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PubMed2005

A treatment algorithm for the management of articular cartilage defects.

The clinical consequences of articular cartilage defects of the knee are pain, swelling, mechanical symptoms, athletic and functional disability, and osteoarthritis. Full thickness articular cartilage defects have a poor capacity to heal. The challenge to restore the articular cartilage surface is multidimensional, faced by basic scientists in the laboratory and orthopedic surgeons in the operating room. This article provides an overview of the contemporary treatment options available for the restoration of articular cartilage defects of the knee.

Algorithms↗

PubMed2004

A type XI collagen mutation leads to increased degradation of type II collagen in articular cartilage.

OBJECTIVE: To determine in articular cartilage whether degraded type II collagen is more abundant in Col11a1 mutant cho/+ than in age-matched +/+ mice and whether collagen degradation occurs in a generalized or localized fashion. DESIGN: Knee joints from cho/+ and +/+ mice at 6, 9, 12 and 15 months of age were dissected, fixed, cryosectioned, and stained with antibody COL2-3/4m against denatured type II collagen using a FITC-conjugated secondary antibody. Sections were viewed and photographed under a fluorescence microscope and areas of staining were quantified. RESULTS: Before 12 months of age, little degraded collagen staining was detectable in +/+ or cho/+ mice. By 15 months, however, cho/+ mice showed significantly more degraded type II collagen than age-matched controls. Degraded collagen staining was localized at the articular surface, not distributed generally throughout the articular cartilage. CONCLUSIONS: The results suggest a model in which cumulative biomechanical stresses trigger increased collagen synthesis and degradation in both +/+ and cho/+ mice at around 12 months of age. Cho/+ mice, however, are less able to synthesize and assemble normal replacement collagen fibrils because of the Col11a1 mutation. Degradation is further activated, resulting in the accumulation of degraded type II collagen in the articular cartilage extracellular matrix. Similar mutations that do not overtly affect skeletal development may likewise predispose humans to increased collagen degradation and resultant osteoarthritis.

Animals↗

PubMed1995

Variations in thickness of articular cartilage in the human sacroiliac joint.

Differences in articular cartilage thickness in the sacroiliac joint were investigated in different regions of the sacral and the iliac articular surfaces in the embalmed cadavers of five males and six females. The mean thickness of the sacral articular cartilage was greater than that of the iliac articular cartilage (P < 0.001) and the sacral articular cartilage of the female was thicker than that of the male (P < 0.02). Differences between thicknesses of the iliac articular cartilage in the male and female and in different regions of the sacral and iliac articular cartilages were found to be not significant.

Age Factors↗

PubMed1999

Composition of the extracellular matrix in human cricoarytenoid joint articular cartilage.

The extracellular matrix of the human cricoarytenoid joint articular cartilage is involved in different pathological changes. Interestingly, in contrast to the limb joints, the extracellular matrix composition of the healthy cricoarytenoid joint articular cartilage has not yet been elucidated except by some light microscopical investigations. The present study investigates the extracellular matrix components of the cricoarytenoid joint articular cartilage by means of light microscopy, immunohistochemistry, transmission electron microscopy and scanning electron microscopy and compares them with the limb joints for a better understanding of their involvement in joint disease. Chondrocytes near the joint surface of the cricoid and arytenoid cartilage differ from chondrocytes of deeper cartilage layers. The extracellular matrix of the articular cartilage contains chondroitin-4-sulfate, chondroitin-6-sulfate and keratansulfate as well as collagen types II, III, VI, IX and XI. Type-III-collagen shows a special distribution throughout the joint cartilage. In deeper cartilage layers, type-III-collagen occurs only pericellularly; in higher cartilage layers type-III-collagen is also located territorially and interterritorialy in small amounts. Scanning and transmission electron microscopy have revealed the articular surface of the cricoid and arytenoid cartilage to consist of a network of irregularly organized collagen fibrils, which are lined by a layer of electron dense material. The network coats subjacent collagen bundles which descend obliquely downward and intermingle at right angles in the middle part of the articular cartilage with collagen bundles of the deeper cartilage zones. The articular cartilage surface shows structural characteristics which differ from the underlying cartilage. The superficial electron dense layer possibly plays a role in the lubrication of the articular cartilage surface. The alignment of the fibrillar structures in the articular cartilage of the cricoarytenoid joint varies from those of the limb joints based on the different strain occurring during arytenoid movement. Nevertheless, the human cricoarytenoid joint articular cartilage can be compared with the joints of the limbs despite its extracellular matrix composition and its involvement in joint pathology. Evidence of type III collagen in the outermost layer of the articular cartilage of the cricoarytenoid joint presents a peculiarity, which has yet not be demonstrated in the articular cartilage of limb joints.

Adult↗

PubMed1975

Evidence of cartilage flow in deep defects in articular cartilage.

Full thickness defects (core defects) violating subchondral bone were created in the weight-bearing area of articular cartilage lining the rabbit medial femoral condyle. The repair reaction that follows has two components: (1) a sliding and flowing of cartilage over the edge of the defect and (2) a filling of the defect by repair tissue arising from the marrow spaces. Past studies have paid little or no attention to cartilage flow but this first scanning electron microscopic study of deep defects shows that it is an important phenomenon which materially affects the changes that occur and also the outcome of such injuries. Briefly, we have found that in most cases the cartilage flows downwards into the core defect. The repair tissue then grows along and over the "toed-in" catilage. In other cases the flowing cartilage rides over the repair tissue from the marrow spaces and as a result of load bearing and joint movement, becomes frayed and drawn out into long ribbons and rope-like structures.

Animals↗

PubMed1997

Current concepts in the treatment of articular cartilage defects.

Over time, articular cartilage loses the capacity to regenerate itself, making repair of articular surfaces difficult. Lavage and debridement may offer temporary relief of pain for up to 4.5 years, but offer no prospect of long-term cure. Likewise, marrow-stimulation techniques such as drilling, microfracture, or abrasion arthroplasty fail to yield long-term solutions because they typically promote the development of fibrocartilage. Fibrocartilage lacks the durability and many of the mechanical properties of the hyaline cartilage that normally covers articular surfaces. Repair tissue resembling hyaline cartilage can be induced to fill in articular defects by using perichondrial and periosteal grafts. However, these techniques are limited by the amount of tissue available for grafting and the tendency toward ossification of the repair tissue. Autogenous osteochondral arthroscopically implanted grafts (mosaicplasty), or open implantation of lateral patellar facet (Outerbridge technique), requires violation of subchondral bone. Osteochondral allografts risk viral transmission of disease and low chondrocyte viability, in addition to removal of host bone for implantation. Autologous chondrocyte implantation offers the opportunity to achieve biologic repair, enabling the surgeon to repair the joint surface with autologous articular cartilage. With this technique, care must be taken to ensure the safety, viability, and microbial integrity of the autologous cells while they are expanded in culture over a 4- to 5-week period prior to implantation. Surgical implantation requires equal attention to meticulous technique. In the future, physiologic repair also may become possible using mesenchymal stem cells or chondrocytes delivered surgically in an ex vivo-derived matrix. This would allow in vitro manipulation of cells with growth factors, mechanical stimuli, and matrix sizing to allow implantation of mature biosynthetic grafts which would allow treatment of larger defects with decreased rehabilitation and morbidity.

Cartilage, Articular↗

PubMed2004

Consolidation responses of delipidized articular cartilage.

OBJECTIVE: To determine the role of articular cartilage lipids in its load-bearing function. DESIGN: Normal and delipidised, bovine articular cartilage specimens were statically loaded and both the hydrostatic excess pore pressure and creep strain were measured. From this the compression stiffness of the skeletal structures of both types of matrices was determined. BACKGROUND: It has been hypothesized that surfactant injection could relief osteoarthritis, but there is no study in the literature relating to the influence of lipids, the main ingredients of such products, on cartilage load-carriage. METHODS: Articular cartilage specimens were obtained from the patellar grooves of 2-3 year old bovine animals. When required specimen delipidization was carried out using chloroform/methanol rinsing. Both normal and delipidised samples were loaded in the consolidometer and the hydrostatic excess pore pressure and strain were measured. RESULTS: The transient patterns of the hydrostatic excess pore pressure were similar for both types of tissue, with a relatively insignificant increase of 2% in the maximum hydrostatic excess pore pressure of the delipidized samples relative to the normal intact specimens. The maximum creep strain of the delipidised specimens decreased by 10% on average relative to their normal intact counterparts, thereby indicating that delipidization causes stiffening of the cartilage matrix. CONCLUSION: The delipidized fluid-saturated articular cartilage is stiffer than its intact counterpart with consequence for cartilage compliance during function. RELEVANCE: Because osteoarthritis can be accompanied by lipid loss in cartilage, this study contributes to the further understanding of the disease with potential benefit for treatment.

Adaptation, Physiological↗

PubMed1999

Autologous mesenchymal progenitor cells in articular cartilage repair.

The lack of repair of articular cartilage where the damage does not penetrate the subchondral bone indicates the importance of marrow components in the repair of the articular cartilage. In adult animals, there is an inability of articular cartilage chondrocytes to heal chondral defects, but if the damage extends beyond the subchondral bone, a repair process ensues in which mesenchymal progenitor cells migrate into the injured site and undergo chondrogenic differentiation. However, analysis of animal models and human biopsy samples indicates that fibrocartilage, rather than true articular cartilage is the predominant tissue synthesized. To improve this outcome, the use of cell based implants of culture expanded progenitor cells from various sources has been proposed and attempted. This paper describes some of the age related differences in the natural repair of osteochondral defects, the in vitro characterization of the chondrogenic potential of certain mesenchymal cell types, and some of the characteristics required of cell and matrix constructs that may be used for repair or regeneration of articular cartilage.

Animals↗

PubMed1989

Articular cartilage lesions of the knee.

The pathogenesis and clinical significance of articular cartilage lesions of the knee persist as topics of considerable interest among orthopedic surgeons. This study was designed to assess the association of articular cartilage degeneration with concomitant intraarticular abnormalities and to correlate the prevalence and severity of articular cartilage damage with preoperative historical and physical exam findings in patients presenting with knee pain. Twenty-six history and physical exam data points were prospectively collected from 192 patients (200 knees), consecutively undergoing arthroscopic knee surgery. During surgery, all articular cartilage lesions were recorded with respect to size, location, and character and were graded according to Oglivie-Harris et al. All concomitant knee joint abnormalities were simultaneously recorded. Of 200 knees examined arthroscopically, 12 knees revealed no demonstrable etiology for the presenting symptoms, 65 knees revealed assorted intraarticular pathology but no articular cartilage degeneration, and the remaining 123 knees revealed a total of 211 articular cartilage lesions (103 femoral, 72 patellar, 36 tibial); 7 femoral, 6 patellar and 0 tibial lesions were completely isolated (no concomitant knee joint pathology). The concomitance of femoral defects with tibial lesions was highly significant (p = 0.01). Femoral and tibial articular cartilage lesions were strikingly correlated with the presence of an unstable torn meniscus (p less than 0.001). Medial compartment articular cartilage lesions were significantly more common (p = 0.001), more closely associated with meniscal derangement, and appreciably more severe than lateral compartment lesions. In 75% of anterior cruciate ligament-deficient knees with concomitant articular cartilage degeneration, the duration from injury to surgery was greater than 9 months, and in each of these cases, a history of reinjury to the knee was elicited. From these data one can conclude that: (a) in some patients with painful knees, isolated articular cartilage lesions may be the only abnormality noted at arthroscopy; (b) unstable meniscal tears are significantly associated with destruction of articular cartilage; (c) the medial compartment is particularly susceptible to articular cartilage degeneration; and (d) in our series, anterior cruciate ligament tears were increasingly associated with articular cartilage destruction as the elapsed time from injury to arthroscopy increased.

Adult↗

PubMed2005

Cryopreservation and biophysical properties of articular cartilage chondrocytes.

In order to successfully cryopreserve articular cartilage chondrocytes, it is important to characterize their osmotic response during the cryopreservation process, as the ice forms and the solutes concentrate. In this study, experimental work was undertaken to determine the osmotic parameters of articular cartilage chondrocytes. The osmotically inactive volume of articular cartilage chondrocytes was determined to be 44% of the isotonic volume. The membrane hydraulic conductivity parameters for water were determined by fitting a theoretical water transport model to the experimentally obtained volumetric shrinkage data; the membrane hydraulic conductivity parameter L(Pg) was found to be 0.0633 microm/min/atm, and the activation energy E, 8.23 kcal/mol. The simulated cooling process, using the osmotic parameters obtained in this study, suggests a cooling rate of 80 degrees C/min for the cryopreservation of the articular cartilage chondrocytes of hogs. The data obtained in this study could serve as a starting point for those interested in cryopreservation of chondrocytes from articular cartilage in other species in which there is clinical interest and there are no parameters for prediction of responses.

Animals↗

PubMed2001

Effect of contact stress in bones of the distal interphalangeal joint on microscopic changes in articular cartilage and ligaments.

OBJECTIVE: To examine articular cartilage of the distal interphalangeal (DIP) joint and distal sesamoidean impar ligament (DSIL) as well as the deep digital flexor tendon (DDFT) for adaptive responses to contact stress. SAMPLE POPULATION: Specimens from 21 horses. PROCEDURE: Pressure-sensitive film was inserted between articular surfaces of the DIP joint. The digit was subjected to a load. Finite element models (FEM) were developed from the data. The navicular bone, distal phalanx, and distal attachments of the DSIL and DDFT were examined histologically. RESULTS: Analysis of pressure-sensitive film revealed significant increases in contact area and contact load at dorsiflexion in the joints between the distal phalanx and navicular bone and between the middle phalanx and navicular bone. The FEM results revealed compressive and shear stresses. Histologic evaluation revealed loss of proteoglycans in articular cartilage from older horses (7 to 27 years old). Tidemark advancement (up to 14 tidemarks) was observed in articular cartilage between the distal phalanx and navicular bone in older clinically normal horses. In 2 horses with navicular syndrome, more tidemarks were evident. Clinically normal horses had a progressive increase in proteoglycans in the DSIL and DDFT. CONCLUSIONS AND CLINICAL RELEVANCE: Load on the navicular bone and associated joints was highest during dorsiflexion. This increased load may be responsible for microscopic changes of tidemark advancement and proteoglycan depletion in the articular cartilage and of proteoglycan production in the DSIL and DDFT Such microscopic changes may represent adaptive responses to stresses that may progress and contribute to lameness.

Animals↗

PubMed2004

Intramatrix events during cryopreservation of porcine articular cartilage using rapid cooling.

Cryopreservation of articular cartilage may improve long-term transplantation results if cell and matrix integrity can be maintained. This study examined intramatrix events in intact porcine articular cartilage that occurred during a rapid-cooling technique with various concentrations of dimethyl sulfoxide (DMSO) (1, 3, 5, 6 and 7 M). Thermocouples were inserted into the solution and in the cartilage matrix to record the temperature during rapid cooling. In addition, scanning electron microscopy of freeze-substituted samples was performed and quantitatively evaluated for the areas representing ice in the matrix. The results of this study showed that low concentrations of DMSO resulted in the largest temperature gradient between the matrix and the surrounding solution, which occurred near the freezing point of the cryoprotectant solution. At higher concentrations of DMSO, the peak temperature gradient occurred near the glass transition temperature. The temperature measurements suggested that a significant amount of ice formed within the matrix at lower DMSO concentrations. At higher DMSO concentrations that resulted in vitrification of the external solution, there was evidence of some ice in the matrix. The scanning electron micrographs demonstrated significantly more matrix disruption (likely due to ice formation) (P<0.02) in the lower DMSO concentrations (1 and 5 M) while the 6 M DMSO concentration demonstrated minimal matrix disruption. Cryopreservation of articular cartilage with a rapid-cooling technique and high concentrations of DMSO resulted in partial vitrification of the matrix and significantly less matrix disruption. It appears that successful cryopreservation of viability and function in articular cartilage will require high concentrations of cryoprotectants and rapid cooling.

Animals↗

PubMed1998

A novel cartilage protein (CILP) present in the mid-zone of human articular cartilage increases with age.

A novel, somewhat basic noncollagenous protein was purified from guanidine hydrochloride extracts of human articular cartilage using cesium chloride density gradient centrifugation, followed by ion-exchange chromatography at pH 5, and gel filtration on two serially coupled columns of Superose 6 and Superdex 200. The protein of 91.5 kDa contains a single polypeptide chain substituted with N-linked oligosaccharides. It appeared unique to cartilage as studied by enzyme-linked immunosorbent assay and immunoblots of various tissue extracts. Its concentration in articular cartilages showed some variability with age being lower in young individuals. It represents a chondrocyte product, since it is synthesized by articular chondrocytes in explant cultures. Interestingly, the distribution of the protein in the articular cartilage provides important information on the nature of chondrocytes at different compartments in the tissue. Thus, chondrocytes in the middle/deeper layers of the tissue in particular, appeared to have produced the protein and deposited it in the interterritorial matrix. The protein was neither seen in the superficial nor in the deepest regions of the articular cartilage. Based on its immunolocalization we have named this protein CILP (cartilage intermediate layer protein).

Adolescent↗

PubMed1997

Evaluation of matrix scaffolds for tissue engineering of articular cartilage grafts.

Injury to articular cartilage predisposes that joint to further degeneration and eventually osteoarthritis. Recent studies have demonstrated the feasibility of using chondrocytes together with different biomaterial carriers as grafts for the repair of cartilage defects. The following study was undertaken to determine the effect of a variety of these materials on chondrocyte growth and extracellular matrix synthesis. We cultured chondrocytes on several commonly used materials and compared their rates of synthesis of proteoglycan and collagen. Additionally, we evaluated them in a closed culture recirculating system on these materials and compared them with standard culture techniques. This was done to see whether such a bioreactor-type system can be used to enhance the quality of in vitro reconstructed tissues. Our results demonstrated marked variability with respect to how chondrocytes responded to culture on the various materials. Bioabsorbable polymers such as polyglycolic acid (PGA)--enhanced proteoglycan synthesis, whereas collagen matrices stimulated synthesis of collagen. The use of the closed culture system, in general, improved the rates of synthesis of collagen and proteoglycan on the different material scaffolds. Exceptions were collagen synthesis on collagen matrices: use of the closed culture system did not enhance the rate of synthesis. Rates of proteoglycan synthesis on PGA scaffold initially was higher in the closed culture system but did not sustain a difference over the entire course of the 3-week culture period. This study demonstrates the importance of carrier material for the purpose of cartilage tissue reconstruction in vitro.

Biocompatible Materials↗

PubMed1987

Healing of experimentally produced lesions in articular cartilage following chondrocyte transplantation.

Articular cartilage is known to have limited ability to heal once injured, and attempts to heal lesions in cartilage have yielded equivocal results. The following experiments were performed to investigate healing in cartilage transplantation of chondrocytes grown in vitro. The knee joint of the New Zealand White rabbit was used as the experimental model. An initial baseline study was made to determine the intrinsic capability of cartilage for healing defects that do not fracture the subchondral plate. A second experiment examined the effects of autologous in vitro grown chondrocytes on the healing rates of these defects. The results were evaluated by qualitative and quantitative light microscopy. In control defects not grafted with chondrocytes, 6 weeks after the initial defect was created, there was little repair. Macroscopic and histological findings were consistent with an osteoarthritic pathology such as synovitis and "cell nests." Macroscopic results from grafted specimens displayed a marked decrease in synovitis and other degenerative changes. Defects which had received transplants had a significant amount of cartilage reconstituted (82%) compared to ungrafted controls (18%). Controls showed a healing rate comparable to that obtained in the initial baseline study.

Animals↗

PubMed1997

Anatomy of the human patellofemoral joint articular cartilage: surface curvature analysis.

Articular cartilage surfaces of 49 human patellae and 24 distal femora were characterized by identifying distinctive features with surface curvature analysis. Paired specimens from the same donor generally exhibited natural symmetry, so only results from nonpaired specimens were considered (39 patellae and 19 femora). In 23 of 39 patellae, proximal median and lateral transverse ridges extended to form an oblique ridge resembling a skewed lambda (lambda). Most of the unpaired patellae (37 of 39) exhibited only a single lateral transverse ridge, and most (32 of 39) had an odd facet. All but one patella exhibited a concave depression in the lateral and medial facets and a sellar area in the proximal region. All distal femoral surfaces exhibited a sellar trochlea. The concavity of the trochlea was greatest in the posterior aspect, near the intercondylar notch.

Adolescent↗

PubMed1993

Development of immortalized human articular cartilage cell lines.

Human articular cartilage cells were transfected with the t.-sensitive polyomavirus large T antigen of SV40. Several immortalized chondrocyte cell lines were obtained. The types of acidic polysaccharides and of collagen synthesized suggest dedifferentiation in the in vitro culture system used afterwards to obtain large numbers of cells.

Antigens, Polyomavirus Transforming↗

PubMed1991

Recombinant human interleukin-1 inhibits plasminogen activator inhibitor-1 (PAI-1) production by human articular cartilage and chondrocytes.

Human articular cartilage and chondrocyte monolayers in culture constitutively produced plasminogen activator inhibitor-1 (PAI-1) protein and mRNA, as assessed by a specific enzyme-linked immunosorbent assay and Northern blotting analysis, respectively. Recombinant human interleukin-1 (IL-1) invoked a dose-dependent inhibition of PAI-1 production in both cartilage and chondrocyte cultures. The inhibitory effect of IL-1 was observed between 2-8h after addition of the cytokine, while the optimal dose was between 10-100U/ml IL-1 alpha (57-570pM IL-1 alpha). Results obtained by Northern analysis of chondrocyte total RNA reflected those found for the PAI-1 antigen, namely, that nontreated chondrocytes showed PAI-1 mRNA which was reduced by IL-1 treatment. To our knowledge, this is the first report where IL-1 has been found to inhibit PAI-1 expression. Since IL-1 has been shown before to cause human cartilage destruction and a correlated change in plasminogen activator activity, it could be that a concomitant reduction in PAI-1 levels by IL-1 may be significant in the control of these changes in cartilage.

Antibodies, Monoclonal↗