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There is no pulp necrosis or calcific metamorphosis of pulp induced by orthodontic treatment: biological basis.

ABSTRACT: To biologically explain why the orthodontic treatment does not induce pulp necrosis and calcific metamorphosis of the pulp, this paper presents explanations based on pulp physiology, microscopy and pathology, and especially the cell and tissue phenomena that characterize the induced tooth movement. The final reflections are as follows: 1) the orthodontic movement does not induce pulp necrosis or calcific metamorphosis of the pulp; 2) there is no literature or experimental and clinical models to demonstrate or minimally evidence pulp alterations induced by orthodontic movement; 3) when pulp necrosis or calcific metamorphosis of the pulp is diagnosed during orthodontic treatment or soon after removal of orthodontic appliances, its etiology should be assigned to concussion dental trauma, rather than to orthodontic treatment; 4) the two pulp disorders that cause tooth discoloration in apparently healthy teeth are the aseptic pulp necrosis and calcific metamorphosis of the pulp, both only induced by dental trauma; 5) the concussion dental trauma still requires many clinical and laboratory studies with pertinent experimental models, to increasingly explain its effects on the periodontal and pulp tissues.

SUBMITTER: Consolaro A

PROVIDER: S-EPMC6150703 | biostudies-other | 2018 Aug

REPOSITORIES: biostudies-other

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There is no pulp necrosis or calcific metamorphosis of pulp induced by orthodontic treatment: biological basis.

Consolaro Alberto A Consolaro Renata Bianco RB

Dental press journal of orthodontics 20180801 4

To biologically explain why the orthodontic treatment does not induce pulp necrosis and calcific metamorphosis of the pulp, this paper presents explanations based on pulp physiology, microscopy and pathology, and especially the cell and tissue phenomena that characterize the induced tooth movement. The final reflections are as follows: 1) the orthodontic movement does not induce pulp necrosis or calcific metamorphosis of the pulp; 2) there is no literature or experimental and clinical models to ...[more]

PMID: 30304152

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Project description:IntroductionDuring normal pulp tissue healing, inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) or interleukins, act in the initial 48 hours (inflammatory phase) and play important roles not only as chemo-attractants of inflammatory cells and stem/progenitor cells but also in inducing a cascade of reactions toward tissue regeneration or reparative dentin formation or both. Previous reports have shown that inflammatory cytokines regulate the differentiation capacity of dental pulp stem/progenitor cells (DPCs), but none has interrogated the impact of these cytokines on the stem cell phenotype of stem/progenitor cells. This study investigated the effects of a short-term treatment with TNF-α on the stem cell phenotype and differentiation ability of human DPCs.MethodsAn in vivo mouse model of pulp exposure was performed for analysis of expression of the mesenchymal stem cell marker CD146 in DPCs during the initial stage of inflammatory response. For in vitro studies, human DPCs were isolated and incubated with TNF-α for 2 days and passaged to eliminate TNF-α completely. Analysis of stem cell phenotype was performed by quantification of cells positive for mesenchymal stem cell markers SSEA-4 (stage-specific embryonic antigen 4) and CD146 by flow cytometry as well as by quantitative analysis of telomerase activity and mRNA levels of OCT-4 and NANOG. Cell migration, colony-forming ability, and differentiation toward odontogenesis and adipogenesis were also investigated.ResultsThe pulp exposure model revealed a strong staining for CD146 during the initial inflammatory response, at 2 days after pulp exposure. In vitro experiments demonstrated that a short-term (2-day) treatment of TNF-α increased by twofold the percentage of SSEA-4+ cells. Accordingly, STRO-1, CD146, and SSEA-4 protein levels as well as OCT-4 and NANOG mRNA levels were also significantly upregulated upon TNF-α treatment. A short-term TNF-α treatment also enhanced DPC function, including the ability to form cell colonies, to migrate, and to differentiate into odontogenic and adipogenic lineages.ConclusionsA short-term treatment with TNF-α enhanced the stem cell phenotype, migration, and differentiation ability of DPCs.

Project description:BackgroundRadiation brain necrosis (RBN) is a serious complication in patients receiving radiotherapy for intracranial disease. Many studies have investigated the efficacy and safety of bevacizumab in patients with RBN. In the present study, we systematically reviewed the medical literature for studies reporting the efficacy and safety of bevacizumab, as well as for studies comparing bevacizumab with corticosteroids.Materials and methodsWe searched PubMed, Cochrane library, EMBASE, and ClinicalTrials.gov from their inception through 1 March, 2020 for studies that evaluated the efficacy and safety of bevacizumab in patients with RBN. Two investigators independently performed the study selection, data extraction, and data synthesis.ResultsOverall, the present systematic review included 12 studies (eight retrospective, two prospective, and two randomized control trials [RCTs]) involving 236 patients with RBN treated who were treated with bevacizumab. The two RCTs also had control arms comprising patients with RBN who were treated with corticosteroids/placebo (n=57). Radiographic responses were recorded in 84.7% (200/236) of patients, and radiographic progression was observed in 15.3% (36/236). Clinical improvement was observed in 91% (n=127) of responding patients among seven studies (n=113). All 12 studies reported volume reduction on T1 gadolinium enhancement MRI (median: 50%, range: 26%-80%) and/or T2 FLAIR MRI images (median: 59%, range: 48%-74%). In total, 46 responding patients (34%) had recurrence. The two RCTs revealed significantly improved radiographic response in patients treated with bevacizumab (Levin et al.: p = 0.0013; Xu et al.: p < 0.001). Both also showed clinical improvement (Levin et al.: NA; Xu et al.: p = 0.039) and significant reduction in edema volume on both T1 gadolinium enhancement MRI (Levin et al.: p=0.0058; Xu et al.: p=0.027) and T2 FLAIR MRI (Levin et al.: p=0.0149; Xu et al.: p < 0.001). Neurocognitive improvement was significantly better after 2 months of treatment in patients receiving bevacizumab than in those given corticosteroids, as assessed by the MoCA scale (p = 0.028). The recurrence rate and side effects of the treatments showed no significant differences.ConclusionsPatients with RBN respond to bevacizumab, which can improve clinical outcomes and cognitive function. Bevacizumab appears to be more efficacious than corticosteroid-based treatment. The safety profile was comparable to that of the corticosteroids.

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There is no pulp necrosis or calcific metamorphosis of pulp induced by orthodontic treatment: biological basis.

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There is no pulp necrosis or calcific metamorphosis of pulp induced by orthodontic treatment: biological basis.

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