DOCSLIB.ORG

Biomaterials and the Foreign Body Reaction: Surface Chemistry Dependent Macrophage Adhesion, Fusion, Apoptosis, and Cytokine Production

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Biomaterials and the Foreign Body Reaction: Surface Chemistry Dependent Macrophage Adhesion, Fusion, Apoptosis, and Cytokine Production BIOMATERIALS AND THE FOREIGN BODY REACTION: SURFACE CHEMISTRY DEPENDENT MACROPHAGE ADHESION, FUSION, APOPTOSIS, AND CYTOKINE PRODUCTION by JACQUELINE ANN JONES Submitted in partial fulfillment of the requirements For the degree of Doctor of Philosophy Dissertation Advisor: James Morley Anderson, M.D., Ph.D. Department of Biomedical Engineering CASE WESTERN RESERVE UNIVERSITY May, 2007 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the dissertation of ______________________________________________________ candidate for the Ph.D. degree *. (signed)_______________________________________________ (chair of the committee) ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ (date) _______________________ *We also certify that written approval has been obtained for any proprietary material contained therein. Copyright © 2007 by Jacqueline Ann Jones All rights reserved iii Dedication This work is dedicated to… My ever loving and ever supportive parents: My mother, Iris Quiñones Jones, who gave me the freedom to be and to dream, inspires me with her passion and courage, and taught me the true meaning of friendship. My father, Glen Michael Jones, a natural-born teacher who taught me to be an inquisitive student of life, inspires me with his strength and perseverance, and gave me his kind, earnest heart that loves deeply and always strives to improve the lives of others. And to my younger siblings: Angie, the yin to my yang whose resoluteness and grace continually inspires me & Jeff, my comrade whose wit and charisma brings me joy …both of whom I am ever proud. Thank you. I am truly blessed to know and love you. iv Table of Contents Chapter I: Introduction Chapter II: Proteomic Analysis and Quantification of Cytokines and Chemokines from Biomaterial Surface-Adherent Macrophages and Foreign Body Giant Cells Chapter III: Matrix Metalloproteinases and Their Inhibitors in the Foreign Body Reaction on Biomaterials Chapter IV: The Effects of Hydrophobic, Hydrophilic, & Ionic Surface Chemistries on Cellular Behaviors Chapter V: In vitro and in vivo Macrophage Behaviors on Surface Modified Polyurethanes Chapter VI: Dynamic Systems Model of Cellular Interactions with Biomaterial Surfaces Chapter VII: Conclusions Appendix: Self-Assembled Monolayers as a Model Material System for Material-Dependant Analysis of Macrophage/FBGC Cellular Behaviors v List of Tables Table 1.1. Adhesive Nature of Common Biomaterials. Table 1.2. Water Contact Angles of Clinically and Experimentally Utilized Polymers Table 1.3. Important Cytokines Involved in Inflammation. Table 1.4. Summary of Previous Findings of Macrophage-Derived Cytokine mRNA Expression. Table 2.1. Surface Chemistries of the Photografted Polymers. Table 2.2. Potential Differences in Cytokines/Chemokines Due to Material, Time, or IL-4 Addition as Analyzed by Cytokine Arrays Table 3.1. Matrix Metalloproteinases and their Functions Table 3.2. MMPs/TIMPs Detected in Cell Cultures at Day 7 using Antibody Arrays Table 3.3. MMP/TIMP Concentrations in Cell Cultures with RGD Substrate Over Time (ng/mL) Table 4.1. Comparison of Alternatively Activated and Classically Activated Macrophages Table 5.1. Chemical Description of Polyurethane Materials Table 5.2. Water Contact Angle Measurements on Polyurethane Materials Table 5.3. Differential Cell Analysis of Cell Layers at Day 4 Table 6.1. Estimated Rate Constants Utilized in Model Simulations Table 6.2. Effects of Material-Dependent Parameters on Cellular Behavior Table 6.3. Sensitivity Ranges for Each Parameter Table A.1. AFM Results for in-house SAM Surfaces Prior to and After Treatment Table A.2. Mixed Monocyte and Lymphocyte Non-Adherent Cell Population vi Table A.3.A. Commonly Used and Chosen Self-Assembled Monolayer Synthesis Techniques (Part I) Table A.3.B. Commonly Used and Chosen Self-Assembled Monolayer Synthesis Techniques (Part II) vii List of Figures Figure 1.1. Biological Responses to an Implanted Biomaterial Device. Figure 1.2. Relationship of Aqueous Contact Angles and Cell Adhesion. Adapted from reference [11]. Conditionally (non)adhesive surfaces will typically depend on the degree of hydration of the hydrophilic surface. Hence, hydrated PEG/PEO is conditionally (non)adhesive, while glass is adhesive. Aqueous adhesion o tension is defined as τ = γlvcosθ(dyne/cm). Figure 1.3. The Progression of Monocytes, Macrophages, and Foreign Body Giant Cells. Figure 1.4. Cascade of Events Involved in Apoptosis. Figure 1.5. The tissue/implant interface with protein adsorption, macrophage adhesion and activation, cytokine and growth factor production, and cellular synthesis and proliferation. Figure 2.1. Cellular/Biomaterial/Cytokine Interactions of Inflammation and Wound Healing. Figure 2.2. Adherent Cell Densities (A) and FBGC Formation (B). Data represents the mean ± the standard error of the mean (n=3). “*” indicates statistical significance in comparison to PET (p<0.05). Figure 2.3. IL-1β (A), IL-6 (B), and IL-10 (C) Cytokine Production from Macrophages and FBGCs Adherent to Photograft Polymers. Mean ± SEM, n=4. Figure 2.4. Effect of IL-4 on IL-10 (A&B), IL-8 (C&D), and MIP-1β (E&F) Production at days 7 and 10. Closed: without IL-4. Open: with added IL-4. Mean ± SEM, n=4. Figure 2.5. Chemokine IL-8 (A) and MIP-1β (B) Expression over Time. “*” indicates a statistical difference in comparison to all other materials, while “^” indicates a statistical difference in comparison to PET. Mean ± SEM, n=4. Figure 2.6. Cellular activation as a Function of IL-1β (A), IL-6 (B) and IL-10 (C) Production per Cell. Mean ± SEM, n=3. Figure 2.7. IL-8 (A) and MIP-1β (B) Production per Cell. Mean ± SEM, n=3. viii Figure 3.1. Macrophage/FBGC Secretion of Matrix Metalloproteinase-9 (A) and Tissue Inhibitors of Matrix Metalloproteinases, TIMP-1 (B) and TIMP-2 (C). Mean ± SEM, n=4. Figure 3.2. Effect of IL-4 on MMP-9 (A&B), TIMP-1 (C&D), TIMP-2 (E&F) Production at Days 7 and 10. Open: with added IL-4. Closed: without IL-4. “*” indicates statistical difference between with and without IL-4. Mean ± SEM, n=4. Figure 3.3. MMP-9 (A), TIMP-1 (B), and TIMP-2 (C) Production per Cell. Mean ± SEM, n=3. Figure 3.4. The Effects of MMP Pharmalogical Inhibitors ECG (A), NNGH (B), CL-82198 (C), and Actinonin (D) on Macrophage Adhesion (■) and Fusion (●). Mean ± SEM, n=3. Figure 4.1. Disparate Effects of Hydrophobic and Hydrophilic Surfaces on Macrophage Adhesion (A) and Fusion (B). Mean ± SEM, n=3. “*” indicates that these values for the hydrophilic surface are statistically less than the hydrophobic surface values (p<0.05). Figure 4.2. Disparate Effects of Hydrophilic Non-Ionic and Ionic Surfaces on Macrophage Adhesion (A) and Fusion (B). Mean ± SEM, n=3. “*” indicates that these values for the hydrophilic/ionic surfaces are statistically greater than the hydrophilic/neutral surface values (p<0.05). Figure 4.3. Direct Comparison of Cellular Adhesion (A), Cytokine Concentration (B), and Cellular Activation (C) on Hydrophobic and Hydrophilic/Neutral Surfaces. Cellular activation equals cytokine concentration measured in 1mL of media normalized to the total number of adherent cells. Mean ± SEM, n=3,4. “*” indicates that these values for the hydrophilic surface are statistically less than the hydrophobic surface values (p<0.05). Figure 4.4. Cytokine/Chemokine Concentration (A-D) and Cellular Activation (E-H) on Hydrophobic and Hydrophilic/Neutral Surfaces. Cellular activation equals cytokine/chemokine concentration measured in 1mL of media normalized to the total number of adherent cells. Notated numbers indicate the x fold increase between the values for BDEDTC and PAAm. Mean ± SEM, n=3. “*” indicates that values statistically greater on the hydrophilic surface compared to the hydrophobic surface values (p<0.05). Figure 4.5. MMP/TIMP Concentration (A-C) and Cellular Activation (D-F) on Hydrophobic and Hydrophilic/Neutral Surfaces. Cellular activation equals cytokine concentration measured in 1mL of media ix normalized to the total number of adherent cells. Notated numbers indicate the x fold change between the values for BDEDTC and PAAm. Mean ± SEM, n=3. “*” indicates that values statistically greater on the hydrophilic surface compared to the hydrophobic surface values (p<0.05). Figure 4.6. Cytokine/Chemokine Concentration (A-E) and Cellular Activation (E-J) on Hydrophilic/Neutral and Hydrophilic/Ionic Surfaces. Cellular activation equals cytokine/chemokine concentration measured in 1mL of media normalized to the total number of adherent cells. Notated numbers indicate the x fold increase between the values for PAAm and PAANa or DMAPAAmMeI. Mean ± SEM, n=3. “*” indicates that values statistically greater on the hydrophilic/neutral surface compared to the hydrophilic/ionic surface values (p<0.05). Figure 4.7. MMP/TIMP Concentration (A-C) and Cellular Activation (D-F) on Hydrophilic/Neutral and Hydrophilic/Ionic Surfaces. Cellular activation equals cytokine/chemokine concentration measured in 1mL of media normalized to the total number of adherent cells. Notated numbers indicate the x fold increase between the values for PAAm and PAANa or DMAPAAmMeI. Mean ± SEM, n=3. “*” indicates that values statistically greater on the hydrophilic/neutral surface compared to the hydrophilic/ionic surface values (p<0.05). Figure 5.1. Monocyte/Macrophage Adhesion on Modified and Unmodified
Load more

Recommended publications
  • Thrombokinetics in Giant Cell Arteritis, with Special Reference to Corticosteroid Therapy
    Ann Rheum Dis: first published as 10.1136/ard.38.3.244 on 1 June 1979. Downloaded from Annals of the Rheumatic Diseases, 38, 1979, 244-247 Thrombokinetics in giant cell arteritis, with special reference to corticosteroid therapy ANNA-LISA BERGSTROM, BENGT-AKE BENGTSSON, LARS-BERTIL OLSSON, BO-ERIC MALMVALL, AND JACK KUTTI From the Departments of Internal Medicine and Infectious Diseases, Eastern Hospital, University of Gothenburg, S-416 85 Gothenburg, Sweden SUMMARY Duplicate platelet survival studies were carried out on 8 patients with giant cell arteritis (GCA), once before the institution of any therapy, and the second time when they were in a com- pletely asymptomatic phase after having received corticosteroid treatment. The time interval be- tween the studies ranged between 5 and 14 months. In the first study the mean peripheral platelet count was 486 ±25 x 109/1 and in the second 326 ±25 x 109/1. The difference between the means was highly significant (P<0 001). The mean life-span of the platelets was normal in the duplicate experiments (6 * 7 ±0 * 3 and 7 *3 ±0 *4 days, respectively). Platelet production rate was significantly (P<0 001) raised in the first experiment but became normal in response to corticosteroid therapy. It is concluded that the thrombocytosis seen in GCA is reactive to the inflammation present in this disease, and it seems reasonable to assume that the reduction in the peripheral platelet count which occurs in response to corticosteroid therapy accurately reflects the clinical improvement of the patient. Thrombocytosis is frequently present in patients Table 1 Eight patients with GCA in whom duplicate platelet sutrvival studies were carried out with untreated giant cell arteritis (GCA) (Olhagen, http://ard.bmj.com/ 1963; Hamrin, 1972; Malmvall and Bengtsson, Patients Age Sex Time interval Maintenance.
    [Show full text]
  • A Case of Discoid Lupus Erythematosus Masquerading As Acne
    Letters to the Editor 175 A Case of Discoid Lupus Erythematosus Masquerading as Acne Anastasios Stavrakoglou, Jenny Hughes and Ian Coutts Department of Dermatology, Hillingdon Hospital, Pield Heath Road, Uxbridge UB8 3NN, UK. E-mail: [email protected] Accepted July 4, 2007. Sir, On examination he had a widespread acneiform eruption, We describe here a case of discoid lupus erythemato- which was distributed on his face, pre-sternal area and back, particularly down the length of his spine. He had multiple sus (DLE) masquerading as acne vulgaris. Cutaneous brown-red follicular papules and open comedones, especially manifestations of lupus erythematosus (LE) are usually on his back, and hypopigmented atrophic scars. There were no characteristic enough to permit straightforward diagnosis. pustules or nodulocystic lesions (Fig. 1). However, occasionally they may be variable and mimic Treatment was started with erythromycin 500 mg bid and other dermatological conditions. adapalene cream once daily to treat a presumed diagnosis of acne vulgaris. He was seen 3 months later with a deterioration Acneiform presentation is one of the most rarely re- of his clinical appearance and increased pruritus. This was ported and one of the most confusing, as it resembles a attributed by the patient to increased sun exposure. The photo- very common inflammatory skin disease and therefore aggravation, the intense pruritus and the absence of pustules can be easily missed clinically. Only 5 cases have been and nodulocystic lesions broadened our differential diagnosis reported in the literature (1–4). The patient described and therefore diagnostic biopsies were obtained. A biopsy from the back where the rash was most suggestive clinically here presented with a widespread pruritic acneiform of acne vulgaris, showed hyperkeratosis with orthokeratosis, rash, which was initially diagnosed and treated as epidermal atrophy and extensive vacuolar degeneration of the acne vulgaris with no response.
    [Show full text]
  • Review Article
    J Clin Pathol: first published as 10.1136/jcp.36.7.723 on 1 July 1983. Downloaded from J Clin Pathol 1983;36:723-733 Review article Granulomatous inflammation- a review GERAINT T WILLIAMS, W JONES WILLIAMS From the Department ofPathology, Welsh National School ofMedicine, Cardiff SUMMARY The granulomatous inflammatory response is a special type of chronic inflammation characterised by often focal collections of macrophages, epithelioid cells and multinucleated giant cells. In this review the characteristics of these cells of the mononuclear phagocyte series are considered, with particular reference to the properties of epithelioid cells and the formation of multinucleated giant cells. The initiation and development of granulomatous inflammation is discussed, stressing the importance of persistence of the inciting agent and the complex role of the immune system, not only in the perpetuation of the granulomatous response but also in the development of necrosis and fibrosis. The granulomatous inflammatory response is Macrophages and the mononuclear phagocyte ubiquitous in pathology, being a manifestation of system many infective, toxic, allergic, autoimmune and neoplastic diseases and also conditions of unknown The name "mononuclear phagocyte system" was aetiology. Schistosomiasis, tuberculosis and leprosy, proposed in 1969 to describe the group of highly all infective granulomatous diseases, together affect phagocytic mononuclear cells and their precursors more than 200 million people worldwide, and which are widely distributed in the body, related by http://jcp.bmj.com/ granulomatous reactions to other irritants are a morphology and function, and which originate from regular occurrence in everyday clinical the bone marrow.' Macrophages, monocytes, pro- histopathology. A knowledge of the basic monocytes and their precursor monoblasts are pathophysiology of this distinctive tissue reaction is included, as are Kupffer cells and microglia.
    [Show full text]
  • 2016 Essentials of Dermatopathology Slide Library Handout Book
    2016 Essentials of Dermatopathology Slide Library Handout Book April 8-10, 2016 JW Marriott Houston Downtown Houston, TX USA CASE #01 -- SLIDE #01 Diagnosis: Nodular fasciitis Case Summary: 12 year old male with a rapidly growing temple mass. Present for 4 weeks. Nodular fasciitis is a self-limited pseudosarcomatous proliferation that may cause clinical alarm due to its rapid growth. It is most common in young adults but occurs across a wide age range. This lesion is typically 3-5 cm and composed of bland fibroblasts and myofibroblasts without significant cytologic atypia arranged in a loose storiform pattern with areas of extravasated red blood cells. Mitoses may be numerous, but atypical mitotic figures are absent. Nodular fasciitis is a benign process, and recurrence is very rare (1%). Recent work has shown that the MYH9-USP6 gene fusion is present in approximately 90% of cases, and molecular techniques to show USP6 gene rearrangement may be a helpful ancillary tool in difficult cases or on small biopsy samples. Weiss SW, Goldblum JR. Enzinger and Weiss’s Soft Tissue Tumors, 5th edition. Mosby Elsevier. 2008. Erickson-Johnson MR, Chou MM, Evers BR, Roth CW, Seys AR, Jin L, Ye Y, Lau AW, Wang X, Oliveira AM. Nodular fasciitis: a novel model of transient neoplasia induced by MYH9-USP6 gene fusion. Lab Invest. 2011 Oct;91(10):1427-33. Amary MF, Ye H, Berisha F, Tirabosco R, Presneau N, Flanagan AM. Detection of USP6 gene rearrangement in nodular fasciitis: an important diagnostic tool. Virchows Arch. 2013 Jul;463(1):97-8. CONTRIBUTED BY KAREN FRITCHIE, MD 1 CASE #02 -- SLIDE #02 Diagnosis: Cellular fibrous histiocytoma Case Summary: 12 year old female with wrist mass.
    [Show full text]
  • Dermatose Degenerativa Induzida Por D-Penicilamina Em Paciente Com Doença De Wilson
    Revista SPDV 76(2) 2018; D-Penicillamine induced degenerative dermopathy; Rui Pedro Santos, Joana Gomes, Celeste Brito. Caso Clínico Dermatose Degenerativa Induzida por D-penicilamina em Paciente com Doença de Wilson Rui Pedro Santos1, Joana Gomes2, Celeste Brito2 1Interno de Dermatovenereologia/Resident, Dermatovenereology, Hospital de Braga, Braga, Portugal 2Especialista de Dermatovenereologia/Specialist of Dermatovenereology, Hospital de Braga, Braga, Portugal RESUMO – As dermatoses degenerativas induzidas por D-penicilamina incluem, entre outras, a elastose perfurante serpiginosa e o pseudo-pseudoxantoma elástico. A elastose perfurante serpiginosa é uma doença perfurante rara caracterizada pela elimi- nação transepidérmica de fibras elásticas anormais. Esta condição pode ser idiopática, reativa ou induzida por D-penicilamina, habitualmente utilizada para o tratamento da doença de Wilson, cistinúria, artrite reumatóide ou esclerose sistémica. Manifesta- ções cutâneas semelhantes a pseudoxantoma elástico mas sem história familiar e mutações do gene ABCC6 foram identificadas como sendo uma dermatose induzida por D-penicilamina e designada de pseudo-pseudoxantoma elástico. Descreve-se o caso de uma mulher de 17 anos tratada por vários anos com D-penicilamina para doença de Wilson, com pápulas assintomáticas, algumas cor de pele e hiperqueratósicas e outras macias e amareladas, na região cervical e face. A histopatolo- gia mostrou a eliminação transepidérmica de fibras elásticas espessadas, em forma de dentes de serra. Estes achados sugeriram uma dermopatia induzida por D-penicilamina e os autores consideraram o diagnóstico de elastose perfurante serpiginosa e pseudo-pseudoxantoma elástico no mesmo paciente. O fármaco foi alterado para acetato de zinco sem lesões novas, mas com manutenção das lesões existentes no seguimento a 1 ano.
    [Show full text]
  • Analysis of Nine Cases of Oral Foreign Body Granuloma Related to Biomaterials
    J Biosci (2019) 44:78 Ó Indian Academy of Sciences DOI: 10.1007/s12038-019-9898-y (0123456789().,-volV)(0123456789().,-volV) Analysis of nine cases of oral foreign body granuloma related to biomaterials 1 1 1 LARISSA SANTOS AMARAL ROLIM ,CAIO CE´ SAR DA SILVA BARROS ,JULIANA CAMPOS PINHEIRO , 2 2 PATRI´CIA TEIXEIRA DE OLIVEIRA ,LE´ LIA BATISTA DE SOUZA and 3 PEDRO PAULO DE ANDRADE SANTOS * 1Oral Pathology Post-Graduation Program Student, Federal University of Rio Grande do Norte, Natal, RN, Brazil 2Oral Pathology Post-Graduation Program, Dentistry Department, Federal University of Rio Grande do Norte, Natal, RN, Brazil 3Oral Pathology Post-Graduation Program, Morphology Department, Federal University of Rio Grande do Norte, Natal, RN, Brazil *Corresponding author (Email, [email protected]) MS received 16 September 2018; accepted 10 April 2019; published online 2 August 2019 Foreign bodies can penetrate the interior of soft and, sometimes, hard, tissues in various ways, including through open wounds, lacerations and traumatic accidents. However over the years, evidence of links between the use of dental materials and lately, significant involvement of aesthetic filler materials as foreign bodies in the oral and perioral region have been reported. Foreign body granulomas (FBGs) may develop from this exogenous material, histopathologically characterized by the presence of chronic inflammation and a high amount of macrophages. This study presents nine FBG cases affecting the oral and perioral regions, and carries out a literature review on the main clinical, histopathological and material characteristics used in dental and dermatological procedures related to the appearance of this type of granuloma. Keywords.
    [Show full text]
  • Malignant Tenosynovial Giant Cell Tumor: the True €Œsynovial Sarcoma?€• a Clinicopathologic, Immunohistochemical
    Modern Pathology (2019) 32:242–251 https://doi.org/10.1038/s41379-018-0129-0 ARTICLE Malignant Tenosynovial Giant Cell Tumor: The True “Synovial Sarcoma?” A Clinicopathologic, Immunohistochemical, and Molecular Cytogenetic Study of 10 Cases, Supporting Origin from Synoviocytes 1 2 1 1 1 3 Alyaa Al-Ibraheemi ● William Albert Ahrens ● Karen Fritchie ● Jie Dong ● Andre M. Oliveira ● Bonnie Balzer ● Andrew L. Folpe1 Received: 5 July 2018 / Revised: 31 July 2018 / Accepted: 1 August 2018 / Published online: 11 September 2018 © United States & Canadian Academy of Pathology 2018 Abstract We present our experience with ten well-characterized malignant tenosynovial giant cell tumors, including detailed immunohistochemical analysis of all cases and molecular cytogenetic study for CSF1 rearrangement in a subset. Cases occurred in 7 M and 3 F (mean age: 52 years; range: 26–72 years), and involved the ankle/foot (n = 1), finger/toe (n = 3), wrist (n = 1), pelvic region (n = 3), leg (n = 1), and thigh (n = 1). There were eight primary and two secondary malignant 1234567890();,: 1234567890();,: tenosynovial giant cell tumors. Histologically, all cases showed definite areas of typical tenosynovial giant cell tumor. The malignant areas varied in appearance. In some cases, isolated malignant-appearing large mononuclear cells with high nuclear grade and mitotic activity were identified within otherwise-typical tenosynovial giant cell tumor, as well as forming larger masses of similar-appearing malignant cells. Occasionally, these nodules of malignant large mononuclear cells showed transition to pleomorphic spindle cell sarcoma, with varying degrees of collagenization and myxoid change. One malignant tenosynovial giant cell tumor was composed of sheets of monotonous large mononuclear cells with high nuclear grade, growing in a hyalinized, osteoid-like matrix, with areas of heterologous osteocartilaginous differentiation.
    [Show full text]
  • The Pathogenesis of Giant Cell Arteritis: Morphological Aspects
    The morphology of GCA / C. Nordborg et al. The pathogenesis of giant cell arteritis: Morphological aspects C. Nordborg1, E. Nordborg2, V. Petursdottir1 1Department of Pathology, 2Department of ABSTRACT in GCA. When studying V-beta families Rheumatology, Sahlgrenska University The light-microscopic, electron-micro- of the T-cell infiltrate with flow cyto- Hospital, Göteborg, Sweden. scopic and immunocytochemical charac- metry, Schaufelberger et al. found that These studies were supported by grants teristics of giant cell arteritis (GCA) the infiltrating lymphocytes are polyclo- from the Göteborg Medical Society, the have been investigated in a number of nal (3). On the other hand, Weyand et Swedish Heart-Lung Foundation, the studies on temporal arteries. Arterial al. (4) demonstrated the identical clonal Swedish Rheumatism Association, Rune atrophy and calcification of the internal expansion of a small proportion of the och Ulla Amlöfs Stiftelse and Syskonen elastic membrane appear to be prere- T-lymphocytes in separate segments of Holmströms Donationsfond. quisites for the evolution of the inflam- the same artery, which indicates antigen Please address correspondence and reprint matory process. Foreign body giant cells stimulation. A correlation between va- requests to: Claes Nordborg, Department form close to calcifications, apparently rious infections and the onset of GCA of Pathology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden. without connection with other inflam- has been reported; it has been speculated E-mail: [email protected] matory cells and probably by the fusion that infectious disorders might trigger the of modified vascular smooth muscle inflammatory process (5). Zoster-vari- Clin Exp Rheumatol 2000: 18 (Suppl. 20): cells.
    [Show full text]
  • Double Layer Continuous Intradermal Sutures in Keloid Operation
    erimenta xp l D E e r & m l a a t c o i l n o i Journal of Clinical & Experimental Wang and Long, J Clin Exp Dermatol Res 2014, 5:1 l g y C f R DOI: 10.4172/2155-9554.1000205 o e l ISSN: 2155-9554 s a e n a r r u c o h J Dermatology Research Research Article Open Access Double Layer Continuous Intradermal Sutures in Keloid Operation Youbin Wang* and Xiao Long Plastic Surgery Department, Peking Union Medical College Hospital, Peking, China Abstract Objective: Keloid offten occurs on chest wall, shoulder and back. Surgical incision and postoperative radiation is an effective method in keloid treatment. Many of the wound in these places can be directly closed after keloids being removed. Recurrence prevention and cosmetic result should all be considered. Operation method especially suture method is one of the key issues which determine the treatment result. Many methods have been developed. However, many of them are designated to prevent recurrence. Cosmetic result is not fully considered. In this article, we reported a new suture method which is with good treatment and cosmetic results in our clinical study. Methods: One hundred and thirty-three patients with chest keloids were treated from 2006 to 2011. Double layer continuous intradermal suture was used in fifty four patients, interrupted epidermal suture was used in forty one patients, and one layer continuous intradermal suture was used in thirty eight patients. All operation sites were treated with radiotherapy on the first and seventh postoperative day. The follow-up time was from 9 to 26 months.
    [Show full text]
  • Foreign Body Granulomatous Reactions to Cosmetic Fillers
    J Clin Exp Dent. 2012;4(4):e244-7. Foreign body granulomatous reactions. Journal section: Oral Medicine and Pathology doi:10.4317/jced.50868 Publication Types: Review http://dx.doi.org/10.4317/jced.50868 Foreign body granulomatous reactions to cosmetic fillers Laura Carlos-Fabuel, Cristina Marzal-Gamarra, Silvia Martí-Álamo, Aisha Mancheño-Franch DDS. Master in Oral Medicine and Surgery. University of Valencia. Valencia (Spain). Correspondence: Clínica Odontológica Gascó Oliag 1 46021 – Valencia (Spain) E-mail: [email protected] Carlos-Fabuel L, Marzal-Gamarra C, Martí-Álamo S, Mancheño-Franch A. Foreign body granulomatous reactions to cosmetic fillers. J Clin Exp Received: 02/05/2012 Dent. 2012;4(4):e244-7. Accepted: 04/05/2012 http://www.medicinaoral.com/odo/volumenes/v4i4/jcedv4i4p244.pdf Article Number: 50868 http://www.medicinaoral.com/odo/indice.htm © Medicina Oral S. L. C.I.F. B 96689336 - eISSN: 1989-5488 eMail: [email protected] Indexed in: Scopus DOI® System Abstract Introduction: The use of different facial cosmetic fillers has increased in recent years. The introduction of appa- rently inert substances in the epidermis can give rise to foreign body granulomatous reactions. Objetives: A literature review is made of the foreign body granulomatous reactions to cosmetic fillers. Material and methods: A PubMed-Medline search was made using the following keywords: “granulomatous reac- tions”, “foreign body reactions”, “esthetic fillers”, “cosmetic fillers”. The search was limited to articles published in English and Spanish during the last 10 years. A total of 22 articles were reviewed. Results: A great variety of substances have been found to give rise to foreign body granulomatous reactions.
    [Show full text]
  • An Unusual Cause of Hyperkeratosis
    An Unusual Cause of Hyperkeratosis Dr. J. White, ST5 Histopathology, Dr. A. Bakshi, Consultant Dematopathologist Clinical Presentation • 43-year-old • Two and a half year history • Pink/light brown papules, some of which appeared scaly and keratotic • Started on her ankle and lower legs and spread to her thighs, arms and neck Clinical Presentation Histology Differential Diagnosis • 1) Keratosis pilaris • 2) Lichen planus • 3) Hyperkeratosis follicularis et parafollicularis in cutem pentetrans (Kyrle’s disease) • 4) Hyperkeratosis lenticularis perstans (Flegel’s disease) • 5) Lichenoid drug reaction Keratosis Pilaris 1 • Peak in adolescence 2 • Association with ichthyosis vulgaris • Pruritic, follicular papules & pustules • Lateral aspect arms & thighs • Histology – follicular dilatation & keratin plugs • May contain distorted hair shafts Lichen Planus 3 • Violaceous papules 4 • Intensely pruritic • Flexor aspects wrists & forearms, extensor aspects hand & ankles • Histology - Interface dermatitis • Irregular acanthosis • (Wedge-shaped) Hypergranulosis Kyrle’s Disease 5 • Similar clinical presentation 6 to our patient (age, gender, distribution), palms & soles classically spared • Histology- epidermal invagination containing keratotic plug & basophilic debris • Eventual perforation into dermis with associated foreign-body reaction & subsequent transepidermal elimination Lichenoid Drug Reaction 7 • Clinically similar presentation to lichen 8 planus • Gold, anti-malarials, penicillamine, captopril, β-blockers, TNF-α inhibitors • May be a
    [Show full text]
  • An Algorithmic Approach to Hypertrophic Scars and Keloids: Maximizing Nonsurgical Options
    AN ALGORITHMIC APPROACH TO HYPERTROPHIC SCARS REVIEW An Algorithmic Approach to Hypertrophic Scars and Keloids: Maximizing Nonsurgical Options Shauna Kranendonk, MD; Suzan Obagi, MD Hypertrophic scars and keloids are very common concerns among dermatologic patients, whether from a medical or cosmetic standpoint. The treatment of these lesions is challenging and associated with variable response or recurrence. The authors of this study review the most current literature on the treatment of hypertrophic scars and keloids ranging from intralesional therapies to laser and surgical modalities. The authors describe a treatment algorithm employing combination therapies while aiming to limit the use of surgical intervention. Representative case reports are presented to illustrate the use of solo orCOS combination therapy. DERM ypertrophic scars and keloids are rou- keloidal scarring and result in superior cosmetic and tinely encountered in the cosmetic der- functional outcomes. matology setting. Patients either present This article will review factors contributing to hyper- Dowith cosmetic concernsNot or have symp- trophic Copyscars and keloids and present an algorithmic toms of pain and/or pruritus associated approach for treatment of these lesions (Figure 1). The Hwith these lesions. Occasionally, there may be a func- emphasis will be on maximizing nonsurgical interven- tional component if the scar interferes with movement tion due to the risk of recurrence associated with exci- of the involved area. sion of these lesions. Intralesional corticosteroids have been a mainstay of treatment, but numerous alternative modalities are BACKGROUND available. Proper sequential use of these modalities, Hypertrophic scars differ clinically from keloids, in that particularly when used early in the course of disease, hypertrophic scars do not grow beyond the boundaries can impede the development of hypertrophic and of the original wound, while keloids grow horizontally beyond the margins of the original wound.1 Hypertro- Dr.
    [Show full text]