Over-suppression of bone turnover: Does it exist?

Compston, Juliet

doi:10.1007/s11914-007-0014-0

Cited by 5 publications

(7 citation statements)

References 45 publications

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“…The outcome of such treatments would be an increase in the age of the bone matrix, eventually leading to accumulation of biochemical alterations in the collagen matrix as well as other aged-related factors [22,23,26,46]. Such effects have raised major concerns within the field of bone research, especially with respect to the massive suppression of bone remodeling, as seen with potent osteoporotic drugs [20,27,68]. Correlation of the change in overall bone turnover, assessed by the αα/ββ CTX ratio, shows that bisphosphonates, which markedly reduce bone resorption and bone turnover, induce a decrease in the αα/ββ CTX ratio, indicating an increase in bone tissue age (Fig.…”

Section: Effects Of Osteoporotic Treatments On Bone Matrix Qualitymentioning

confidence: 99%

Is bone quality associated with collagen age?

et al. 2009

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The World Health Organization defines osteoporosis as a systemic disease characterized by decreased bone tissue mass and microarchitectural deterioration, resulting in increased fracture risk. Since this statement, a significant amount of data has been generated showing that these two factors do not cover all risks for fracture. Other independent clinical factors, such as age, as well as aspects related to qualitative changes in bone tissue, are believed to play an important role. The term "bone quality" encompasses a variety of parameters, including the extent of mineralization, the number and distribution of microfractures, the extent of osteocyte apoptosis, and changes in collagen properties. The major mechanism controlling these qualitative factors is bone remodeling, which is tightly regulated by the osteoclast/osteoblast activity. We focus on the relationship between bone remodeling and changes in collagen properties, especially the extent of one posttranslational modification. In vivo, measurements of the ratio between native and isomerized C-telopeptides of type I collagen provides an index of bone matrix age. Current preclinical and clinical studies suggests that this urinary ratio provides information about bone strength and fracture risk independent of bone mineral density and that it responds differently according to the type of therapy regulating bone turnover.

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Section: Effects Of Osteoporotic Treatments On Bone Matrix Qualitymentioning

confidence: 99%

Is bone quality associated with collagen age?

et al. 2009

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“…There are few reports in the literature describing bone morphometry in patients with ABD. Patients with the adynamic bone type of renal osteodystrophy generally tended to have lower bone volume in their iliac crest biopsies compared to normal controls [25]; while treatment of postmenopausal women with bisphosphonates has been shown to preserve trabecular bone microarchitecture [26]. The deterioration in trabecular bone volume and micro-architecture in ROD-ABD may be a function of altered calciumphosphorous homeostasis in CKD patients.…”

Section: Discussionmentioning

confidence: 98%

“…In recent years, severe suppression of bone turnover has become a possible cause for concern in the treatment and management of * p<0.05 compared to DTK Control § p<0.01 compared to No Resorption osteoporosis [26,28,38,39]. There is a worry that long-term antiresorptive use can result in bones becoming brittle despite having an improved bone mineral density [35,40,41].We had expected the bones of our ABD mice to require less energy to fracture than the bones of our cnotrol animals.…”

Section: Discussionmentioning

confidence: 99%

“…In the adynamic bone condition secondary mineralization may proceed uninterrupted for long periods of time. Previous studies have found increased degree of mineralization in iliac crest biopsies of patients with ROD-ABD [23], as well as in the cortical and cancellous bone of postmenopausal women treated with bisphosphonates and other antiresorptive drugs [26,35,36]. We used qBEI to investigate the degree of mineralization in our mouse model of ABD.…”

Section: Discussionmentioning

confidence: 99%

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Development, validation and characterization of a novel mouse model of Adynamic Bone Disease (ABD)

Willett

Alman

et al. 2014

Bone

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“…(7,8) In the past decade, there have been increasing concerns regarding the effects of long-term bisphosphonate use on bone metabolism. (9,10) Long-term use of bisphosphonates may suppress bone turnover to the point where bone remodeling and repair becomes impaired. (6,11) Our laboratory previously established a novel mouse model of adynamic bone that directly targeted the actions of osteoblasts and osteoclasts.…”

Section: Introductionmentioning

confidence: 99%

Adynamic Bone Decreases Bone Toughness During Aging by Affecting Mineral and Matrix

Omelon

Variola

et al. 2015

Journal of Bone and Mineral Research

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Adynamic bone is the most frequent type of bone lesion in patients with chronic kidney disease; long-term use of antiresorptive therapy may also lead to the adynamic bone condition. The hallmark of adynamic bone is a loss of bone turnover, and a major clinical concern of adynamic bone is diminished bone quality and an increase in fracture risk. Our current study aims to investigate how bone quality changes with age in our previously established mouse model of adynamic bone. Young and old mice (4 months old and 16 months old, respectively) were used in this study. Col2.3Dtk (DTK) mice were treated with ganciclovir and pamidronate to create the adynamic bone condition. Bone quality was evaluated using established techniques including bone histomorphometry, microcomputed tomography, quantitative backscattered electron imaging, and biomechanical testing. Changes in mineral and matrix properties were examined by powder X-ray diffraction and Raman spectroscopy. Aging controls had a natural decline in bone formation and resorption with a corresponding deterioration in trabecular bone structure. Bone turnover was severely blunted at all ages in adynamic animals, which preserved trabecular bone loss normally associated with aging. However, the preservation of trabecular bone mass and structure in old adynamic mice did not rescue deterioration of bone mechanical properties. There was also a decrease in cortical bone toughness in old adynamic mice that was accompanied by a more mature collagen matrix and longer bone crystals. Little is known about the effects of metabolic bone disease on bone fracture resistance. We observed an age-related decrease in bone toughness that was worsened by the adynamic condition, and this decrease may be due to material level changes at the tissue level. Our mouse model may be useful in the investigation of the mechanisms involved in fractures occurring in elderly patients on antiresorptive therapy who have very low bone turnover.

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Over-suppression of bone turnover: Does it exist?

Cited by 5 publications

References 45 publications

Is bone quality associated with collagen age?

Is bone quality associated with collagen age?

Development, validation and characterization of a novel mouse model of Adynamic Bone Disease (ABD)

Adynamic Bone Decreases Bone Toughness During Aging by Affecting Mineral and Matrix

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