Age-related bone loss: A hypothesis and initial assessment in mice

A. J. Kahn*, R. Gibbons, S. Perkins, D. Gazit

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

106 Scopus citations

Abstract

The osteopenia associated with advanced age appears to be a universal phenomenon in humans and animals, but the mechanisms by which it occurs are understood incompletely. However, the explanation must lie in an absolute or relative diminution in the level of osteoblastic bone-forming activity when compared with osteoclastic bone-resorbing activity. The authors postulated that with old age there would be a reduction in the number or function or both of osteoblastic stem cells that could account for part of the diminution in bone formation. They further postulated that there would be either no change or an increase in osteoclastic potential and bone resorption. To test these concepts, bone marrow cells were isolated from 4- to 6-month-old or 24- month-old mice and cultured in vitro under a variety of circumstances that permitted an assessment of the stromal osteogenic cells and marrow hemopoietic progenitor cells belonging to the monocyte and osteoclast series. These data show a marked reduction in the number and in vitro activity of stromal osteogenic cells from old animals. There is an increase in old mice in the number of marrow cells capable of forming osteoclasts in coculture and responsive to the growth factors believed operational in the monocyte and osteoclast series. The authors now are exploring the hypothesis that an age- related diminution in transforming growth factor-β levels is responsible for these changes in progenitor cell levels in marrow and their functional status as expressed in vitro. The data to date are consistent with age-related changes in osteoblast and osteoclast precursor pools contributing to the loss of bone mass in Type II osteoporosis (osteopenia).

Original languageEnglish
Pages (from-to)69-75
Number of pages7
JournalClinical Orthopaedics and Related Research
Volume313
StatePublished - 1995
Externally publishedYes

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