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Remobilization does not fully restore immobilization induced articular cartilage atrophy.

Haapala, Jussi (författare)
Department of Surgery, Kuopio University Hospital, Kuopio, Finland; Department of Rehabilitation Clinic, Kuopio University Hospital, Kuopio, Finland
Arokoski, Jari (författare)
Department of Rehabilitation Clinic, Kuopio University Hospital, Kuopio, Finland
Hyttinen, Mika (författare)
Department of Anatomy, University of Kuopio, Kuopio, Finland
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Lammi, Mikko, 1961- (författare)
Department of Anatomy, University of Kuopio, Kuopio, Finland,Chondrogenic and Osteogenic Differentiation Group
Tammi, Markku (författare)
Department of Anatomy, University of Kuopio, Kuopio, Finland
Kovanen, Vuokko (författare)
Department of Health Sciences, University of Jyväskylä, Jyväskylä, Finland
Helminen, Heikki (författare)
Department of Anatomy, University of Kuopio, Kuopio, Finland
Kiviranta, Ilkka (författare)
Department of Surgery, Jyväskylä Central Hospital, Jyväskylä, Finland
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 (creator_code:org_t)
Lippincott Williams & Wilkins, 1999
1999
Engelska.
Ingår i: Clinical Orthopaedics and Related Research. - : Lippincott Williams & Wilkins. - 0009-921X .- 1528-1132. ; :362, s. 218-229
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • The recovery of articular cartilage from immobilization induced atrophy was studied. The right hind limbs of 29-week-old beagle dogs were immobilized for 11 weeks and then remobilized for 50 weeks. Cartilage from the immobilized knee was compared with tissue from age matched control animals. After the immobilization period, uncalcified articular cartilage glycosaminoglycan concentration was reduced by 20% to 23%, the reduction being largest (44%) in the superficial zone. The collagen fibril network showed no significant changes, but the amount of collagen crosslinks was reduced (13.5%) during immobilization. After remobilization, glycosaminoglycan concentration was restored at most sites, except for in the upper parts of uncalcified cartilage in the medial femoral and tibial condyles (9% to 17% less glycosaminoglycans than in controls). The incorporation of 35SO4 was not changed, and remobilization also did not alter the birefringence of collagen fibrils. Remobilization restored the proportion of collagen crosslinks to the control level. The changes induced by joint unloading were reversible at most sites investigated, but full restoration of articular cartilage glycosaminoglycan concentration was not obtained in all sites, even after remobilization for 50 weeks. This suggests that lengthy immobilization of a joint can cause long lasting articular cartilage proteoglycan alterations at the same time as collagen organization remains largely unchanged. Because proteoglycans exert strong influence on the biomechanical properties of cartilage, lengthy immobilization may jeopardize the well being of articular cartilage.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Ortopedi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Orthopaedics (hsv//eng)
NATURVETENSKAP  -- Biologi -- Biokemi och molekylärbiologi (hsv//swe)
NATURAL SCIENCES  -- Biological Sciences -- Biochemistry and Molecular Biology (hsv//eng)

Nyckelord

Articular cartilage
dog
immobilzation
remobilization
proteoglycans
biokemi
Biochemistry
ortopedi
Orthopaedics

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