Bone three-dimensional microstructural features of the common osteoporotic fracture sites

Chen, Huayue; Kubo, Kin‐ya

doi:10.5312/wjo.v5.i4.486

Cited by 44 publications

(24 citation statements)

References 67 publications

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“…Since the earliest changes of bone loss occur in the radius, it may be a more sensitive indicator of risk for asymptomatic fractures . Also, the lower end of the radius is composed predominantly of cancellous bone, and hence may be reflective of similar changes in the cancellous bones of the vertebrae . Some studies in lupus have also shown poor correlation of BMD with fracture incidence.…”

Section: Discussionmentioning

confidence: 99%

Prevalence and predictors of asymptomatic vertebral fractures in inflammatory myositis

et al. 2018

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Section: Discussionmentioning

confidence: 99%

Prevalence and predictors of asymptomatic vertebral fractures in inflammatory myositis

et al. 2018

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“…Diminished OB activity associated with aging contributes to thinner and fewer trabeculae resulting in a loss of trabecular microarchitecture [42]. The consequent failure of the trabecular reinforcement of the inner cortical bone surface triggers cortical bone porosity, ultimately increasing the risk of fragility factures such as those involving the distal radius, distal tibia and proximal femur [42, 43]. Bone anabolic activity stimulated in older mice by the acute inhibition of CaMKK2 significantly improves trabecular microarchitecture while enhancing cortical bone geometry.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of CaMKK2 reverses age-associated decline in bone mass

Pritchard

Cary

Yang

et al. 2015

Bone

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Decline in bone formation is a major contributing factor to the loss of bone mass associated with aging. We previously showed that the genetic ablation of the tissue-restricted and multifunctional Ca2+/calmodulin (CaM)-dependent protein kinase kinase 2 (CaMKK2) stimulates trabecular bone mass accrual, mainly by promoting anabolic pathways and inhibiting catabolic pathways of bone remodeling. In this study, we investigated whether inhibition of this kinase using its selective cell-permeable inhibitor STO-609 will stimulate bone formation in 32 week old male WT mice and reverse age-associated of decline in bone volume and strength. Tri-weekly intraperitoneal injections of saline or STO-609 (10 μM) were performed for six weeks followed by metabolic labeling with calcein and alizarin red. New bone formation was assessed by dynamic histomorphometry whereas micro-computed tomography was employed to measure trabecular bone volume, microarchitecture and femoral mid-shaft geometry. Cortical and trabecular bone biomechanical properties were assessed using three-point bending and punch compression methods respectively. Our results reveal that as they progress from 12 to 32 weeks of age, WT mice sustain a significant decline in trabecular bone volume, microarchitecture and strength as well as cortical bone strength. However, treatment of the 32 week old WT mice with STO-609 stimulated apposition of new bone and completely reversed the age-associated decrease in bone volume, quality, as well as trabecular and cortical bone strength. We also observed that regardless of age, male Camkk2−/− mice possessed significantly elevated trabecular bone volume, microarchitecture and compressive strength as well as cortical bone strength compared to age-matched WT mice, implying that the chronic loss of this kinase attenuates age-associated decline in bone mass. Further, whereas STO-609 treatment and/or the absence of CaMKK2 significantly enhanced the femoral midshaft geometry, the midshaft cortical wall thickness and material bending stress remained similar among the cohorts, implying that regardless of treatment, the material properties of the bone remain similar. Thus, our cumulative results provide evidence for the pharmacological inhibition of CaMKK2 as a bone anabolic strategy in combating age-associated osteoporosis.

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“…GC was proved to inhibit osteoblastic function, causing bone loss [26]. Several lines of evidence indicate the sympathetic nervous system in central regulation of bone remodeling [17,18,43]. Chronic stress is associated with pronounced and an enduring central and peripheral hyper-noradrenergic state [44].…”

Section: Possible Mechanisms For Bone Fragility Induced By Chronic Psmentioning

confidence: 99%

“…As the proportion of elderly persons has increased substantially and will continue to do so, osteoporotic fracture is a serious global health problem. Osteoporotic fractures might affect body movement, inducing disability, limiting daily activities and affecting the quality of life [2,17].…”

Section: Bone Homeostasis Regulated By the Central Nervous Systemmentioning

confidence: 99%

Chronic Psychological Stress as a Risk Factor of Osteoporosis

Chen

Adachi

Hayashi

et al. 2015

J UOEH

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: Osteoporosis, the most common metabolic skeletal disease, is characterized by decreased bone mass and deteriorated bone quality, leading to increased fracture risk. With the aging of the population, osteoporotic fracture is an important public health issue. Organisms are constantly exposed to various stressful stimuli that affect physiological processes. Recent studies showed that chronic psychological stress is a risk factor for osteoporosis by various signaling pathways. The purpose of this article is to review the recent progress of the association between chronic psychological stress and osteoporosis. Increasing evidence confirms the physiological importance of the central nervous system, especially the hypothalamus, in the regulation of bone metabolism. Both animal and human studies indicate that chronic psychological stress induces a decrease of bone mass and deterioration of bone quality by influencing the hypothalamic-pituitary-adrenocortical (HPA) axis, sympathetic nervous system, and other endocrine, immune factors. Active mastication, proven to be an effective stress-coping behavior, can attenuate stress-induced neuroendocrine responses and ameliorate stress-induced bone loss. Therefore, active mastication may represent a useful approach in preventing and/or treating chronic stress-associated osteoporosis. We also discuss several potential mechanisms involved in the interaction between chronic stress, mastication and osteoporosis. Chronic stress activates the HPA axis and sympathetic nervous system, suppresses the secretion of gonadal hormone and growth hormone, and increases inflammatory cytokines, eventually leading to bone loss by inhibiting bone formation and stimulating bone resorption.

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Bone three-dimensional microstructural features of the common osteoporotic fracture sites

Cited by 44 publications

References 67 publications

Prevalence and predictors of asymptomatic vertebral fractures in inflammatory myositis

Prevalence and predictors of asymptomatic vertebral fractures in inflammatory myositis

Inhibition of CaMKK2 reverses age-associated decline in bone mass

Chronic Psychological Stress as a Risk Factor of Osteoporosis

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