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PubMed2003

Outcome of untreated traumatic articular cartilage defects of the knee: a natural history study.

BACKGROUND: Articular cartilage damage has been reported in 23% of knees with an acute anterior cruciate ligament (ACL) injury and 54% of those with chronic ACL laxity. Because the purpose of surgery is to reconstruct the ACL, the chondral lesion is usually an incidental finding. It is not known if any of the numerous treatments that have been recommended for chondral defects alters the natural history of the untreated lesion. We sought to determine what effect, if any, an isolated articular cartilage defect observed at the time of ACL reconstruction would have on the radiographic, subjective, and objective results after surgery if no intervention was performed on the cartilage lesion itself. METHODS: From 1987 to 1999, 2770 ACL reconstructions were performed, and 125 of them were done in patients who had an articular cartilage defect of Outerbridge grade 3 or 4 but had both menisci intact. The mean defect size was 1.7 cm (2) (range, 0.5 to 6.5 cm (2) ). Postoperative rehabilitation was not altered because of the chondral defect, and patients were allowed full weight-bearing and the full range of motion of which they were capable. A control group of patients matched on the basis of sex and age at surgery was identified from the database. No patient in the control group had a chondral defect or meniscal tear. Patients were evaluated at one, two, and five years after surgery and every five years thereafter with use of the IKDC (International Knee Documentation Committee) criteria, modified Noyes subjective questionnaire, and radiographs. RESULTS: Subjective follow-up was carried out more than two years after surgery (mean time, 8.7 years after surgery) for 101 patients. The results of objective evaluation were available for fifty-two patients, at a mean of 6.3 years. The patients in the control group had significantly higher subjective scores than did the patients with a defect in the medial compartment (mean, 95.2 points versus 94.0 points; p = 0.0451) and those with a defect in the lateral compartment (mean, 95.9 points versus 92.8 points; p = 0.0047). There was no significant correlation between larger defect size and lower subjective scores (p = 0.2543). The distribution of IKDC radiographic ratings was not significantly different between the groups. At least 79% of the patients in both groups returned to jumping, twisting, and pivoting sports at least at the recreational level. CONCLUSIONS: While statistical analysis revealed a difference in subjective scores between the defect and control groups, an average of 93 points for the patients with a lateral defect and 94 points for those with a medial defect indicates that most patients have very few symptoms. This study provides a baseline of information that can be used to compare the results of procedures designed to treat articular cartilage defects.

Adult↗
PubMed1998

Age-related changes in the articular cartilage of human sacroiliac joint.

Iliac and sacral articular cartilage of 25 human sacroiliac joints (1-93 years) are examined by light microscopy and immunohistochemistry in order to gain further insight into the nature and progress of degenerative changes appearing during aging. These changes can already be seen in younger adults as compared to cartilage degeneration known in other diarthrodial joints. Structural differences between sacral and iliac cartilage can already be observed in the infant: the sacral auricular facet is covered with a hyaline articular cartilage, reaching 4 mm in thickness in the adult and staining intensely blue with alcian blue at pH1. Iliac cartilage of the newborn is composed of a dense fibrillar network of thick collagen bundles, crossing each other at approximately right angles. A faint staining with alcian blue suggests a low content of acidic glycosaminoglycans. In the adult, iliac cartilage becomes hyaline and its maximal thickness reaches 1-2 mm. Both articular facets exhibit morphological changes during aging that are more pronounced in the iliac cartilage and resemble osteoarthritic degeneration; the staining pattern of the extracellular matrix becomes inhomogenous, chondrocytes are arranged in clusters and the articular surface develops superficial irregularities and fissures. Sometimes fibrous tissue fills up these defects. Nevertheless, large areas of iliac cartilage remain hyaline in nature. Sacral articular cartilage often remains largely unaltered until old age. The sacral subchondral bone plate is usually thin and shows spongiosa trabeculae inserted at right angles, suggesting a perpendicular load on the articular facet. Iliac subchondral spongiosa shows no definite alignment and joins the thickened subchondral bone plate in an oblique direction. The iliac cartilage therefore seems to be stressed predominantly by shearing forces, arising from the changing monopodal support of the pelvis during locomotion. The subchondral bone plate on both the iliac and sacral auricular facet is penetrated by blood vessels that come into close contact with the overlying articular cartilage. These vessels may contribute to the high incidence of rheumatoid and inflammatory diseases in the human sacroiliac joint. Immunolabelling with an antibody against type II collagen reveals a diminished immunoreactivity in the upper half of adult sacral cartilage and only a faint and irregular labelling in the iliac cartilage. Type I collagen can be detected in a superficial layer on the sacral articular surface and around chondrocyte clusters in iliac cartilage, as in dedifferentiating chondrocytes during the development of osteoarthritis.

Adolescent↗
PubMed1987

Charge-charge interactions between articular cartilage and cationic antibodies, antigens, and immune complexes.

Bovine articular cartilage was used to examine the binding of cationized antibodies, antigens, and immune complexes to articular cartilage by charge-charge interactions. Rabbit antibodies to human serum albumin (anti-HSA) and HSA were cationized to various degrees by the addition of amino groups. When approximately 20 or more new amino groups were added to HSA and approximately 25 or more amino groups were added to anti-HSA, the proteins readily bound to cartilage and penetrated into the matrix. Soluble immune complexes made with the cationic antibodies, including small-latticed complexes, bound only to the surface of the cartilage. When cationic HSA was bound to the matrix of the cartilage, unaltered antibodies bound only to the antigen at the surface and did not penetrate the matrix. This model system defines the manner in which cationic antigens and antibodies bind to and penetrate into the articular cartilage.

Animals↗
PubMed2002

Articular cartilage injuries.

The acute and repetitive impact and torsional joint loading that occurs during participation in sports can damage articular surfaces causing pain, joint dysfunction, and effusions. In some instances, this articular surface damage leads to progressive joint degeneration. Three classes of chondral and osteochondral injuries can be identified based on the type of tissue damage and the repair response: (1) damage to the joint surface that does not cause visible mechanical disruption of the articular surface, but does cause chondral damage and may cause subchondral bone injury; (2) mechanical disruption of the articular surface limited to articular cartilage; and (3) mechanical disruption of articular cartilage and subchondral bone. In most instances, joints can repair damage that does not disrupt the articular surface if they are protected from additional injury. Mechanical disruption of articular cartilage stimulates chondrocyte synthetic activity, but it rarely results in repair of the injury. Disruption of subchondral bone stimulates chondral and bony repair, but it rarely restores an articular surface that duplicates the biologic and mechanical properties of normal articular cartilage. In selected patients, surgeons have used operative treatments including penetrating subchondral bone, soft tissue grafts, and cell transplants and osteochondral autografts and allografts to restore articular surfaces after chondral injuries. Experimental studies indicate that use of artificial matrices and growth factors also may promote formation of a new joint surface. However, an operative treatment of an articular surface injury that will benefit patients must not just provide a new joint surface, it must produce better long-term joint function than would be expected if the injury was left untreated or treated by irrigation and debridement alone. Therefore, before selecting a treatment for a patient with an articular cartilage injury, the surgeon should define the type of injury and understand its likely natural history.

Cartilage, Articular↗
PubMed2005

MRI of articular cartilage: revisiting current status and future directions.

OBJECTIVE: The purpose of this article is to review the current understanding of the MRI appearance of articular cartilage and its relationship to the microscopic and macroscopic structure of articular cartilage, the optimal pulse sequences to be used in imaging, the appearance of both degenerative and traumatic chondral lesions, the appearance of the most common cartilage repair procedures, and future directions and developments in cartilage imaging. CONCLUSION: Articular cartilage plays an essential role in the function of the diarthrodial joints of the body but is frequently the target of degeneration or traumatic injury. The recent development of several surgical procedures that hold the promise of forming repair tissue that is hyaline or hyalinelike cartilage has increased the need for accurate, noninvasive assessment of both native articular cartilage and postoperative repair tissue. MRI is the optimal noninvasive method for assessment of articular cartilage.

Cartilage Diseases↗
PubMed1997

Chondrocyte transplantation and experimental treatment options for articular cartilage defects.

Current treatment options for injured articular cartilage have resulted in temporary improvements in clinical symptoms and functional levels. None of these modalities, however, has resulted in restoration of an articular surface that is able to withstand long-term joint loading and function. As a result, numerous investigators have attempted to devise alternative therapies. The limited regnerative potential of articular cartilage has led investigators to attempt using cells with the potential for differentiation and proliferation to repair chondral defects. Chondrocyte transplantation, both allogeneic and autogenous, has shown early promising results in regenrating hyaline-like tissue in both animals and humans. Encouraging results in animals have also been demonstrated with alternative sources of osteoprogenitor cells as grafts, as well as with natural/synthetic implants and the use of growth factors and cytokines. However, despite encouraging short-term results, long-term data concerning the regenerate tissue are still needed. As more research is being conducted to understand the processes of cartilage maintenance and healing, there is hope that cartilage regeneration and neochondrogenesis will be possible in the future.

Animals↗
PubMed2026

Mapping articular cartilage maturation across postnatal development by proteomics.

OBJECTIVE: Articular cartilage has a specialised extracellular matrix that provides tensile strength and resistance to compression, but repair capacity is limited. Matrix remodelling during growth is essential for long-term tissue function, yet the underlying protein-level adaptations remain poorly characterised in large-animal models relevant to human joint biology. DESIGN: Using non-targeted, label-free mass spectrometry-based proteomics, we profiled full-thickness articular cartilage from goats across seven postnatal ages from neonatal to adult (n = 3 per age). Cartilage proteins were extracted using guanidine-based solubilisation and analysed by mass spectrometry. Selected proteins were further examined by immunohistochemistry. RESULTS: We identified 799 proteins across the seven ages, of which 157 matrisome components grouped into six categories. Development was associated with increased abundance of proteins involved in matrix organisation and stabilisation, including COL6A1, LOX, TIMP3 and CILP. Enrichment analysis revealed a shift from collagen biosynthesis and fibrillogenesis in early postnatal cartilage to elastic fibre organisation, integrin-matrix interactions and glycosaminoglycan metabolism in mature tissue, consistent with transition from matrix assembly to maintenance. Lysozyme increased with age, suggesting a structural role that warrants further study. Several proteins enriched in mature cartilage, including CILP, HTRA1, FN1 and SPP1, have also been implicated in osteoarthritis, suggesting that some molecular features of mature ECM maintenance are shared with diseased tissue. Immunohistochemistry confirmed stable COL2 localisation, loss of deep-zone COL10 staining with maturation and emergence of superficial PRG4 expression in adult cartilage. CONCLUSIONS: Our findings define the proteomic trajectory of cartilage maturation and provide a molecular reference for joint development and matrix ageing.

Animals↗