomolecular characteristics of mandibular condylar cartilage. The purpose of this study was to determine the age-related changes in the morphology and immunolocalization of glycosaminoglycans (GAGs) in mandibular condyles. The mandibular condylar cartilages from 4-, 8-, 16-, 32-, and 64-week-old Wistar male rats were examined to verify the localization of chondroitin-4-sulfate (Ch-4S), chondroitin-6-sulfate (Ch-6S) and keratan sulfate (KS) using an indirect immunofluorescent technique with three monoclonal antibodies for glycosaminoglycans, 2-B-6, 3-B-3 and 5-D-4, respectively. Morphologically, the condylar cartilage was a growth cartilage during growing periods, began to differentiate into articular cartilage from the central area of 16-week-old condyles, and became mature articular cartilage at 32 weeks of age. A regional difference was found in the morphological features and distribution of GAGs between the anterior, central, postero-superior and posterior areas of the condyles at each age. The immunohistochemical localizations of these three glycosaminoglycans showed age-related, morphology-dependent changes, from growth cartilage to articular cartilage-like cartilage. Immunoreactions for all of the antibodies decreased progressively with age in the interterritorial matrix, while the pericellular and territorial matrix in the condylar cartilage of the mandible maintained relatively higher immunoreactivity. In conclusion, age-related and regional differences in the localization of glycosaminoglycans Ch-4S, Ch-6S, and KS were found in the mandibular condyles in rats, and these changes are believed to be related to functional and developmental requirements.

Aging↗
PubMedDate not supplied

What's new in cartilage?

Magnetic resonance (MR) imaging of articular cartilage is important in evaluation of new surgical and pharmacologic treatments for cartilage damage. Many techniques exist for MR imaging of articular cartilage. Standard techniques for morphologic imaging of cartilage include fast spin-echo and spoiled gradient-echo imaging. These methods provide high-resolution morphologic images of cartilage but are time-consuming in the clinical setting. New methods for faster or higher-resolution morphologic imaging include techniques based on steady-state free precession imaging. These fast techniques will allow detailed evaluation of cartilage in the routine clinical setting. There are also several MR imaging methods that may provide information about the structure and physiology of cartilage. Physiologic imaging may allow detailed evaluation of the glycosaminoglycan matrix or collagen network of articular cartilage and may be the most sensitive method for detection of early changes. With the development of new therapies for osteoarthritis and cartilage injury, MR imaging of articular cartilage is of increasing clinical importance. MR imaging will play an important role in evaluation of the effectiveness of these therapies.

Cartilage Diseases↗
PubMedDate not supplied

Bronchial cartilage atrophy in chronic bronchitis: observations on chondrolytic processes.

The status of bronchial cartilage degeneration in chronic bronchitis is unclear, and little is known about the chondrolytic mechanisms involved. The potential contributions of various inflammatory cells, chondrocytes and cartilage-degrading enzymes to cartilage atrophy have been examined. Bronchial cartilage specimens were obtained at autopsy from lobar secondary bronchi from chronic bronchitics and age-matched controls; each was examined by light microscopy and immunohistology for the distributions of mast cells, macrophages, eosinophils, collagenase 1, collagenase 3, and degradation products of cartilage collagen. Most bronchitic specimens showed hypertrophic chondrocytes, some of which were immunostained for collagenase 3, and occasionally for collagenase 1. Evidence for collagen degradation products was demonstrated around the lacunae of a proportion of chondrocytes, and both collagenases were also observed in the soft inflammatory tissues in close association with the cartilage surface, together with variable distributions of mast cells and macrophages. Such observations were generally absent or very much reduced in the control, non-bronchitic specimens. Degenerative changes, atrophy and loss of bronchial cartilage were common features of most chronic bronchitic specimens, this usually being related to intrinsic changes in the chondrocyte phenotype, including proliferative and matrix-degrading properties. Mast cells and macrophages were often observed in close association with the bronchial cartilage, suggesting that inflammatory cells may also contribute to the mechanisms of bronchial cartilage degradation and loss. These observations of bronchial cartilage degeneration were generally lacking in age-matched non-bronchitic control specimens.

Atrophy↗
PubMed2006

Effects of calcified cartilage on healing of chondral defects treated with microfracture in horses.

BACKGROUND: Microfracture of full-thickness articular defects has been shown to significantly enhance the amount of repair tissue. However, there is a suggestion that leaving calcified cartilage inhibits this repair response. HYPOTHESIS: Removal of the calcified cartilage with retention of subchondral bone enhances the amount of attachment of the repair tissue compared with retention of the calcified cartilage layer. STUDY DESIGN: Controlled laboratory study. METHODS: There were 1-cm(2) articular cartilage defects made in 12 skeletally mature horses on the axial weightbearing portion of both medial femoral condyles. Using a custom measuring device and direct arthroscopic observation of the subchondral bone beneath the calcified cartilage layer, the authors removed the calcified cartilage from 1 defect of each horse. The repair was assessed with arthroscopy, clinical examination, radiographic and magnetic resonance imaging examinations, biopsy at 4 months, gross and histopathologic examinations at 12 months, as well as mRNA and immunohistochemical evaluations. RESULTS: Removal of calcified cartilage with retention of the subchondral bone plate increased the overall repair tissue as assessed by arthroscopic (4 months) and gross evaluation (12 months). An increase in the level of the subchondral bone was also observed with removal of the calcified cartilage layer. The clinical pain, radiographic examinations, magnetic resonance imaging evaluations, histologic character, matrix proteins, or mRNA expression do not appear to differ based on level of defect debridement. CLINICAL RELEVANCE: Removal of the calcified cartilage layer appears to provide optimal amount and attachment of repair tissue. Therefore, close arthroscopic visualization is recommended for debridement of clinical lesions to ensure removal of the calcified cartilage layer.

Animals↗
PubMed2002

Mechanical resistance of biological repair cartilage: comparative in vivo tests of different surgical repair procedures.

The former common knowledge that cartilage lesions do not heal has been modified over the last few years due to new technologies. For repair of deeper circumscribed lesions osteochondral press-fit grafting and tissue engineering are used in clinical application. The histological data of the hyaline-like tissue obtained by engineering are just as satisfactory as the surviving grafted hyaline cartilage on top of osteochondral cylinders. But comparative studies are still lacking. To fill the gap and with a view to repairing larger osteoarthritic defects we have performed an in vivo study on 16 goats. Three months after the creation of a full thickness wide cartilage defect on the femoral condyle with harvesting of cartilage samples for tissue cultures we performed secondary cartilage repair procedures on the installed osteoarthritis areas: 1) grafting with autogenic osteochondral press-fit cylinders from the opposite knee, 2) autologous engineered chondrocyte grafting under periosteal flaps, 3) both in combination. The harvesting defects were either left as controls or filled with a hyaluronate fleece. After eight months the repaired areas and the harvesting defects were examined for cartilage stiffness as a novel comparative parameter. Compared to normal the cartilage on top of osteochondral grafts is considerably stiffer. Engineered cartilage is weaker than normal. Spontaneously ingrown fibrous cartilage is much weaker even with a carrier fleece. A combination of osteochondral press-fit grafts with engineered autologous cells restores biomechanical qualities to repaired larger degenerative cartilage defects.

Animals↗
PubMed1992

Neoplastic infiltration of laryngeal cartilages: histocytochemical study.

The relationship between cartilage and invading neoplastic cells was studied in 32 cases of laryngeal cancer by histological and cytochemical methods. Cartilage invasion was present in 12 cases, 10 of which were in proximity or in contact with areas of calcification and ossification. It was significantly correlated only to tobacco consumption (P less than .05) and, in regard to glottic tumors, to tumor diameter greater than 3 cm (P less than .01). Histologically, neoplastic invasion in cartilage was massive in 2 cases, occurred in areas of ossification in 4, between cartilage and bone in 4, and in epiglottic cartilage in 2. In 3 of the cases with bone invasion, there was also new bone formation. Hyaline cartilage and bone resorption was due to tartrate-resistant acid phosphatase (TRAP)-positive giant cells; in epiglottic cartilage only mononuclear cells were present, some of which were TRAP-positive. These results show that neoplastic cells can promote not only resorption and formation of bone, but also resorption of cartilage, which is considered resistant to neoplastic invasion. The different types of resorbing cells in contact with hyaline cartilage and bone in laryngeal cancer, and elastic cartilage in epiglottic cancer, suggest that the structure of the tissue being resorbed can influence the type of resorbing cells.

Acid Phosphatase↗
PubMed2003

[Value of autologous chondrocyte transplantation in the reconstruction of experimental cartilage defects. Part I. Extent of defect, macroscopic appearance of reconstructed articular surface and microscopic analysis of predominant tissue].

Articular cartilage defect is one of the main reasons of osteoarthritis. Currently, tissue engineering techniques are the methods concerning better cartilage reconstruction. The aim of this part of the study was macroscopic evaluation of degree of defect feeling, macroscopic appearance of repair tissue and microscopic analysis of predominant tissue after autologous chondrocytes transplantation. Repair of partial thickness cartilage defect on distal part of femur was evaluated (25 adolescent rabbits). Procedures were performed in II groups: I--autologous chondrocytes transplantation under periosteal flap, II--periosteal graft. Chondrocytes were isolated from the cartilage specimens by enzymatic digestion and cultured in vitro. The regenerates were inspected 4, 8 and 12 weeks after the operation. Macroscopic analysis in group I, in most cases revealed filling of the defect with tissue resembling surrounding cartilage. In group II the defect was partially filled, and there was many fissures and cracks in all regenerates. In microscopic analysis in group I, after 4 and 8 weeks following the transplantation the tissue similar to juvenile hyaline cartilage predominated. After 12 weeks it resembled mature hyaline cartilage. In group II, in all cases fibrous cartilage was observed after 4, 8, 12 weeks. Obtained results indicate, that macroscopic and microscopic characteristics of repair tissue after autologous chondrocytes transplantation more closely resembled hyaline cartilage, than in periosteal graft group. 12 weeks after autologous chondrocytes transplantation the repair tissue reached maturity, and demonstrated microscopic characteristics of hyaline-like cartilage. The method of autologous chondrocytes transplantation provides potential for clinical application.

Animals↗
PubMed2005

[Mesenchymal stem cells as potential source cartilage repair].

Articular cartilage damaged by disease or trauma has a limited capacity for regeneration. The end stage of cartilage loss frequently leads to osteoarthritis resulting in a significantly decreased quality of life in millions of people. The surgical treatment of articular cartilage injury has always posed difficult problems for orthopedic surgeons and regarding long-term outcomes the currently available methods are unsatisfactory. The main lack of the applied methods is the appearance of the mechanically inadequate resident fibrocartilage instead of hyalin cartilage in the place of the cartilage defect. To find reliable methods for early repair of cartilage injuries seems of huge importance. Using techniques of tissue engineering, artificial cartilage fabricated in vitro has been applied for the repair and regeneration of damaged cartilage. Mesenchymal stem cells provide a source of cells for the repair of musculoskeletal tissue. Mesenchymal stem cells are multipotent cells that are capable of differentiating into cartilage, tendon, muscle, cartilage or hematopoiesis supporting marrow stroma. To ensure the successful durable integration and function of the engineered tissue requires suitable biomechanical and biochemical circumstances, and poses the challenge of handling in vitro culture of human cells, cell biology and molecular biology.

Animals↗
PubMed1984

Topographical variation in the calcified zone of upper femoral articular cartilage.

A series of 27 adult human femoral heads has been examined for topographical variation in 'remodelling' and other histological features of the calcified zone at the base of the articular cartilage. The specimens were obtained from necropsies; hip joints with osteoarthritic bone exposure were excluded. A tissue sample from the inferomedial aspect was compared with one from the femoral zenith, using a standard length along the articular contour at each site. Histological sections were cut in a plane vertical to that of the articular surface. A study was made of the various patterns seen within cartilage tidemarks when these were examined at high magnification in paraffin sections stained with Ehrlich's haematoxylin and eosin. Special attention was paid to the identification of tidemark segments which stained faintly and were not readily apparent. The tidemarks were mapped on a photomicrographic montage from each of the tissue samples. When a sample showed evidence of one or more extra phases of cartilage calcification, as indicated by the presence of more than one tidemark, the spatial extent of the extra calcification was quantified by linear measurement and by point counting on the photomicrographic montage. The mean of the results for the spatial extent of extra-phase calcification of the cartilage was greater for the inferomedial than for the zenith samples. However, it was also greater for samples where the articular surface showed minimal fibrillation than for samples where the surface was still intact, and it was noted that surface fibrillation was much more common in the inferomedial than in the zenith samples. Where there was more than one tidemark, the lowest sometimes showed gaps where it had been breached by an advance of ossification into the calcified cartilage. The mean value of the tangential extent of such gaps was similar at the two sites sampled. Focal contacts, where the uncalcified articular cartilage was in contiguity with calcified zone 'defects' containing tissue other than calcified hyaline cartilage, were more numerous at the femoral zenith than inferomedial to the fovea. Counts were also made of tangential shearing splits at the interface of the calcified and uncalcified cartilage. Subject to the reservation that genuine splitting may be difficult to distinguish from technical artifact, the mean number was closely similar at the two sites sampled. The interpretation of the findings is discussed in relation to remodelling changes in the cartilage base and to degenerative changes in the overlying articular cartilage.

Adult↗
PubMed1983

Proteoglycans from rabbit articular and growth plate cartilage. Ultracentrifugation, gel chromatography, and electron microscopy.

Proteoglycans are considered to be important for the mechanical properties of articular cartilage and growth plate and for the regulation of calcification of growth plate. We have used ultracentrifugation, gel chromatography, and electron microscopy to characterize and compare proteoglycans isolated from rabbit articular cartilage, uncalcified growth plate, and calcified cartilage. We found that proteoglycans from articular cartilage were more resistant to extraction than were proteoglycans from uncalcified growth plate and calcified cartilage. Long term neutral decalcification of calcified cartilage resulted in degraded proteoglycans. The chondroitin sulfate chains from all three tissues had similar size distribution. Gel chromatography and electron microscopy of proteoglycan monomers suggested that those from uncalcified growth plate were largest, those from articular cartilage intermediate, and those from calcified cartilage smallest. Proteoglycan aggregates from articular cartilage were longer than those from uncalcified growth plate. Both biochemical and quantitative electron microscopic data suggested the existence in mineralizing cartilage of at least two different sized populations of proteoglycan aggregates.

Animals↗
PubMed1982

A functional-morphological study of the tidemark region of articular cartilage maintained in a non-viable physiological condition.

Composite samples consisting of articular and calcified cartilage maintained in a non-viable physiological condition have been subjected to static compression using a system of simultaneous micromechanical testing and interference light microscopy. This, combined with transmission electron microscopy following glutaraldehyde fixation of the tissue under sustained load, has provided a unique observation of the response of the collagen framework in the tidemark region of articular cartilage to sustained compression loading. The tidemark in mature articular cartilage is seen to be highly variable in its morphological features, when viewed ultrastructurally. It incorporates variable amounts of internal stress which are relieved when the articular cartilage is separated from the calcified cartilage. Deformation of the articular cartilage can terminate abruptly at the tidemark. There is no evidence that the tidemark or calcified cartilage provided an intermediate layer between the complaint articular cartilage and the rigid subchondral bone. However, morphological evidence presented suggests that a smooth transfer of stress from the complaint to the rigid tissues could be achieved through changes in orientation and packing density of the collagen fibres in the articular cartilage adjacent to the tidemark. A variety of morphological responses of the collagen framework was observed in the tidemark region of articular cartilage following static compressive loading. In any given region, these responses were determined by (a) the local form and orientation of the tidemark; (b) the organisation of the collagen fibres; (c) the position of this region with respect to the compressive anvil. No evidence was obtained which suggested that the collagen fibres near the tidemark had a predominantly tensile role during direct compression. The observed process of compaction and collapse via a 'crimp' formation is clearly non-tensile. However, deformation involving lateral shear in regions nearer the extremities of joint contact would require that the collagen fibres provide an anchoring role and thus be subjected to tensile loading.

Animals↗