HISTOLOGICAL ANALYSIS OF THE NUMBER AND WEIGHT OF VESSELS OF OSTEONECROSIS OF THE FEMORAL HEAD

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  • HARADA Kenji
    Department of Pathology, Showa University School of Medicine
  • SAITO Koji
    Department of Pathology, Showa University School of Medicine
  • HIRABAYASHI Kodai
    Department of Pathology, Showa University School of Medicine
  • MURAKAMI Yuto
    Department of Pathology, Showa University School of Medicine
  • YAMAOKA Keita
    Department of Pathology, Showa University School of Medicine
  • MOROHOSHI Toshio
    Department of Pathology, Showa University School of Medicine
  • KUNIMURA Toshiaki
    Department of Clinical Diagnostic Pathology, Showa University Northern Yokohama Hospital
  • YAMANO Yuko
    Department of Hygiene and Preventive Medicine, Showa University School of Medicine
  • ASTUMI Takashi
    Department of Orthopaedic Surgery, Showa University Fujigaoka Hospital

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Other Title
  • 特発性大腿骨頭壊死症における血管形態の組織学的評価
  • トクハツセイ ダイタイコツトウ エシショウ ニ オケル ケッカン ケイタイ ノ ソシキガクテキ ヒョウカ

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Abstract

Aseptic necrosis of the femoral head is caused by a circulatory disorder in the feeding artery. This report investigates the morphological abnormality in the vessel that causes the disorder. We studied 28 hip joints of 21 males and 7 females (avg. age 47 years; range 27 to 66) that had been resected during total hip arthroplasty. Of the 28, 6 hips were Stage 3A, 16 Stage 3B, and 6 Stage 4. We investigated four areas: the band lesion, the distal-lateral part close to the band lesion, the proximal-lateral part close to the band lesion, and the normal part of each femoral head. The vessel number was greater in the band lesion and the distal-lateral part than in the normal part and the proximal-lateral part. This fact confirms that the ingression of reparative vessels occurs at the lateral part in the head following osteonecrosis. The diameter of the vessels in the band lesion and in the distal-lateral part was significantly less in Stage 4 than in Stage 3. This result indicates that the load stress delays the reparative vessel ingression compared to the interstitial fibrosis during the delay.

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