From this work it may be concluded that persistent compression affects the growth plate by interference with the blood flow on one or both sides of the growth cartilage.

Despite exertion of the same pressure upon both sides of the growth plate, only the metaphysial side was readily affected in the early stages, for, as long as no damage was caused to the epiphysial side of the growth cartilage, the lesions were fully reversible.

Interference with growth was directly proportionate to the damage caused by compression to the epiphysial side of the growth plate and, in general, to the duration of compression.

The first signs of interference with the metaphysial side of the plate were the lack of vascular progression and concomitant retardation of calcification.

When severe degeneration was not present the growth cartilage recovered within four days.

The matrix was ready for calcification all the time, as shown by the extremely rapid calcification occurring soon after the compression had ceased and the vessels were able to reach their proper place.

It seems justified to believe that the first hypertrophic cell not to be calcified after removal of the clamp is the one around which the matrix has not yet changed sufficiently to have an affinity for the apatite crystals. As in moderate compression, the division of the proliferative cells continues and it seems it must be the age, or even more likely the distance from the transudate coming from the epiphysial side of the growth cartilage that conditions the maturity of the cell, which prepares the field for calcification and thus initiates the osteogenic process.

Views similar to this have been advanced by Ham (1957) and his school.

The effects on articular cartilage of continuous and intermittent excessive pressures have been studied in the knees of rabbits. Severe degenerative changes in the cartilage were observed; these resembled the typical lesions seen in osteoarthritis in man. They included fibrillation of cartilage, death of chondrocytes, eburnation of joint surfaces, sclerosis of bone and the production of "bone cysts." Regeneration of cartilage was common and it was brought about either by the deeply situated chondrocytes which had escaped death or by metaplasia of young connective tissue cells of the bone marrow.