Influence of prednisolone-induced osteoporosis on bone mass and bone quality of the mandible in rats

Kozai, Yusuke; Kawamata, Ryota; Sakurai, Takashi; Kanno, M; Kashima, Isamu

doi:10.1259/dmfr/28859075

Cited by 15 publications

(15 citation statements)

References 29 publications

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“…A total of 10 papers investigated the effect of mechanical loading, through diet texture modification and mastication [7], [11], [13], [19], [27], [29], [31], [36], [37], [38] on the bone micro-architecture, while 8 addressed the effect of drug intervention [3], [12], [32], [34], [39], [40], [41], [42]. One paper investigated the mandibular bone architecture in the ovariectomy-induced osteoporotic animal [43].…”

Section: Resultsmentioning

confidence: 99%

“…The literature search also identified 16 reports dealing with interventions which potentially impact the bone micro-architecture and the bone healing or regeneration, with 6 studies applying to the maxilla [3], [4], [8], [15], [16], [23], 6 to the mandible [3], [11], [32], [40], [41], [43] and 4 to the condyle region [10], [22], [28], [46]. It is evident that the control groups included in these studies offer the possibility to extract bone micro-architectural parameters that characterize the physiological bone micro-architectural state.…”

Section: Discussionmentioning

confidence: 99%

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Micro-CT analysis of the rodent jaw bone micro-architecture: A systematic review

et al. 2015

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IntroductionKnowledge about macro- and micro-structural characteristics may improve in vivo estimation of the quality and quantity of regenerated bone tissue. For this reason, micro-CT imaging has been applied to evaluate alveolar bone remodelling, alterations of periodontal ligament thickness and cortical and trabecular bone changes in rodent jaw bones. In this paper, we provide a systematic review on the available micro-CT literature on jaw bone micro-architecture.MethodologyA detailed search through the PubMed database was performed. Articles published up to December 2013 and related to maxilla, mandible and condyle with quantitatively analysed bone micro-architectural parameters were considered eligible for inclusion. Two reviewers assessed the search results according to inclusion criteria designed to identify animal studies quantifying the bone micro-architecture of the jaw rodent bones in physiological or drug-induced disease status, or in response to interventions such as mechanical loading, hormonal treatment and other metabolic alterations. Finally, the reporting quality of the included publications was evaluated using the tailored ARRIVE guidelines outlined by Vignoletti and Abrahamsson (2012).ResultsDatabase search, additional manual searching and assessment of the inclusion and exclusion criteria retrieved 127 potentially relevant articles. Eventually, 14 maxilla, 20 mandible and 12 condyle articles with focus on bone healing were retained, and were analysed together with 3 methodological papers. Each study was described systematically in terms of subject, experimental intervention, follow-up period, selected region of interest used in the micro-CT analysis, parameters quantified, micro-CT scanner device and software. The evidence level evaluated by the ARRIVE guidelines showed high mean scores (between 18 and 25; range: 0–25), indicating that most of the selected studies are well-reported. The major obstacles identified were related to sample size calculation, absence of adverse event descriptions, randomization or blinding procedures.ConclusionsThe evaluated studies are highly heterogeneous in terms of research topic and the different regions of interest. These results illustrate the need for a standardized methodology in micro-CT analysis. While the analysed studies do well according to the ARRIVE guidelines, the micro-CT procedure is often insufficiently described. Therefore we recommend to extend the ARRIVE guidelines for micro-CT studies.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Micro-CT analysis of the rodent jaw bone micro-architecture: A systematic review

et al. 2015

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“…Studies showed that long-term GCs administration induced alveolar bone loss in mice; diminished the cortical bone mineral substance, as well as bone area and strength of rats' mandibles (16,17). Likewise, GIOP can potentiate the destructive impacts of experimental periodontitis on the alveolar bone of rats (18).…”

Section: Introductionmentioning

confidence: 99%

Effect of Bisphosphonates on the Alveolar Bone of Rats With Glucocorticoids Induced Osteoporosis

Sherif

Masry

Kawana

et al. 2019

Alexandria Dental Journal

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INTRODUCTION: Bone is a unique tissue that undergoes frequent remodeling. An imbalance between bone formation and resorption results in osteoporosis. Glucocorticoids (GCs) are widely used clinically as anti-inflammatory and immunomodulatory. However, their prolonged use may induce osteoporosis. Currently, evidences revealed that also the alveolar processes are subject to osteoporosis. Bisphosphonates, such as Alendronate, Risedronate and Zoledronate, are recommended by several international guidelines as the first-line therapy for the prevention and treatment of generalized glucocorticoids induced osteoporosis (GIOP). OBJECTIVES: To evaluate the effect of bisphosphonates (Risedronate) on the alveolar bone of rats with glucocorticoids induced osteoporosis. MATERIALS AND METHODS: Thirty female albino rats were divided into 3 equal groups (10 rats each) as follows: Group I: control group. Group II: glucocorticoids group (Dexamethasone 0.6mg/kg twice/week subcutaneously). Group III: Risedronate treated group; rats were given Dexamethasone (0.6mg/kg twice/week subcutaneously) and Risedronate (1mg/kg/day orally). After 12 weeks, rats were euthanized, and the mandibular alveolar bone was evaluated histologically by light microscope and ultra-structurally by scanning electron microscopy and energy dispersive X-ray (EDX) microanalysis. RESULTS: Group II showed deterioration of the alveolar bone in comparison to the control group I. The alveolar bone structure in Group III rats, treated by bisphosphonates (Risedronate), showed remarkable improvement both histologically and ultrastructurally in comparison to group II. Moreover, EDX analysis revealed a significant decrease of calcium levels in group II in comparison to group I. However, in group III calcium levels were restored to normal levels comparable to the control group I. CONCLUSIONS: Glucocorticoids intake induces loss of the alveolar bone; which, could be counterbalanced by bisphosphonates.

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“…Among the many effects of glucocorticoids on bone, they are known to suppress PLR in trabecular and cortical bone of the femur, which likely plays a causal role in glucocorticoid-induced osteonecrosis of the femoral head ( Fowler et al, 2017 ). In the mandible, glucocorticoids alter the biomechanical behavior of the bone as well as decrease overall cortical bone mass and strength ( Bozzini et al, 2015 ; Kozai et al, 2009 ). However, the extent to which PLR in the mandible is sensitive to glucocorticoids has yet to be studied.…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids cause mandibular bone fragility and suppress osteocyte perilacunar-canalicular remodeling

et al. 2018

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Osteocytes support dynamic, cell-intrinsic resorption and deposition of bone matrix through a process called perilacunar/canalicular remodeling (PLR). In long bones, PLR depends on MMP13 and is tightly regulated by PTH, sclerostin, TGFβ, and glucocorticoids. However, PLR is regulated differently in the cochlea, suggesting a mechanism that is anatomically distinct. Unlike long bones, the mandible derives from neural crest and exhibits unique susceptibility to medication and radiation induced osteonecrosis. Therefore, we sought to determine if PLR in the mandible is suppressed by glucocorticoids, as it is in long bone. Hemimandibles were collected from mice subcutaneously implanted with prednisolone or vehicle containing pellets for 7, 21, or 55 days (n = 8/group) for radiographic and histological analyses. Within 21 days, micro-computed tomography revealed a glucocorticoid-dependent reduction in bone volume/total volume and trabecular thickness and a significant decrease in bone mineral density after 55 days. Within 7 days, glucocorticoids strongly and persistently repressed osteocytic expression of the key PLR enzyme MMP13 in both trabecular and cortical bone of the mandible. Cathepsin K expression was significantly reduced only after 55 days of glucocorticoid treatment, at which point histological analysis revealed a glucocorticoid-dependent reduction in the lacunocanalicular surface area. In addition to reducing bone mass and suppressing PLR, glucocorticoids also reduced the stiffness of mandibular bone in flexural tests. Thus, osteocyte PLR in the neural crest-derived mandible is susceptible to glucocorticoids, just as it is in the mesodermally-derived femur, highlighting the need to further study PLR as a target of drugs, and radiation in mandibular osteonecrosis.

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Influence of prednisolone-induced osteoporosis on bone mass and bone quality of the mandible in rats

Abstract: These findings suggest that steroid treatment decreases the cortical BMC, bone area and bone strength of the mandible.

Cited by 15 publications

References 29 publications

Micro-CT analysis of the rodent jaw bone micro-architecture: A systematic review

Micro-CT analysis of the rodent jaw bone micro-architecture: A systematic review

Effect of Bisphosphonates on the Alveolar Bone of Rats With Glucocorticoids Induced Osteoporosis

Glucocorticoids cause mandibular bone fragility and suppress osteocyte perilacunar-canalicular remodeling

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