Low Bone Mineral Density in Rotating-Shift Workers

Quevedo, Iván; Zuniga, Ana M.

doi:10.1016/j.jocd.2010.07.004

Cited by 52 publications

(40 citation statements)

References 10 publications

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“…Using the Per1,2 −/− double knockout mouse model of circadian disruption, Fu et al demonstrated that the circadian clock is involved in leptin dependent regulation of osteoblast proliferation, and that the absence of the clock resulted in increased proliferation and bone formation (Fu et al, 2005). At the same time, it was reported that shift work (circadian disruption) results in lower bone mineral density and increases the risk of osteoporosis in humans (Freskanich et al, 2009; Quevedo & Zuniga, 2010). Therefore, these lines of evidence are seemingly at odds and suggest the connection between the circadian clock and bone homeostasis is more complicated than first thought arguing for the need of additional study.…”

Section: 0 Introductionmentioning

confidence: 99%

Deficiency of circadian clock protein BMAL1 in mice results in a low bone mass phenotype

Samsa

Vasanji

Midura

et al. 2016

Bone

100

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The circadian clock is an endogenous time keeping system that controls the physiology and behavior of many organisms. The transcription factor Brain and Muscle ARNT-like Protein 1 (BMAL1) is a component of the circadian clock and necessary for clock function. Bmal1−/− mice display accelerated aging and many accompanying age associated pathologies. Here, we report that mice deficient for BMAL1 have a low bone mass phenotype that is absent at birth and progressively worsens over their lifespan. Accelerated aging of these mice is associated with the formation of bony bridges occurring across the metaphysis to the epiphysis, resulting in shorter long bones. Using micro-computed tomography we show that Bmal1−/− mice have reductions in cortical and trabecular bone volume and other micro-structural parameters and a lower bone mineral density. Histology shows a deficiency of BMAL1 results in a reduced number of active osteoblasts and osteocytes in vivo. Isolation of bone marrow derived mesenchymal stem cells from Bmal1−/− mice demonstrate a reduced ability to differentiate into osteoblasts in vitro, which likely explains the observed reductions in osteoblasts and osteocytes, and may contribute to the observed osteopenia. Our data support the role of the circadian clock in the regulation of bone homeostasis and shows that BMAL1 deficiency results in a low bone mass phenotype.

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Section: 0 Introductionmentioning

confidence: 99%

Deficiency of circadian clock protein BMAL1 in mice results in a low bone mass phenotype

Samsa

Vasanji

Midura

et al. 2016

Bone

100

View full text Add to dashboard Cite

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“…These working schedules result in a misalignment between the sleep-wake cycle and the internal biological clock, which is under control of the suprachiasmatic nucleus (SCN) in the hypothalamus, also referred to as the central "master" clock. [6][7][8] In addition, shift work has been associated with a low bone mineral density and increased fracture risk, 9,10 which are both hallmarks of the bone disease osteoporosis. These tissue rhythms are driven by circadian clock genes, which promote rhythmic expression of many important tissue-specific genes and proteins.…”

Section: Introductionmentioning

confidence: 99%

Circadian disruption by shifting the light‐dark cycle negatively affects bone health in mice

et al. 2019

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The past decade, it has become evident that circadian rhythms within metabolically active tissues are very important for physical health. However, although shift work has also been associated with an increased risk of fractures, circadian rhythmicityhas not yet been extensively studied in bone. Here, we investigated which genes are rhythmically expressed in bone, and whether circadian disruption by shifts in lightdark cycle affects bone turnover and structure in mice. Our results demonstrate diurnal expression patterns of clock genes (Rev-erbα, Bmal1, Per1, Per2, Cry1, Clock), as well as genes involved in osteoclastogenesis, osteoclast proliferation and function (Rankl, Opg, Ctsk), and osteocyte function (c-Fos) in bone. Weekly alternating lightdark cycles disrupted rhythmic clock gene expression in bone and caused a reduction in plasma levels of procollagen type 1 amino-terminal propeptide (P1NP) and tartrate-resistant acidic phosphatase (TRAP), suggestive of a reduced bone turnover.These effects coincided with an altered trabecular bone structure and increased cortical mineralization after 15 weeks of light-dark cycles, which may negatively affect

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“…2 We categorized the study population (persons aged 50 years and above) into two groups based on their pattern of daily work schedule. All the daytime workers were classified as regular workers and others (night-shift, evening-shift, and rotating-shift) were classified as shiftworkers.…”

Section: Methodsmentioning

confidence: 99%

“…1 In another cross-sectional study involving 70 post-menopausal nurses, it was found that rotating-shift workers had a higher prevalence of osteopenia (T score ¼ À1.0 to À2.5) than the daytime workers (46.2% vs 35.5%, respectively) and lower BMD in trabecular and cortical bones. 2 The purpose of this short study was to investigate the effect of shiftwork on femoral neck bone mineral parameters from the National Health and Nutrition Examination Survey data from 2010 to 2011. 2 …”

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confidence: 99%