Effects of Active Mastication on Chronic Stress-Induced Bone Loss in Mice

Chen, Huayue; Furuzawa, Manabu; Fujiwara, Shu; Yamada, Kumiko; Kubo, Kin‐ya

doi:10.7150/ijms.13298

Cited by 13 publications

(14 citation statements)

References 34 publications

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“…In contrast to our study, decreased bone mass was reported in mice following exposure to chronic mild stress ( Yirmiya et al, 2006 ; Furuzawa et al, 2014 ; Azuma et al, 2015 ; Lertsinthai et al, 2015 ), an accepted stress model for inducing a depressive-like phenotype and increased plasma GC and NE concentrations. Because GCs are established inhibitors of bone formation by increasing osteoblast and decreasing osteoclast apoptosis ( Weinstein et al, 2004 , 1998 ; O'Brien et al, 2004 ), the difference in the HPA axis activity might contribute to the different effects of CSC and chronic mild stress on bone metabolism and formation.…”

Section: Discussioncontrasting

confidence: 99%

“…Preclinical studies revealed reduced bone mass in murine models of chronic mild stress, in which mice were subjected to a series of mild and unpredictable physical and/or psychological stressors, resulting in a depressive-like phenotype ( Liu and Liu, 2017 ), basal hypercorticism and sympathetic nervous system (SNS) activation ( Azuma et al, 2015 ; Furuzawa et al, 2014 ; Yirmiya et al, 2006 ; Baldock et al, 2014 ). However, these models might have limitations in trying to reflect the situation in PTSD patients, who suffer from hypo- rather than hypercorticism ( Yehuda and Seckl, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

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Chronic psychosocial stress disturbs long-bone growth in adolescent mice

Foertsch¹,

Haffner‐Luntzer²,

Kroner³

et al. 2017

Disease Models &Amp; Mechanisms

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Although a strong association between psychiatric and somatic disorders is generally accepted, little is known regarding the interrelationship between mental and skeletal health. Although depressive disorders have been shown to be strongly associated with osteoporosis and increased fracture risk, evidence from post-traumatic stress disorder (PTSD) patients is less consistent. Therefore, the present study investigated the influence of chronic psychosocial stress on bone using a well-established murine model for PTSD. C57BL/6N mice (7 weeks old) were subjected to chronic subordinate colony housing (CSC) for 19 days, whereas control mice were singly housed. Anxiety-related behavior was assessed in the open-field/novel-object test, after which the mice were euthanized to assess endocrine and bone parameters. CSC mice exhibited increased anxiety-related behavior in the open-field/novel-object test, increased adrenal and decreased thymus weights, and unaffected plasma morning corticosterone. Microcomputed tomography and histomorphometrical analyses revealed significantly reduced tibia and femur lengths, increased growth-plate thickness and reduced mineral deposition at the growth plate, suggesting disturbed endochondral ossification during long-bone growth. This was associated with reduced Runx2 expression in hypertrophic chondrocytes in the growth plate. Trabecular thicknesses and bone mineral density were significantly increased in CSC compared to singly housed mice. Tyrosine hydroxylase expression was increased in bone marrow cells located at the growth plates of CSC mice, implying that local adrenergic signaling might be involved in the effects of CSC on the skeletal phenotype. In conclusion, chronic psychosocial stress negatively impacts endochondral ossification in the growth plate, affecting both longitudinal and appositional bone growth in adolescent mice.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chronic psychosocial stress disturbs long-bone growth in adolescent mice

Foertsch¹,

Haffner‐Luntzer²,

Kroner³

et al. 2017

Disease Models &Amp; Mechanisms

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“…Chronic physical and psychological stress has become a major health issue across the world. Both clinical and animal studies have confirmed that stress is an important risk or aggravating factor for several diseases, including hypertension, cardiovascular disease, bone loss, neurodegenerative diseases, and cancer [ 1 – 5 ]. In fact, females are easier targets of stress compared with males [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Chronic restraint stress induces excessive activation of primordial follicles in mice ovaries

Xu¹,

Sun²,

Wang³

et al. 2018

PLoS ONE

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Chronic stress is an important factor influencing people’s health. It usually causes endocrinal disorders and a decline in reproduction in females. Although studies of both human and animals suggest a detrimental effect of stress on reproduction, the influence of chronic stress on the ovarian reservation and follicular development is still not clear. In this study, a chronic restraint stress (CRS) mouse model was used to investigate the effect of stress on ovarian reservation and follicular development and explore the underlying mechanism. In this study, after 8 weeks of CRS, primordial follicles were excessively activated in the ovaries of the CRS group compared with the control group. Further results showed that the activation of primordial follicles induced by CRS was involved in the increasing expression level of Kit ligand and its receptor Kit and the activation of phosphatidylinositol 3-kinase (PI3K)/phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/protein kinase B (Akt) pathway. The corticotropin-releasing hormone (CRH) is a neuropeptide released due to stress, which plays an important role in regulating follicle development. A high level of serum CRH was detected in the CRS mouse model, and the real-time polymerase chain reaction assay showed that the mRNA level of its main receptor CRHR1increased in the ovaries of the CRS mouse group. Moreover, 100nM CRH significantly improved the activation of primordial follicles in newborn mouse ovaries in vitro. These results demonstrated that CRS could induce immoderate activation of primordial follicles accompanied by the activation of Kit-PI3K signaling, in which CRH might be an important endocrine factor.

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“…Chewing is an effective stress-coping behavior 30 - 32 . In humans, gum chewing relieves stress and improves task performance, and in rodents chewing or biting under restraint or immobilization stress ameliorates stress-induced diseases such as gastric ulcer, and osteoporosis, and attenuates stress-induced cognitive and emotional impairment 30 , 33 - 35 . Chewing under restraint stress rescues the increase in plasma corticosterone levels, deficits in spatial learning ability 36 , and suppression of cell proliferation in the hippocampal DG 37 .…”

Section: Introductionmentioning

confidence: 99%

Chewing during prenatal stress prevents prenatal stress-induced suppression of neurogenesis, anxiety-like behavior and learning deficits in mouse offspring

Kubo¹,

Kotachi²,

Suzuki³

et al. 2018

Int. J. Med. Sci.

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Prenatal stress (PS) induces learning deficits and anxiety-like behavior in mouse pups by increasing corticosterone levels in the dam. We examined the effects of maternal chewing during PS on arginine vasopressin (AVP) mRNA expression in the dams and on neurogenesis, brain-derived neurotrophic factor (BDNF) mRNA expression, learning deficits and anxiety-like behavior in the offspring. Mice were divided into control, stress and stress/chewing groups. Pregnant mice were exposed to restraint stress beginning on day 12 of pregnancy and continuing until delivery. Mice in the stress/chewing group were given a wooden stick to chew during restraint stress. PS significantly increased AVP mRNA expression in the paraventricular nucleus (PVN) of the hypothalamus in the dams. PS also impaired learning ability, suppressed neurogenesis and BDNF mRNA expression in the hippocampus, and induced anxiety-like behavior in the offspring. Chewing during PS prevented the PS-induced increase in AVP mRNA expression of the PVN in the dams. Chewing during PS significantly attenuated the PS-induced learning deficits, anxiety-like behavior, and suppression of neurogenesis and BDNF mRNA expression in the hippocampus of the offspring. Chewing during PS prevented the increase in plasma corticosterone in the dam by inhibiting the hypothalamic-pituitary-adrenal axis activity, and attenuated the attenuated the PS-induced suppression of neurogenesis and BDNF expression in the hippocampus of the pups, thereby ameliorating the PS-induced learning deficits and anxiety-like behavior. Chewing during PS is an effective stress-coping method for the dam to prevent PS-induced deficits in learning ability and anxiety-like behavior in the offspring.

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Effects of Active Mastication on Chronic Stress-Induced Bone Loss in Mice

Cited by 13 publications

References 34 publications

Chronic psychosocial stress disturbs long-bone growth in adolescent mice

Chronic psychosocial stress disturbs long-bone growth in adolescent mice

Chronic restraint stress induces excessive activation of primordial follicles in mice ovaries

Chewing during prenatal stress prevents prenatal stress-induced suppression of neurogenesis, anxiety-like behavior and learning deficits in mouse offspring

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