DOCSLIB.ORG

Responses to Metal Implants

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Responses to Metal Implants /s£.llVIC£.t,(t<t, ( -I_ rffl.l U.S. FOOD & DRUG "-<..,,~~ - ADMINISTRATION Biological Responses to Metal Implants U.S. Food and Drug Administration Center for Devices and Radiological Health Office of Product Evaluation and Quality Office of Science Engineering and Laboratories September 2019 i | Page TABLE OF CONTENTS 1 Introduction ...................................................................................................................................... 1 2 Background: Definitions, History, and Landscape ............................................................................ 3 3 Metals in Human Physiology and Pathology ..................................................................................... 5 3.1 Introduction .................................................................................................................................. 5 3.2 Essential Trace Metal Elements .................................................................................................... 6 3.3 Non-Essential Metals .................................................................................................................... 7 4 Current nonclinical pre-market evaluation of metal implants ......................................................... 9 4.1 Introduction .................................................................................................................................. 9 4.2 Biocompatibility .......................................................................................................................... 10 4.2.1 Sensitization ........................................................................................................................ 10 4.2.2 Implantation ........................................................................................................................ 12 4.2.3 Inflammatory Response ...................................................................................................... 12 4.2.4 Genotoxicity and Carcinogenicity ....................................................................................... 13 4.2.5 Systemic Toxicity ................................................................................................................. 14 4.3 CDRH’s Immunotoxicity Guidance .............................................................................................. 16 5 Corrosion and metal ion release ..................................................................................................... 17 5.1 Introduction ................................................................................................................................ 17 5.2 Corrosion susceptibility ............................................................................................................... 19 5.2.1 Physiological Environment .................................................................................................. 19 5.2.2 Mechanical Interactions ...................................................................................................... 20 5.2.3 Active Devices ..................................................................................................................... 20 5.2.4 Processing ........................................................................................................................... 22 5.3 In vitro corrosion testing ............................................................................................................. 22 5.3.1 General Corrosion ............................................................................................................... 22 5.3.2 General Corrosion - Active Implants ................................................................................... 23 5.3.3 Pitting Corrosion ................................................................................................................. 24 5.3.4 Crevice Corrosion ................................................................................................................ 25 5.3.5 Fretting ................................................................................................................................ 25 5.3.6 Galvanic Corrosion .............................................................................................................. 25 5.4 In-vivo corrosion ......................................................................................................................... 26 i | Page Immunological responses to metal implants 5.4.1 Corrosion in Cardiovascular Devices ................................................................................... 27 5.4.2 Corrosion in Orthopedic Devices ........................................................................................ 27 5.4.3 Corrosion in Active Devices ................................................................................................. 28 5.4.4 Correlation to In Vitro Testing ............................................................................................. 28 6 Subclinical response to metal implants .......................................................................................... 31 6.1. Introduction ................................................................................................................................ 31 6.1 Wound Healing ........................................................................................................................... 32 6.1.1 Foreign Body Response (FBR) ............................................................................................. 33 6.2. Innate Immune Responses To Metal Implants ........................................................................... 34 6.2.1. Innate Immune Recognition of Metals ............................................................................... 34 6.2.2. Innate Cellular Responses to Metals ................................................................................... 35 6.3. Adaptive Immune Responses to Metal Implants ........................................................................ 37 6.4. Tissue and Organ Localization of Inflammatory Responses to Metal Implants .......................... 39 6.4.1. Orthopedic Devices ............................................................................................................. 39 6.4.2. Neurologic Devices .............................................................................................................. 40 6.4.3. Cardiovascular Devices ....................................................................................................... 41 6.4.4. Oral and Dental Implants .................................................................................................... 42 6.4.5. Urogenital Devices .............................................................................................................. 43 6.5. Conclusions, Summary, Inflammatory regulation underlying clinical outcomes ....................... 43 7 Clinical response to metal implants ................................................................................................ 45 7.1 Introduction ................................................................................................................................ 46 7.2 Terminology Pertaining to Potential Clinical, Imaging, and Morphological Manifestations of Metal Implant-Related Adverse Outcomes ............................................................................................ 46 7.2.1 Systemic ARMDs ................................................................................................................. 48 7.2.2 Elevated Metal Ion Levels ................................................................................................... 48 7.2.3 Different manifestations of systemic hypersensitivity and inflammation .......................... 49 7.3 Sex-related issues in clinical responses to metal implants ......................................................... 51 7.4 Clinical observations and investigations of systemic responses to metal implants ................... 51 7.4.1 Cardiotoxicity ...................................................................................................................... 51 7.4.2 Neurotoxicity ....................................................................................................................... 52 7.4.3 Thyroid toxicity ................................................................................................................... 52 7.4.4 Cancer ................................................................................................................................. 52 7.5 Specific Device Areas .................................................................................................................. 54 ii | Page Introduction 7.5.1 Orthopedic devices ............................................................................................................. 54 7.5.2 Cardiac and Endovascular Implants .................................................................................... 57 7.5.3 Dental and Oral/Maxillofacial Devices ................................................................................ 60 7.5.4 Neurological Devices ........................................................................................................... 62 7.5.5 Gastroenterological Devices ..............................................................................................
Load more

Recommended publications
  • Differentiation and Bone Resorption Role of CX3CL1/Fractalkine In
    Role of CX3CL1/Fractalkine in Osteoclast Differentiation and Bone Resorption Keiichi Koizumi, Yurika Saitoh, Takayuki Minami, Nobuhiro Takeno, Koichi Tsuneyama, Tatsuro Miyahara, This information is current as Takashi Nakayama, Hiroaki Sakurai, Yasuo Takano, Miyuki of September 29, 2021. Nishimura, Toshio Imai, Osamu Yoshie and Ikuo Saiki J Immunol published online 18 November 2009 http://www.jimmunol.org/content/early/2009/11/18/jimmuno l.0803627.citation Downloaded from Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 29, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published November 18, 2009, doi:10.4049/jimmunol.0803627 The Journal of Immunology Role of CX3CL1/Fractalkine in Osteoclast Differentiation and Bone Resorption1 Keiichi Koizumi,2* Yurika Saitoh,* Takayuki Minami,* Nobuhiro Takeno,* Koichi Tsuneyama,†‡ Tatsuro Miyahara,§ Takashi Nakayama,¶ Hiroaki Sakurai,*† Yasuo Takano,‡ Miyuki Nishimura,ʈ Toshio Imai,ʈ Osamu Yoshie,¶ and Ikuo Saiki*† The recruitment of osteoclast precursors toward osteoblasts and subsequent cell-cell interactions are critical for osteoclast dif- ferentiation.
    [Show full text]
  • Acting on the CCR1 Receptor Mediates Neutrophil Migration in Immune Inflammation Via Sequential ␣ Release of TNF- and LTB4 Cleber D
    MIP-1␣[CCL3] acting on the CCR1 receptor mediates neutrophil migration in immune inflammation via sequential ␣ release of TNF- and LTB4 Cleber D. L. Ramos,* Claudio Canetti,*,† Janeusa T. Souto,‡,§ Joa˜ o S. Silva,‡ Cory M. Hogaboam,¶ Sergio H. Ferreira,* and Fernando Q. Cunha*,1 Departments of *Pharmacology and ‡Biochemistry and Immunology, School of Medicine of Ribeira˜o Preto, University of Sa˜o Paulo, Brazil; §Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, RN, Brazil; and †Division of Pulmonary & Critical Care Medicine and ¶Department of Pathology, University of Michigan, Ann Arbor Abstract: In the present study, we investigated nists might have a therapeutic potential. J. Leukoc. the involvement of macrophage-inflammatory pro- Biol. 78: 167–177; 2005. tein-1␣ (MIP-1␣)[CC chemokine ligand 3 (CCL3)], MIP-1␤[CCL4], regulated on activation, normal Key Words: chemokines ⅐ chemokine receptors ⅐ chemotaxis T expressed and secreted (RANTES)[CCL5], and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- INTRODUCTION ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor Neutrophil migration is a complex process, which results ␣ ␣ mainly from the release of neutrophil chemotactic factors by (TNF- ) and leukotriene B4 (LTB4). Herein, we show increased mRNA expression for MIP- resident cells, inducing rolling and adhesion of neutrophils on 1␣[CCL3], MIP-1␤[CCL4], RANTES[CCL5], and endothelial cells, followed by their transmigration to the ex- travascular space [1, 2]. Apart from its importance in host CCR1 in peritoneal cells harvested from OVA-chal- defense, the migration of neutrophils to the inflammatory site lenged, immunized mice, as well as MIP-1␣[CCL3] is, at least in part, responsible for tissue damage observed in and RANTES[CCL5] but not MIP-1␤[CCL4] proteins several inflammatory diseases such as rheumatoid arthritis, in the peritoneal exudates.
    [Show full text]
  • Metallosis and Pseudotumor Around Ceramic-On-Polyethylene Total Hip Arthroplasty; Case Report and Literature Review
    Available online at www.ijmrhs.com Special Issue 9S: Medical Science and Healthcare: Current Scenario and Future Development International Journal of Medical Research & ISSN No: 2319-5886 Health Sciences, 2016, 5, 9S:518-524 Metallosis and Pseudotumor around Ceramic-On-Polyethylene Total Hip Arthroplasty; Case Report and Literature Review Afshin Taheriazam 1* and Amin Saeidinia 2,3 1Hip Surgeon, Assistant Professor, Department of Orthopedics Surgery, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran 2General Practitioner, Assistant Researcher, Mashhad University of Medical Sciences, Mashhad, Iran 3Member of Young Researchers Club, Rasht Branch, Islamic Azad University, Rasht, Iran *Corresponding Email: [email protected] _____________________________________________________________________________________________ ABSTRACT Polyethylene failure is a rare complication of ceramic-on-polyethylene total hip arthroplasty due to characteristics of ceramic. Complications associated with ceramic-on-polyethylene articulations have been studied extensively, however, only few reports have described its catastrophic wear and concurrent pseudotumor formation. The etiology of this biological reaction and concurrency of pseudotumor formation with metallosis remain unclear. We report two cases of wear of the acetabular liner in a ceramic-on-polyethylene prosthesis due to total hip arthroplasty (THA) long time ago. They came back to the clinic with the history of worsening hip pain and abnormal radiological and clinical findings. Then they underwent surgery and metallosis and pseudotumors were detected and revisions were performed for them. It is necessary to evaluate patients underwent THA complaining of hip pain for component wear and be checked the cup appear well fixing and fairly oriented on follow-up radiographies. Close follow ups can prevent accelerated polyethylene wear in ceramic-on-polyethylene coupling THA.
    [Show full text]
  • Mice in Inflammation Psoriasiform Skin IL-22 Is Required for Imiquimod-Induced
    IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice Astrid B. Van Belle, Magali de Heusch, Muriel M. Lemaire, Emilie Hendrickx, Guy Warnier, Kyri This information is current as Dunussi-Joannopoulos, Lynette A. Fouser, Jean-Christophe of September 29, 2021. Renauld and Laure Dumoutier J Immunol published online 30 November 2011 http://www.jimmunol.org/content/early/2011/11/30/jimmun ol.1102224 Downloaded from Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 29, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2011 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published November 30, 2011, doi:10.4049/jimmunol.1102224 The Journal of Immunology IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice Astrid B. Van Belle,*,† Magali de Heusch,*,† Muriel M. Lemaire,*,† Emilie Hendrickx,*,† Guy Warnier,*,† Kyri Dunussi-Joannopoulos,‡ Lynette A. Fouser,‡ Jean-Christophe Renauld,*,†,1 and Laure Dumoutier*,†,1 Psoriasis is a common chronic autoimmune skin disease of unknown cause that involves dysregulated interplay between immune cells and keratinocytes.
    [Show full text]
  • The Chemokine System in Innate Immunity
    Downloaded from http://cshperspectives.cshlp.org/ on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press The Chemokine System in Innate Immunity Caroline L. Sokol and Andrew D. Luster Center for Immunology & Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114 Correspondence: [email protected] Chemokines are chemotactic cytokines that control the migration and positioning of immune cells in tissues and are critical for the function of the innate immune system. Chemokines control the release of innate immune cells from the bone marrow during homeostasis as well as in response to infection and inflammation. Theyalso recruit innate immune effectors out of the circulation and into the tissue where, in collaboration with other chemoattractants, they guide these cells to the very sites of tissue injury. Chemokine function is also critical for the positioning of innate immune sentinels in peripheral tissue and then, following innate immune activation, guiding these activated cells to the draining lymph node to initiate and imprint an adaptive immune response. In this review, we will highlight recent advances in understanding how chemokine function regulates the movement and positioning of innate immune cells at homeostasis and in response to acute inflammation, and then we will review how chemokine-mediated innate immune cell trafficking plays an essential role in linking the innate and adaptive immune responses. hemokines are chemotactic cytokines that with emphasis placed on its role in the innate Ccontrol cell migration and cell positioning immune system. throughout development, homeostasis, and in- flammation. The immune system, which is de- pendent on the coordinated migration of cells, CHEMOKINES AND CHEMOKINE RECEPTORS is particularly dependent on chemokines for its function.
    [Show full text]
  • Haplotypes in CCR5-CCR2, CCL3 and CCL5 Are Associated with Natural Resistance to HIV-1 Infection in a Colombian Cohort Jorge A
    Biomédica 2017;37:267-73 Haplotypes associated with resistance to HIV-1 doi: http://dx.doi.org/10.7705/biomedica.v37i3.3237 BRIEF COMMUNICATION Haplotypes in CCR5-CCR2, CCL3 and CCL5 are associated with natural resistance to HIV-1 infection in a Colombian cohort Jorge A. Vega1,2,3, Simón Villegas-Ospina1, Wbeimar Aguilar-Jiménez1, María T. Rugeles1, Gabriel Bedoya3, Wildeman Zapata1,4 1 Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia 2 Laboratorio de Genética, Dirección Regional Noroccidente, Instituto Nacional de Medicina Legal y Ciencias Forenses, Medellín, Colombia 3 Genética Molecular, Instituto de Biología, Universidad de Antioquia, Medellín, Colombia 4 Grupo Infettare, Facultad de Medicina, Universidad Cooperativa de Colombia, Medellín, Colombia Introduction: Variants in genes encoding for HIV-1 co-receptors and their natural ligands have been individually associated to natural resistance to HIV-1 infection. However, the simultaneous presence of these variants has been poorly studied. Objective: To evaluate the association of single and multilocus haplotypes in genes coding for the viral co-receptors CCR5 and CCR2, and their ligands CCL3 and CCL5, with resistance or susceptibility to HIV-1 infection. Materials and methods: Nine variants in CCR5-CCR2, two SNPs in CCL3 and two in CCL5 were genotyped by PCR-RFLP in 35 seropositive (cases) and 49 HIV-1-exposed seronegative Colombian individuals (controls). Haplotypes were inferred using the Arlequin software, and their frequency in individual or combined loci was compared between cases and controls by the chi-square test. A p’ value <0.05 after Bonferroni correction was considered significant. Results: Homozygosis of the human haplogroup (HH) E was absent in controls and frequent in cases, showing a tendency to susceptibility.
    [Show full text]
  • Ccl17-Dependent Release of Ccl3 Restrains Regulatory T Cells Thereby Aggravating Atherosclerosis
    From the Institute for Cardiovascular Prevention (IPEK) of the Ludwig-Maximilians-Universität München Director: Univ.-Prof. Dr. med. Christian Weber Ccl17-dependent release of Ccl3 restrains regulatory T cells thereby aggravating atherosclerosis Dissertation zum Erwerb des Doctor of Philosophy (Ph.D.) an der Medizinischen Fakultät der Ludwig-Maximilians-Universität München Submitted by M.Sc. Carlos Neideck from Taió in Santa Catarina, Brazil on 21.03.2018 Supervisor: Prof. Dr. med. Christian Weber Second evaluator: Prof. Dr. rer. nat. Jürgen Bernhagen Dean: Prof. Dr. Reinhard Hickel Date of oral defense: 23.07.2018 Affidavit Neideck, Carlos ______________________________________________________________________ Name, Surname ______________________________________________________________________ Street ______________________________________________________________________ Zip Code, Town ______________________________________________________________________ Country I hereby declare, that the submitted thesis entitled: “Ccl17-dependent release of Ccl3 restrains regulatory T cells thereby aggravating atherosclerosis.” is my own work. I have only used the sources indicated and have not made unauthorized use of services of a third party. Where the work of others has been quoted or reproduced, the source is always given. I further declare that the submitted thesis or parts thereof have not been presented as part of an examination degree to any other university. Munich, 25.07.2018 Carlos Neideck Place, date Signature doctoral candidate Confirmation
    [Show full text]
  • Exploration of Prognostic Biomarkers and Therapeutic Targets in the Microenvironment of Bladder Cancer Based on CXC Chemokines
    Exploration of Prognostic Biomarkers and Therapeutic Targets in The Microenvironment of Bladder Cancer Based on CXC Chemokines Xiaoqi Sun Department of Urology, Kaiping Central Hospital, Kaiping, 529300, China Qunxi Chen Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China Lihong Zhang Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China Jiewei Chen Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China Xinke Zhang ( [email protected] ) Sun Yat-sen University Cancer Center Research Keywords: Bladder cancer, Biomarkers, CXC Chemokines, Microenvironment Posted Date: February 24th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-223127/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/29 Abstract Background: Bladder cancer (BLCA) has a high rate of morbidity and mortality, and is considered as one of the most malignant tumors of the urinary system. Tumor cells interact with surrounding interstitial cells, playing a key role in carcinogenesis and progression, which is partly mediated by chemokines. CXC chemokines exert anti‐tumor biological roles in the tumor microenvironment and affect patient prognosis. Nevertheless, their expression and prognostic values patients with BLCA remain unclear. Methods: We used online tools, including Oncomine, UALCAN, GEPIA, GEO databases, cBioPortal, GeneMANIA, DAVID 6.8, Metascape, TRUST (version 2.0), LinkedOmics, TCGA, and TIMER2.0 to perform the relevant analysis. Results: The mRNA levels of C-X-C motif chemokine ligand (CXCL)1, CXCL5, CXCL6, CXCL7, CXCL9, CXCL10, CXCL11, CXCL13, CXCL16, and CXCL17 were increased signicantly increased, and those of CXCL2, CXCL3, and CXCL12 were decreased signicantly in BLCA tissues as assessed using the Oncomine, TCGA, and GEO databases.
    [Show full text]
  • With Immunoregulatory Invariant NK T Cells Schwann Cells and Potential Interactions Expression of Cd1d Molecules by Human
    Expression of CD1d Molecules by Human Schwann Cells and Potential Interactions with Immunoregulatory Invariant NK T Cells This information is current as Jin S. Im, Nikos Tapinos, Gue-Tae Chae, Petr A. Illarionov, of September 27, 2021. Gurdyal S. Besra, George H. DeVries, Robert L. Modlin, Peter A. Sieling, Anura Rambukkana and Steven A. Porcelli J Immunol 2006; 177:5226-5235; ; doi: 10.4049/jimmunol.177.8.5226 http://www.jimmunol.org/content/177/8/5226 Downloaded from References This article cites 60 articles, 23 of which you can access for free at: http://www.jimmunol.org/content/177/8/5226.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 27, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Expression of CD1d Molecules by Human Schwann Cells and Potential Interactions with Immunoregulatory Invariant NK T Cells1 Jin S.
    [Show full text]
  • Role of Chemokines in Hepatocellular Carcinoma (Review)
    ONCOLOGY REPORTS 45: 809-823, 2021 Role of chemokines in hepatocellular carcinoma (Review) DONGDONG XUE1*, YA ZHENG2*, JUNYE WEN1, JINGZHAO HAN1, HONGFANG TUO1, YIFAN LIU1 and YANHUI PENG1 1Department of Hepatobiliary Surgery, Hebei General Hospital, Shijiazhuang, Hebei 050051; 2Medical Center Laboratory, Tongji Hospital Affiliated to Tongji University School of Medicine, Shanghai 200065, P.R. China Received September 5, 2020; Accepted December 4, 2020 DOI: 10.3892/or.2020.7906 Abstract. Hepatocellular carcinoma (HCC) is a prevalent 1. Introduction malignant tumor worldwide, with an unsatisfactory prognosis, although treatments are improving. One of the main challenges Hepatocellular carcinoma (HCC) is the sixth most common for the treatment of HCC is the prevention or management type of cancer worldwide and the third leading cause of of recurrence and metastasis of HCC. It has been found that cancer-associated death (1). Most patients cannot undergo chemokines and their receptors serve a pivotal role in HCC radical surgery due to the presence of intrahepatic or distant progression. In the present review, the literature on the multi- organ metastases, and at present, the primary treatment methods factorial roles of exosomes in HCC from PubMed, Cochrane for HCC include surgery, local ablation therapy and radiation library and Embase were obtained, with a specific focus on intervention (2). These methods allow for effective treatment the functions and mechanisms of chemokines in HCC. To and management of patients with HCC during the early stages, date, >50 chemokines have been found, which can be divided with 5-year survival rates as high as 70% (3). Despite the into four families: CXC, CX3C, CC and XC, according to the continuous development of traditional treatment methods, the different positions of the conserved N-terminal cysteine resi- issue of recurrence and metastasis of HCC, causing adverse dues.
    [Show full text]
  • Fas Ligand Elicits a Caspase-Independent Proinflammatory Response in Human Keratinocytes: Implications for Dermatitis Sherry M
    CORE Metadata, citation and similar papers at core.ac.uk Provided by Serveur académique lausannois ORIGINAL ARTICLE See related commentary on pg 2364 Fas Ligand Elicits a Caspase-Independent Proinflammatory Response in Human Keratinocytes: Implications for Dermatitis Sherry M. Farley1, Anjali D. Dotson1, David E. Purdy1, Aaron J. Sundholm1, Pascal Schneider2, Bruce E. Magun1 and Mihail S. Iordanov1 Fas ligand (FasL) causes apoptosis of epidermal keratinocytes and triggers the appearance of spongiosis in eczematous dermatitis. We demonstrate here that FasL also aggravates inflammation by triggering the expression of proinflammatory cytokines, chemokines, and adhesion molecules in keratinocytes. In HaCaT cells and in reconstructed human epidermis (RHE), FasL triggered a NF-kB-dependent mRNA accumulation of inflammatory cytokines (tumor necrosis factor-a, IL-6, and IL-1b), chemokines (CCL2/MCP-1, CXCL1/GROa, CXCL3/GROg, and CXCL8/IL-8), and the adhesion molecule ICAM-1. Oligomerization of Fas was required both for apoptosis and for gene expression. Inhibition of caspase activity abolished FasL-dependent apoptosis; however, it failed to suppress the expression of FasL-induced genes. Additionally, in the presence of caspase inhibitors, but not in their absence, FasL triggered the accumulation of CCL5/RANTES (regulated on activation normal T cell expressed and secreted) mRNA. Our findings identify a novel proinflammatory role of FasL in keratinocytes that is independent of caspase activity and is separable from apoptosis. Thus, in addition to causing spongiosis, FasL may play a direct role in triggering and/or sustaining inflammation in eczemas. Journal of Investigative Dermatology (2006) 126, 2438–2451. doi:10.1038/sj.jid.5700477; published online 20 July 2006 INTRODUCTION increased local concentration of procaspase 8 allows for Apoptosis (Kerr et al., 1972), the principal mechanism for its spontaneous autocatalytic cleavage and activation by elimination of damaged cells in metazoan organisms (Edinger ‘‘induced proximity’’ (Muzio et al., 1998).
    [Show full text]
  • Metallosis After Reverse Total Shoulder Arthroplasty
    Edorium J Orthop 2017;3:17–23. Rondon et al. 17 www.edoriumjournaloforthopedics.com CASE REPORT PEER REVIEWED OPEN| OPEN ACCESS ACCESS Metallosis after reverse total shoulder arthroplasty Alexander J. Rondon, Tyler R. Clark, Felix H. Savoie ABSTRACT environment. Conclusion: Future consideration must be given to the size and angle of the Introduction: We present a case of metallosis humeral and glenoid components in reverse following a reverse total shoulder arthroplasty. total shoulder arthroplasties. It is our hope that We are not aware of any cases described in our case emphasizes the importance of proper literature of metallosis following reverse total prosthetic placement and establishes a higher shoulder arthroplasty with well-fixed implants. level of suspicion for metallosis as a complication To date, there have been four cases described in for reverse total shoulder arthroplasties. literature that have found metallosis following shoulder replacement surgery: three following Keywords: Arthroplasty, Metallosis, Reverse, hemiarthroplasty and one following total shoulder Shoulder arthroplasty. Case Report: Our patient dislocated seven months postoperatively, and with concern How to cite this article of further instability as noted on examination, the patient was taken to the operating room for Rondon AJ, Clark TR, Savoie FH. Metallosis after glenosphere and liner exchange. During surgery, reverse total shoulder arthroplasty. Edorium J severe metallic staining was discovered in the Orthop 2017;3:17–23. joint as well as significant inferomedial wear to the polyethylene insert. This was likely due to instability as a result of inadequate tension on Article ID: 100007O03AR2017 the deltoid muscle, inadequate liner size, early hypermobility, downward tilt of the glenoid, and failure to lateralize the component sufficiently.
    [Show full text]