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The fine structure of proliferating cartilage cells: structural changes in an experimental model
Journal of Anatomy
|July 1, 1975
Summary
Cartilage cells near defects showed extensive rough endoplasmic reticulum and myelin figures, suggesting unused membrane material. Cortisone may impair membrane development in chondrocytes.
Area of Science:
- Cell biology
- Biochemistry
- Orthopedics
Background:
- Cartilage defects can alter chondrocyte morphology and function.
- Intra-articular injections of papain and cortisone are used to induce cartilage damage.
- The role of endoplasmic reticulum and Golgi apparatus in chondrocyte response to injury is not fully understood.
Purpose of the Study:
- To investigate the ultrastructural changes in chondrocytes near experimentally induced cartilage defects.
- To explore the formation and potential origin of myelin-like figures in these cells.
- To assess the potential impact of cortisone on chondrocyte membrane development.
Main Methods:
- Induction of cartilage defects in animal models using intra-articular papain and cortisone injections.
- Histological examination of chondrocyte clusters in the vicinity of defects.
- Ultrastructural analysis using electron microscopy to observe cellular organelles and membrane structures.
Main Results:
- Chondrocytes exhibited significant proliferation of rough endoplasmic reticulum.
- Golgi membranes were comparatively less developed in these cells.
- Myelin-like membranous figures were frequently observed, associated with cell membranes, intercellular spaces, nuclear envelope, or endoplasmic reticulum.
Conclusions:
- The observed myelin figures may represent unused material from membrane synthesis.
- Cortisone's known interference with metabolic processes could explain the observed deficiencies in membrane differentiation and transfer.
- These findings suggest a specific cellular response to injury and pharmacological intervention in cartilage.