Effect of sex steroids on peak bone density of growing rabbits

Gilsanz, Vicente; Roe, Thomas; Gibbens, D T; Schulz, Eloy; Carlson, Michael; Gonzalez, Orlando R.; Boechat, M. Ines

doi:10.1152/ajpendo.1988.255.4.e416

Cited by 105 publications

(100 citation statements)

References 30 publications

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“…There have been surprisingly few studies using the ovariectomized rabbit to study the effect of ovarian insufficiency on bone mass although this animal seems more popular to study bone ingrowth into implants and bone-implant interfaces. To determine the effect of testosterone and estrogen on bone density during bone growth, New Zealand White rabbits were selected because of their short developmental period and their faster bone turnover than primates (Gilsanz et al, 1988). Unlike other mammals such as the rat, mouse and guinea pig, rabbits achieve skeletal maturity (closure of epiphyseal plates) shortly after reaching complete sexual development at approximately 6 months (Gilsanz et al, 1988), and they show significant intracortical remodelling (Kimmel, 1996).…”

Section: Rabbitsmentioning

confidence: 99%

“…To determine the effect of testosterone and estrogen on bone density during bone growth, New Zealand White rabbits were selected because of their short developmental period and their faster bone turnover than primates (Gilsanz et al, 1988). Unlike other mammals such as the rat, mouse and guinea pig, rabbits achieve skeletal maturity (closure of epiphyseal plates) shortly after reaching complete sexual development at approximately 6 months (Gilsanz et al, 1988), and they show significant intracortical remodelling (Kimmel, 1996). Female growing rabbits were given prednisolone (0.7 mg/kg per day for 5 months) to study corticosteroid-induced osteoporosis.…”

Section: Rabbitsmentioning

confidence: 99%

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Animal models of osteoporosis - necessity and limitations

2001

eCM

243

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There is a great need to further characterise the available animal models for postmenopausal osteoporosis, for the understanding of the pathogenesis of the disease, investigation of new therapies (e.g. selective estrogen receptor modulators (SERMs)) and evaluation of prosthetic devices in osteoporotic bone. Animal models that have been used in the past include non-human primates, dogs, cats, rodents, rabbits, guinea pigs and minipigs, all of which have advantages and disadvantages. Sheep are a promising model for various reasons: they are docile, easy to handle and house, relatively inexpensive, available in large numbers, spontaneously ovulate, and the sheep's bones are large enough to evaluate orthopaedic implants. Most animal models have used females and osteoporosis in the male has been largely ignored. Recently, interest in development of appropriate prosthetic devices which would stimulate osseointegration into osteoporotic, appendicular, axial and mandibular bone has intensified. Augmentation of osteopenic lumbar vertebrae with bioactive ceramics (vertebroplasty) is another area that will require testing in the appropriate animal model. Using experimental animal models for the study of these different facets of osteoporosis minimizes some of the difficulties associated with studying the disease in humans, namely time and behavioral variability among test subjects. New experimental drug therapies and orthopaedic implants can potentially be tested on large numbers of animals subjected to a level of experimental control impossible in human clinical research.

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Section: Rabbitsmentioning

confidence: 99%

Section: Rabbitsmentioning

confidence: 99%

Animal models of osteoporosis - necessity and limitations

2001

eCM

243

View full text Add to dashboard Cite

show abstract

“…The rabbit is also convenient as they reach skeletal maturity shortly after sexual maturity at around 6 months of age. 4 Guidelines are provided for the dimensions of implants for in vivo studies, based on the size of animal and bone chosen and on the implant design, in order to avoid pathological fracture of the test site. 5 At least four rabbits and at least two of each of the other species mentioned above should be used for each treatment at each implantation period, though appropriate power calculations should be performed.…”

Section: Introductionmentioning

confidence: 99%

Rabbits as Animal Models in Contemporary Implant Biomaterial Research

Arora¹,

Nafria²,

Kanase³

2011

World Journal of Dentistry

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Development of an optimal interface between bone and orthopedic or dental implants has taken place for many years. In order to determine whether a newly developed implant material conforms to the requirements of biocompatibility, mechanical stability and safety, it must undergo rigorous testing both in vitro and in vivo. Results from in vitro studies can be difficult to extrapolate to the in vivo situation. For this reason the use of animal models is often an essential step in the testing of orthopedic and dental implants prior to clinical use in humans. This review discusses the reasons, the importance, and the research carried out in rabbits in our quest to develop a dental implant ideally suited for human bone.

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“…We then stopped the glucocorticoid treatment and assessed markers of growth plate senescence to determine whether senescence had, in fact, been delayed by the previous growth inhibition. (10) and undergo epiphyseal fusion by approximately 6 mo of age (11). Treatment was begun at 5 wk of age to allow sufficient time for induction of growth retardation and recovery before epiphyseal fusion occurs.…”

mentioning

confidence: 99%

Catch-Up Growth Is Associated with Delayed Senescence of the Growth Plate in Rabbits

et al. 2001

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In mammals, release from growth-inhibiting conditions results in catch-up growth. To explain this phenomenon, we proposed the following model: 1) The normal senescent decline in growth plate function depends not on age per se, but on the cumulative number of replications that growth plate chondrocytes have undergone. 2) Conditions that suppress growth plate chondrocyte proliferation therefore slow senescence. 3) After transient growth inhibition, growth plates are thus less senescent and hence show a greater growth rate than expected for age, resulting in catch-up growth. To test this model, we administered dexamethasone to growing rabbits to suppress linear growth.After stopping dexamethasone, catch-up growth occurred. In distal femoral growth plates of untreated controls, we observed a senescent decline in the growth rate and in the heights of the proliferative zone, hypertrophic zone, and total growth plate. During the period of catch-up growth, in the animals previously treated with dexamethasone, the senescent decline in all these variables was delayed. Prior treatment with dexamethasone also delayed epiphyseal fusion. These findings support our model that linear catch-up growth is caused, at least in part, by a delay in growth plate senescence. More than 35 y ago, Prader, Tanner, and von Harnack observed that children undergo supranormal linear growth after release from growth-inhibiting conditions (1). This phenomenon, termed catch-up growth, was attributed to a CNS mechanism that compares the individual's actual body size with an age-appropriate set-point and then adjusts the growth rate accordingly (2). However, this neuroendocrine hypothesis has not been subjected to a definitive experimental test.More recently, we demonstrated that transient growth inhibition within a single growth plate is followed by local catch-up growth (3). This local catch-up growth cannot be readily explained by a systemic mechanism, which would have affected all the growth plates equally. Instead, it suggests that catch-up growth is due, at least in part, to a mechanism intrinsic to the growth plate.To account for this finding, we speculated that catch-up growth might be caused by a delay in the process of growth plate senescence. The growth plate, a layer of cartilage located between the epiphysis and the metaphysis of mammalian long bones, is composed of three distinct zones: the resting zone, proliferative zone, and hypertrophic zone. With increasing age, the growth plate undergoes a program of structural and functional changes. These senescent changes include a progressive decline in the growth rate accompanied by a decrease in the heights of the proliferative zone (4), the hypertrophic zone (5), and the overall growth plate (6). In some mammals, including humans and rabbits, the senescent growth plates are eventually replaced by bone tissue, a process termed epiphyseal fusion.Specifically, to explain the mechanism underlying local catch-up growth, we hypothesized that growth plate senescence is not a function of age per s...

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Effect of sex steroids on peak bone density of growing rabbits

Cited by 105 publications

References 30 publications

Animal models of osteoporosis - necessity and limitations

Animal models of osteoporosis - necessity and limitations

Rabbits as Animal Models in Contemporary Implant Biomaterial Research

Catch-Up Growth Is Associated with Delayed Senescence of the Growth Plate in Rabbits

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