Hall Cartilage

Biomedical Aspects
1. Auflage 2013
ISBN: 978-1-4832-6690-9
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 366 Seiten

Cartilage, Volume 3: Biomedical Aspects is a compilation of articles that covers the various aspects of age-related cartilage deterioration, bone disease, and genetic mutation. The book is composed of 10 chapters that highlight different subjects related to the diseases and malformations of cartilage. Relevant topics that are discussed in each chapter include the formation of cartilage outside the confines of the skeleton; aspects of age-related changes in cartilage; tumors that invade cartilage; molecular and biochemical bases of cartilage mutations; and the immunological and bioelectrical properties of cartilage. Physicians, pathologists, orthopedic surgeons, and those working on the human skeletal system will find this text a very good reference material.

Autoren/Hrsg.

Hall, Brian K.

Leseproben

2

Mechanisms of Resorption and Remodeling of Cartilage

James A. Albright and R.P. Misra

Publisher Summary

This chapter discusses the mechanisms of resorption and remodeling of cartilage. The ability to limit or prevent cartilage breakdown and to stimulate effective remodeling activity continue to be a major unsolved problem in the treatment of patients with musculoskeletal disease. The term “remodeling” indicates the process whereby cartilage defects are reshaped in the adult animal. The three-dimensional changes that occur during growth are directed by a different set of control mechanisms. As the physical properties of cartilage include only a limited ability to deform elastically and to creep, remodeling must be accomplished primarily through tissue regeneration. In a healthy adult, cartilage is a relatively inert tissue containing a sparse number of cells—chondrocytes—that, once formed, are not replaced during the life of the animal. On a cellular basis, chondrocytes are dynamic structures that carry on metabolic activities similar to the other types of connective tissue cells. This chondrocyte activity serves a maintenance function with little or no evidence that remodeling of cartilage occurs in the normal state. In contrast, bone remodeling is a continuous process wherein new bone constantly replaces older bone and therefore, bone remodeling limits the life span of most cellular and structural skeletal elements. Bone, however, can not only renew itself but also demonstrates a remarkable power of recovery from drastic insults such as comminuted fractures or infections. In the diseased state, numerous stimuli such as infection, trauma, rheumatoid arthritis, or even prolonged immobilization can lead to the destruction of cartilage. This process probably follows a common pathway at the microscopic and ultrastructural levels regardless of the precipitating event, type of cartilage, or its location.

I. Introduction

II. Response of Cartilage to lnjury

A. Superficial Lesions

B. Deep Lesions

III. Resorption

A. Pathophysiology

B. Pressure

C. Immobilization

D. Relief of Cartilage-to-Cartilage Contact

E. Septic Arthritis

F. Antigen-Induced Arthritis

G. Chondrocyte Death

IV. Remodeling

A. Physical Forces

B. Oxygen Tension

C. Tissue and Cellular Factors

D. Miscellaneous Factors

E. Implants

V. Cartilage Transplants

VI. Hormones, Vitamins, and Drugs

A. Hormones

B. Vitamin A

C. Drugs

VII. Concluding Remarks

References

I INTRODUCTION

The ability to limit or prevent cartilage breakdown and to stimulate effective remodeling activity continues to be a major unsolved problem in the treatment of patients with musculoskeletal disease. To discuss these questions, this chapter will concentrate on hyaline cartilage, particularly articular cartilage, a tissue long known for its durability, its relative resistance to resorption, and its limited remodeling and regeneration potential.

The term will be used to indicate the process whereby cartilage defects are reshaped in the adult animal. The three-dimensional changes that occur during growth are directed by a different set of control mechanisms and will not be included in this discussion (see Volume 2, Chapter 7). These changes are part of a separate subject more properly termed modeling, not remodeling. Since the physical properties of cartilage include only a limited ability to deform elastically and to creep, remodeling must be accomplished primarily through tissue regeneration.

In the healthy adult, cartilage has proven to be a relatively inert tissue containing a sparse number of cells (chondrocytes) that, once formed, are not replaced during the life of the animal (Fig. 1a,b). On a cellular basis chondrocytes themselves are dynamic structures that carry on metabolic activities similar to other types of connective tissue cells. This chondrocyte activity serves a maintenance function with little or no evidence that remodeling of cartilage occurs in the normal state. In contrast, bone remodeling is a continuous process wherein new bone constantly replaces older bone. Therefore, bone remodeling in effect limits the life span of most cellular and structural skeletal elements. Bone, however, not only can renew itself, it demonstrates a remarkable power of recovery from drastic insults, such as comminuted fractures or infections.

Fig. 1 Photomicrographs of normal articular cartilage of rabbit knee joint. (a) Low-power view shows normal distribution of chondrocytes and matrix in the four ill-defined zones of cartilage. The arrow points to an artifact. Magnification 40×. (b) High-power view emphasizes the sparcity of cells and abundance of matrix in the upper three (A, superficial; B, transitional; and C, deep) zones of cartilage. Magnification 100× (stained with toluidine blue).

In the diseased state, numerous stimuli such as infection, trauma, rheumatoid arthritis, or even prolonged immobilization can lead to the destruction of cartilage. This process probably follows a common pathway at the microscopic and ultrastructural levels, regardless of the precipitating event, the type of cartilage or its location.

The ability of cartilage to regenerate has often been questioned, due in part to a dearth of knowledge on ways to stimulate cartilage formation in diseased joints. It is known that injury to cartilage, whether traumatic or metabolic, often stimulates a limited repair process, but cartilage formation is not directly coupled with resorption as it is in bone. Even so, abundant evidence indicates that cartilage has a definite, if latent, regeneration potential. For instance, a pseudarthrosis may contain hyaline cartilage, growth hormone can reactivate growth in articular cartilage, and exercise can stimulate hyaline cartilage regrowth in surface defects of joints. The overriding problem, therefore, concerns the control of cartilage regrowth in joint surface remodeling, that is, methods of activating and directing the process of articular cartilage replacement.

II RESPONSE OF CARTILAGE TO INJURY

This section will outline the overall response of cartilage to injury in order to provide background information for more detailed discussions of resorption and remodeling in subsequent sections. The response of osteoarthritic cartilage appears to be similar to that described in this section, very likely because trauma is probably the most common cause of osteoarthritis (see Chapter 4 in this volume).

The classical studies utilized linear scalpel cuts into articular cartilage perpendicular to the surface. Subsequently, many investigators have used drill holes through cartilage into subchondral bone. The response of cartilage to such injuries varies dramatically, depending on the depth of the injury and whether or not it violates the deeper layers of cartilage to expose the vasculature in the bone.

A Superficial Lesions

The response of cartilage to injury can best be seen after a superficial injury that does not reach bone. Such an injury produces no inflammatory response due to the absence of vessels, nor does the cartilage show more than a minimal attempt at repair. Histologically, the first change occurs in the matrix with a loss of proteoglycans along the margins of the injury, as determined with metachromatic stains. This stimulates an attempt at repair with increased glycosaminoglycan synthesis as indicated by enhanced metachromasia adjacent to many superficial chondrocytes and by increased 35SO4 uptake (Meachim, 1963). Collagen synthesis has also been found to increase (Repo and Mitchell, 1971). Other than the death of some of the chondrocytes lining the injury, little cellular response is evident histologically, although occasional clusters of cells may be seen in a few weeks. Soon after the injury the cells adjacent to the injured surfaces may show a brief burst of reproductive activity with an increased uptake of tritiated thymidine (Mankin, 1962), or they may fail to respond (DePalma 1966).

The long term response varies depending upon the type of defect, and more important, whether the injury leads to progressive degeneration of the surrounding cartilage. A linear defect often shows little or no long term change, and 6 months to 1 year later may look the same as it did immediately following injury (Fig. 2). Thompson (1975) found that linear defects at the periphery of the patella showed more evidence of healing than those located...