Effect of puberty on rates of bone growth and mineralisation: with observations in male delayed puberty.

Krabbe, S; Christiansen, Claus; Rødbro, P.; Transbøl, Ib

doi:10.1136/adc.54.12.950

Cited by 125 publications

(59 citation statements)

References 14 publications

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“…The lag between growth in length and growth in strength should be exaggerated when longitudinal growth accelerates (19). In fact, the dissociation between bone's growth in length and in mass is a well-documented phenomenon during the pubertal growth spurt in both sexes (5,52,(57)(58)(59)(60), and could explain the increased fracture rate during that period in life (61)(62)(63). Because the timing of the maximal increase in bone length and muscle mass differs among musculoskeletal regions (64,65), it is not unexpected that the increase in bone mass also follows a region-specific pattern during puberty (52).…”

Section: Clinical and Experimental Observations Related To The Mechanmentioning

confidence: 99%

The Developing Bone: Slave or Master of Its Cells and Molecules?

2001

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A large number of molecular, cellular, and epidemiologic factors have been implicated in the regulation of bone development. A major unsolved problem is how to integrate these disparate findings into a concept that explains the development of bone as an organ. Often events on the organ level are simply presented as the cumulative effect of all factors that individually are known to influence bone development. In such a cumulative model it must be assumed that each bone cell carries the construction plan of the entire skeletal anatomy in its genes. This scenario is implausible, because it would require an astronomical amount of positional information. We therefore propose a functional model of bone development, which is based on Frost's mechanostat theory. In this model the genome only provides positional information for the basic outline of the skeleton as a cartilaginous template. Thereafter, bone cell action is coordinated by the mechanical requirements of the bone. When mechanical challenges exceed an acceptable level (the mechanostat set point), bone tissue is added at the location where it is mechanically necessary. The main mechanical challenges during growth result from increases in bone length and in muscle force. Hormones, nutrition, and environmental factors exert an effect on bone either directly by modifying the mechanostat system or indirectly by influencing longitudinal bone growth or muscle force. Predictions based on this model are in accordance with observations on prenatal, early postnatal, and pubertal bone development. We propose that future studies on bone development should address topics that can be derived from the mechanostat model. Bone development is one of the key processes of intrauterine and postnatal growth. Indeed, major abnormalities in bone development are incompatible with survival. Elucidating the mechanisms of this process, therefore, is an important task in biology and medicine. Similar to other fields of biomedical investigation, current research in bone biology heavily relies on the reductionist approach, which excludes the physiologic context as far as possible and focuses on the role of individual factors (1). Methods based on this approach have led to spectacular new insights into the molecular and cellular events occurring during bone development. A rapidly increasing number of factors, commonly called determinants or regulators of bone development, have been implicated in this process. To the list of molecular and cellular factors must be added the many environmental and behavioral factors identified by epidemiology, such as nutritional aspects and physical activity.Thus, the reductionist approach has been extremely useful in identifying individual parts of the developing bone's machinery. The problem is how to put the individual pieces back into place. This is an essential task when it comes to explaining bone development on the level that interests patients and physicians most-the organ level. Confronted with a maze of molecular and cellular pathways, one may easily...

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Section: Clinical and Experimental Observations Related To The Mechanmentioning

confidence: 99%

The Developing Bone: Slave or Master of Its Cells and Molecules?

2001

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“…By the age of 16 yr most epiphyses are closed, and endosteal bone apposition is ceasing as well (8). Most of the cross sectional studies which have related BM to age either ended by the late adolescence or early 20s (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25) or started by the beginning of third decade , thereby perhaps missing an important phase ofthe timing ofPBM. There is also no study where multiple skeletal sites were measured in the same individuals between childhood and adulthood.…”

Section: Introductionmentioning

confidence: 99%

Timing of peak bone mass in Caucasian females and its implication for the prevention of osteoporosis. Inference from a cross-sectional model.

et al. 1994

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To determine the timing of peak bone mass and density, we conducted a cross-sectional study of bone mass measurements in 265 premenopausal Caucasian females, aged 8-50 yr. Bone mass and bone mineral density were measured using dual X-ray absorptiometry and single-photon absorptiometry at the spine (anteroposterior, lateral), proximal femur, radius shaft, distal forearm, and the whole body. Bone mass parameters were analyzed using a quadratic regression model and segmented regression models with quadratic-quadratic or quadratic-linear form. The results show that most of the bone mass at multiple skeletal locations will be accumulated by late adolescence. This is particularly notable for bone mineral density of the proximal femur and the vertebral body. Bone mass of the other regions of interest is either no different in women between the age of 18 yr and the menopause or it is maximal in 50-yr-old women, indicating slow but permanent bone accumulation continuing at some sites up to the time of menopause. This gain in bone mass in premenopausal adult women is probably the result ofcontinuous periosteal expansion with age. Since rapid skeletal mineral acquisition at all sites occurs relatively early in life, the exogenous factors which might optimize peak bone mass need to be more precisely identified and characterized. (J. Clin. Invest.

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“…Moreover, sex steroids can act centrally by regulating GH secretion and peripherally modulating GH responsiveness (Figure 1). Higher levels of GH and of sexual steroids during the prepubertal period have a positive influence on bone mineral density and the accumulation of calcium in the skeleton (Krabbe et al, 1979). The effects of GH on bone turnover may be partly mediated by locally produced IGF-1, which is a beneficial factor on skeletal development and bone formation.…”

Section: Bone Physiology During Adolescencementioning

confidence: 99%