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Lamellar bone turnover system and its effector organ.

作者信息

Jaworski Z F

出版信息

Calcif Tissue Int. 1984;36 Suppl 1:S46-55. doi: 10.1007/BF02406133.

Abstract

Juxtaposition of cell kinetics in the asymmetric, self-renewing osteoclast and osteoblast populations in the evolving secondary Haversian systems, which are in neutral balance, disclosed their genetically determined fixed and flexible or variable properties, the latter controllable. These jointly controlled cell populations (coupling) at local and organ level, constitute the Effector Organ of Lamellar Bone Turnover Systems (EO LBTS). In part genetically preprogrammed, this system also responds during growth and maturity to environmental (mainly biomechanical) factors that adjust structure to function. Since the pattern of signals and stimuli generated within the bones under the conditions of mechanical loads differs during growth and maturity, the two major expressions of the LBTS (i.e., modeling of bones during growth and their remodeling during growth and maturity) can be explained by the appropriate response of its EO to those patterns. Since normal physical activity has a limited range and bones sustain more or less predictable deforming forces, the signals and stimuli so generated must preserve more or less similar patterns. Considering also the constraints on the system (constants of the EO LBTS), modeling and remodeling patterns, as well as the gross and microscopic organization of bones, would vary little from one individual to another under normal circumstances. For its proper function, the EO LBTS requires the presence in the cell environment of specific and nonspecific permissive factors (as any cell or tissue in the organism) and it may be influenced further by modulatory factors which link it with the system maintaining calcium ion homeostasis in the body fluids. Mechanical failure of the skeleton in metabolic bone disease can be explained by the alterations in the biochemical or biomechanical milieu due to disorders of other organs and systems which interfere with the primary (structural) function of the EO LBTS.

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