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PubMed1989

Effects of intramuscular polysulfated glycosaminoglycan on chemical and physical defects in equine articular cartilage.

The effect of intramuscular polysulfated glycosaminoglycan (PSG) on repair of cartilage injury was evaluated in eight horses. In each horse, one middle carpal joint had both a partial-thickness and a full-thickness articular cartilage defect created. In the contralateral middle carpal joint, chemical articular cartilage injury was created by intra-articular injection of 50 mg sodium monoiodoacetate (MIA). Horses were divided into two groups for treatment. Group 1 horses (control) received an intramuscular injection of normal saline every four days for a total of seven injections starting seven days after cartilage injury. Group 2 horses received 500 mg of PSG intramuscularly every four days for seven treatments starting seven days after cartilage injury. Horses were maintained for 12 weeks. Horses were evaluated clinically, and their middle carpal joints were evaluated radiographically and arthroscopically at the end of the study. Joint tissues were also collected and examined microscopically. The only significant difference between groups was slightly greater matrix staining intensity for glycosaminoglycans in the radiate articular cartilage layer in MIA injected and PSG treated joints. Partial-thickness defects had not healed and the predominant repair tissue in full-thickness defects was fibrous tissue. It was concluded that using this joint injury model, 500 mg PSG administered intramuscularly had no effect on the healing of articular cartilage lesions, and minimal chondroprotective effect from chemically induced articular cartilage degeneration.

Animals↗
PubMed1987

[Results of autopsy examination of knee cartilage in 120 patients dying in the hospital. I. Femoro-patellar joint].

The authors have performed the pathological examination of the knees of 57 women and 63 men or 112 patients over the age of 50, who died in the hospital. The lesions of the patellar and trochlear cartilages were studied and classified according to four categories: stage I: non extended fissures; stage II: fissures extending over 25 p. cent of the articular surface; stage III: fissures associated with small deep ulcerations of the cartilage; stage IV: deeps and extended ulcerations of the articular cartilage exposing the sub-chondral bone. Cartilage alterations were found in 93.3 p. cent of the patellas; 26.2 p. cent of stage I; 22.5 p. cent of stage II, 27.1 p. cent of stage III; 17.5 p. cent of stage IV. These alterations are bilateral and symmetrical, most of the time. Their frequency and severity increase with age. Thus, deep and extended ulcerations (stage IV) of the patellar cartilage have a frequency of 1.9 p. cent before the age of 60.8 p. cent between 60 and 70 years, 13.6 p. cent between 70 and 80 years and 38.9 p. cent after 80 years. Alterations of the patellar cartilage are more frequent and more severe in women than in men. In 85.7 of the patellas they occupy both facets, overriding the patellar crest; more seldom, they are exclusively localized to the medial patellar facet (11.6 p. cent) or lateral facet (3.1 p. cent). Alterations of the trochlear cartilage, although more common are less frequent than that of the patellar cartilages. Patellar osteophytosis is very frequent.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Clonal proliferation and cell density of chondrocytes isolated from human fetal epiphyseal, human adult articular and nasal septal cartilage. Influence of hormones and growth factors.

The present study characterizes the cell density and cellular growth characteristics of functionally and morphogenetically different human cartilages. In fetal epiphyseal, in postnatal nasal septal and in articular cartilage the influence of aging on cell density and in vitro growth characteristics were investigated. Cell density was highest in fetal epiphyseal cartilage and lowest in articular cartilage. In vitro growth of isolated chondrocytes as measured by clonal growth in a semisolid assay was almost identically high in fetal epiphyseal and septal cartilage and significantly lower in articular cartilage. Cell density increased with age in the nasal septal cartilage whereas no age dependency was found in the other cartilages. The stimulatory effects of human biosynthetic insulin, human growth hormone and partially purified IGF I on clonal growth of chrondrocytes were assessed. Only IGF I stimulated clonal growth of chondrocytes and its stimulatory effect was significantly higher in postnatal than in fetal chondrocytes.

Adolescent↗
PubMed1984

Interaction of malignant cells with salt-extracted cartilage in vitro.

A salt-extractable low-molecular-weight fraction has been held responsible for the resistance of cartilage to invasion by malignant cells. To test this hypothesis, we have confronted in vitro fragments from bovine articular cartilage, from bovine nasal septum, from chick embryonic tibia, or from human knee meniscus with cells from the following malignant lines: LICR-HN-4 human squamous cell carcinoma; B16BL6 mouse melanoma; Hu-456 human transitional cell carcinoma; TE-85 and SAOS-2 human osteosarcoma; and MO4 mouse fibrosarcoma. Human embryo lung cells and chick embryonic heart cells were used as nonmalignant counterparts. Confronting cultures using living cartilage and cartilage extracted with 3 M guanidinium hydrochloride were examined light microscopically and ultrastructurally after 1 to 14 days. Neither invasion of malignant cells into the matrix of living or salt-extracted cartilage nor breakdown of collagen was observed in these cultures. In contrast, both malignant and nonmalignant cells occupied preexisting spaces in the matrix, namely, cut chondrocyte lacunae, cartilage canals, and fibrillation clefts. We concluded from these experiments that salt extraction did not alter the resistance of cartilage to invasion by malignant cells in vitro. This conclusion does not support the opinion that salt-extractable factors are solely responsible for the resistance of cartilage.

Animals↗
PubMed1976

[On the metabolic heterogenity of the cartilage tissue (author's transl)].

Autoradiografic studies with 3H-thymidine, 3H-proline and 35S-sulfate in different cartilage tissues from rabbits and rats (articular and epiphyseal cartilage of the knee; costal, xiphoid and tracheal cartilage) were performed. The following results were obtained: The proliferative zone of the epiphyseal plate of young and adult animals is limited to the superior part of the columnar cartilage. The articular cartilage shows no proliferative zones but single S-phase-nuclei in all layers seldom were found. In the adult animals a decrease of DNA-synthetising chondrocytes in all investigated cartilage tissues and a narrowing of the proliferative zone could be detected. 3H-proline and 35S-sulfate in proliferating chondrocytes of the bone cartilage border line and in chondrocytes of the subperichondrial area increasingly were incorporated. Possible causes of the regional differences in the uptake of the used precursors were discussed and the significance of the metabolic heterogenity of the cartilage tissue for aging and pathological processes was pointed to.

Aging↗
PubMedDate not supplied

The fate of fresh, layered, nonsutured and sutured, autogenous cartilage in the rabbit model.

OBJECTIVE: To compare the thickness, area, and volume of sutured and nonsutured multilayered cartilage grafts in a rabbit population. DESIGN: Autogenous rabbit cartilage grafts were harvested, layered, and placed in the contralateral auricle. Half the grafts were sutured; the other half were nonsutured. Graft thickness, area, and volume were measured before implantation, after 90 days in vivo, and after explantation. RESULTS: The area and volume of the cartilage grafts increased during the 90-day period. Histologically, this was caused by increased fibrous tissue around the cartilage grafts. Minimal cartilage resorption was observed. No differences were noted between sutured and nonsutured grafts. CONCLUSIONS: Autogenous, fresh, uncrushed, layered nonsutured or sutured cartilage grafts are well tolerated. Statistically significant increases in the area and volume of autogenous, fresh, uncrushed, layered cartilage grafts occurred primarily because of fibrous tissue formation at the margins of the layered grafts. Suturing had no effect on the postoperative volume retention of these layered grafts. This information will be helpful to the facial plastic surgeon when using fresh-layered autogenous cartilage grafts during cosmetic or reconstructive procedures. Arch Facial Plast Surg. 2000;2:256-259

Animals↗
PubMed1996

Inhibition of in vitro limb cartilage differentiation by syndecan-3 antibodies.

The transmembrane heparan sulfate proteoglycan syndecan-3 is transiently expressed in high amounts during the cellular condensation process that characterizes the onset of limb cartilage differentiation. During condensation, limb mesenchymal cells become closely juxtaposed and undergo cell-cell and cell-matrix interactions that are necessary to trigger cartilage differentiation and cartilage-specific gene expression. To test directly the possible involvement of syndecan-3 in regulating the onset of limb chondrogenesis, we examined the effect of polyclonal antibodies against a syndecan-3 fusion protein on the chondrogenic differentiation of chick limb mesenchymal cells in micromass culture. Syndecan-3 antiserum elicits a dose-dependent inhibition of the accumulation of Alcian blue-stainable cartilage matrix by high density limb mesenchymal cell micromass cultures (2 x 10(5) cells/10 microliters) and a corresponding reduction in steady-state levels of mRNAs for cartilage-characteristic type II collagen and the core protein of the cartilage proteoglycan aggrecan. In preimmune serum-treated control cultures proliferating cells are limited to the periphery of areas of cartilage matrix deposition, whereas large numbers of proliferating cells are uniformly distributed throughout the undifferentiated cultures supplemented with syndecan-3 antiserum. Limb mesenchymal cells cultured at lower densities (1 x 10(5) cells/10 microliters) in the presence of preimmune serum form extensive precartilage condensations characterized by the close juxtaposition of rounded cells by day 2 of culture. In contrast, in the presence of syndecan-3 antiserum, the cells fail to aggregate but rather remain flattened and spatially separated from one another, suggeting that syndecan-3 antibodies impair the formation of precartilage condensations. These results indicate that syndecan-3 plays an important role in regulating the onset of limb chondrogenesis, perhaps by mediating the cell-cell and cell-matrix interactions required for condensation and subsequent cartilage differentiation.

Aggrecans↗
PubMed1998

Chondrocyte apoptosis increases with age in the articular cartilage of adult animals.

BACKGROUND: Apoptosis in vivo has been identified in developing cartilage from embryonic chick sterna and avian and murine growth plates. To date, no evidence exists that chondrocytes in articular cartilage undergo apoptosis. METHODS: We examined the distribution of cells demonstrating fragmented DNA in the articular knee cartilage of C57BL/6 mice (aged 11, 18, 24, and 30 months) and Wistar rats (aged 6, 12, and 24 months) using a DNA end-labeling technique. RESULTS: Control experiments utilizing retinoic acid-induced apoptosis in a chondrocyte cell line, established that DNA end-labeling correlated with DNA ladder formation. In vivo, apoptotic cells were detected in articular cartilage tissue in both species examined. The percentage of apoptotic cells increased significantly (P < 0.05 with age) for all joint surfaces in both species. No significant difference was found between the medial and lateral or femoral and tibial joint surfaces of the knee. Apoptotic cells were observed in both the calcified and uncalcified regions of the articular cartilage of C57 mice. In the rat, only the calcified region of articular cartilage contained apoptotic cells. CONCLUSIONS: These results suggest that apoptosis plays a role in some aspect of maintenance, remodeling, or turnover of mature articular cartilage. In addition, the increase in apoptosis associated with aging could contribute to the greater risk for cartilage degeneration.

Aging↗
PubMed1999

Differential responses to parathyroid hormone-related protein (PTHrP) deficiency in the various craniofacial cartilages.

PTHrP null mutant mice exhibit skeletal abnormalities both in the craniofacial region and limbs. In the growth plate cartilage of the null mutant, a diminished number of proliferating chondrocytes and accelerated chondrocytic differentiation are observed. In order to examine the effect of PTHrP deficiency on the craniofacial morphology and highlight the differential feature of the composing cartilages, we examined the various cartilages in the craniofacial region of neonatal PTHrP deficient mice. The major part of the cartilaginous anterior cranial base appeared to be normal in the homozygous PTHrP deficient mice. However, acceleration of chondrocytic differentiation and endochondral bone formation was observed in the posterior part of the anterior cranial base and in the cranial base synchondroses. Ectopic bone formation was observed in the soft tissue-running mid-portion of the Meckel's cartilage, where the cartilage degenerates and converts to ligament in the course of normal development. The zonal structure of the mandibular condylar cartilage was scarcely affected, but the whole condyle was reduced in size. These results suggest the effect of PTHrP deficiency varies widely between the craniofacial cartilages, according to the differential features of each cartilage.

Animals↗
PubMed1998

Osteogenic protein (OP-1, BMP-7) stimulates cartilage differentiation of human and goat perichondrium tissue in vitro.

The objective of this study was to examine in vitro the influence of recombinant human osteogenic protein-1 [rhOP-1, or bone morphogenetic protein-7 (BMP-7)] on cartilage formation by human and goat perichondrium tissue containing progenitor cells with chondrogenic potential. Fragments of outer ear perichondrium tissue were embedded in clotting autologous blood to which rhOP-1 had been added or not added (controls), and the resulting explant was cultured for 3 weeks without further addition of rhOP-1. Cartilage formation was monitored biochemically by measuring [35S]-sulphate incorporation into proteoglycans and histologically by monitoring the presence of metachromatic matrix with cells in nests. The presence of rhOP-1 in the explant at the beginning of culture stimulated [35S]-sulphate incorporation into proteoglycans in a dose-dependent manner after 3 weeks of culture. Maximal stimulation was reached at 40 microg/mL (human explants: +148%; goat explants: +116%). Histology revealed that explants treated with 20-200 microg/mL of rhOP-1, but not untreated control explants, contained areas of metachromatic-staining matrix with chondrocytes in cell nests. It was concluded that rhOP-1 stimulates differentiation of cartilage from perichondrium tissue. The direct actions of rhOP-1 on perichondrium cells in the stimulation of chondrocytic differentiation and production of cartilage matrix in vitro provides a cellular mechanism for the induction of cartilage formation by rhOP-1 in vivo. Thus rhOP-1 may promote early steps in the cascade of events leading to cartilage formation and could prove to be an interesting factor in the regeneration of cartilage in articular cartilage defects.

Animals↗
PubMed1997

Interleukin-1beta-stimulated invasion of articular cartilage by rheumatoid synovial fibroblasts is inhibited by antibodies to specific integrin receptors and by collagenase inhibitors.

OBJECTIVE: To study the role of integrin receptors in the invasion of cartilage by rheumatoid synovial fibroblasts (RSF). METHODS: RSF were cocultured with cartilage slices alone or in the presence of various potential activators or inhibitors. The penetration of the cartilage surface by RSF was determined by live-cell imaging of fluorescent-labeled cells. RESULTS: Interleukin-1beta (IL-1beta) and IL-8 stimulated the RSF invasion of cartilage. Invasion was specific for RSF and required a concentration gradient of IL-1beta. The IL-1beta-activated invasion of cartilage was inhibited by anti-IL-1 antibodies, IL-1 receptor antagonist, and collagenase inhibitors. RSF invasion was also inhibited by antibodies to alpha4, alpha5, alphaV, and beta1 integrins. CONCLUSION: In this study, an IL-1beta concentration gradient was required for RSF invasion into cartilage, raising the possibility that in vivo invasion may be induced by IL-1beta released by chondrocytes. The IL-1beta activation of RSF assayed in vitro may contribute to the RSF invasion of cartilage in vivo. Cartilage invasion requires the availability of beta1 and alpha4, alpha5, and alphaV integrins and the presence of collagenase activity.

Antibodies↗
PubMed1998

Linkage of chondrocyte apoptosis and cartilage degradation in human osteoarthritis.

OBJECTIVE: To examine the occurrence of apoptosis in human osteoarthritis (OA) cartilage, and to determine its relationship to cartilage degradation. METHODS: Knee cartilage was obtained from subjects at autopsy, from a tissue bank, and from OA patients undergoing total joint replacement surgery. Chondrocytes were isolated and the number of apoptotic cells was analyzed by flow cytometry. Apoptotic cells in cartilage sections were identified by the detection of DNA strand breaks. Electron microscopy was applied to demonstrate morphologic changes, and Safranin O staining was performed to analyze the relationship between apoptosis and proteoglycan depletion. RESULTS: Flow cytometry on cell suspensions prepared from collagenase digests of cartilage showed that approximately 22.3% of OA chondrocytes and 4.8% of normal chondrocytes were undergoing apoptosis. Staining of cartilage sections demonstrated the presence of apoptotic cells in the superficial and middle zones. Cartilage areas that contained apoptotic cells showed proteoglycan depletion, and the number of apoptotic cells was significantly correlated with the OA grade. CONCLUSION: These observations demonstrate increased chondrocyte apoptosis in OA cartilage. Chondrocyte apoptosis and proteoglycan depletion are anatomically linked and may be mechanistically related.

Adult↗
PubMed1999

Staphylococcus aureus stimulates inducible nitric oxide synthase in articular cartilage.

OBJECTIVE: To determine if Staphylococcus aureus stimulates the L-arginine-nitric oxide (NO) synthase pathway in articular cartilage. METHODS: A heat-killed and sonicated (denatured) S. aureus preparation was added to cultures of bovine articular cartilage. NO production was measured as accumulated nitrite in the culture medium and by the NO synthase-dependent conversion of 3H-L-arginine to 3H-L-citrulline in cartilage homogenates. Inducible NO synthase (iNOS) messenger RNA (mRNA) expression was analyzed by Northern blot. Proteoglycan synthesis was measured by 35SO4 incorporation into glycosaminoglycan. RESULTS: Nitrite accumulation and 3H-L-citrulline formation in cartilage were elevated by denatured S. aureus (compared with unstimulated control cartilage) and inhibited by the NO synthase inhibitor N(G)-monomethyl-L-arginine. Northern blot analysis revealed increased iNOS mRNA expression in bovine chondrocytes in response to denatured S. aureus stimulation. Denatured S. aureus suppressed the accumulation of 35SO4-labeled macromolecules representing newly synthesized proteoglycans in bovine articular cartilage. The suppressed proteoglycan synthesis was due to the presence of NO. CONCLUSION: These findings support the hypothesis that a component of S. aureus can stimulate iNOS in articular cartilage, and that NO generated from this enzyme down-regulates cartilage matrix proteoglycan synthesis.

Animals↗
PubMed2001

Matrix metalloproteinase and proinflammatory cytokine production by chondrocytes of human osteoarthritic cartilage: associations with degenerative changes.

OBJECTIVE: To examine by immunohistochemistry the relative distributions of 6 matrix metalloproteinases (MMPs 1, 2, 3, 8, 9, and 13) and the 2 proinflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha) in osteoarthritic (OA) cartilage compared with normal, age-matched articular cartilage. METHODS: Articular cartilage samples were obtained from the tibial plateau of OA knees removed at arthroplasty and from normal, nonarthritic, knees obtained at autopsy. Specimens were promptly fixed in Carnoy's fixative, processed, embedded in paraffin, sectioned, and examined by immunohistochemistry for MMP and cytokine production. In addition, human articular chondrocytes (HAC) were treated in vitro with either IL-1beta, TNFalpha, or phorbol myristate acetate (PMA) to assess their potential to produce each of the MMPs, as determined by Western blotting and gelatin zymography. RESULTS: Immunodetection of the collagenases (MMPs 1, 8, and 13) and stromelysin 1 (MMP-3) was demonstrated in a proportion of chondrocytes in the superficial zone of almost all of the OA specimens that had degenerative matrix changes. The gelatinases (MMPs 2 and 9) were also demonstrated by immunohistochemistry but were not so prominent. IL-1beta- and TNFalpha-positive chondrocytes were also observed in a proportion of cells in the superficial zones of OA specimens. Much less immunostaining for MMPs and cytokines was observed in the deep zone of all OA specimens, where the cartilage matrix and chondrocyte morphology appeared normal. In contrast, full-thickness normal cartilage specimens showed virtually no immunostaining for these MMPs or cytokines. Confirmation that chondrocytes can produce these 6 MMPs was obtained from HAC cultures treated with either IL-1beta, TNFalpha, or PMA; conditioned medium from activated HAC contained all the MMPs demonstrated by immunohistochemistry. Dual immunolocalization studies of OA cartilage specimens demonstrated the coexpression of IL-1 with MMP-8 by individual chondrocytes in situ. CONCLUSION: These results indicate that the superficial zone of OA cartilage specimens, which is characterized by fibrillations, chondrocyte clusters, and degenerative matrix changes, contains a variable proportion of cells that immunostain for IL-1beta, TNFalpha, and 6 different MMPs. These observations support the concept that cytokine-MMP associations reflect a modified chondrocyte phenotype and an intrinsic process of cartilage degradation in OA.

Aged↗
PubMed2001

Production of the chemokine RANTES by articular chondrocytes and role in cartilage degradation.

OBJECTIVE: To examine the expression of the chemokine RANTES and its receptors in normal and osteoarthritic (OA) human cartilage and to analyze its effects on chondrocyte function. METHODS: The expression of RANTES and its receptors were examined by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. The effect of RANTES on gene expression of other cytokines and on the release of mediators of cartilage degradation was also examined by PCR and enzyme-linked immunosorbent assay. RESULTS: The expression of RANTES was undetectable in normal chondrocytes until after stimulation with interleukin-1beta (IL-1beta) or IL-18. Cultures of normal cartilage also produced RANTES in response to IL-1beta, as demonstrated by immunohistochemistry. All OA cartilage samples analyzed expressed RANTES messenger RNA (mRNA); RANTES protein was detected by immunohistochemistry in the superficial and mid zones of the tissue. OA chondrocytes produced elevated levels of RANTES constitutively and after IL-1beta stimulation. Normal cartilage expressed the RANTES receptors CCR3 and CCR5, but not CCR1. CCR1 was expressed in OA cartilage, and CCR3 and CCR5 were increased. In normal chondrocytes, RANTES induced the expression of inducible nitric oxide synthase and IL-6. RANTES stimulated the release of matrix metalloproteinase 1 in normal and OA chondrocytes as effectively as IL-1beta. Treatment of normal articular cartilage with RANTES increased the release of glycosaminoglycans and profoundly reduced the intensity of Safranin O staining. CONCLUSION: Chondrocytes produce RANTES and express RANTES receptors. RANTES and CCR5 were markedly increased in OA and after in vitro treatment of normal chondrocytes with IL-1. Chondrocyte activation and cartilage degradation were identified as novel biologic and pathogenetic activities of this chemokine.

Cartilage, Articular↗
PubMed2001

The osteoprotegerin/receptor activator of nuclear factor kappaB/receptor activator of nuclear factor kappaB ligand system in cartilage.

OBJECTIVE: The receptor activator of nuclear factor kappaB (RANK) is a member of the tumor necrosis factor receptor family. It is activated by the secreted or cell surface-bound RANK ligand (RANKL). Osteoprotegerin (OPG) is a soluble nonsignaling receptor for RANKL and interferes with RANK activation. This receptor-ligand system regulates the differentiation of osteoclasts and dendritic cells. The present study examined human articular cartilage for the expression of these molecules and the role of RANKL in the regulation of chondrocyte function. METHODS: Normal and osteoarthritic (OA) human articular cartilage was used for explant tissue culture or for isolation of chondrocytes and cell culture. Expression of RANK, RANKL, and OPG was analyzed by immunohistochemistry, Western blotting, or reverse transcription-polymerase chain reaction. Recombinant RANKL was added to cartilage or chondrocyte cultures, and gene expression, collagenase and nitric oxide production, and NF-kappaB activation were determined. RESULTS: RANK, RANKL, and OPG messenger RNA (mRNA) were expressed in normal cartilage. By immunohistochemistry, RANK, RANKL, and OPG were detected in the superficial zone of normal cartilage. OA cartilage contained increased levels of OPG mRNA, and expression of the 3 proteins extended into the midzone of OA cartilage. OPG was detected by Western blotting, and was increased in response to interleukin-1beta stimulation. OPG, RANK, and RANKL protein were also detected in cultured chondrocytes. Addition of exogenous RANKL did not activate NF-kappaB, induce expression of genes encoding proinflammatory mediators in chondrocytes, or stimulate the production of collagenase and nitric oxide. CONCLUSION: These results demonstrate the expression of OPG, RANK, and RANKL in cartilage. However, RANKL does not activate human articular chondrocytes.

Carrier Proteins↗
PubMed1976

The development of the elastic cartilage of the mouse pinna.

The development of the elastic cartilage in the mouse pinna was studied with the electron microscope. For descriptive purposes, the developmental process was divided into five stages. These begin with the onset of cartilage matrix production by chondroblasts. The second stage is the major mitotic stage although the cells now resemble chondrocytes and cartilage matrix production evidently continues. This is followed by a period during which cartilage matrix production appears to be the major activity of the chondrocytes. In Stage IV, the cells continue to produce cartilage matrix but at the same time they also produce lipid which comes to occupy most of the cell as a large lipid droplet. In the adult, Stage V, matrix production appears to be at an end and each cell contains a lipid droplet which is so large that the cells bear some resemblance to white fat cells and might be designated as lipochondrocytes. The adult cartilage matrix contains elastic plates in a three-dimensional honeycomb pattern. Between the elastic plates and the cells, the matrix contains elements similar to those seen in hyaline cartilage but it does not contain matrix vesicles such as those which have been associated with the calcification of cartilage. Two types of filaments differing in appearance, size, and location are seen within the chondrocytes. They have been designated cytofilaments and cortical filaments. Cytofilaments are dispersed throughout the cell and also contact the substance of the lipid droplet; cortical filaments (sub-plasmalemmal microfilaments) are located directly under the plasma membrane. They are thought to be involved in movement of the plasma membrane as a concomitant to extracellular fibrogenesis.

Age Factors↗
PubMed1988

Trabecular, nasal, branchial, and pericardial cartilages in the sea lamprey, Petromyzon marinus: fine structure and immunohistochemical detection of elastin.

Immunohistochemical and ultrastructural methods were used to examine the distribution of elastin and the fine structure of the trabecular, nasal, branchial, and pericardial cartilages in the sea lamprey, Petromyzon marinus. The cells and matrix, as well as the overall organization of these components, in larval and adult trabecular cartilage resemble those of adult annular and piston cartilages (Wright and Youson: Am. J. Anat., 167:59-70, 1983) Chondrocytes are similar to those in hyaline cartilage. Lamprin fibrils and matrix granules, but no collagen fibrils, are found in a matrix arranged into pericellular, territorial, and interterritorial zones. Branchial, pericardial, and nasal cartilages differ from trabecular, annular, and piston cartilages in the organization of their matrix and in the structural components of their matrix and perichondria. Furthermore, immunoreactive elastin-like material is present within the perichondria and peripheral matrices of nasal, branchial, and pericardial cartilages in both larval and adult lampreys. Oxytalan, elaunin, and elastic-like fibers are dispersed between collagen fibers in the perichondrium. The matrix contains lamprin fibrils, matrix granules, and a band of amorphous material, which is reminiscent of elastin, in the periphery bordering the perichondrium. The presence of elastic-like fibers and elastin-like material within some lamprey cartilages implies that this protein may have evolved earlier in vertebrate history than has been previously suggested.

Animals↗