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Stevens, D.G.; Boyer, Martin I.; Bowen, C. Vaughan A.

doi:10.1097/00004694-199905000-00022

Cited by 26 publications

(9 citation statements)

References 30 publications

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“…That decrease in growth plate function appears to be due to a mechanism intrinsic to the growth plate rather than a hormonal or other systemic mechanism; in growth plate transplantation experiments, the growth rate of the transplanted growth plate depends on the age of the donor animal, not the age of the recipient [6]. The term growth plate senescence [7] has been used to describe this intrinsic process that involves both a decline in the function and cellularity of the growth plate.…”

Section: Basic Principles Of Growth Plate Physiologymentioning

confidence: 99%

Endocrine Regulation of the Growth Plate

et al. 2005

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Longitudinal bone growth occurs at the growth plate by endochondral ossification. Within the growth plate, chondrocyte proliferation, hypertrophy, and cartilage matrix secretion result in chondrogenesis. The newly formed cartilage is invaded by blood vessels and bone cells that remodel the newly formed cartilage into bone tissue. This process of longitudinal bone growth is governed by a complex network of endocrine signals, including growth hormone, insulin-like growth factor I, glucocorticoid, thyroid hormone, estrogen, androgen, vitamin D, and leptin. Many of these signals regulate growth plate function, both by acting locally on growth plate chondrocytes and also indirectly by modulating other endocrine signals in the network. Some of the local effects of hormones are mediated by changes in paracrine factors that control chondrocyte proliferation and differentiation. Many human skeletal growth disorders are caused by abnormalities in the endocrine regulation of the growth plate. This review provides an overview of the endocrine signals that regulate longitudinal bone growth, their interactions, and the mechanisms by which they affect growth plate chondrogenesis.

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Section: Basic Principles Of Growth Plate Physiologymentioning

confidence: 99%

Endocrine Regulation of the Growth Plate

et al. 2005

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“…A similar process occurs in other mammals including humans (2-9). Based on growth plate transplantation experiments, the senescent decline in growth rate appears not to be due to a hormonal or other systemic mechanism but rather to a mechanism intrinsic to the growth plate (27). Indirect evidence suggests that growth plate chondrocytes have a finite proliferative capacity that is gradually exhausted, causing growth to slow and eventually halt (28,29).…”

Section: Fig 2 Effect Of Estrogen Treatment On Mean (ϯSem) Tibial Gmentioning

confidence: 99%

Effects of estrogen on growth plate senescence and epiphyseal fusion

Weise

De-Levi

Barnes

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

270

202

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Estrogen is critical for epiphyseal fusion in both young men and women. In this study, we explored the cellular mechanisms by which estrogen causes this phenomenon. Juvenile ovariectomized female rabbits received either 70 g/kg estradiol cypionate or vehicle i.m. once a week. Growth plates from the proximal tibia, distal tibia, and distal femur were analyzed after 2, 4, 6, or 8 weeks of treatment. In vehicle-treated animals, there was a gradual senescent decline in tibial growth rate, rate of chondrocyte proliferation, growth plate height, number of proliferative chondrocytes, number of hypertrophic chondrocytes, size of terminal hypertrophic chondrocytes, and column density. Estrogen treatment accelerated the senescent decline in all of these parameters. In senescent growth plates, epiphyseal fusion was observed to be an abrupt event in which all remaining chondrocytes were rapidly replaced by bone elements. Fusion occurred when the rate of chondrocyte proliferation approached zero. Estrogen caused this proliferative exhaustion and fusion to occur earlier. Our data suggest that (i) epiphyseal fusion is triggered when the proliferative potential of growth plate chondrocytes is exhausted; and (ii) estrogen does not induce growth plate ossification directly; instead, estrogen accelerates the programmed senescence of the growth plate, thus causing earlier proliferative exhaustion and consequently earlier fusion.

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“…For example, the concentration of IGF-I actually increases with age during childhood (5). Furthermore, growth plates have been transplanted between rabbits of different ages, and the growth rate of the transplanted growth plates depends on the age of the donor, not the recipient, suggesting that the decline in growth rate is due to a local, growth plate mechanism, rather than a systemic mechanism (6). …”

Section: Linear Growth Is Rapid In Infancy But Subsequently Slows Duementioning

confidence: 99%