scholarly journals Preliminary Histological Evaluation of the Application of Ozone in the First Days of Orthodontic Force Induction in Animal Model

2021 ◽  
Author(s):  
Melissa Faccini ◽  
Felipe Agostini ◽  
Tassio Drieu ◽  
Francisco Ubiratan Ferreira de Campos ◽  
Aguinaldo Garcez ◽  
...  
Keyword(s):  
Animal Model ◽  
Blood Vessels ◽  
Mononuclear Cells ◽  
Root Resorption ◽  
Histological Evaluation ◽  
Polymorphonuclear Cells ◽  
Pressure Side ◽  
Ozone Therapy ◽  
Orthodontic Force ◽  
Maxillary Central Incisor

Abstract Objectives The aim of the study is to histologically evaluate the effect of ozone therapy on orthodontic force induction in an animal model. Materials and Methods Twenty-four Wistar rats were divided into three groups (n = 8). A NiTi coil spring was installed from the maxillary first molar to the maxillary central incisor. G1 was control and G2/G3 received 1 mL of ozonated gas at concentrations of 10 and 60 µg/mL, in the buccal mucosa above the first molar roots. The animals were euthanized 3 and 5 days after the procedure. Histological sections were obtained, longitudinally of the first molar’ long axis, in the mesiodistal direction. The number of osteoclasts, osteoblasts, blood vessels, polymorphonuclear and mononuclear cells, formation of osteoid tissue and hyaline areas, and root resorption were evaluated with light microscope, in tension and pressure sides. Intergroup comparisons were performed with Kruskal–Wallis, Dunn, and Chi-square tests. Results At 3-days pressure side, a greater number of osteoclasts was observed in ozone groups and greater number of blood vessels and polymorphonuclear cells were observed in G2. On the tension side, there was a significantly greater number of blood vessels, osteoblasts, and mononuclear cells in G2. At 5-days pressure side, there was a significantly greater number of osteoclasts in G2, blood vessels and osteoblasts in the ozone groups, and lesser number of polymorphonuclear cells in G3. Conclusion Ozone therapy increased the number of osteoclasts on the pressure side and osteoblasts on tension side, in 10 µg/mL concentration, demonstrating histological parameters favorable to bone remodeling. The 60 µg/mL ozone concentration accelerated the periodontal ligament reorganization process.

scholarly journals Endoscopic and Histopathological Findings of the Esophagus, Stomach, and Duodenum in Patients with Crohn’s Disease from a Reference Center in Bahia, Brazil

2021 ◽  
Vol 11 (2) ◽  
pp. 374-385
Author(s):  
Andrea Maia Pimentel ◽  
Luiz Antônio Rodrigues de Freitas ◽  
Rita de Cássia Reis Cruz ◽  
Isaac Neri de Novais Silva ◽  
Laíla Damasceno Andrade ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Mononuclear Cells ◽  
Erosive Esophagitis ◽  
Gastric Body ◽  
Polymorphonuclear Cells ◽  
Cross Sectional ◽  
Histopathological Findings ◽  
Focally Enhanced Gastritis ◽  
H Pylori

(1) The aim of the present study was to describe the endoscopic and histopathological findings in the esophagus, stomach, and duodenum in patients with Crohn’s disease. (2) Methods: This was a cross-sectional study that included patients receiving treatment from the inflammatory bowel disease outpatient clinic. Esophagogastroduodenoscopies with biopsies of the stomach and proximal duodenum were performed. Presence of Helicobacter pylori bacteria was assessed by Giemsa staining. (3) Results: We included 58 patients. Erosive esophagitis was identified in 25 patients (43.1%), gastritis was diagnosed in 32 patients (55.2%) and erosive duodenitis was found in eight (13.8%). The most frequent histopathological finding in the H. pylori-positive group was increased inflammatory activity in the gastric body and antrum, with a predominance of mononuclear and polymorphonuclear cells. In turn, the most frequent finding in the H. pylori-negative group was chronic inflammation with predominance of mononuclear cells. Focally enhanced gastritis was identified in four patients (6.9%), all of whom were negative for H. pylori. Granulomas were not observed. H. pylori infection was present in 19 patients (32.8%). (4) Conclusions: Nonspecific endoscopic and histological findings were frequent in patients with Crohn’s disease. Focally enhanced gastritis was uncommon and observed only in H. pylori-negative patients. The time from the diagnosis, patient age, and therapy in use may have influenced the nondetection of epithelioid granuloma.

scholarly journals Bone Marrow Homeostasis Is Impaired via JAK/STAT and Glucocorticoid Signaling in Cancer Cachexia Model

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1059
Author(s):  
Jinyeong Yu ◽  
Sanghyuk Choi ◽  
Aran Park ◽  
Jungbeom Do ◽  
Donghyun Nam ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Animal Model ◽  
Bone Loss ◽  
Cancer Cachexia ◽  
Mononuclear Cells ◽  
Bone Homeostasis ◽  
Bone Marrow Mscs ◽  
Hematopoietic Stem ◽  
Glucocorticoid Signaling

Cancer cachexia is a multifactorial systemic inflammation disease caused by complex interactions between the tumor and host tissues via soluble factors. However, whether cancer cachexia affects the bone marrow, in particular the hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs), remains unclear. Here, we investigated the bone marrow and bone in a cancer cachexia animal model generated by transplanting Lewis lung carcinoma cells. The number of bone marrow mononuclear cells (BM-MNCs) started to significantly decrease in the cancer cachectic animal model prior to the discernable loss of muscle and fat. This decrease in BM-MNCs was associated with myeloid skewing in the circulation and the expansion of hematopoietic progenitors in the bone marrow. Bone loss occurred in the cancer cachexia animal model and accompanied the decrease in the bone marrow MSCs that play important roles in both supporting HSCs and maintaining bone homeostasis. Glucocorticoid signaling mediated the decrease in bone marrow MSCs in the cancer cachectic environment. The cancer cachexia environment also skewed the differentiation of the bone marrow MSCs toward adipogenic fate via JAK/STAT as well as glucocorticoid signaling. Our results suggest that the bone loss induced in cancer cachexia is associated with the depletion and the impaired differentiation capacity of the bone marrow MSCs.

Fifteen-year Clinical Follow-up of Restoration of Extensive Cervical Resorption in a Maxillary Central Incisor

2017 ◽  
Vol 42 (2) ◽  
pp. E55-E58 ◽  
Author(s):  
EG Reston ◽  
RPR Bueno ◽  
LQ Closs ◽  
J Zettermann
Keyword(s):  
Root Resorption ◽  
Treatment Options ◽  
Glass Ionomer Cement ◽  
Central Incisor ◽  
Endodontically Treated Teeth ◽  
Maxillary Central Incisor ◽  
External Root Resorption ◽  
Fixed Prosthodontics ◽  
Single Structure ◽  
The One

SUMMARY Internal bleaching in endodontically treated teeth requires care and protection to prevent harm to the periodontal ligament due to peroxide and may result in external root resorption. There is a myriad of treatment options when this occurs, such as monitoring, extraction, and subsequent rehabilitation with implants or fixed prosthodontics. In some cases, such as the one described here, a conservative attempt to maintain the tooth as a single structure can be made by sealing the resorptive defect. In the present case, we show a multidisciplinary approach where orthodontics, periodontics, and restorative dentistry were involved in treating the maxillary right central incisor (#8) of a 65-year-old patient with extensive cervical resorption, whose chief complaint was esthetics. The proposed treatment was extrusion of the tooth followed by curettage and restoration of the defect with glass ionomer cement. The patient has been followed for 15 years with no signs of recurrence, maintenance of periodontal health, and patient satisfaction with the esthetic outcome.

Effects of diabetes on tooth movement and root resorption after orthodontic force application in rats

2016 ◽  
Vol 19 (2) ◽  
pp. 83-92 ◽  
Author(s):  
K. Arita ◽  
H. Hotokezaka ◽  
M. Hashimoto ◽  
T. Nakano-Tajima ◽  
T. Kurohama ◽  
...  
Keyword(s):  
Tooth Movement ◽  
Root Resorption ◽  
Orthodontic Force ◽  
Force Application

scholarly journals Enhanced plasminogen-activator production by leukocytes in the human and murine Chediak-Higashi syndrome

Blood ◽  
1985 ◽  
Vol 65 (5) ◽  
pp. 1275-1281 ◽  
Author(s):  
G de Saint Basile ◽  
A Fischer ◽  
MD Dautzenberg ◽  
A Durandy ◽  
F Le Deist ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Mononuclear Cells ◽  
Chronic Phase ◽  
Polymorphonuclear Cells ◽  
Clotting Factors ◽  
Coagulation Abnormalities ◽  
Life Threatening ◽  
Coagulation Status ◽  
Chediak Higashi Syndrome

Abstract We have studied the coagulation status of eight patients with the Chediak-Higashi syndrome (CHS), both in the chronic and the accelerated phase of the disease. It has been shown that during the accelerated phase there are coagulation abnormalities. These abnormalities include a peripheral thrombocytopenia, minor alterations of liver clotting factors, and mainly a profound hypofibrinogenemia and hypoplasminogenemia, which cause life-threatening bleedings. These disorders are of complex origin, but a fibrinolytic process, possibly primary, appears to play a significant role, since the present evidence for intravascular coagulation is not definitive. The accelerated phase of the CHS is characterized by a visceral infiltration by macrophages and lymphocytes. Therefore, we have investigated the possible role of the macrophages in the fibrinolytic process. We have found an excessive plasminogen activator (PA) production by CHS mononuclear cells in the accelerated phase and to a lesser extent in the chronic phase, except in one patient in whom no anomaly was found. Single-cell studies revealed an increased number of PA-producing cells among the monocyte- macrophage lineage rather than a higher level of production per cell. Polymorphonuclear cells (PMN) from patients with CHS were also shown to contain more PA. Slight but significant abnormalities in PA production were observed in obligatory heterozygotes (five out of nine), indicating the inherited nature of the excessive PA production. Finally, an enhanced PA production was similarly demonstrated using beige mice macrophages. The exacerbated production of PA by macrophages in the accelerated phase of the CHS can account to some extent for the coagulation abnormalities that have been observed.

scholarly journals Enhanced plasminogen-activator production by leukocytes in the human and murine Chediak-Higashi syndrome

Blood ◽  
1985 ◽  
Vol 65 (5) ◽  
pp. 1275-1281
Author(s):  
G de Saint Basile ◽  
A Fischer ◽  
MD Dautzenberg ◽  
A Durandy ◽  
F Le Deist ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Mononuclear Cells ◽  
Chronic Phase ◽  
Polymorphonuclear Cells ◽  
Clotting Factors ◽  
Coagulation Abnormalities ◽  
Life Threatening ◽  
Coagulation Status ◽  
Chediak Higashi Syndrome

We have studied the coagulation status of eight patients with the Chediak-Higashi syndrome (CHS), both in the chronic and the accelerated phase of the disease. It has been shown that during the accelerated phase there are coagulation abnormalities. These abnormalities include a peripheral thrombocytopenia, minor alterations of liver clotting factors, and mainly a profound hypofibrinogenemia and hypoplasminogenemia, which cause life-threatening bleedings. These disorders are of complex origin, but a fibrinolytic process, possibly primary, appears to play a significant role, since the present evidence for intravascular coagulation is not definitive. The accelerated phase of the CHS is characterized by a visceral infiltration by macrophages and lymphocytes. Therefore, we have investigated the possible role of the macrophages in the fibrinolytic process. We have found an excessive plasminogen activator (PA) production by CHS mononuclear cells in the accelerated phase and to a lesser extent in the chronic phase, except in one patient in whom no anomaly was found. Single-cell studies revealed an increased number of PA-producing cells among the monocyte- macrophage lineage rather than a higher level of production per cell. Polymorphonuclear cells (PMN) from patients with CHS were also shown to contain more PA. Slight but significant abnormalities in PA production were observed in obligatory heterozygotes (five out of nine), indicating the inherited nature of the excessive PA production. Finally, an enhanced PA production was similarly demonstrated using beige mice macrophages. The exacerbated production of PA by macrophages in the accelerated phase of the CHS can account to some extent for the coagulation abnormalities that have been observed.

scholarly journals Il6/Sil6R Regulates Tnfα-Inflammatory Response In Synovial Fibroblasts Through Modulation of Transcriptional and Post-Transcriptional Mechanisms

2020 ◽  
Author(s):  
Alvaro Valin ◽  
Manuel J. Del Rey ◽  
Cristina Municio ◽  
Alicia Usategui ◽  
Marina Romero ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mononuclear Cells ◽  
De Novo ◽  
Inflammatory Cells ◽  
Synovial Fibroblasts ◽  
Matrix Metalloproteases ◽  
P Value ◽  
Polymorphonuclear Cells ◽  
Expression Of Genes

Abstract Introduction: The clinical efficacy of specific interleukin-6 inhibitors has confirmed the central role of IL6 in rheumatoid arthritis (RA). However the local role of IL6, in particular in synovial fibroblasts (SF) as a direct cellular target to IL6/sIL6R signal is not well characterized. The purpose of the study was to characterize the crosstalk between TNFα and IL6/sIL6R signaling to the effector pro-inflammatory response of SF. Methods SF lines were stimulated with either TNFα or IL6 and sIL6R for the time and dose indicated for each experiment, and where indicated, cells were treated with inhibitors actinomycin D, adalimumab, ruxolitinib and cicloheximide. mRNA expression of cytokines, chemokines and matrix metalloproteases (MMPs) were analyzed by quantitative RT-PCR. Level of IL8 and CCL8 in culture supernatants was measured by ELISA. Mononuclear and polymorphonuclear cells migration assays were assesed by transwell using conditioned medium from SF cultures. Statistical analyses were performed as indicated in the corresponding figure legends and a p-value < 0.05 was considered statistically significant. Results IL6/sIL6R stimulation of TNFα treated SF cooperatively promotes the expression of mono- and lymphocytic chemokines such as IL6, CCL8 and CCL2, as well as matrix degrading enzymes such as MMP1, while inhibiting the induction of central neutrophil chemokines such as IL8. These changes in the pattern of chemokines expression resulted in reduced polymorphonuclear (PMN) and increased mononuclear cells (MNC) chemoattraction by SF. Mechanistic analyses of the temporal expression of genes demonstrated that the cooperative regulation mediated by these two factors is mostly induced through de novo transcriptional mechanisms activated by IL6/sIL6R. Furthermore, we also demonstrate that TNFα and IL6/sIL6R cooperation is partially mediated by the expression of secondary factors signaling through JAK/STAT pathways. Conclusions These results point out to a highly orchestrated response to IL6 in TNFα-induced SF and provide additional insights into the role of IL6/sIL6R in the context of RA, highlighting the contribution of IL6/sIL6R to the interplay of SF with other inflammatory cells.

scholarly journals Concurrent helminthosis engendered gastroenteritis in a leopard Panthera pardus

2019 ◽  
Vol 56 (4) ◽  
pp. 323-328
Author(s):  
R. Kumar ◽  
A. D. Moudgil ◽  
A. Sharma ◽  
R. Sharma ◽  
R. Masand ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Inflammatory Cells ◽  
Toxocara Canis ◽  
Intestinal Content ◽  
Detailed Examination ◽  
Pathological Examination ◽  
Polymorphonuclear Cells ◽  
Panthera Pardus ◽  
Parasitic Gastroenteritis ◽  
Present Case Study

SummaryThe necropsy of a leopard (Panthera pardus), succumbed to a chronic ailment exhibited a mixed parasitic gastroenteritis. Gross internal examination of carcass revealed the presence of round and tapeworms in the stomach and intestines with diffuse catarrhal and hemorrhagic gastroenteritis. The detailed examination of the intestinal content revealed the presence of Toxocara canis and Spirometra species eggs. Also, the gross morphological investigation of round and tapeworms approved the presence of both species. Histo-pathological examination showed sloughing of intestinal epithelium, hemorrhages, and ulcerative areas with the infiltration of polymorphonuclear cells admixed with mononuclear cells. Lungs revealed the accumulation of eosinophilic edematous fl uid in the alveolar spaces along with inflammatory cells. These parasites are pathogenic to precious wild felids and often pose a threat of zoonotic transmission due to spill-over infections. The present case study is an attempt to put on record a case of parasitic gastroenteritis in a captive leopard.

Various adhesion molecules impair microvascular leukocyte kinetics in ventilator-induced lung injury

2006 ◽  
Vol 290 (6) ◽  
pp. L1059-L1068 ◽  
Author(s):  
Naoki Miyao ◽  
Yukio Suzuki ◽  
Kei Takeshita ◽  
Hiroyasu Kudo ◽  
Makoto Ishii ◽  
...  
Keyword(s):  
Lung Injury ◽  
Fluorescence Microscopy ◽  
Adhesion Molecules ◽  
Mononuclear Cells ◽  
Tissue Injury ◽  
Laser Fluorescence ◽  
Confocal Laser ◽  
Polymorphonuclear Cells ◽  
Ventilator Induced Lung Injury ◽  
Endothelial Adhesion Molecules

Although the endothelial expression of various adhesion molecules substantially differs between pulmonary microvessels, their importance for neutrophil and lymphocyte sequestration in ventilator-induced lung injury (VILI) has not been systematically analyzed. We investigated the kinetics of polymorphonuclear cells (PMN) and mononuclear cells (MN) in the acinar microcirculation of the isolated rat lung with VILI by real-time confocal laser fluorescence microscopy, with or without inhibition of ICAM-1, VCAM-1, or P-selectin by monoclonal antibodies (MAb). Adhesion molecules in each microvessel were estimated by intravital fluorescence microscopy or immunohistochemical staining. In high tidal volume-ventilated lungs, 1) ICAM-1, VCAM-1, and P-selectin were differently upregulated in venules, arterioles, and capillaries; 2) venular PMN rolling was improved by inhibition of ICAM-1, VCAM-1, or P-selectin, whereas arteriolar PMN rolling was improved by ICAM-1 or VCAM-1 inhibition; 3) capillary PMN entrapment was ameliorated only by anti-ICAM-1 MAb; and 4) MN rolling in venules and arterioles and MN entrapment in capillaries were improved by ICAM-1 and VCAM-1 inhibition. In conclusion, the contribution of endothelial adhesion molecules to abnormal leukocyte behavior in VILI-injured microcirculation is microvessel and leukocyte specific. ICAM-1- and VCAM-1-dependent, but P-selectin-independent, arteriolar PMN rolling, which is expected to reflect the initial stage of tissue injury, should be taken as a phenomenon unique to ventilator-associated lung injury.

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