scholarly journals Immunological and physiological responses related to orthodontic treatment

2021 ◽  
Author(s):  
Rehab Fuad Bawyan ◽  
Ahmed Jamil Baajajah ◽  
Haitham Abdullah Alzahrani ◽  
Mohammed Abdulkader Murad ◽  
Hattan Mohammed Hisham Jamalellail ◽  
...  
Keyword(s):  
Immune Cells ◽  
Orthodontic Treatment ◽  
Inflammatory Process ◽  
Tooth Movement ◽  
Physiological Responses ◽  
Mechanical Forces ◽  
Cytokines And Chemokines ◽  
Tnf Α ◽  
Ifn Γ ◽  
Orthodontic Forces

Orthodontic treatment is usually approached to achieve better aesthetics by influencing tooth movement in different positions within the jaw. The application of mechanical forces during the process of treatment is the main responsible for these events. Remarkable changes in the vascularity of the underlying tissues were also reported to occur secondary to applying orthodontic forces. This significantly leads to the synthesis and release of many metabolites and signaling molecules. Furthermore, it might be associated with various immunological and physiological responses that enhance or deteriorate the prognosis. Therefore, the present study reviewed the literature to identify the different immunological and physiological responses secondary to orthodontic treatment. Our findings indicate that different immune cells and immunoglobulins are usually involved in orthodontic treatment-related events. Moreover, we found that cytokines and chemokines have an important role in the post-treatment inflammatory process, leading to bone resorption or bone formation. Various cytokines were reported in this context, including TNF-α, IFN-γ, IL-13, IL-12, IL-8, IL-6, and IL-1β. The roles of these modalities have been discussed based on their effects on bone remodeling following orthodontic treatment.

scholarly journals Is Inflammation a Friend or Foe for Orthodontic Treatment?: Inflammation in Orthodontically Induced Inflammatory Root Resorption and Accelerating Tooth Movement

2021 ◽  
Vol 22 (5) ◽  
pp. 2388
Author(s):  
Masaru Yamaguchi ◽  
Shinichi Fukasawa
Keyword(s):  
Inflammatory Mediators ◽  
Orthodontic Treatment ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Root Resorption ◽  
Orthodontic Tooth Movement ◽  
Tnf Α ◽  
Orthodontic Forces ◽  
Necrosis Factor

The aim of this paper is to provide a review on the role of inflammation in orthodontically induced inflammatory root resorption (OIIRR) and accelerating orthodontic tooth movement (AOTM) in orthodontic treatment. Orthodontic tooth movement (OTM) is stimulated by remodeling of the periodontal ligament (PDL) and alveolar bone. These remodeling activities and tooth displacement are involved in the occurrence of an inflammatory process in the periodontium, in response to orthodontic forces. Inflammatory mediators such as prostaglandins (PGs), interleukins (Ils; IL-1, -6, -17), the tumor necrosis factor (TNF)-α superfamily, and receptor activator of nuclear factor (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) are increased in the PDL during OTM. OIIRR is one of the accidental symptoms, and inflammatory mediators have been detected in resorbed roots, PDL, and alveolar bone exposed to heavy orthodontic force. Therefore, these inflammatory mediators are involved with the occurrence of OIIRR during orthodontic tooth movement. On the contrary, regional accelerating phenomenon (RAP) occurs after fractures and surgery such as osteotomies or bone grafting, and bone healing is accelerated by increasing osteoclasts and osteoblasts. Recently, tooth movement after surgical procedures such as corticotomy, corticision, piezocision, and micro-osteoperforation might be accelerated by RAP, which increases the bone metabolism. Therefore, inflammation may be involved in accelerated OTM (AOTM). The knowledge of inflammation during orthodontic treatment could be used in preventing OIIRR and AOTM.

scholarly journals The Effects of Oral Liposomal Glutathione and In Vitro Everolimus in Altering the Immune Responses against Mycobacterium bovis BCG Strain in Individuals with Type 2 Diabetes

2021 ◽  
Vol 12 (1) ◽  
pp. 16-26
Author(s):  
Kimberly To ◽  
Ruoqiong Cao ◽  
Aram Yegiazaryan ◽  
James Owens ◽  
Kayvan Sasaninia ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Immune Cells ◽  
Mycobacterial Infection ◽  
Drug Resistant ◽  
Tnf Α ◽  
Resistant Strains ◽  
Ifn Γ ◽  
Drug Resistant Strains

Abstract Tuberculosis (TB) caused by Mycobacterium tuberculosis (M. tb) still remains a devastating infectious disease in the world. There has been a daunting increase in the incidence of Type 2 Diabetes Mellitus (T2DM) worldwide. T2DM patients are three times more vulnerable to M. tb infection compared to healthy individuals. TB-T2DM coincidence is a challenge for global health control. Despite some progress in the research, M. tb still has unexplored characteristics in successfully evading host defenses. The lengthy duration of treatment, the emergence of multi-drug-resistant strains and extensive-drug-resistant strains of M. tb have made TB treatment very challenging. Previously, we have tested the antimycobacterial effects of everolimus within in vitro granulomas generated from immune cells derived from peripheral blood of healthy subjects. However, the effectiveness of everolimus treatment against mycobacterial infection in individuals with T2DM is unknown. Furthermore, the effectiveness of the combination of in vivo glutathione (GSH) supplementation in individuals with T2DM along with in vitro treatment of isolated immune cells with everolimus against mycobacterial infection has never been tested. Therefore, we postulated that liposomal glutathione (L-GSH) and everolimus would offer great hope for developing adjunctive therapy for mycobacterial infection. L-GSH or placebo was administered to T2DM individuals orally for three months. Study subjects’ blood was drawn pre- and post-L-GSH/or placebo supplementation, where Peripheral Blood Mononuclear Cells (PBMCs) were isolated from whole blood to conduct in vitro studies with everolimus. We found that in vitro treatment with everolimus, an mTOR (membrane target of rapamycin) inhibitor, significantly reduced intracellular M. bovis BCG infection alone and in conjunction with L-GSH supplementation. Furthermore, we found L-GSH supplementation coupled with in vitro everolimus treatment produced a greater effect in inhibiting the growth of intracellular Mycobacterium bovis BCG, than with the everolimus treatment alone. We also demonstrated the functions of L-GSH along with in vitro everolimus treatment in modulating the levels of cytokines such as IFN-γ, TNF-α, and IL-2 and IL-6, in favor of improving control of the mycobacterial infection. In summary, in vitro everolimus-treatment alone and in combination with oral L-GSH supplementation for three months in individuals with T2DM, was able to increase the levels of T-helper type 1 (Th1) cytokines IFN-γ, TNF-α, and IL-2 as well as enhance the abilities of granulomas from individuals with T2DM to improve control of a mycobacterial infection.

Exploration of beneficial and deleterious effects of inflammation in stroke: dynamics of inflammation cells

2009 ◽  
Vol 367 (1908) ◽  
pp. 4699-4716 ◽  
Author(s):  
Taïssia Lelekov-Boissard ◽  
Guillemette Chapuisat ◽  
Jean-Pierre Boissel ◽  
Emmanuel Grenier ◽  
Marie-Aimée Dronne
Keyword(s):  
Immune Cells ◽  
Blood Cells ◽  
Inflammatory Process ◽  
Living Cells ◽  
Therapeutic Strategies ◽  
Brain Parenchyma ◽  
Brain Cell ◽  
Cytokines And Chemokines ◽  
The Brain

The inflammatory process during stroke consists of activation of resident brain microglia and recruitment of leucocytes, namely neutrophils and monocytes/macrophages. During inflammation, microglial cells, neutrophils and macrophages secrete inflammatory cytokines and chemokines, and phagocytize dead cells. The recruitment of blood cells (neutrophils and macrophages) is mediated by the leucocyte–endothelium interactions and more specifically by cell adhesion molecules. A mathematical model is proposed to represent the dynamics of various brain cells and of immune cells (neutrophils and macrophages). This model is based on a set of six ordinary differential equations and explores the beneficial and deleterious effects of inflammation, respectively phagocytosis by immune cells and the release of pro-inflammatory mediators and nitric oxide (NO). The results of our simulations are qualitatively consistent with those observed in experiments in vivo and would suggest that the increase of phagocytosis could contribute to the increase of the percentage of living cells. The inhibition of the production of cytokines and NO and the blocking of neutrophil and macrophage infiltration into the brain parenchyma led also to the improvement of brain cell survival. This approach may help to explore the respective contributions of the beneficial and deleterious roles of the inflammatory process in stroke, and to study various therapeutic strategies in order to reduce stroke damage.

Aspirin Blocks Orthodontic Relapse via Inhibition of CD4+ T Lymphocytes

2017 ◽  
Vol 96 (5) ◽  
pp. 586-594 ◽  
Author(s):  
Y. Liu ◽  
T. Zhang ◽  
C. Zhang ◽  
S.S. Jin ◽  
R.L. Yang ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Relapse Rate ◽  
Immune Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Th1 Cells ◽  
Tnf Α ◽  
Inflammatory Drugs ◽  
Ifn Γ ◽  
Anti Inflammatory

Immunologic response plays an important role in orthodontic tooth movement (OTM) and relapse. Nonsteroidal anti-inflammatory drugs, such as aspirin, affect immune cells and clinical orthodontic treatment. However, the mechanisms by which nonsteroidal anti-inflammatory drugs regulate immune cells to affect orthodontic relapse are unclear. In this study, male Sprague-Dawley rats were grouped as relapse and relapse + aspirin for 10 d after 14 d of OTM. Silicone impressions of the rats’ maxillary dentitions were obtained to record the distance of OTM at the indicated time point. CD4+ T lymphocytes in spleen were examined by flow cytometry. Serum levels of type 1 T-helper (Th1) cell–associated cytokines tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ) were determined through enzyme-linked immunosorbent assay. The effects of aspirin on CD4+ T and Th1 cells were also analyzed in vitro. Aspirin treatment significantly reduced the relapse rate. More interestingly, injection of CD25 neutralizing antibody basiliximab or TNF-α inhibitor etanercept can significantly reduce the relapse rate as well. Correspondingly, aspirin treatment significantly accelerated the decrease of orthodontic force–induced secretion of TNF-α and IFN-γ in serum and the expression of TNF-α and IFN-γ in periodontal ligament during relapse. Furthermore, aspirin treatment in vitro significantly repressed the differentiation of CD4+ T and Th1 cells. Overall, results indicated that aspirin treatment can block orthodontic relapse by regulating Th1 cells.

scholarly journals Regulation of human NK-cell cytokine and chemokine production by target cell recognition

Blood ◽  
2010 ◽  
Vol 115 (11) ◽  
pp. 2167-2176 ◽  
Author(s):  
Cyril Fauriat ◽  
Eric O. Long ◽  
Hans-Gustaf Ljunggren ◽  
Yenan T. Bryceson
Keyword(s):  
Nk Cells ◽  
Target Cell ◽  
Cell Activation ◽  
Nk Cell ◽  
Cell Recognition ◽  
Chemokine Production ◽  
Relative Contribution ◽  
Cytokines And Chemokines ◽  
Tnf Α ◽  
Ifn Γ

AbstractNatural killer (NK)–cell recognition of infected or neoplastic cells can induce cytotoxicity and cytokine secretion. So far, it has been difficult to assess the relative contribution of multiple NK-cell activation receptors to cytokine and chemokine production upon target cell recognition. Using Drosophila cells expressing ligands for the NK-cell receptors LFA-1, NKG2D, DNAM-1, 2B4, and CD16, we studied the minimal requirements for secretion by freshly isolated, human NK cells. Target cell stimulation induced secretion of predominately proinflammatory cytokines and chemokines. Release of chemokines MIP-1α, MIP-1β, and RANTES was induced within 1 hour of stimulation, whereas release of TNF-α and IFN-γ occurred later. Engagement of CD16, 2B4, or NKG2D sufficed for chemokine release, whereas induction of TNF-α and IFN-γ required engagement of additional receptors. Remarkably, our results revealed that, upon target cell recognition, CD56dim NK cells were more prominent cytokine and chemokine producers than CD56bright NK cells. The present data demonstrate how specific target cell ligands dictate qualitative and temporal aspects of NK-cell cytokine and chemokine responses. Conceptually, the results point to CD56dim NK cells as an important source of cytokines and chemokines upon recognition of aberrant cells, producing graded responses depending on the multiplicity of activating receptors engaged.

scholarly journals Cytokine regulation of stem cells

2016 ◽  
Author(s):  
Gyanesh Singh ◽  
Hasan Korkaya
Keyword(s):  
Stem Cells ◽  
Dendritic Cells ◽  
Stem Cell ◽  
Immune Cells ◽  
Interferon Γ ◽  
Gm Csf ◽  
Cell Functions ◽  
Tnf Α ◽  
Different Types ◽  
Ifn Γ

Different types of stem cells are targeted by a number of cytokines that alter proliferation, differentiation, or other properties of stem cells. Stem cells are known to express various cytokine genes. As IL-12, IL-14, G-CSF, and GM-CSF expression is lost after the differentiation of MSCs, these factors might have major contribution to pluripotency. Several other cytokines that are produced by immune cells, frequently target stem cells. Modulation of stem cell functions by cytokines can be a cause of various diseases including cancer. Stem cells can show immunosuppressive properties by a number of mechanisms. MSC-induced immunosuppression is often mediated by IFN-γ, TNF-α, IL-1α, or IL-1β. In co-culture experiments, MSCs were able to control T cells IL-2 response, or, dendritic cells TNF-α and IL-10 secretion. MSCs are also known to cause decreased interferon γ (IFN-γ) and increased IL-4 production by immune cells. However, the outcome in most of the cases depends on the presence of various factors that might synergize or antagonize with each other.

scholarly journals Uncontrolled diabetes mellitus: a current understanding of the mechanisms underlying the disease that affect orthodontic tooth movement

2021 ◽  
Vol 69 ◽  
Author(s):  
Daniela Gomides SAMARTINI ◽  
Manuela Ortega Marques RODRIGUES ◽  
Carina de Sousa SANTOS
Keyword(s):  
Diabetes Mellitus ◽  
Bone Remodeling ◽  
Orthodontic Treatment ◽  
Tooth Movement ◽  
Healing Process ◽  
Orthodontic Tooth Movement ◽  
Study Protocols ◽  
Uncontrolled Diabetes ◽  
Orthodontic Forces ◽  
A Current

ABSTRACT With improvements in dental aesthetic requirements an increasing number of adults are seeking orthodontic treatment that, along with current lifestyle and eating habits of the adult population, makes orthodontists more likely to encounter patients with metabolic disorders such as diabetes mellitus. Speculated that the diabetic patient during orthodontic treatment may not experience a physiological healing process as a healthy patient. Therefore, the objective of this work is to present a current and contextualized review of the mechanisms by which uncontrolled diabetes mellitus impacts on bone remodeling and orthodontic tooth movement during the application of orthodontic forces. The following databases were searched MEDLINE (via PubMed), Scopus, Web of Science, SciELO, LILACS and open grey with these MeSH “bone remodeling”, “diabetes mellitus”, “orthodontic” and “tooth movement”. Five articles remained after search strategy and were analyzed. In sum, no clinical studies were found, the evidence was limited to animal studies (rats). The results suggest that there are differences in bone remodeling and tooth movement during the application of orthodontic forces in animals with diabetes mellitus when compared to healthy animals, especially when the disease is associated with periodontal disease. However, the results are still controversial and may be due to different study protocols.

scholarly journals Tooth movement, orofacial pain, and leptin, interleukin-1β, and tumor necrosis factor–α levels in obese adolescents

2021 ◽  
Author(s):  
Rafaela Carolina Soares Bonato ◽  
Marta Artemisa Abel Mapengo ◽  
Lucas José de Azevedo-Silva ◽  
Guilherme Janson ◽  
Silvia Helena de Carvalho Sales-Peres
Keyword(s):  
Tumor Necrosis Factor ◽  
Orthodontic Treatment ◽  
Tumor Necrosis ◽  
Tooth Movement ◽  
Orofacial Pain ◽  
Obese Group ◽  
Subjective Report ◽  
Obese Adolescents ◽  
Tnf Α ◽  
Necrosis Factor

ABSTRACT Objectives To evaluate tooth movement, orofacial pain, and leptin, interleukin (IL)–1β, and tumor necrosis factor (TNF)–α cytokine levels in the gingival crevicular fluid (GCF) during orthodontic treatment in obese adolescents. Materials and Methods Participants included adolescent patients aged 12–18 years: group 1, obese (n = 30), and group 2, nonobese controls (n = 30). They were evaluated before (T0) and after 1 hour (T1), 24 hours (T2), and 1 week (T3) of fixed appliance bonding. Periodontal examination (T0), collection of GCF (T1, T2, T3), and evaluation of Little's irregularity index (T0, T3) were performed, and a visual analog scale was used to measure pain (T1, T2, T3). Evaluation of IL-1β, TNF-α, and leptin cytokines was performed using a Luminex assay. Mann-Whitney and t-tests were used for intergroup comparisons, and a generalized estimating equation and cluster analyses were used for comparisons among observation times (P < .05). Results The obese group had a higher prevalence of probing depth of ≥4 mm and bleeding on probing. Orthodontic tooth movement was similar in both groups. Peak of pain was at T2 in both groups and was higher in the obese patients. TNF-α showed a slight increase at T1, followed by a gradual decrease at T2 and T3 in both groups. The obese group had a higher concentration of IL-1β before and during orthodontic treatment. There was no difference in tooth movement between obese and control patients during the first week of orthodontic treatment. Conclusions Obese adolescents had a greater subjective report of orofacial pain after 24 hours of orthodontic treatment and higher concentrations of IL-1β proinflammatory cytokine before and during tooth movement as compared with nonobese control adolescents.

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