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Cartilage in normal and osteoarthritis conditions

https://doi.org/10.1016/j.berh.2008.02.001Get rights and content

The preservation of articular cartilage depends on keeping the cartilage architecture intact. Cartilage strength and function depend on both the properties of the tissue and on their structural parameters. The main structural macromolecules are collagen and proteoglycans (aggrecan). During life, cartilage matrix turnover is mediated by a multitude of complex autocrine and paracrine anabolic and catabolic factors. These act on the chondrocytes and can lead to repair, remodeling or catabolic processes like those that occur in osteoarthritis. Osteoarthritis is characterized by degradation and loss of articular cartilage, subchondral bone remodeling, and, at the clinical stage of the disease, inflammation of the synovial membrane. The alterations in osteoarthritic cartilage are numerous and involve morphologic and metabolic changes in chondrocytes, as well as biochemical and structural alterations in the extracellular matrix macromolecules.

Introduction

Articular cartilage is a specialized, avascular, aneural connective tissue that provides covering for the osseous components of diarthrodial joints. It serves as a load-bearing material, absorbs impact and is capable of sustaining shearing forces. The unique properties of this tissue are related to the composition and structure of its extracellular matrix, which is composed mainly of a high concentration of proteoglycans (aggrecan) entangled in a dense network of collagen fibers and a large amount of water. This tissue allows the frictionless motion of the joint, in which it absorbs and dissipates load. The articular cartilage is composed of a sparse population of cells, named chondrocytes, which are responsible for the synthesis and maintenance of the extracellular matrix.

Osteoarthritis (OA) is characterized by degradation and loss of articular cartilage, hypertrophic bone changes with osteophyte formation, subchondral bone remodeling, and, at the clinical stage of the disease, chronic inflammation of the synovial membrane. Its etiology, although not yet completely understood, appears to result from a complex system of interacting mechanical, biological, biochemical, molecular, and enzymatic feedback loops. The final common pathway of cartilage destruction results from a failure of chondrocytes to maintain a homeostatic balance between matrix synthesis and degradation. As the disease progresses, the degradative process eventually exceeds the anabolic one, leading to a progressive loss of cartilage and eburnation of bone. This appears to occur when the physiologic balance between the synthesis and degradation of the extracellular matrix favors catabolism. At the clinical stage of the disease, an inflammatory reaction involving the synovial membrane is often present. This process favors the synthesis of inflammatory mediators, which impact on cartilage matrix homeostasis by altering chondrocyte metabolism to enhance catabolism and reduce anabolism.

This chapter summarizes the pertinent data related to the molecules and factors involved in cartilage maintenance, remodeling, and during the progression of OA.

Section snippets

Structural organization

The cartilage matrix consists of macromolecules in which collagen and proteoglycans (aggrecan) are the main representatives. These components are highly ordered from the cartilage surface to the deepest layers. Cartilage is divided into four zones with different functions: the superficial, middle or transitional, deep or radial, and calcified cartilage zones. Interestingly, there is no sharp boundary between the first three zones.

The superficial zone, the thinnest of the four, consists of fine

Subchondral bone and cartilage crosstalk in osteoarthritis

Although the initiating event responsible for the degradation of cartilage in OA patients remains elusive, the concept of a key role of the subchondral bone tissue in OA is gaining strong support. A plausible hypothesis is that cytokines, growth factors, and eicosanoids produced locally by subchondral bone tissue seep through the bone–cartilage interface and induce changes in the cartilage metabolism. Although it was previously thought that the calcified cartilage layer was an impenetrable

Biological markers of cartilage

When a component of joint tissue is released, measuring its concentration in the joint fluid is theoretically the most reliable approach. However, joint fluid collection is difficult in many OA patients and can be obtained readily only in the knee. Moreover, joint lavage results in significant errors to the concentration of the markers because of uncontrolled sample dilution. The best use of biomarkers in OA is their determination in serum or urine. However, their use in clinical practice has

Conclusion

Cartilage matrix turnover is mediated by a multitude of factors that act on the chondrocytes and could lead to repair, remodeling or catabolic processes. The molecules and factors involved in cartilage repair and maintenance have been the subject of intensive research and significant progress has been made in the understanding of the interactions of the components of this tissue. At a certain point, these processes are altered, resulting in matrix changes including local abnormal biochemical

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