The changes in quality of mandibular bone mineral in otherwise totally immobilized Rhesus monkeys

Grynpas, Marc D.; Patterson-Allen, Patricia; Simmons, David J.

doi:10.1007/bf02553291

Cited by 35 publications

(7 citation statements)

References 14 publications

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“…X-ray diffraction has produced results for crystal length from 1 Dnm to 36nm (Myers and Engstrb'm, 1 965;Jackson et al, 1978;Engstrbm, 1972;Bonar et al, 1983;Boskey et al, 1985;Grynpas et al, 1986;Arsenault and Grynpas, 1988).…”

Section: Biological Apatitementioning

confidence: 99%

A correlation between the distribution of biological apatite and amino acid sequence of type I collagen

Maitland

Arsenault

1991

Calcif Tissue Int

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We have determined the localization of apatite within type I collagen fibrils of calcifying turkey leg tendons by both bright field and selected-area dark field (SADF) electron microscopy and have compared this to computer-modeled, chick type I collagen amino acid sequence data. Apatite crystals occur in both the gap and overlap zones at early stages of mineralization in an asymmetric pattern that corresponds to the polarity, N- to C- orientation, of the collagen molecule. Based on comparisons with computer-generated models of known amino acid sequence of collagen, it was determined for early stages of mineral deposition that apatite is restricted by areas of high hydrophobicity. The gap zone is less hydrophobic than the overlap zone on average but each of these zones had areas of high hydrophobicity that correlated with sites of low localization of mineral. Possible interactions between hydrophobic regions and the process of mineral deposition are discussed.

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Section: Biological Apatitementioning

confidence: 99%

A correlation between the distribution of biological apatite and amino acid sequence of type I collagen

Maitland

Arsenault

1991

Calcif Tissue Int

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“…However, several studies have suggested that a large component of the bone loss associated with disuse induced by HS is related to decreased bone formation, inhibition of mineralization, and delay in bone maturation (5,13,25,39,43,64,67). These changes in bone formation and maturation appear to be due, in part, to decreased proliferation and differentiation of osteoblast progenitors (26,33,56,57,71).…”

mentioning

confidence: 99%

Aging alters the skeletal response to disuse in the rat

Perrien¹,

Akel²,

Dupont‐Versteegden³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Perrien DS, Akel NS, Dupont-Versteegden EE, Skinner RA, Siegel ER, Suva LJ, Gaddy D. Aging alters the skeletal response to disuse in the rat. Am J Physiol Regul Integr Comp Physiol 292: R988 -R996, 2007. First published October 26, 2006; doi:10.1152/ajpregu.00302.2006.-Disuse has been shown to cause a rapid and dramatic loss of skeletal mass and strength in the loadbearing bones of young and mature animals and humans. However, little is known about the skeletal effects of disuse in aged mammals. The present study was designed to determine whether the skeletal effects of disuse are maintained with extreme age. Fischer 344/Brown Norway male rats (6 and 32 mo old) were hindlimb suspended (HS) or housed individually for 2 wk. Trabecular volume and microarchitecture in the proximal tibia were significantly decreased by HS only in young rats. HS significantly reduced cortical bone mineral density and increased cortical porosity only in old rats by inducing new pore formation. Cortical pore diameter was also increased in old rats, regardless of loading condition. Ex vivo osteogenic and adipogenic cultures established from each group demonstrated that age and HS decreased osteoblastogenesis. Age, but not HS, decreased sensitivity to endogenous bone morphogenetic protein stimulation, as measured by treatment with exogenous Noggin. Adipocyte development increased with age, whereas HS suppressed sensitivity to peroxisome proliferator-activated receptor-␥-induced differentiation. Serum insulin-like growth factor I levels were reduced with HS in young rats and with age in control and HS rats. These results suggest that the site of bone loss due to disuse is altered with age and that the loss of osteogenic potential with disuse in the old rats may be due to the combined effects of decreased insulin-like growth factor I levels and sensitivity, as well as diminished bone morphogenetic protein production. hindlimb suspension; osteopenia; osteoblast; bone morphogenetic protein; insulin-like growth factor I AGING IS ASSOCIATED WITH FUNCTIONAL changes in many tissues, such as a decline in muscle mass and strength and reduced bone density (8,16,30,38,42,59). With aging, bone and muscle mass regress in a parallel fashion (51). The osteopenia has far-reaching consequences on the ability of the elderly to perform tasks of daily living and to be functionally independent. Indeed, one of the major concerns of aging is the loss of bone mass and strength, which is associated with an increased risk of fractures (1,9,18,51). Moreover, the elderly are often subjected to periods of inactivity, such as bed rest, due to diseases or surgeries. The association of inactivity with decreases in muscle mass and bone density in young people and animals is well documented, and the mechanisms responsible for these losses have been the subject of intense investigation (2,20,23,39,40,49,51).Recent evidence suggests that the increased bone fragility that occurs with aging is multifactorial: decreased bone mineral density (BMD), as well as changes in bone m...

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“…By x-ray diffraction, crystal size has been found to range in its long dimension (c-axis) from 10-25 nm (Boskey et al, 1985;Grynpas et al, 1986). By electron microscopy, bone crystal length has been found to vary from 30-70 nm (Landis et al, 1978).…”

Section: Bone Mineralsmentioning

confidence: 98%