ArticleCalcified tissue international1992
Light and electron microscopic abnormalities in diastrophic dysplasia growth cartilage.
Article in Calcified tissue international, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 22 citations in OpenAlex.
- Microscale mapping of extracellular matrix elasticity of mouse joint cartilage: an approach to extracting bulk elasticity of soft matter with surface roughness.Soft matter · 2018Article
- Matrix disruptions, growth, and degradation of cartilage with impaired sulfation.The Journal of biological chemistry · 2012Article
- A mutation in the alpha 3 chain of type IX collagen causes autosomal dominant multiple epiphyseal dysplasia with mild myopathy.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
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1 author at 1 institution in 1 country.
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Abstract
Light and electron microscopic studies of diastrophic dysplasia iliac crest growth cartilage performed on five occasions in two patients from 1 to 10 years of age reveal extensive cell and matrix abnormalities at each time period. Light microscopy shows atypical chondrocytes with extreme variation in size and shape, and premature cytoplasmic degeneration, and formation of target ghost cells. Prominent, densely staining fibrotic foci are present throughout the cartilage. Ultrastructure reveals some structurally intact chondrocytes with a single large fat inclusion, slightly dilated rough endoplasmic reticulum, and abundant glycogen. As early as 1 year of age cystic degeneration of chondrocyte cytoplasm is evident with indistinct organelles seen. The cartilage matrix demonstrates a general increase in fibrous tissue as well as the fibrotic foci. The collagen in these foci is remarkably abnormal. It is composed of short, extremely broad fibrils ranging from 150 to 950 nm in width which are separated at their terminal ends but fused to each other centrally in random fashion. On cross-section there are very few round fibrils but rather a marked irregularity in shape giving the appearance of having fibrils randomly added to others to form enlarged nonuniform fibril aggregates. On longitudinal sectioning, regular cross-banding across the entire fibril width is seen but fibril splitting and aggregation are highly irregular.(ABSTRACT TRUNCATED AT 250 WORDS)
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Registered trials
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