Cell Kinetics of Growth Cartilage in the Rat Tibia Ii. Measurements During Ageing

Walker, K. V. R.; Kember, N. F.

doi:10.1111/j.1365-2184.1972.tb00379.x

Cited by 50 publications

(45 citation statements)

References 11 publications

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“…The bone loss is even enhanced in this study by the growth of the animals that results in a "flow" of the screw and the surrounding volume of interest towards the less trabecularized diaphyseal region. Normally, the growth of rats slows down and ceases around 26 weeks of age [52], this corresponds in this study with day 31 after screw implantation. When comparing bone resorption with formation in the Control-group, it can be seen that, beside the early bone formation peak, the BRR clearly exceeded the BFR in all bone regions most of the time and leveled out only towards the end of the study.…”

Section: Discussionsupporting

confidence: 77%

Does locally delivered Zoledronate influence peri-implant bone formation? – Spatio-temporal monitoring of bone remodeling in vivo

Kettenberger

Ston

Thein³

et al. 2014

Biomaterials

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a b s t r a c tBisphosphonates are known for their strong inhibitory effect on bone resorption. Their influence on bone formation however is less clear. In this study we investigated the spatio-temporal effect of locally delivered Zoledronate on peri-implant bone formation and resorption in an ovariectomized rat femoral model. A cross-linked hyaluronic acid hydrogel was loaded with the drug and applied bilaterally in predrilled holes before inserting polymer screws. Static and dynamic bone parameters were analyzed based on in vivo microCT scans performed first weekly and then biweekly. The results showed that the locally released Zoledronate boosted bone formation rate up to 100% during the first 17 days after implantation and reduced the bone resorption rate up to 1000% later on. This shift in bone remodeling resulted in an increase in bone volume fraction (BV/TV) by 300% close to the screw and 100% further away. The double effect on bone formation and resorption indicates a great potential of Zoledronateloaded hydrogel for enhancement of peri-implant bone volume which is directly linked to improved implant fixation.

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Section: Discussionsupporting

confidence: 77%

Does locally delivered Zoledronate influence peri-implant bone formation? – Spatio-temporal monitoring of bone remodeling in vivo

Kettenberger

Ston

Thein³

et al. 2014

Biomaterials

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“…In vivo, the decline in proliferation largely explains the decline in growth rate with age (Walker & Kember 1972), but a decline in cell hypertrophy, matrix production, and possibly an increase in apoptosis may also contribute to the decrease in growth rate (Walker & Kember 1972, Chrysis et al 2002.…”

Section: Figurementioning

confidence: 99%

“…Longitudinal bone growth, in turn, results from chondrocyte proliferation in the growth plates. With age, this proliferation slows down, causing longitudinal bone growth to slow and eventually stop (Walker & Kember 1972). Also with increasing age, the growth plate undergoes structural changes including a decrease in the height of the growth plate, a decrease in the number of chondrocytes in the individual zones, as well as a decrease in the size of the individual hypertrophic chondrocytes.…”

Section: Introductionmentioning

confidence: 99%

Growth plate senescence is associated with loss of DNA methylation

Nilsson¹,

Mitchum²,

Schrier³

et al. 2005

Journal of Endocrinology

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The overall body size of vertebrates is primarily determined by longitudinal bone growth at the growth plate. With age, the growth plate undergoes programmed senescence, causing longitudinal bone growth to slow and eventually cease. Indirect evidence suggests that growth plate senescence occurs because stem-like cells in the growth plate resting zone have a finite proliferative capacity that is gradually exhausted. Similar limits on replication have been observed when many types of animal cells are placed in cell culture, an effect known as the Hayflick phenomenon. However, we found that the number of population doublings of rabbit resting zone chondrocytes in culture did not depend on the age of the animal from which the cells were harvested, suggesting that the mechanisms limiting replicative capacity of growth plate chondrocytes in vivo are distinct from those in vitro. We also observed that the level of DNA methylation in resting zone chondrocytes decreased with age in vivo. This loss of methylation appeared to occur specifically with the slow proliferation of resting zone chondrocytes in vivo and was not observed with the rapid proliferation of proliferative zone chondrocytes in vivo (i.e. the level of DNA methylation did not change from the resting zone to the hypertrophic zone), with proliferation of chondrocytes in vitro, or with growth of the liver in vivo. Thus, the overall level of DNA methylation decreases during growth plate senescence. This finding is consistent with the hypothesis that the mechanism limiting replication of growth plate chondrocytes in vivo involves loss of DNA methylation and, thus, loss of DNA methylation might be a fundamental biological mechanism that limits longitudinal bone growth in mammals, thereby determining the overall adult size of the organism.

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“…the time period over which longitudinal bone growth was measured; Walker & Kember, 1972a;Smith et al 1981;Kember, 1983), and it is thus a measure of cell turnover. Mean cell turnover per column per day can thus be calculated from the daily cell elimination rate, which is equal to daily linear growth rate divided by final mean cell height (Steel, 1967;Walker & Kember, 1972b;Kember, 1983 Although the fate of these cells is unknown (Hunziker, Herrmann, Schenk, Muller & Moor, 1984), they certainly do not persist as chondrocytes.…”

Section: Quantification Of Chondrocyte Performancementioning

confidence: 99%

Physiological mechanisms adopted by chondrocytes in regulating longitudinal bone growth in rats.

Hunziker

Schenk

1989

The Journal of Physiology

279

310

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SUMMARY1. Chondrocyte activities within growth plate cartilage are the principal determinants of longitudinal bone growth, and it was the aim of this investigation to assess how these cell activities are modulated under various growth rate conditions.Using proximal tibial growth plates from rats of different ages, growth rate was determined by fluorochrome labelling and incident light fluorescence microscopy. Various cellular parameters contributing to longitudinal bone growth were quantified by light microscopic stereology. The size of the proliferating cell population ('growth fraction') was estimated by autoradiography (using [3H]thymidine labelling).2. A comparison between data for suckling (21-day-old) and fast-growing (35-dayold) rats revealed that growth acceleration is achieved almost exclusively by cellshape modelling, namely by an increase in final cell height and a decrease in lateral diameter, whereas final cell volume and surface area are slightly reduced. Cell proliferation rate in the longitudinal direction and net matrix production per cell remain unchanged. The physiological increase in linear growth rate thus appears to be based principally upon a controlled structural modulation of the chondrocyte phenotype. On the other hand, a physiological reduction in growth rate (i.e. growth deceleration) effected during the transition from pre-puberty (35-day-old rats) to maturity (80-day-old rats) is achieved by simultaneous decreases in several chondrocyte parameters, including cell height (i.e. phenotype modulation), cell volume and proliferation rate (in the longitudinal direction

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Cell Kinetics of Growth Cartilage in the Rat Tibia Ii. Measurements During Ageing

Cited by 50 publications

References 11 publications

Does locally delivered Zoledronate influence peri-implant bone formation? – Spatio-temporal monitoring of bone remodeling in vivo

Does locally delivered Zoledronate influence peri-implant bone formation? – Spatio-temporal monitoring of bone remodeling in vivo

Growth plate senescence is associated with loss of DNA methylation

Physiological mechanisms adopted by chondrocytes in regulating longitudinal bone growth in rats.

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