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[Biochemical study of human articular cartilage and meniscus on aging and joint disease (author's transl)].

We studied biochemically the changes associated with aging and disease in the collagen of articular cartilages and menisci. Pepsin soluble and insoluble collagen were obtained by the method of Miller (1971) from the articular cartilages of seven healthy young and adult, six healthy aged subjects, and of six osteoarthritic and six rheumatoid arthritic patients. One portion of pathological cartilage was histologically examined to eliminate any possible contamination of the fibrous tissue and subchondral bone, and to classify the pathological findings. By the method of Miller, the pepsin soluble and insoluble collagen were also obtained from four adult and six aged menisci. Amino acid composition and carbohydrate contents were studied in insoluble collagen. The type of soluble collagen were analyzed with SDS disc electrophoresis. The amount of crosslinks in insoluble collagen was analyzed by the method of Masuda (1976) using automatic amino acid analyzer. The results obtained where shown as follow: 1) Solubility of collagen by pepsin decreased with aging on articular cartilages and menisci. In osteoarthritis and rheumatoid arthritis, the solubility of collagen by pepsin was different between the samples, and generally higher than that of collagen from the aged articular cartilages. 2) In respect to aldimine crosslinks of insoluble collagen, the dihydroxylysinonorleucine (DHLNL), hydroxylysinonorleucine (HLNL) and lysinonorleucine (LNL) increased with aging. DHLNL and HLNL were present in the nonreduced collagen in vitro. It was shown that the aldimine crosslinks had been already reduced in vivo. 3) The contents of carbohydrate of insoluble collagen from articular cartilage showed lower values than that of type II collagen as described previously. The hexosamine contents increased and those of uronic acid and hexose decreased with aging. In osteoarthritic and rheumatoid arthritic articular cartilages, the contents of uronic acid were lower than that of healthy aged group. The carbohydrate contents of menisci were similar to that of type I collagen. 4) concerning the type of collagen, healthy articular cartilages consisted of type II collagen. In collagen of aged cartilages and those of fibrillated and osteophytic cartilages in osteoarthritic and rheumatoid arthritic patients, the type II collagen were mixed with type I collagen ranging from 13.8% to 64.5%, although the analysis of articular cartilages in this study showed histological characteristics of hyaline cartilage. The type of soluble collagen in adult and aged menisci were composed of type I collagen in spite of aging.

Adolescent↗

The development of articular cartilage: I. The spatial and temporal patterns of collagen types.

Articular cartilage is both morphologically and biochemically heterogeneous. Its susceptibility to degenerative diseases such as arthritis and its limited repair capacity have made cartilage the focus of intense study; surprisingly, little is known of its development. Using a panel of specific antibodies, we have documented the temporal and spatial patterns of collagen types I, II, III, VI and X in the developing knee cartilage of the marsupial Monodelphis domestica from parturition to adulthood. Type I collagen was initially detected in the presumptive articular cartilage of the epiphyses in addition to the perichondrium. By 14 d postparturition, type I collagen was not detectable in the epiphyseal cartilage apart from insertion sites of ligaments and tendons of the joint. Similarly, type III collagen was detected at insertion sites of the major ligaments and tendons and within the perichondrium/periosteum but was never detected in the cartilage per se. Type II collagen was predictably distributed throughout the cartilage matrix and was also detected in the perichondrium. Type VI collagen was widely distributed throughout the cartilage matrix at parturition, but during development became restricted to a pericellular location particularly towards the presumptive articular cartilage, i.e. the epiphysis. Interestingly, generalised matrix immunopositivity was only retained in the hypertrophic cartilage of the secondary centre of ossification. After the formation of the secondary centre, type VI collagen became localised pericellularly in the deeper regions of the articular cartilage but was absent in the cartilage of the growth plate. Type X collagen showed a novel distribution pattern. In addition to being synthesised by hypertrophic chondrocytes, this collagen type was also expressed transiently by some cells at the presumptive articular surface. Furthermore, these surface chondrocytes also stained histochemically for alkaline phosphatase, suggesting that they were terminally differentiated. The fate of these terminally differentiated cells is unknown.

Alkaline Phosphatase↗

Differences in submicroscopic structure of the extracellular matrix of canine femoral and tibial condylar articular cartilages as revealed by polarization microscopical analysis.

The submicroscopic orientation patterns of sulfated glycosaminoglycan side chains of proteoglycan molecules and collagen fibrils were compared in different extracellular matrix areas of femoral and tibial articular cartilages of young adult beagle dogs using qualitative and quantitative polarization microscopic analytical methods. Paraffin sections were cut perpendicularly to the articular surfaces from the femoral and tibial condyles and stained. Picrosirius red F38 staining combined with an antecedent digestion with testicular hyaluronidase was used to enhance the optical anisotropy of collagen. Birefringence of sulfated glycosaminoglycan molecules was selectively amplified by a combination of carboxymethylation with CH3I and a subsequent staining with toluidine blue. The specimens were analysed in a polarization microscope equipped with compensator plates, and retardation values of birefringence were determined in territorial and interterritorial matrix areas of different zones using monochromatic plane polarized light. It was found that besides some similarities there were significant differences in the submicroscopic organization of extracellular matrix between femoral and tibial articular cartilages. Common structural features of the femoral and tibial cartilages were the sulfated glycosaminoglycans and collagen fibrils which were circularly oriented in the territorial matrix, and these components were longitudinally arranged within the trabeculae of the interterritorial matrix. Furthermore, the territorial matrix was a more densely packed structure than the interterritorial matrix. Our results revealed the following major differences between the two cartilages: The degree of orientation of sulfated glycosaminoglycans was higher in the femoral cartilage matrix areas as compared to the identical structures of the tibial cartilage; the collagen structure was more densely packed in the interterritorial matrix of the superficial and mineralization zones of the femoral cartilage than in the tibial cartilage, and except for the zone of mineralization, the degree of collagen orientation was higher in the territorial matrix of the femoral than the tibial cartilage. These findings suggest that the extracellular matrix of femoral condylar cartilage has a more densely packed molecular structure than the softer tibial cartilage matrix. This structural difference may have an influence on the pathogenesis of diseases involving articular cartilage.

Animals↗

Osteoclast differentiation at growth plate cartilage-trabecular bone junction in newborn rat femur.

Using 3-day-old newborn rats, we examined the differentiation processes of osteoclasts associated with the destruction of the femoral growth plate cartilage and primary trabecular bone. In the growth plate cartilage, thin mineralized areas were detected solely in the longitudinal septal cartilage matrix in the hypertrophic zone, but the transverse septal cartilage matrix between adjacent chondrocytic lacunae within a row of chondrocytes remained unmineralized. The longitudinal septal cartilage between adjacent rows of chondrocytes appeared to persist, forming the walls of opened lacunar canals. Consistent with the removal of the transverse septal cartilage matrix, the longitudinal canals of opened chondrocytic lacunae were deeply invaded by capillary vessels, mononuclear cells and multinucleated pre-osteoclasts lacking a ruffled border. CD34-positive endothelial cells of capillary vessels deeply penetrated into the transverse septal cartilage matrix facing the medullary cavity and the opened chondrocytic lacunae. ED1-positive monocytes/macrophages were distributed at the chondro-osseous junction, but they were distant from the erosive front of the transverse septa. Tartrate-resistant acid phosphatase-positive multinucleated pre-osteoclasts lacking a ruffled border and differentiated osteoclasts with a ruffled border were localized mainly at two locations: the chondro-osseous junction and the growth front of primary bone trabeculae. Osteoclasts were located on the type-I collagen-positive bone trabeculae close to the growth plate, but they appeared to be distant from the type-II collagen-positive cartilage matrix. Even within opened chondrocytic lacunae, when osteoclasts were distant from the cartilage and bone matrix, they lacked polarized cytoplasmic organization and a ruffled border. The osteoclasts located in the remaining septal cartilage also exhibited neither a ruffled border nor a clear zone. Osteoclasts with a prominent ruffled border and clear zone were located in bone matrix covering the remaining septal cartilage. These results suggest that osteoclasts require hydroxyapatite crystals and bone matrix constituents for ruffled border formation and are not involved in resorption of the unmineralized transverse and mineralized longitudinal septal cartilage without covering bone matrix at the chondro-osseous junction.

Animals↗

Experimentally Induced Articular Cartilage Injury: The Combined Use of Misoprostol and Diclofenac as Therapeutic Agents.

Injection of chymopapain (CP) into the rabbit knee causes rapid depletion of proteoglycans (PGs) in the articular cartilage. Successful repair of the articular cartilage follows injection of only 0.2 mg CP whereas in animals injected with 0.2 mg CP, the repair phase fails leading to cartilage destruction within 21 days. Previous work by the authors indicated that daily oral diclofenac reduced the severity and incidence of CP-induced cartilage injury after 21 days. The present study was designed to determine if administration of diclofenac promoted articular cartilage repair after CP injury over a longer period of time and if coadministration with misoprostol could reduce the concentration of diclofenac needed to promote repair as well as confer protection to the gastric mucosa. Adolescent male New Zealand white rabbits received CP-induced cartilage injury (2.0 mg) followed by daily oral diclofenac, diclofenac/misoprostol or misoprostol. Control animals received diclofenac, diclofenac/misoprostol, or misoprostol or no drug treatment with no cartilage injury. All animals were sacrificed after 2 months. Examination of the stomachs from animals receiving no drug or misoprostol only were completely normal. Most animals receiving diclofenac only had abnormal gastric mucosa. In contrast, coadministration of diclofenac/misoprostol revealed significantly fewer abnormalities. Analysis of the composite histologic score of patellae and measurements of cartilage PG content revealed no significant differences in groups which received CP injury with and without drug treatment. Histology scores and cartilage PG content from animals in groups which did not receive CP injury, but were treated with diclofenac/misoprostol, diclofenac or misoprostol were within normal limits and thus did not differ significantly from untreated control cartilage. The results of this study indicate that daily administration of diclofenac, diclofenac/misoprostol or misoprostol has no protective effect on CP-induced cartilage injury after 2 months. Administration of diclofenac only results in severe gastric abnormalities which are significantly reduced if diclofenac is coadministered with misoprostol. Administration of diclofenac, diclofenac/misoprostol or misoprostol has no effect on PG content of cartilage from otherwise normal joints.

Journal Article↗

Characterization of collagen types XII and XIV from fetal bovine cartilage.

The structurally related type XII-like collagen molecules TL-A and TL-B were recently identified in fetal bovine epiphyseal cartilage and subsequently shown to be collagen types XII and XIV, respectively. By indirect immunofluorescent staining of cartilage using monoclonal antibodies to the NC3 domains of each molecule, it was shown that type XII collagen was present predominantly around cartilage canals, the articular surface, subperichondrial margins, and the perichondrium, was less so in the remaining cartilage matrix, and was absent from the growth plate region. In the permanent cartilage of trachea, type XII stained somewhat more intensely in the margins beneath the loose connective tissue. Type XIV collagen localized more uniformly throughout the articular cartilage and was also absent from the growth plate region, whereas in tracheal cartilage, its distribution was similar to type XII. We have characterized the structure of these cartilage molecules and compared them with those from fetal bovine skin. Extraction of cartilage with 1 M NaCl and differential NaCl precipitation yields a fraction enriched for these two collagens. Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting with monoclonal antibodies to the large amino-terminal non-triple-helical domain, NC3, revealed the presence in cartilage of two forms of type XII collagen: type XIIB, the molecule previously identified in chick and bovine tissues, and type XIIA, a much larger form equivalent to the molecule recently identified in WISH-transformed epithelial cell culture medium (Lunstrum, G. P., McDonough, A. M., Marinkovich, M. P., Keene, D. R., Morris, N. P., and Burgeson, R. E. (1992) J. Biol. Chem. 267, 20087-20092). Digestion with bacterial collagenase shows that the increased mass is present in the NC3A domain. Additional purification by velocity sedimentation and observation of rotary-shadowed images demonstrates molecules with extended non-triple-helical arms approximately 80 nm in length analogous to the WISH cell molecules. Electrophoretic mobilities of bands corresponding to type XIIA, but not type XIIB, are sensitive to chondroitinase ABC, indicating that type XIIA is a chondroitin sulfate proteoglycan and that modification occurs predominantly within the NC3A domain distal to NC3B. Neither type XIIB from skin nor type XIIA from WISH cells are chondroitinase-sensitive. By similar analysis, a portion of the type XIV collagen chains in cartilage was also sensitive to chondroitinase digestion. Chondroitin sulfate is apparently not located on its NC3 domain. As in skin, collagen types XII and XIV have subtly different distributions within cartilage and type XII may have a tissue-specific structure.

Animals↗

Response of the donor and recipient cells in mesenchymal cell transplantation to cartilage defect.

To facilitate the repair of articular cartilage defects, autologous mesenchymal cells from bone marrow or periosteum were transplanted in a rabbit model. Two weeks after the transplantation of the mesenchymal cells, the whole area of the original defect was occupied by cartilage. From the deep area of the reparative cartilage, which contacted with host bone, chondrocytes became hypertrophic and the invasion of bone with vasculature started, until the replacement reached the natural junction of the host cartilage and the subchondral bone about 4 weeks after transplantation. Twelve weeks after the transplantation, the repair cartilage in the defect became a little thinner than the adjacent normal cartilage, which became a little thinner 24 weeks after the transplantation (the longest observation period in the study). Large, full-thickness defects of the weight-bearing region of the articular cartilage were repaired with hyaline-like cartilage after implantation of autologous mesenchymal cells. The repair process by mesenchymal cell transplantation was explained as follows: The donor transplanted cell differentiated into cartilage and the defects were completely filled with cartilage. Then, mesenchymal cells that entered the chondrogenic lineage rapidly progressed through this lineage to the hypertrophic state, which was then the target for erosion and vascular invasion. Although this vasculature and the newly formed bone were considered to be host-derived, there was no evidence to that effect. To prove this, suitable experimental marking of these donor cells is needed. In the case of chondrocyte transplantation, the repair cartilage maintained its thickness to the full depth of the original defect; the tissue derived from the implanted chondrocytes was not invaded by vessels or replaced by subchondral bone.

Animals↗

Destructive cartilage loss in the joints of adult male broiler breeding fowls.

Patterns of destructive cartilage loss were studied in 60 male broiler breeding fowls. All showed destructive lesions in their hip or intertarsal joints and were between 18 and 62 weeks old when killed. Although surface regressive changes in articular cartilage were common, deep fibrillation, as seen in human and mammalian osteoarthrosis, was not identified. This difference probably reflects the more fibrous nature of articular cartilage in birds, but a number of similarities to hyaline cartilage degeneration were noted. Destructive cartilage loss resulted from partial or full thickness detachment of uncalcified cartilage. Clefts in deep cartilage preceded segmental detachment and occurred in cartilage with an intact articular surface. Detachment of segments of uncalcified cartilage may be the principal method of destructive cartilage loss in all avian species. It is concluded that clefts and destructive cartilage loss in adult broiler fowls can be a consequence of articular osteochondrosis or may result from osteoarthrosic lesions.

Acetabulum↗

Nonuniform swelling-induced residual strains in articular cartilage.

Swelling effects in cartilage originate from an interstitial osmotic pressure generated by the presence of negatively charged proteoglycans in the tissue. This swelling pressure gives rise to a non-zero residual strain in the cartilage solid matrix in the absence of externally applied loads. Previous studies have quantified swelling effects in cartilage as volumetric or dimensional change of excised samples in varying osmotically active solutions. This study presents a new optical technique for measuring two-dimensional swelling-induced residual strain fields in planar samples of articular cartilage attached to the bone (i.e., in situ). Osmotic loading was applied to canine cartilage bone samples by equilibration in external baths of varying NaCl concentration. Non-zero swelling-induced strains were measured in physiological saline, giving evidence of the existence of residual strains in articular cartilage. Only one component of planar strain (i.e., in thickness direction) was found to be non-zero. This strain was found to be highly non-uniform in the thickness direction, with evidence of compressive strain in the deep zone of cartilage and tensile strain in the middle and surface zones. The obtained results can be used to characterize the material properties of the articular cartilage solid matrix, with estimated values of 26 M Pa for the tensile modulus for middle zone cartilage. The method provides the basis to obtain material properties of the cartilage solid matrix from a simple, free-swelling test and may be useful for quantifying changes in cartilage properties with injury, degeneration and repair.

Analysis of Variance↗

Overuse of hyaline cartilage and imaging.

Traumatic injury to joints may involve articular cartilage alone or result in osteochondral fractures which may impair mechanical properties of articular cartilage. Injuries of articular cartilage alone with visible tissue disruption and osteochondral fractures are now visualized by MRI which is the only modality for direct non-invasive visualization of articular cartilage. Three-dimensional T1-weighted gradient-echo sequences with fat-suppression provide high accuracy in the detection of cartilage surface defects. Fast spin echo imaging with heavy T2-weighting demonstrates cartilage defects in the presence of joint effusion accurately too, but minimal slice thickness in 2D-imaging is limited. For correct staging of osteochondral fractures, which determines further therapy, intraarticular administration of contrast media may be necessary. Repetitive direct blunt trauma or high-energy joint loading can cause cartilage damage without visible tissue disruption. To demonstrate this early stage of chondral injury special techniques and agents are necessary. These include diffusion weighted imaging, measurements of magnetization transfer as a function of collagen concentration, proton density mapping to plot the distribution of water in hyaline cartilage and sodium imaging to visualize ions bound to proteoglycans or intraarticular application of Mangan selectively bound to proteoglycans. Although promising techniques, they are still experimental. With recent developments of repair of cartilage defects by cartilage grafts, osteochondral autografts and transplantation, MRI becomes the method of choice in the noninvasive evaluation of injured articular cartilage and follow-up studies.

Cartilage, Articular↗

The biomechanical, morphologic, and histochemical properties of the costal cartilages in children with pectus excavatum.

BACKGROUND/PURPOSE: The cause of the pectus excavatum (PE) remains unclear, although some results of research have indicated that the disturbance of the sternum or costal cartilage might be responsible for this deformity. But no decisive evidence has been gained. The authors have analyzed the biomechanical, morphologic, and histochemical properties of the cartilage in PE and intend to support the belief that the disturbance of the cartilage might contribute to the development of PE. METHODS: Thirty-eight specimens of the sixth cartilage were obtained at operation for the PE group (aged from 3 to 6 years; mean, 4.2 years). And 28 specimens of the control group (aged from 3 to 6 years; mean, 4.4 years) were gained from routine postmortem examinations in which the cause of death was unlikely to have affected the cartilage. The biomechanical test was carried out in a material testing machine (Shimadzu AG-10TA, Tokyo, Japan). The relation curve of load-deformation in tensile and compressive tests and the curve of load-time in the flexuous test were recorded automatically. The values of the ultimate strength and strain were calculated from this relation curve. The specimens also underwent H&E staining. The values of the area, circumference, mean diameter, maximal diameter, and morphologic factor of the cell and the nucleus of the cartilage in superficial and deep area were determined with the help of image analysis software (GT-2 model, China). The superficial zone (SZ) and deep zone (DZ) of the cartilage were examinated with electron microscopy (JEM-100SX, Japan). The distribution and intensity of type II collagen was shown by immunohistochemistry staining and analyzed with the image analysis software (GT-2 model, Huakang Co, Chengdu, China). The extent and distribution of proteoglycan were analyzed after Safranin-O and periodic acid shiff (PAS) staining. RESULTS: The mean strength of the costal cartilage in the experimental group was less than that in the control group in terms of tension, compression, and flexure (P <.05). The shape of the stress-strain curve for tension and compression in the experimental group was different from the control group. The fracture load in the experimental group was less than in the control group in tension (1.5 MPa versus 2.8 MPa) and in compression (.2 MPa versus 8.3 MPa). The time of fracture in experimental group was 30 seconds compared with 38 seconds in control group. No denaturation or necrosis could be found in light microscopical examination. There was no manifestation of hyperplasia or hypoplasia in the costal cartilage of the PE group. In SZ and DZ areas, the pattern and the number of mitochondria, endoplasmic reticulum, and Golgi in the experimental group were the same as the control group in transmission electron microscopy. Furthermore, the distribution and the number of proteoglycan in the 2 groups did not show a significant difference both in SZ and DZ areas. Although the distribution of the collagen in SZ areas was normal, this pattern was disturbed in DZ areas in the experiment group. The results of type II collagen immunohistochemistry examination was concordant with that change. No significant difference between control and experimental group could be seen in Safranin-O and PAS staining for proteoglycan. CONCLUSIONS: The biomechanical stability of the cartilage was decreased in the PE group. This might be caused by the disorderly arrangement and distribution of the collagen in the cartilage of PE patients. J Pediatr Surg 36:1770-1776.

Biomechanical Phenomena↗

Depth-resolved phase retardation measurements for laser-assisted non-ablative cartilage reshaping.

Since polarization-sensitive optical coherence tomography (PS-OCT) is emerging as a new technique for determining phase retardation in biological materials, we measured phase retardation changes in cartilage during local laser heating for application to laser-assisted cartilage reshaping. Thermally-induced changes in phase retardation of nasal septal cartilage following Nd:YAG laser irradiation were investigated using a PS-OCT system. A PS-OCT system and infrared imaging radiometer were used to record, respectively, depth-resolved images of the Stokes parameters of light backscattered from ex vivo porcine nasal septal cartilage and radiometric temperature changes following laser irradiation. PS-OCT images of cartilage were recorded before (control), during and after laser irradiation. From the measured Stokes parameters (I, Q, U and V), an estimate of the relative phase retardation between two orthogonal polarizations was computed to determine birefringence in cartilage. Phase retardation images of light backscattered from cartilage show significant changes in retardation following laser irradiation. To investigate the origin of retardation changes in response to local heat generation, we differentiated two possible mechanisms: dehydration and thermal denaturation. PS-OCT images of cartilage were recorded after dehydration in glycerol and thermal denaturation in heated physiological saline. In our experiments, observed retardation changes in cartilage are primarily due to dehydration. Since dehydration is a principal source for retardation changes in cartilage over the range of heating profiles investigated, our studies suggest that the use of PS-OCT as a feedback control methodology for non-ablative cartilage reshaping requires further investigation.

Animals↗

Tibial and femoral cartilage changes in knee osteoarthritis.

BACKGROUND: Despite the increasing interest in using knee cartilage volume as an outcome measure in studies of osteoarthritis (OA), it is unclear what components of knee cartilage will be most useful as markers of structure in the tibiofemoral (TF) joint. OBJECTIVE: To compare the changes that occur in femoral and tibial cartilage volume in normal and osteoarthritic knees and how they relate to radiological grade. METHODS: 82 subjects (44 female, 38 male, age range 35-69 years) with a spectrum of radiological knee OA were examined. Each subject had femoral and tibial cartilage volume in the medial and lateral TF joint determined from T(1) weighted fat saturated magnetic resonance images of the knee. Radiological grade of OA was determined from standing knee radiographs. RESULTS: There was strong correlation between femoral and tibial cartilage volume measured in both the medial (R=0.75, p<0.001) and lateral TF joint (R=0.77, p<0.001). Similar correlations persisted when those with normal and those with OA joints were examined separately at both the medial and lateral TF joint. For each increase in radiological grade of joint space narrowing (0-3), there was a mean (SD) reduction in tibial cartilage volume of 1.00 (0.32) ml in the medial compartment and 0.53 (0.25) ml in the lateral compartment, after adjusting for differences in bone size. Similar changes were seen in the femoral cartilage. CONCLUSIONS: The amounts of tibial and femoral cartilage are strongly related. It may be that for TF joint disease, measuring tibial cartilage alone may be adequate, given that measurements of the total femoral cartilage are less reproducible and the difficulties inherent in identifying the most appropriate component of femoral cartilage to measure.

Adult↗

Age related changes and osteochondrosis in swine articular and epiphyseal cartilage: light ane electron microscopy.

Age related changes and osteochondrosis in swine were studied using light microscopy and electron microscopy in articular cartilage and light microscopy and epiphyseal cartilage of swine from three days to 30 weeks of age. Thickness, cellularity and vascularity of both the epiphyseal and articular cartilage, decreased as the swine aged. Osteochondrotic changes included formation of "plugs" of cartilage indicating localized failure of ossification and separation and space formation in epiphyseal cartilage. Eosinophilic streaks and space formation in epiphyseal cartilage was observed in relation to epiphyseal separation. Electron microscopy showed a continuous fibrillar layer on the surface of the cartilage corresponding to the lamina splendens of light microscopy. This layer increased in the thickness and showed accumulation of amorphous material between the fibrils with aging. In the matrix, the orientation and distribution of the collagen fibers changed with growth and thicker fibers with clear sub banding were more common in older age groups. Also, necrotic cells, glycogen containing bodies and cellular debris were noticed in the matrix of normal cartilage in old animals. Chondrocytes in the younger cartilage showed accumulation of organelles responsible for protein synthesis; while Golgi bodies, vesicles, lysosomes, well developed foot processes and other inclusions were noticed in older cartilage. Cartilage erosions had a clumped and disrupted lamina splendens on the surface and electron lucent patches in the ground substances of the matrix and chondrocyte cytoplasm.

Aging↗

Neoplastic invasion of the laryngeal cartilage: reassessment of criteria for diagnosis at CT.

PURPOSE: To evaluate eight different diagnostic criteria to help detect neoplastic invasion of laryngeal cartilage at computed tomography (CT). MATERIALS AND METHODS: In a prospective series, 111 patients with carcinoma of the larynx or hypopharynx underwent thin-section, contrast material-enhanced CT before total or partial laryngectomy. The following CT criteria were evaluated: extralaryngeal tumor, sclerosis, tumor adjacent to nonossified cartilage, serpiginous contour, erosion or lysis, obliteration of marrow space, cartilaginous blowout, and bowing. Histologic findings were correlated with findings on CT scans obtained at each level. RESULTS: Histologically, 122 of 412 cartilages were invaded. Depending on the diagnostic criteria and each specific cartilage, there was great variation in sensitivity (7%-83%) and specificity (40%-100%). Sclerosis was the most sensitive criteria in all cartilages but often corresponded to reactive inflammation in the thyroid cartilage. Extralaryngeal tumor and erosion or lysis yielded the highest specificity. Tumor adjacent to nonossified cartilage, serpiginous contour, and obliteration of marrow space were specific although not sensitive signs of invasion in the arytenoid and cricoid cartilage and were nonspecific in the thyroid cartilage. Blowout and bowing were not useful. Selection of the appropriate combination of criteria enabled an overall sensitivity of 91% (associated specificity, 68%) or an overall specificity of 79% (associated sensitivity, 82%). CONCLUSION: Detection of neoplastic cartilage invasion with CT greatly depended on the appropriate use of individual and combined CT criteria.

Adult↗

The effects of resorbable plates on rabbit ear cartilage.

BACKGROUND: When performing septorhinoplasty, deviated segments of septal cartilage can be straightened using cartilage or bone as splinting grafts. In some cases, autologous material is not available without an additional surgical procedure to harvest cartilage or bone. It is possible that resorbable plates can be used to splint and straighten deviated cartilage. Experience using bioresorbable rigid fixation devices on cartilage has been limited. OBJECTIVE: To examine early histopathologic changes of rabbit ear cartilage and adjacent soft tissue following implantation with bioresorbable plates. DESIGN: Nonrandomized, placebo-controlled trial. SUBJECTS: Twelve adult New Zealand white rabbits. MATERIALS AND METHODS: Ten adult New Zealand white rabbits (20 ears) underwent stenting of intact ear cartilage with LactoSorb plates (Lorenz, Jacksonville, Fla). Rabbits were killed 28 days after implantation, and the soft tissue, plates, and cartilage were harvested and prepared for histological examination. As controls, 2 rabbits (4 ears) underwent dissection and closure without stenting. RESULTS: Six rabbits experienced superficial skin breakdown on the ventral surface of the ear caused by excessive wound tension of the implant. The cartilage-plate interface and the surrounding soft tissues stenting the dorsal side of the ear remained free of inflammation or necrosis for all animals. Simple elevation of the perichondrium revealed no differences in the appearance of the cartilage between the control and test rabbits. CONCLUSIONS: Resorbable plates have no deleterious effects on cartilage during the first month of implantation. While short-term studies have documented the safety and efficacy of using bioresorbable plates, further studies are recommended.

Absorbable Implants↗

Natural history of knee cartilage defects and factors affecting change.

BACKGROUND: Knee cartilage defects may play an important role in early osteoarthritis, but little is known about their natural history. METHODS: Knee cartilage defect score (range, 0-4), cartilage volume, and bone surface area were determined using T1-weighted fat-saturated magnetic resonance imaging in 325 subjects (mean age, 45 years) at baseline and 2 years later. RESULTS: Thirty-three percent of the subjects had a worsening (>or=1-point increase) and 37% of the subjects had an improvement (>or=1-point decrease) in cartilage defect score in any knee compartment during 2.3 years. A worsening in cartilage defect score was significantly associated with female sex (odds ratio [OR], 3.09 and 3.64 in the medial and lateral tibiofemoral compartments) and baseline factors, including age (OR, 1.05 per year in the medial tibiofemoral compartment), body mass index (OR, 1.08 in the lateral tibiofemoral compartment), tibiofemoral osteophytes (OR, 6.22 and 6.04 per grade), tibial bone area (OR, 1.24 and 2.07 per square centimeter), and cartilage volume (OR, 2.91 and 1.71 per milliliter in the medial tibiofemoral and patellar compartments). An improvement in cartilage defect score had similar but reversed associations with these factors (except for sex), including a decrease in body mass index (OR, 1.23 in the medial tibiofemoral compartment). CONCLUSIONS: Knee cartilage defects are variable, and changes are associated with female sex, age, and body mass index. Increases are associated with baseline cartilage volume, bone size, and osteophytes, suggesting a role for these in the pathogenesis of cartilage defects. Interventions such as weight loss may improve knee cartilage defects.

Adult↗

Autogenous tissue-engineered cartilage: evaluation as an implant material.

OBJECTIVES: To determine whether autogenous tissue-engineered cartilage grafts can be synthesized in predetermined shapes, to compare tissue-engineered cartilage with native cartilage with respect to histological characteristics and biomechanical properties, and to demonstrate how multiple transplantations affect tissue-engineered cartilage. DESIGN: Controlled, prospective animal study. SUBJECTS: Twenty New Zealand white rabbits, 3 weeks old. INTERVENTIONS: Autogenous chondrocytes were seeded onto biodegradable polyglycolic acid-poly-L-lactic acid copolymer templates in 1 of 3 shapes (cross, nasal tip graft, or auricle). Grafts and controls of sculpted cartilage were divided among 3 groups: short-term implantation (4 or 8 weeks), long-term implantation (6 or 12 months), and a reimplantation group. The gross morphological features, histological findings, and tensile strength of grafts were assessed. RESULTS: Production of tissue-engineered cartilage was confirmed in 30 of 31 implants. Histological evaluation demonstrated characteristic cartilaginous matrix, but with prominent vascular and fibrous tissue ingrowth. In long-term implantation grafts (n=4), foci of osteoid were evident by 6 months. In the subset of transplanted grafts (n=7), 5 of 7 demonstrated significant loss of cartilage viability. Tensile strength measurements demonstrated values 24% and 41% of those of controls at 4 and 8 weeks, respectively. CONCLUSIONS: Tissue-engineered autogenous cartilage can be reliably produced, and predetermination of graft shape is possible. Histologically, grafts represent composites of mature cartilage infiltrated by vasculature and fibrous tissue, with delayed osteoid formation. Graft viability is compromised by early transplantation, and tensile strength is less than that of native cartilage. These results demonstrate the feasibility of tissue-engineered cartilage as a future graft material.

Animals↗