Proliferation, Regeneration, and Repair of Articular Cartilage of Immature Animals

¹ Campbell Foundation and the Division of Pathology and Microbiology, University of Tennessee College of Medicine, Memphis

Repair of articular cartilage of the femoral condyles in immature dogs was studied histologically at various time intervals after injury in thirty complete (full-thickness) and ten incomplete (one-third to one-half thickness) defects in the weight-bearing surface and in six incomplete defects in the patellar ridge.

In the complete defects, the following changes were observed:

At two weeks, there was a pale-staining, cell-free zone of cartilage necrosis around the defect, and the matrix of the intermediate zone of the articular cartilage had flowed into the defect, producing an overhanging shelf.

At four to six weeks, there was marked proliferation of the superficial cells of the cartilage with the formation, over the surface of the defect, of a layer of flattened and compacted cells with a collagenous stroma. This layer was continuous with the superficial cell layer of the adjacent cartilage.

The most striking feature of the repair process in the complete defects was the active growth of granulation tissue into the defect from the subchondral bone. This ingrowth was sufficient to fill almost completely the defect beneath the previously described layer of flattened cells and collagenous stroma. The vascular tissue so formed seemed to inhibit the formation of new cartilage. However, some hyaline cartilage was observed in almost every complete defect more than three weeks old which was not filled completely by fibrous or fibrocartilaginous tissue. This cartilage was immature and embryonal in appearance and seemed to be derived from the superficial cell layer. In only three of the thirty full-thickness defects was complete repair with hyaline cartilage observed.

A few new chondrons were seen near the margins of the complete defects. Whether these were the result of regeneration or degeneration in the marginal cartilage could not be determined.

Three general types of repair were observed in the complete defects: repair by fibrous tissue, by fibrocartilage, and by hyaline cartilage. In the first two types, the tissue was obviously derived from the granulation tissue growing in from the base; in these types of repair a new subchondral plate was formed. In the third type, the defect was bridged with mature hyaline cartilage which was continuous with the articular cartilage at the margins of the defect, and no subchondral plate was formed. The mechanism of this third type of repair was not apparent. One explanation is that the flow of matrix into these defects was so extensive that the defect was completely covered.

In the incomplete defects, the repair processes were similar to those observed in the complete defects with the following exceptions:

When the walls of the incomplete defects were sloping, there was no flow of the matrix into the defects—an observation suggesting that this is a purely mechanical phenomenon.

In the incomplete defects, there was no ingrowth of granulation tissue from the base and no apparent interference with the proliferation of the superficial layer of the surrounding articular cartilage.

There was an increase in the number of blood vessels in the cartilage beneath the incomplete defects. This change in the intracartilaginous blood vessels was not observed in relation to the complete defects.

The findings in this study appear to indicate that the articular cartilage of the femoral condyle of immature dogs is capable of proliferation, regeneration, and even complete repair with hyaline cartilage, although the conditions leading to this desirable type of repair are not understood. The differences in repair of complete and incomplete defects suggest that granulation tissue from the subchondral bone inhibits cartilage formation and that if this could be prevented the full potential of cartilage repair might be realized.

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