Bone mineral density of the mandible in ovariectomized rats: analyses using dual energy X‐ray absorptiometry and peripheral quantitative computed tomography

Kuroda, Shinji; Mukohyama, Hitoshi; Kondo, Hiroyo; Aoki, Kazuhiro; Ohya, Keiichi; Ohyama, Takahiro; Kasugai, Shohei

doi:10.1034/j.1601-0825.2003.01810.x

Cited by 62 publications

(50 citation statements)

References 22 publications

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“…Clinical observations in postmenopausal women have confirmed an increased prevalence of periodontal disease with low estrogen levels, even when oral hygiene remains unchanged (Krall et al 1994;Reinhardt et al 1999). Animal experiments with ovariectomized (OVX) rats have also clarified that estrogen deficiency may result in low mineral density in the mandible (Kuroda et al 2003). However, the precise effects of estrogen depletion on periodontal tissues at the molecular level are unknown, so we would like to provide more valuable clues to discover the mechanism of the effects of estrogen deficiency on periodontal regeneration.…”

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confidence: 88%

Estrogen Deficiency Leads to Impaired Osteogenic Differentiation of Periodontal Ligament Stem Cells in Rats

Zhang

Liu

Zhou

et al. 2011

Tohoku J. Exp. Med.

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Estrogen deficiency in post-menopausal women is considered as one of the risk factors for periodontal diseases. The periodontal ligament is a connective tissue that connects cementum and alveolar bone to constrain teeth within the jaw. Periodontal ligament stem cells (PDLSCs) isolated from the periodontal ligament can differentiate into many types of specialized cells, including osteoblast-like cells that can be used to regenerate alveolar bone. However, little is known about the effect of estrogen-deficient microenvironment on the osteogenic differentiation of PDLSCs. The aim of this study was to explore the role of estrogen on the potential for osteogenic differentiation of PDLSCs using a rat model of osteoporosis. Three-month-old female Sprague-Dawley rats were divided into two groups (n = 6 for each): ovariectomized (OVX) and sham-operated rats (Sham). Then the characteristics of PDLSCs isolated from these rats were investigated. Real-time PCR analysis showed the lower expression levels of estrogen receptors (ERα and ERβ) mRNAs in PDLSCs of OVX animals compared to Sham control. Mineralization assay demonstrated fewer calcium deposits in PDLSCs from OVX group than those from Sham group. Treatment with 17β-estradiol (E2) significantly enhanced the osteogenic differentiation of PDLSCs from both groups in vitro. Furthermore, by means of lentivirus-mediated siRNA targeting ERα or ERβ, the expression of ERα or ERβ was down-regulated (> 50% reduction), which impaired the estrogen-induced osteogenic differentiation of PDLSCs from both groups (> 50% reduction). These results indicate that estrogen plays an important role in maintaining osteogenic differentiation of PDLSCs, which acts through both ERα and ERβ.

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confidence: 88%

Estrogen Deficiency Leads to Impaired Osteogenic Differentiation of Periodontal Ligament Stem Cells in Rats

Zhang

Liu

Zhou

et al. 2011

Tohoku J. Exp. Med.

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“…A lack of functional occlusion may induce active alveolar bone loss, including decreasing bone mass and volume (7,8). In addition, in certain pathological conditions, such as estrogen deficiency, functional occlusion has been revealed to slow down the rate of bone loss (9), whereas occlusal hypofunction was reported to accelerate bone loss (10,11). However, the cellular and molecular mechanisms underlying bone loss have yet to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Sclerostin is essential for alveolar bone loss in occlusal hypofunction

Wang

Sun

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Bone loss is caused by occlusal hypofunction and is a serious health concern. This is particularly true of tooth loss, which is common in the elderly. However, the cellular and molecular mechanisms underlying bone loss have yet to be fully elucidated. Sclerostin and Wnt/β-catenin signaling have previously been reported to serve important roles in regulating bone remodeling. Therefore, the present study aimed to investigate the involvement of sclerostin and Wnt/β-catenin signaling in occlusal hypofunction-induced alveolar bone remodeling. The unilateral maxillary molars of 14 male Sprague-Dawley rats were extracted in order to establish a model of occlusal hypofunction. For each rat, the non-extraction side was treated as the control group for comparisons with the extraction side. At 8 weeks after tooth extraction, the rats were sacrificed and alveolar bone specimens were harvested for X-ray radiography, micro-computed tomography (CT) and histological and immunohistochemical examinations. Bone loss and architecture deterioration were observed at the occlusal hypofunction side. The bone mineral density was markedly decreased and the ratio of bone volume to total volume was significantly decreased at the hypofunction side, as compared with the control side (P<0.001). In addition, the number of osteoclasts at the hypofunction side were significantly increased compared with that in the control side (P<0.001), as demonstrated using tartrate-resistant acid phosphatase staining. Furthermore, the protein expression levels of sclerostin and receptor activator of nuclear factor-κB ligand were increased, whereas those of β-catenin were decreased, at the hypofunction side when compared with the control side. In conclusion, the results of the present study suggested that occlusal hypofunction-induced bone loss may be associated with upregulated expression of sclerostin, which, in turn, may inhibit the activity of the Wnt/β-catenin signaling pathway. IntroductionTooth loss is a common and serious health concern, particularly in the elderly. Although the incidence of tooth loss has declined in industrialized countries, the goal established by the World Health Organization of retaining 20 teeth at the age of 80 years has not been widely achieved (1,2). Mechanical stress has a crucial role in bone remodeling (3,4) and bone loss may occur as a result of reduced mechanical force, which is defined as disuse osteoporosis (5). Occlusal hypofunction due to tooth loss has a negative impact on jaw bone homeostasis (6). Tooth loss may lead to a reduced bite force in the antagonistic tooth and underlying alveolar bone during chewing. A lack of functional occlusion may induce active alveolar bone loss, including decreasing bone mass and volume (7,8). In addition, in certain pathological conditions, such as estrogen deficiency, functional occlusion has been revealed to slow down the rate of bone loss (9), whereas occlusal hypofunction was reported to accelerate bone loss (10,11). However, the cellular and molecular mechanisms under...

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“…*p < 0.05 was regarded as statistically significant. (S. Kuroda et al, 2003) 2.2 Guided bone regeneration with a collagen membrane 2.2.1 Background Guided Bone Regeneration (GBR) technique is clinically used to acquire the sufficient bone volume, which has been developed by Nyman and Dahlin (C. Dahlin et al, 1988Dahlin et al, , 1989Dahlin et al, , 1990. The concept of this technique is that the application of a membrane creates a secluded space to facilitate proliferation of angiogenic and osteogenic cells from the basal bone into the defect without interference by fibroblasts.…”

Section: Resultsmentioning

confidence: 99%