Dr. Kevin Yip

Dr Kevin Yip
Orthopaedic Surgeon
MBBS(UK), FRCS(EDIN), FAM(SING), FHKCOS(ORTHO)

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Cartilage Healing

It generally is agreed that intrinsic healing of cartilage lesions does not occur. There may be a response of the chondrocyte to injury, but this response does not result in cartilage repair.

The obvious example is seen in degenerative arthritis [degenerative joint disease (DJD) osteoarthrosis, and osteoarthritis (OA)], in which chondrocytes often form clones of cells that demonstrate an increased rate of synthesis of matrix components in an attempt to repair damaged surfaces.

The synthesized components are not retained within the matrix, however, and newly synthesized molecules, such as proteoglycans, are reduced in concentration despite the increased rate of synthesis. In reported experimental studies of mammalian joints, linear incisions created on articular cartilage surfaces remained indefinitely.

Efforts at surgical reconstruction of articular defects therefore have shifted focus to allografts or cartilage autografts developed from cultured cells. These techniques will be addressed in subsequent chapters. Historically, most surgical attempts at cartilage healing involved exposure of marrow cells to mount a repair response.

This was achieved by subchondral bone resection (e.g., cup arthroplasty) or by drilling, abrasion, or microfracture of the subchondral plate. When examined histologically a few days after surgery, the response to injury mounted by primitive marrow cells produces an outgrowth of a granulation-type tissue .

This cellular response consists for the most part of immature vascular cells, fibroblasts, and macrophages. With the passage of time, maturation of the surface into fibrocartilage occurs, provided that the surface is protected from compressive and shear forces during the early stages of repair.

The fibrocartilage so formed is remarkably different from hyaline articular cartilage. The fibrocartilage surface is deficient in both the precise morphology and the composition of normal articular cartilage, as documented earlier in this chapter.

The fibrocartilage cells vary in shape from place to place in the matrix. Occasionally, they are seen as round cells in a lacunalike structure, but they tend more commonly to be spindle shaped. The fibrous matrix lacks both the precise morphology of arcades in the deeper layers and the packing of thin, parallel fiber organization at the surface, and it is not anchored securely into the subchondral plate.

Strikingly, the proteoglycan content is only a fraction of that in normal articular cartilage. Not surprisingly, this reconstituted surface is not an efficient load-bearing organ.

Mechanical tests done on experimental arthroplasty surfaces show a resistance to compression of only one third that of normal articular cartilage. As a result, the durability of regenerated arthroplasty surfaces of this type is limited, and the fibrocartilage surface is gradually worn away.

The consequence of the unsatisfactory outcome of the biological healing response was the relatively rapid abandonment of procedures such as cup arthroplasty of the hip in the late 1960s and early 1970s in favor of total hip replacement constructs using artificial components.

Similarly, arthroscopic debridement of degenerative knee joints using abrasion techniques on exposed bone to stimulate fibrocartilage formation is presently being applied principally as a temporizing procedure to defer total knee replacement.

A related problem encountered surgically is the localized osteochondral defect exemplified by osteochondritis dissecans of the knee or ankle. Frequently, the necrotic fragment with its overlying cartilage is damaged and/or displaced and is not suitable for replacement and fixation in the cavity from which it originated. In such cases, the surgeon is confronted with a defect of sufficient size to jeopardize long-term survival of the joint because of incongruity of the opposing surfaces. In the past, this defect was “repaired” by curettage of the cavity and drilling the base of the exposed bone. The expectation was that the cavity would be filled with repair tissue and that a new surface would be regenerated.

The rationale for this approach was partially derived from experimental studies with small animals that indicated drill holes in articular cartilage could heal. The model commonly used in such experiments was the rabbit knee joint in which a 1- to 2-mm drill hole was created that penetrated the subchondral plate.

However, the absolute geometry of the larger defects in the human knee—often 2 cm in diameter—respond quite differently from the response seen in size of defects studied in the small animal models. Experiments performed in large animals, however, represent a more realistic model. The experiments of Convery et al.On the horse’s knee, in which defects of 1.5 to 2.5 cm diameter were created, demonstrated grossly imperfect healing in all cases. Other studies have confirmed the limitation of healing large osteochondral defects .

Such results motivated the search for more realistic solutions, such as allografting, to the Osteochondritis Dessicans (OCD) lesion in humans. Some of the newer surgical approaches to this question are reviewed in a later chapter.

The implication of the evolving knowledge of normal articular cartilage is the recognition of its phenomenal genius as a biologically engineered construct. It follows that all the evolving surgical attempts at reconstruction are faced with the daunting challenge of the precise requirements for replicating articular cartilage.

Normal articular cartilage remains the exacting benchmark against which all new therapeutic concepts must be measured. Current efforts seeking a biological solution to repair are exciting. Clearly, however, the hurdles that remain are large, and the race to the ultimate biological solution has just begun.

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