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Articular chondrocytes of achondroplastic mice (cn/cn) resemble ultrastructurally those of their non-achondroplastic siblings (Cn/Cn or Cn/cn), except for premature deposition of glycogen and a tendency to undergo regression. The latter may be slight or extreme. The ultimate cause of the vulnerability of the chondrocytes and the cause of the heterogeneity of the reaction could not be determined with the method employed. Nevertheless, increased vulnerability accounts for cell death under conditions which are usually not injurious, and which may be either physiologic or altered by endogenous or exogenous factors.

10 days’ to 3 months’ consumption of a diet containing 4% cholesterol causes a minor and transitory stimulation of articular chondrocytes of mice. The transitory disturbance is accompanied by a more permanent increase in glycogen, by abnormal deposition of cytoplasmic lipid and by an increase in the fibrillarity of the pericellular matrix. The changes are consistent with the failure of the cholesterol diet to influence the course of osteoarthrosis if fed to mice from an early age through life.

Articular chondrocytes of 1-year-old male mice of strain C57B1 were stimulated by injections of a cartilage-bone marrow extract to undergo hypertrophy, intensified organellar development and hyperplasia. This response was attenuated as compared with that of growing animals treated similarly. The morphological findings are consistent with some increase in synthetic activity on the part of the chondrocytes. The increased cell death observed was attributed to overstimulation and subsequent exhaustion, and was considered responsible for the prominence of microscars in the matrix.

Young adult male mice of strain Cδ7Bl were treated with somatotrophin, thyroxine or estradiol benzoate and were observed for 24 h, 2, 4 days or 1 or 2 weeks. The articular cartilage of the femoral head reacted to the treatment with ultra-structural changes in cells and matrix. Chondrocytes were relatively less and the matrix was relatively more conspicuously altered than in growing mice treated similarly. The changes observed are consistent with accelerated passage of cell products into the matrix and with altered cellular activity in regard to the production of components of the matrix. Early effects were followed by intensified degeneration and death of chondrocytes.