論文

2015年7月

Degenerative changes of the cranial cruciate ligament harvested from dogs with cranial cruciate ligament rupture.

The Journal of veterinary medical science
  • Tom Ichinohe
  • ,
  • Nobuo Kanno
  • ,
  • Yasuji Harada
  • ,
  • Takuya Yogo
  • ,
  • Masahiro Tagawa
  • ,
  • Satoshi Soeta
  • ,
  • Hajime Amasaki
  • ,
  • Yasushi Hara

77
7
開始ページ
761
終了ページ
70
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1292/jvms.14-0383

Degenerative cranial cruciate ligament (CCL) rupture is characterized histologically by degenerating extracellular matrix (ECM) and chondroid metaplasia. Here, we describe the progression of chondroid metaplasia and the changes in the expression of ECM components in canine CCL rupture (CCLR). CCLs from 26 stifle joints with CCLR (CCLR group) and normal CCLs from 12 young beagles (control group) were examined histologically and immunohistochemically for expression of type I (COLI), type II (COLII), type III collagen (COLIII) and Sry-type HMG box 9 (SOX9). Cell density and morphology of CCLs were quantified using hematoxylin-eosin staining. The percentage of round cells was higher in the CCLR group than in controls. COLI-positive areas were seen extensively in the connecting fibers, but weakly represented in the cytoplasm of normal CCLs. In the CCLR group, there were fewer COLI-positive areas, but many COLI-positive cells. The percentages of COLII-, COLIII- and SOX9-positive cells were higher in the CCLR group than in controls. The number of spindle cells with perinuclear halo was high in the CCLR group, and most of these cells were SOX9-positive. Deposition of COLI, the main ECM component of ligaments, decreased with increased COLIII expression in degenerated CCL tissue, which shows that the deposition of the ECM is changed in CCLR. On the contrary, expression of SOX9 increased, which may contribute to the synthesis of cartilage matrix. The expression of COLII and SOX9 in ligamentocytes showed that these cells tend to differentiate into chondrocytes.

リンク情報
DOI
https://doi.org/10.1292/jvms.14-0383
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/25716871
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4527496
ID情報
  • DOI : 10.1292/jvms.14-0383
  • PubMed ID : 25716871
  • PubMed Central 記事ID : PMC4527496

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