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Fibromodulin-null murine knee joints display increased incidences of osteoarthritis and alterations in tissue biochemistry

Gill, MR ; Oldberg, Åke LU and Reinholt, FP (2002) In Osteoarthritis and Cartilage 10(10). p.751-757
Abstract
Objective: To elucidate variations in tissue ultrastructure and incidence of pathology between fibromodulin (FM)-null mice and wild-type (WT) animals. Design: FM-null and WT siblings from different age groups were compared. Serial sections were made through paraffin-embedded whole knees and investigated histologically. Additionally, medial femoral condyle peaks from sibling pairs were investigated ultrastructurally using transmission electron microscopy. Results: Histological findings demonstrated a clear and increasing disparity between tissue degeneration in WT and FM-null animal knees with progressing age. Distinct differences were apparent by 36 weeks. Around the 80 week period and onward these differences became profound. However,... (More)
Objective: To elucidate variations in tissue ultrastructure and incidence of pathology between fibromodulin (FM)-null mice and wild-type (WT) animals. Design: FM-null and WT siblings from different age groups were compared. Serial sections were made through paraffin-embedded whole knees and investigated histologically. Additionally, medial femoral condyle peaks from sibling pairs were investigated ultrastructurally using transmission electron microscopy. Results: Histological findings demonstrated a clear and increasing disparity between tissue degeneration in WT and FM-null animal knees with progressing age. Distinct differences were apparent by 36 weeks. Around the 80 week period and onward these differences became profound. However, qualitative ultrastructural investigation did not indicate either any aberrant tissue ultrastructure or any abnormal collagen fibril forms in FM-null articular cartilage compared with WT. Biochemical and immunohistochemical investigation of FM-null articular cartilage showed a significant increase in tissue levels of lumican (LUM). Conversely, the cruciate ligaments of the knee showed both an increase in LUM content and considerable structural abnormalities including the tendency towards rupture. Conclusion: This report indicates for the first time that FM-null mice have a higher propensity towards degenerative changes in their knee joints than comparable WT animals. Interestingly, no underlying ultrastructural or fibril abnormalities within the articular cartilage could be identified to explain why FM-null cartilage is more prone to pathological changes than wild-type tissue. We conclude that alterations in ligaments, and possibly other tissues within the knee, are of considerable importance in the pathogenesis of the observed articular cartilage degeneration. (C) 2002 OsteoArthritis Research Society International. Published by Elsevier Science Ltd. All rights reserved. (Less)
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author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
electron microscopy, transmission, knock-out mice, lumican, osteoarthritis, fibromodulin, articular cartilage, ligaments
in
Osteoarthritis and Cartilage
volume
10
issue
10
pages
751 - 757
publisher
Elsevier
external identifiers
  • wos:000178548100001
  • pmid:12359160
  • scopus:0036795456
ISSN
1063-4584
DOI
10.1053/joca.2002.0527
language
English
LU publication?
yes
id
3520e969-c1b2-4def-9cdb-42576787e264 (old id 325503)
date added to LUP
2016-04-01 12:14:21
date last changed
2022-01-27 00:49:44
@article{3520e969-c1b2-4def-9cdb-42576787e264,
  abstract     = {{Objective: To elucidate variations in tissue ultrastructure and incidence of pathology between fibromodulin (FM)-null mice and wild-type (WT) animals. Design: FM-null and WT siblings from different age groups were compared. Serial sections were made through paraffin-embedded whole knees and investigated histologically. Additionally, medial femoral condyle peaks from sibling pairs were investigated ultrastructurally using transmission electron microscopy. Results: Histological findings demonstrated a clear and increasing disparity between tissue degeneration in WT and FM-null animal knees with progressing age. Distinct differences were apparent by 36 weeks. Around the 80 week period and onward these differences became profound. However, qualitative ultrastructural investigation did not indicate either any aberrant tissue ultrastructure or any abnormal collagen fibril forms in FM-null articular cartilage compared with WT. Biochemical and immunohistochemical investigation of FM-null articular cartilage showed a significant increase in tissue levels of lumican (LUM). Conversely, the cruciate ligaments of the knee showed both an increase in LUM content and considerable structural abnormalities including the tendency towards rupture. Conclusion: This report indicates for the first time that FM-null mice have a higher propensity towards degenerative changes in their knee joints than comparable WT animals. Interestingly, no underlying ultrastructural or fibril abnormalities within the articular cartilage could be identified to explain why FM-null cartilage is more prone to pathological changes than wild-type tissue. We conclude that alterations in ligaments, and possibly other tissues within the knee, are of considerable importance in the pathogenesis of the observed articular cartilage degeneration. (C) 2002 OsteoArthritis Research Society International. Published by Elsevier Science Ltd. All rights reserved.}},
  author       = {{Gill, MR and Oldberg, Åke and Reinholt, FP}},
  issn         = {{1063-4584}},
  keywords     = {{electron microscopy; transmission; knock-out mice; lumican; osteoarthritis; fibromodulin; articular cartilage; ligaments}},
  language     = {{eng}},
  number       = {{10}},
  pages        = {{751--757}},
  publisher    = {{Elsevier}},
  series       = {{Osteoarthritis and Cartilage}},
  title        = {{Fibromodulin-null murine knee joints display increased incidences of osteoarthritis and alterations in tissue biochemistry}},
  url          = {{http://dx.doi.org/10.1053/joca.2002.0527}},
  doi          = {{10.1053/joca.2002.0527}},
  volume       = {{10}},
  year         = {{2002}},
}