Bone “mass” and the “mechanostat”: A proposal

Wiley - Tập 219 Số 1 - Trang 1-9 - 1987
Harold M. Frost1,2
1Department of Anatomy, Purdue University, West Lafayette, IN 47907
2Southern Colorado Clinic, Pueblo, CO 81004

Tóm tắt

AbstractThe observed fit of bone mass to a healthy animal's typical mechanical usage indicates some mechanism or mechanisms monitor that usage and control the three longitudinal growth, bone modeling, and BMU‐based remodeling activities that directly determine bone mass. That mechanism could be named a mechanostat. Accumulated evidence suggests it includes the bone itself, plus mechanisms that transform its mechanical usage into appropriate signals, plus other mechanisms that detect those signals and then direct the above three biologic activities. In vivo studies have shown that bone strains in or above the 1500–3000 microstrain range cause bone modelling to increase cortical bone mass, while strains below the 100–300 microstrain range release BMU‐based remodeling which then removes existing cortical‐endosteal and trabecular bone. That arrangement provides a dual system in which bone modeling would adapt bone mass to gross overloading, while BMU‐based remodeling would adapt bone mass to gross underloading, and the above strain ranges would be the approximate “setpoints” of those responses.The anatomical distribution of those mechanical usage effects are well known. If circulating agents or disease changed the effective setpoints of those responses their bone mass effects should copy the anatomical distribution of the mechanical usage effects. That seems to be the case for many agents and diseases, and several examples are discussed, including postmenopausal osteoporosis, fluoride effects, bone loss in orbit, and osteogenesis imperfecta.The mechanostat proposal is a seminal idea which fits diverse evidence but it requires critique and experimental study.

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Tài liệu tham khảo

Albright J. A., 1987, The Scientific Basis of Orthopaedics

Anderson C.(1986) Three studies of oophorectomy and estrogen and progestone replacement in Beagle dogs. Reviewed at the 1986 University of Utah‐sponsored Hard Tissue Workshop. Calcif. Tissue Int. (in press).

10.1002/ajpa.1330280513

Briançon D. andMeunier P. J. (1979) Le Traitement de l'Ostéoporose par l'Association Fluorure de Sodium Calcium Vitamine D. Univ. Claude Bernard Lyon.

10.1016/8756-3282(85)90001-8

Van Cochran G. B., 1982, A Primer of Orthopaedic Biomechanics

Courpron P., 1981, Bone tissue mechanisms underlying osteoporoses, Orthop. Clin. N. Am., 12, 513, 10.1016/S0030-5898(20)31369-9

10.1115/1.3138584

Cruess R. L., 1982, Embryology, Biochemistry and Physiology

10.1515/9781400853724

DeLuca H. F., 1981, Recent Advances in Pathogenesis and Treatment

Enlow D. H., 1963, Principles of Bone Remodeling

Frame B., 1973, Clinical Aspects of Metabolic Bone Disease

Frame B., 1983, Clinical Disorders of Bone and Mineral Metabolism, 10.7326/0003-4819-99-5-725

Frost H. M., 1964, The Laws of Bone Structure

Frost H. M., 1983, A determinant of bone architecture, The minimum effective strain. Clin. Orthop., 175, 286

Frost H. M., 1985, The pathomechanics of osteoporoses, Clin. Orthop., 200, 198, 10.1097/00003086-198511000-00027

Frost H. M., 1986, Intermediary Organization of the Skeleton

10.1007/978-3-642-70709-4_30

10.1007/978-3-642-70709-4_19

Frost H. M.(1987) Vital biomechanics. Proposed general concepts for skeletal adaptations to mechanical usage. Calcif. Tissue Int. (in press).

Heaney R. P., 1978, Menopausal changes in bone remodeling, J. Lab. Clin. Med., 92, 964

10.1007/BF02406133

Jaworski Z. F. G., 1980, Effect of long term immobilization on the pattern of bone loss in older dogs, J. Bone Joint Surg., 62, 104, 10.1302/0301-620X.62B1.6985912

Jee W. S. S., 1983, Histology, 200, 10.1007/978-1-349-06859-3_6

Jee W. S. S., 1983, Effects of spaceflight on trabecular bone in rats, Am. J. Physiol., 13, 310

Johnston C. C., 1986, A review of pre‐, intra‐ and postmenopausal bone loss in women

Kuhlencordt F., 1980, Klinische Osteologie

10.1007/BF02406134

Lips P.(1982)Metabolic Causes and Prevention of Femoral Neck Fractures. PhD Thesis. University of Amsterdam Amsterdam.

Martin B.(1986)Comparison of bone turnover and bone mass findings in oophorectomized and estrogen treated oophorectomized dogs. Reviewed at the 1986 University of Utah‐sponsored Hard Tissue Workshop. Calcif. Tissue Int. (in press).

Melton L. J.(1986)Epidemiology of pre‐ and postmenopausal bone loss in women. A review of recent studies in the U.S. and Europe. Given at the 1986 University of Utah‐sponsored Hard Tissue Workshop.

Minnaire P.(1973) L'Ostéoporose d'Immobilization. Données Biologiques et Histologiques Quantitatives. PhD Thesis. Ediprim Lyon.

10.1016/8756-3282(85)90317-5

10.1016/8756-3282(86)90019-0

1975, Orthopaedic Research Society Abstracts

10.1002/jor.1100030308

Parfitt A. M.(1986) Review of bone mass and turnover in pre‐ intra‐and postmenopausal women. Given at the 1986 University of Utah‐Sponsored Hard Tissue Workshop.

10.1007/BF02406132

10.1007/BF02406145

Peck W., 1984, Bone and Mineral Research/3 (Ed)

Recker R. R., 1983, Techniques and Interpretation

Recker R. R., 1978, Effect of estrogens and calcium carbonate on bone loss in postmenopausal women, Metab. Bone Dis. Relat. Res., 1, 7

10.1007/BF02406128

Sillence D., 1981, Osteogenesis imperfecta, An expanding panorama of variants. Clin. Orthop., 159, 11

10.1007/BF02406146

10.1007/978-3-642-70709-4

10.1302/0301-620X.60B3.681422

Urist M. R., 1980, Fundamental and Clinical Bone Physiology

10.1007/BF02406148

10.1016/0221-8747(82)90011-X

Wronski T. J., 1983, Inhibition of cortical and trabecular bone formation in the long bones of immobilized monkeys, Clin. Ortho., 181, 269, 10.1097/00003086-198312000-00042

Wronski T. J., 1983, Effect of spaceflight on periosteal bone formation in rats, Am. J. Physiol., 13, 305

10.1016/8756-3282(86)90683-6

10.1016/8756-3282(86)90682-4

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Wiley

Tập 219 Số 1

1-9

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