By Susanne Grässel, Attila Aszódi

ISBN-10: 3319295667

ISBN-13: 9783319295664

ISBN-10: 3319295683

ISBN-13: 9783319295688

In 3 Volumes this mini e-book sequence provides present wisdom and new views on cartilage as a really expert but flexible tissue. this primary quantity offers a finished review at the uncomplicated composition and improvement of cartilaginous tissues by means of the outline of the most important signaling pathways which keep watch over cartilage morphogenesis and function.
This e-book addresses Professors, researchers and PhD scholars who're drawn to musculoskeletal and cartilage biology.

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Extra resources for Cartilage: Volume 1: Physiology and Development

Sample text

Recently, similar degenerative alterations in the intervertebral disks and end plates of the spine in mice lacking the entire collagen IX protein were reported. Boyd et al. detected cellular changes such as mucous degeneration, cell death, fibrochondrocyte degeneration, and cell clustering in 3–12-month-old Col9a1-deficient mice. The vertebral end plates of 6-month-old mice showed a more severe degeneration than in wild-type mice (Boyd et al. 2008). Notably, growth cartilage abnormalities have only been assigned to mouse strains lacking the entire collagen IX protein as comparable irregularities have not been described for the mice harboring a mutated collagen IX.

Their results show that collagen III molecules accumulate in mature human articular cartilage cross-linked to the surface of collagen II fibrils. The amount presumably varies between individual joints, anatomical location, and tissue microanatomy, perhaps dependent on the history of injuries and the wear and tear experienced by a normal joint during life. If so, the content will tend to increase with age.

Heterozygous cho/+ mice have a much less severe phenotype characterized by age-dependent osteoarthritis, demonstrating that Col11a1 haploinsufficiency has a deleterious effect on articular connective tissue. The diameter of collagen fibrils in articular cartilage of knee joints from heterozygous cho/+ mice was increased relative to that in control cartilage, and histologic analysis showed OA-like degenerative changes in knee and temporomandibular (TM) joints, starting at the age of 3 months which became more severe with aging (Xu et al.

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Cartilage: Volume 1: Physiology and Development by Susanne Grässel, Attila Aszódi

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