On the Estrogen–Bone Relationship and Postmenopausal Bone Loss: A New Model


  • Harold M. Frost

    Corresponding author
    1. Department of Orthopaedic Surgery, Southern Colorado Clinic, Pueblo, Colorado, U.S.A.
    • Address reprint requests to: Dr. Harold Frost, Department of Orthopaedic Surgery, Southern Colorado Clinic, 2002 Lake Avenue, Pueblo, CO 81004 U.S.A.
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In this model of estrogen effects on bone, a postulated mediator mechanism in marrow would affect modeling and remodeling only of bone next to or close to it. That mediator mechanism could sense estrogen. In response to that hormone, it would let remodeling of bone next to marrow proceed in its conservation mode. This would minimize losses of that bone and tend to prevent an osteopenia. But acute estrogen deficiency would make that mechanism switch remodeling of bone next to marrow to its disuse mode. Meanwhile, conservation-mode remodeling would continue for haversian and subperiosteal bone. The resulting losses of bone next to marrow would expand marrow cavities, thin cortices, and reduce trabecular bone “mass,” but would not reduce outside bone diameters. That scheme could explain the osteopenia that follows natural or experimental estrogen deficiency in mammalian females. If so, as estrogen secretion rises in girls at puberty they should begin accumulating more bone next to marrow. They do. Also if so, at menopause women should begin to lose that bone. They do. Those effects would exist in addition to known effects of estrogen on existing osteoclasts and osteoblasts.