The ability of<scp>H</scp><sub>1</sub>or<scp>H</scp><sub>2</sub>receptor antagonists or their combination in counteracting the glucocorticoid‐induced alveolar bone loss in rats

Ezzat, Bassant A.; Abbass, Marwa M. S.

doi:10.1111/jop.12104

Cited by 11 publications

(21 citation statements)

References 47 publications

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“…However, GCs are strictly controlled for use due to its severe side effects, including metabolic disease, cardiovascular disease, avascular necrosis and osteoporosis [1, 2]. GCs can also cause a series of health problems in the periodontal apparatus.…”

Section: Introductionmentioning

confidence: 99%

“…Glucocorticoids (GCs) are widely used in the clinic for their potent anti-inflammatory and immunomodulatory activities to treat a variety of disorders including inflammatory, pulmonary, gastrointestinal and autoimmune diseases. However, GCs are strictly controlled for use due to its severe side effects, including metabolic disease, cardiovascular disease, avascular necrosis and osteoporosis [ 1 , 2 ]. GCs can also cause a series of health problems in the periodontal apparatus.…”

Section: Introductionmentioning

confidence: 99%

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Blockade of cyclophilin D rescues dexamethasone-induced oxidative stress in gingival tissue

Zhang

Zhu

et al. 2017

PLoS ONE

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Glucocorticoids (GCs) are frequently used for the suppression of inflammation in chronic inflammatory diseases. Excessive GCs usage is greatly associated with several side effects, including gingival ulceration, the downward migration of the epithelium, attachment loss and disruption of transeptal fibers. The mechanisms underlying GCs-induced impairments in gingival tissue remains poorly understood. Mitochondrial dysfunction is associated with various oral diseases, such as chronic periodontitis, age-related alveolar bone loss and hydrogen peroxide-induced cell injury in gingival. Here, we reported an unexplored role of cyclophilin D (CypD), the major component of mitochondrial permeability transition pore (mPTP), in dexamethasone (Dex)-induced oxidative stress accumulation and cell dysfunctions in gingival tissue. We demonstrated that the expression level of CypD significantly increased under Dex treatment. Blockade of CypD by pharmaceutical inhibitor cyclosporine A (CsA) significantly protected against Dex-induced oxidative stress accumulation in gingival tissue. And the protective effects of blocking CypD in Dex-induced gingival fibroblasts dysfunction were evidenced by rescued mitochondrial function and suppressed production of reactive oxygen species (ROS). In addition, blockade of CypD by pharmaceutical inhibitor CsA or gene knockdown also restored Dex-induced cell toxicity in HGF-1 cells, as shown by suppressed mitochondrial ROS production, increased CcO activity and decreased apoptosis. We also suggested a role of oxidative stress-mediated p38 signal transduction in this event, and antioxidant N-acety-l-cysteine (NAC) could obviously blunted Dex-induced oxidative stress. These findings provide new insights into the role of CypD-dependent mitochondrial pathway in the Dex-induced gingival injury, indicating that CypD may be potential therapeutic strategy for preventing Dex-induced oxidative stress and cell injury in gingival tissue.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Blockade of cyclophilin D rescues dexamethasone-induced oxidative stress in gingival tissue

Zhang

Zhu

et al. 2017

PLoS ONE

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“…LiCl has been used for decades for the treatment of bipolar disorder by increasing â-catenin signaling through the inhibition of GSK-3â. 49,50 The canonical Wnt/â-catenin pathway increases bone mass in several ways, including the renewal of stem cells, stimulation of preosteoblast replication, induction of osteogenesis and inhibition of osteoblast and osteocyte apoptosis. 51 Since orthodontic tooth movement involves the repeated process of alveolar bone remodeling, LiCl has the potential to affect tooth movement during orthodontic treatment by affecting the process of bone formation.…”

Section: F Lithiumchloridementioning

confidence: 99%

An Extensive Review of Literature: Considering Bone Reaction To Different Agents In Orthodontically Induced Root And Alveolar Resorption

2017

IJDA

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ABSTRACT:Orthodontically induced root resorption is a common problem in day to day practice. If such root resorption could be prevented, it would be an important contribution toward reducing risk factors in orthodontic treatment. The aim of the review is to focus on different agents which can be therapeutically useful in orthodontic tooth movement. The article reviews various agents inhibiting as well as promoting root and alveolar bone resorption to orthodontic tooth movement based on advanced PUBMED, Cochrane database, Wiley online search of the English language literature from the year 1951 to present in order to help us select the most suitable among them fulfilling the desired criteria of being safe, having less adverse effects, minimal contraindications, rare cross reactions, economically viable, having a scope to be used for successful prognosis and possibly not requiring any special considerations to interpret the results.Forty-nine articles were included in the review, but their interpretation was hindered by the variability in experimental design, magnitude of force applied during tooth movement, and medication regimens. Corticosteroid hormones, parathyroid hormone, and thyroxin have all been shown to increase tooth movement. Bisphosphonates had a strong inhibitory effect.By this review, we conclude that low laser therapy and RGD peptide emerges as the clear winner and can result in better prognosis in orthodontic treatment. These techniques are new and cannot replace the conventional agents as a whole.

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“…LiCl has been used for decades for the treatment of bipolar disorder by increasing β-catenin signaling through the inhibition of GSK-3β. (49,50) The canonical Wnt/βcatenin pathway increases bone mass in several ways, including the renewal of stem cells, stimulation of preosteoblast replication, induction of osteogenesis and inhibition of osteoblast and osteocyte apoptosis. (51) Since orthodontic tooth movement involves the repeated process of alveolar bone remodeling, (52,53) LiCl has the potential to affect tooth movement during orthodontic treatment by affecting the process of bone formation.…”

Section: Fig 2: Intraoral Application Of Llltmentioning

confidence: 99%

An extensive review of literature: considering bone reaction to different agents in orthodontically induced root and alveolar resorption

2017

IJODR

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Objective: Orthodontically induced root resorption is a common problem in day to day practice. If such root resorption could be prevented, it would be an important contribution toward reducing risk factors in orthodontic treatment. The aim of the review is to focus on different agents which can be therapeutically useful in orthodontic tooth movement. Methods and Materials: The article reviews various agents inhibiting as well as promoting root and alveolar bone resorption to orthodontic tooth movement based on advanced PubMed Central (PMC), Cochrane database, Wiley online search of the English language literature from the year 1951 to present in order to help us select the most suitable among them fulfilling the desired criteria of being safe, having less adverse effects, minimal contraindications, rare cross reactions, economically viable, having a scope to be used for successful prognosis and possibly not requiring any special considerations to interpret the results. Results: Forty-nine articles were included in the review, but their interpretation was hindered by the variability in experimental design, magnitude of force applied during tooth movement, and medication regimens. Corticosteroid hormones, parathyroid hormone, and thyroxin have all been shown to increase tooth movement. Bisphosphonates had a strong inhibitory effect. Conclusion: By this review, we conclude that low laser therapy and arginylglycylaspartic acid (RGD) peptide emerges as the clear winner and can result in better prognosis in orthodontic treatment. These techniques are new and cannot replace the conventional agents as a whole.

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The ability ofH₁orH₂receptor antagonists or their combination in counteracting the glucocorticoid‐induced alveolar bone loss in rats

Abstract: In a rat model, the administration of H1 or H2 receptor antagonists separately could minimize the alveolar bone loss caused by the administration of glucocorticoids while concomitant administration of both H1 and H2 receptor antagonists deteriorated the bone condition.

Cited by 11 publications

References 47 publications

Blockade of cyclophilin D rescues dexamethasone-induced oxidative stress in gingival tissue

Blockade of cyclophilin D rescues dexamethasone-induced oxidative stress in gingival tissue

An Extensive Review of Literature: Considering Bone Reaction To Different Agents In Orthodontically Induced Root And Alveolar Resorption

An extensive review of literature: considering bone reaction to different agents in orthodontically induced root and alveolar resorption

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The ability ofH1orH2receptor antagonists or their combination in counteracting the glucocorticoid‐induced alveolar bone loss in rats

Abstract: In a rat model, the administration of H1 or H2 receptor antagonists separately could minimize the alveolar bone loss caused by the administration of glucocorticoids while concomitant administration of both H1 and H2 receptor antagonists deteriorated the bone condition.

Cited by 11 publications

References 47 publications

Blockade of cyclophilin D rescues dexamethasone-induced oxidative stress in gingival tissue

Blockade of cyclophilin D rescues dexamethasone-induced oxidative stress in gingival tissue

An Extensive Review of Literature: Considering Bone Reaction To Different Agents In Orthodontically Induced Root And Alveolar Resorption

An extensive review of literature: considering bone reaction to different agents in orthodontically induced root and alveolar resorption

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The ability ofH₁orH₂receptor antagonists or their combination in counteracting the glucocorticoid‐induced alveolar bone loss in rats