An osteopenic/osteoporotic phenotype delays alveolar bone repair

Chih Hao Chen, Liao Wang, U. Serdar Tulu, Masaki Arioka, Melika Maghazeh Moghim, Benjamin Salmon, Chien Tzung Chen, Waldemar Hoffmann, Jessica Gilgenbach, John B. Brunski, Jill A. Helms

研究成果: Contribution to journalArticle査読

26 被引用数 (Scopus)

抄録

Aging is associated with a function decline in tissue homeostasis and tissue repair. Aging is also associated with an increased incidence in osteopenia and osteoporosis, but whether these low bone mass diseases are a risk factor for delayed bone healing still remains controversial. Addressing this question is of direct clinical relevance for dental patients, since most implants are performed in older patients who are at risk of developing low bone mass conditions. The objective of this study was to assess how an osteopenic/osteoporotic phenotype affected the rate of new alveolar bone formation. Using an ovariectomized (OVX) rat model, the rates of tooth extraction socket and osteotomy healing were compared with age-matched controls. Imaging, along with molecular, cellular, and histologic analyses, demonstrated that OVX produced an overt osteoporotic phenotype in long bones, but only a subtle phenotype in alveolar bone. Nonetheless, the OVX group demonstrated significantly slower alveolar bone healing in both the extraction socket, and in the osteotomy produced in a healed extraction site. Most notably, osteotomy site preparation created a dramatically wider zone of dying and dead osteocytes in the OVX group, which was coupled with more extensive bone remodeling and a delay in the differentiation of osteoblasts. Collectively, these analyses demonstrate that the emergence of an osteoporotic phenotype delays new alveolar bone formation.

本文言語英語
ページ(範囲)212-219
ページ数8
ジャーナルBone
112
DOI
出版ステータス出版済み - 7 2018

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Histology
  • Physiology

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