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THE PRODUCTION OF CHRONIC ARTHRITIS BY THE INJECTION OF WEAK ACIDS, ALKALIES, DISTILLED WATER, AND SALT SOLUTION INTO JOINTS.

KEY, J. ALBERT
The Journal of Bone & Joint Surgery: January 1933
Archive: PDF Only

Postmortem cultures of the joints yielded no growth; consequently, it may be assumed that the pathological changes which occurred in the injected joints were caused by the injected material. These changes can be summarized as follows:

1.Synovial Exudate: The acute joints (one and three days) contained a moderate excess of cloudy, straw-colored fluid and this fluid contained large numbers of leucocytes and macrophages. The subacute joints (five and ten days) also contained a moderate excess of cloudy, straw-colored fluid, but the leucocytes had largely disappeared and most of the cells were macrophages. In the chronic joints (twenty-eight to eighty-five days) the excess fluid was decreased in amount, relatively clear, and contained only a moderate number of cells (mostly macrophages.

2. Synovial Tissues: In the acute joints the areolar and adipose areas of the synovial surface exhibited a rather acute inflammatory reaction with hypertrophy and hyperplasia of the fixed tissue cells and infiltration of the tissues with leucocytes and small and medium-sized round cells. In the subacute joints the leucocytes had largely disappeared, but the round-cell infiltration of the loose subsynovial tissues was more marked and the hyperplastic synovial tissues tended to invade and overlap the margins of the articular cartilage. In the chronic joints the fixed tissue cells were about normal in size, but the synovial tissues were moderately thickened and infiltrated with small and medium-sized round cells (Fig. 2).

The fibrous areas of the synovial surface (including the fibrocartilage) showed relatively slight changes in any of the joints.

3.Articular Cartilage: A variable number of the cartilage cells were killed and the death of the cells was followed by fibrillation, cleavage, and disintegration of the matrix, and occasionally by separation of the superficial cartilage from the deep calcified zone. Where only a portion of the cells in a given area were killed, the small superficial cells tended to survive, while the larger cells in the deeper zones died (Fig. 3). When some of the deeper cells remained alive, they tended to proliferate and form cell columns and cell nests and the larger cell nests were surrounded [SEE FIG. 5, 6, 7 IN SOURCE PDF] by zones of newly formed hyaline matrix (Figs. 3, 4, and 6). The Small cells near the articular surface exhibited relatively little tendency to proliferate.

Occasionally the cartilage necrosis was sharply localized (Fig. 4, Right), but as a rule it was diffuse and was especially marked over the bearing surfaces of the joint. Here the surface tended to disintegrate and the cartilage was in many instances eroded and the subchondral bone was exposed (Figs. 6 and 7). In joints with considerable cartilage necrosis there was a variable amount of marginal proliferation of the articular cartilage.

4. Bone: When the articular cartilage was eroded the underlying bone became eburnated and the bone cells near the exposed surface died. Necrosis and erosion of the cartilage over the bearing surface of the joint were usually accompanied by proliferation of cartilage and bone around the margins of the cartilage (marginal osteophytes) and beneath the adjacent periosteum (exostoses) (Fig. 9). The combination of central necrosis and marginal proliferation caused deformities of the joint. These joints did not tend to ankylose by fibrous tissue or bone.

(C) 1933 All Rights Reserved.The Journal of Bone and Joint Surgery, Inc.

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