Publications by authors named "Fauvel F"

Medication related osteonecrosis of the jaws (MRONJ) and osteoradionecrosis of the jaws (ORNJ) are two different diseases of quite similar appearance. MRONJ is mainly due to antiresorptive or antiangiogenic drug therapy and ORNJ to radiotherapy. The present work aimed at presenting and comparing the current knowledge on MRONJ and ORNJ.

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Background: The aim of this network meta-analysis (NMA) was to compare the clinical results obtained after primary reconstruction of orbital floor fractures (OFF) using different materials.

Methods: PubMed, Cochrane, and Google Scholar databases were screened from 1989 to 2019. For a study to be eligible, it had to evaluate two or more materials and report the following clinical parameters: diplopia and/or enophthalmos and/or other complications.

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Complications with bilateral sagittal split osteotomy (BSSO) can sometimes result from surgical inexperience. Our aim was to present a 3-dimensional printed mandibular model for BSSO training in a maxillofacial surgical education programme. A polymethacrylate mandibular model obtained from mandibular cone-beam computed tomographic (CT) images was designed and printed for use in training.

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Spontaneous regeneration of bone tissue after mandibular resection is rare in adults, although it does often take place in children. Periosteum conservation appears to play a major role in this healing process. We here report regarding a 5-year-old boy who exhibited a large mandibular trabecular juvenile ossifying fibroma.

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Introduction: Several surgical procedures have been proposed for the treatment of hyperdivergent dentoskeletal deformities. We propose a new osteotomy technique allowing for lengthening and advancement of the mandibular ramus by intra-oral approach.

Surgical Procedure: This technique differs from the conventional sagittal split osteotomyin that which the anterior osteotomy line is not continued until the basilar edge but stopped 5-6mm above it.

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Objective: The aim of this study is to present and discuss the results of a European multicentre prospective study about pediatric maxillofacial trauma epidemiology during a year.

Study Design: The following data were recorded: gender, age, etiology, site of fracture, date of injury. Of the 3396 patients with maxillofacial fractures admitted within the study period, 114 (3.

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Introduction: Oral impalement injuries are common in children. We report a case of severe pharyngeal toothbrush perforation in a 15-month-old infant.

Observation: A 15-month-old child was admitted for a penetrating oral injury caused by a toothbrush.

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Kindlin-3 (FERMT-3) is known to be central in hemostasis and thrombosis control and its deficiency disrupts platelet aggregation and causes Leukocyte Adhesion Deficiency disease. Here we report that Kindlin-3 has a tumor suppressive role in solid cancer. Our present genetic and functional data show that Kindlin-3 is downregulated in several solid tumors by a mechanism involving gene hypermethylation and deletions.

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Fragments of five rrp genes encoding response regulators (RRs) in Lactobacillus sakei were amplified by PCR using degenerate oligonucleotide primers. The five rrp genes were part of distinct loci that also comprised hpk genes encoding histidine protein kinases (HPKs). The putative RRs belonged to the OmpR-PhoB subclass of response regulators that consist of N-terminal receiver and C-terminal DNA-binding domains.

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Previous works demonstrated that microfibrils stimulate blood platelets to aggregate. The present study compares the activation of platelets by human placental and bovine aortic microfibrils and by type III collagen. We studied the morphological changes occurring in in platelets during their activation and aggregation, as well as the kinetics of the release reaction and thromboxane B2 formation.

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The culture medium of bovine aortic endothelial cells contains proteins which inhibit the aggregation of platelets induced by aortic microfibrils but not by type III collagen. From this medium, fibronectin, thrombospondin and a glycoprotein with MW of 128 Kd (GP 128), similar to a glycoprotein described in a microfibrillar extract from bovine aorta were separated by affinity and ion exchange chromatography. GP 128 was further purified by molecular sieve chromatography on SW 3000 column.

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Biochemical methods involving chemical and enzymatic cleavage of type III collagen (characteristic of arterial subendothelium) have led to the identification of a nonapeptide common to different overlapping collagen fragments capable of interacting with platelets. This nonapeptide has been synthesized; it specifically inhibits platelet aggregation and secretion of endogenous platelet serotonin by type III collagen from which it originates. Its effect on platelet adhesion is moderate.

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The effect of normal and nonenzymatically glycosylated rat type I acid-soluble collagen on normal human platelets was investigated. Glycosylated collagen was obtained either after in vitro incubation with glucose or from rats made diabetic by streptozotocin. The amount of nonenzymatically bound glucose was as follows: normal 2.

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Adult bovine aortic tissue was treated with 6 M guanidinium chloride in the presence of proteinase inhibitors to obtain an extract that was essentially devoid of collagenous components and appeared homogeneous by electron microscopy. When this extract was dispersed by sonication it was found to be a very potent inducer of human platelet aggregation. This interaction required the presence of von Willebrand factor and of its receptor (glycoprotein Ib) on platelet membrane.

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Two different subendothelial macromolecules have been identified as being thrombogenic: collagen and the microfibrils associated with elastin. The interaction between platelets and collagen involves the binding of platelet membrane receptors by numerous sites repeatedly staggered along a collagen fiber: this explains why the preservation of ordered structures (quaternary and tertiary structures) is so important in the reactivity of collagen towards platelets. In the case of Type III collagen, a nonapeptide has been identified as possibly being part of these repetitive sites.

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Thrombogenicity of the vessel wall: role of the microfibrils and collagen. The study of platelet adhesion to rabbit aortic subendothelium preincubated with highly specific collagenase has revealed that platelets adhere to the microfibrils of the elastic lamina. To certify that an interaction between microfibrils and platelets can occur, microfibrils from two different origins were isolated: placental microfibrils extracted from the villi of human placenta, and aortic microfibrils extracted from adult bovine aorta.

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The interaction of human blood platelets with collagenase-treated rabbit subendothelium was studied by histochemical ultrastructural methods and by morphometric semi-quantitative analysis. Aortas were deendothelialized and incubated: 1) with a highly purified bacterial collagenase whose specificity was controlled; and 2) with the same collagenase followed by chymotrypsin. For histochemical studies, tannic acid, ruthenium red, and peroxidase-labeled Ricinus communis and concanavalin A were used.

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In view of its anatomical position, physical characteristics and metabolism, the endothelial cell plays a major part in maintaining the integrity of the vascular system and in the relation between the blood content, both plasma and blood cells, and the wall structure. Where this continuous single layer undergoes anatomical or functional changes, a new equilibrium is set up, an equilibrium which is multifactorial and dynamic. It is governed by the vascular and blood components and by their interrelation; it varies as a function of time and of the biorheological conditions.

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This review deals with some structural features of the collagen molecules involved in the adhesion of platelets representing the initial step of hemostasis, thrombosis, and (partly) atherosclerosis. The adhesion occurs at the level of a vascular lesion or deendothelialized area, whatever the genetic type of collagen. In vitro experiments with purified collagens have shown that vascular interstitial collagens (types I and III, the latter present in subendothelium) as well as basement membrane-derived collagens (types IV and V) induce an adhesion of platelets, provided that an ordered arrangement linked to the quaternary and tertiary structures of their molecule is preserved.

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A quantitative method (Sepharose test) was devised to measure the adhesion of blood platelets to fibrillar collagen. [14C]5HT-labeled platelets were isolated from plasma, resuspended in EDTA buffer, and incubated with buffer (control) or with fibrillar collagen for 150 sec at 33 degrees C. The mixtures were then filtered through Sepharose 2B columns.

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