DOCSLIB.ORG

Research Article Ki-67 and MCM-2 in Dental Follicle and Odontogenic Cysts: the Effects of Inflammation on Proliferative Markers

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Research Article Ki-67 and MCM-2 in Dental Follicle and Odontogenic Cysts: the Effects of Inflammation on Proliferative Markers The Scientific World Journal Volume 2012, Article ID 946060, 8 pages The cientificWorldJOURNAL doi:10.1100/2012/946060 Research Article Ki-67 and MCM-2 in Dental Follicle and Odontogenic Cysts: The Effects of Inflammation on Proliferative Markers Nurhan Guler,¨ 1 Nil C¸omunoglu,˘ 2, 3 and Fatih Cabbar1 1 Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Yeditepe University, No. 238 Bagdat Cd, 34728 Goztepe, Istanbul, Turkey 2 Pathology Service, Haydarpas¸a Hospital, 34668 Uskudar, Istanbul, Turkey 3 Department of Pathology, Faculty of Medicine, Yeditepe University, 34755 Istanbul, Turkey Correspondence should be addressed to Nurhan Guler,¨ [email protected] Received 25 February 2012; Accepted 12 April 2012 Academic Editors: A. Baldi and S. E. Hiscox Copyright © 2012 Nurhan Guler¨ et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The aim of this study was to investigate whether there is any association between inflammation and the expression of markers of cell cycle entry (Ki-67 and MCM-2) in dental follicle (DF) of asymptomatic impacted teeth and odontogenic cysts. The study consisted of 70 DFs and 20 odontogenic cysts (radicular cyst (RC), dentigerous cyst (DC) and keratocytic odontogenic tumor (KCOT) located at posterior mandibular region. Histological findings of inflammation for all specimen and mucous cell prosoplasia, squamous metaplasia, glandular epithelium for all DFs were stained with hematoxyline and eosin, periodic acid schiff, alcian blue, and mucin. Epithelial cell proliferation was determined by using immunohistochemical labeling for Ki-67 and MCM-2. The histologic examinations showed 16% mucous cell prosoplasia, 54% squamous metaplasia, 20% glandular epithelium, 37% inflammation. Inflammation was detected in all RCs and %62 in DF, %43 in DC and KCOT. Positive correlation was found between the inflammation of DF and odontogenic cysts (P<0.01). The mean Ki-67 and MCM-2 expressions were found 9, 64 ± 5, 99 and 6, 34 ± 3, 81 in DF, 11, 85 ± 9, 01 and 13, 6 ± 9, 94 in odontogenic cysts, respectively. While the mean Ki-67 expressions were statistically significant in DF and KCOT (P<0.01), MCM-2 were significant in RC and KCOT (P<0.01). MCM-2 expresion in RCs were statistically significant than KCOT (P<0.01). The results of this study indicated that the higher MCM-2 expressions in RC than the KCOT might be related to the inflammation and this protein might be more sensitive to inflammation. 1. Introduction is an odontogenic cyst of inflammatory stimulation of the epithelial rests of Malassez [5]. DC presents clinically as an Odontogenic cysts, osteodestructive lesions affecting jaws, aymptomatic unilocular radiolucency enclosing the crown of are arise from epithelial cells of dental follicle (DF) or from an unerupted or impacted tooth [3], and it can transform the remnants of odontogenic epithelium such as reduced into more serious lesions, such as unicystic ameloblastoma enamel epithelium, malessez, hertwig epithelial shield, or [6]. Keratocystic odontogenic tumor (formerly odontogenic rests of serres [1]. The most common cysts originated keratocysts, KOCT) is a unique cyst because of its locally from these odontogenic cells are dentigerous cyst (DCs), aggressive behavior, high recurrence rate, and characteristic keratocytic odontogenic tumor (KCOTs), and calcified odon- histological appearance [4]. RCs, DCs, and KCOTs show togenic tumor [2, 3]. It is well known that the epithelial distinct growth patterns and biological behaviors. Increased linings of both inflammatory and developmental cysts of activity of the epithelium, confirmed by previous study that odontogenic origin are primarily composed of squamous has compared KCOTs with other odontogenic cysts, may epithelium, but various forms of metaplasia and degenera- explain the high recurrence rates of KCOTs [7]. tion are observed in these epithelial linings such as mucous Cell proliferation plays an important role in several cells, ciliated cells, para and/or ortho-hyperkeratinization, biological and pathological events such as oral cysts and and formation of hyaline bodies [4]. Radicular cyst (RC) tumors [5, 7, 8]. The proliferative potential can be assessed by 2 The Scientific World Journal immunohistochemistry using monoclonal antibodies against enlarged tissues surrounding impacted third molars and 20 specific cell cycle associated proteins. The proliferative activ- inflammatory and developmental odontogenic cysts located ity of the epithelial lining of odontogenic cysts more particu- at the posterior mandibular region (of 6 RCs, 7 DCs and 7 larly in KCOTs has been the subject of various investigations KCOTs) were included. Fifty females and 20 males (mean age examining the expressions of p53, proliferating cell nuclear 27 years, range 16–68 years) were included in DFs group and antigen (PCNA), Ki-67, as well as nucleolar organiser regions seven females and 13 males (mean age 39 years, range 22–67 (AgNORs) [5, 7–10]. Among the immunohistochemical cell years) were included in odontogenic cysts group. The study cycle markers, the monoclonal antibody Ki-67 has been the was approved by Yeditepe University clinical investigations most widely used, which labels all active parts of the cell cycle, ethic committee (2006) and informed consent was obtained rises during the second half of the S phase, reaches a peak from all participating patients. in the G2 and M phases, and rapidly degrades after mitosis DFs of impacted teeth were carried out under local with a half life of detectable antigen being an hour or less. It anesthesia by conventional third molar surgery and biopsy can be expressed actively in proliferating cells, in particular, taken from odontogenic cyst. All specimens were placed neoplasms and its immunoreactivity, has been found to immediately in 10% buffered formalin and processed to correlate closely with other variables of cell proliferation paraffin wax. Sections (5 µ thick) were cut from each [7, 11]. block containing the DF and cysts specimens and stained Minichromosome maintenance proteins (MCM) expres- with hematoxylin and eosin (H&E) for routine histologic sion can be used as a new marker in the determination of examination. All slides were stained with periodic acid the proliferating cells. The main function of MCM proteins is Schiff (PAS), Alcian blue, and mucin for the evaluation of cooperation with other factors in molecular mechanisms that mucous cell prosoplasia. Histologic appearance of normal form the replication fork and in regulation of DNA synthesis. DF described by Glosser and Campbell [16]wasused MCM proteins form a ring-shaped complex, which is and any soft tissue specimens with squamous epithelium activated when other factors are bound. MCM 2–7 complex spreading along the surface of the DF were considered as is one of the prereplication factors. Association of MCM 2–7 cystic [9]. Histologically, the epithelial components consisted complex is a crucial moment initiating the replication fork. of mucous cell prosoplasia, basal epithelial cells, squamous MCM proteins play a role in maintaining genome integrity epithelium, and glandular epithelium, while mesenchymal and prevent rereplication once per cell cycle. Proliferating components were inflammation, rests of the odontogenic cells have high levels of MCM, whereas they are not detected epithelium, and calcified follicles. in quiescent, differentiated or senescent cells. Recent results Immunohistochemical method was described in our also indicate that the presence or absence of licensed origins previous study [9]. Briefly, 5 µ thickness sections were has even deeper implications for cell biology, as it might prepared for incubations of Ki-67 (ScyTek, Logan, UT; play a role in determining the proliferative capacity of 7 mL) and MCM-2 (MCM-2; CRCT2.1 [D1.9H5]; 1/100 cells [12–14]. They are also potential useful markers of dilution) antibodies according to manufacture’s instructions. cell proliferation. This protein can be observed both in Dysplastic cervix epithelium was used as a positive control cells coming out of the cell cycle and during the cellular for Ki-67 and tonsillary tissue for MCM-2. Each slide was proliferation in the normal, premalignant, and neoplastic examined under a multihead light microscope and scored cells [14, 15]. Recent studies suggested that MCMs are good by pathologist. For each of the specimens, intensity and markers of proliferation activity degree, because they are extent of Ki-67 and MCM-2 expression were evaluated by highly expressed in a variety of tumors [12]. a comprehensive scoring formula. One hundred nuclei were Under the influence of pathologic changes, however, assessed in each specimen and scored as a percentage of dental follicles that possess reduced epithelium can prolif- positively stained nuclei out of the total number of nuclei erate into stratified squamous epithelium as far as originate reprehensive microscopic fields counted. dental cysts [16]. In this way, the microscopic analysis Histologic and immunohistochemical characteristics of concomitant to immunohistochemical markers is relevant epithelial and mesenchymal components of DF and odon- for understanding the behavior of DF in and odontogenic togenic cysts were recorded and the Kruskal-Wallis test cysts. It appears that assessing the proliferative capacity of was used to compare data between groups. Two-tailed epithelial cells
Load more

Recommended publications
  • (12) Patent Application Publication (10) Pub. No.: US 2015/0353527 A1 Zisman (43) Pub
    US 20150353527A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2015/0353527 A1 Zisman (43) Pub. Date: Dec. 10, 2015 (54) NON-SELECTIVE KINASE INHIBITORS Publication Classification (71) Applicant: arence ZIAMAN, Slingerlands, NY (51) Int. Cl. (US) C07D 40/12 (2006.01) (72) Inventor: Lawrence S Zisman, Slingerlands, NY C07D 24/20 (2006.01) (US) C07D 403/2 (2006.01) (73) Assignee: PULMOKINE, INC. Slingerlands, NY (52) U.S. Cl. (US) CPC ............ C07D401/12 (2013.01); C07D 403/12 (21) Appl. No.: 14f76O139 (2013.01); C07D 241/20 (2013.01) y x- - - 9 (22) PCT Filed: Jan. 9, 2014 (57) ABSTRACT (86). PCT No.: PCT/US1.4/10778 T.S. ). L. 9, 2015 Disclosed herein are compounds, compositions, and methods e 19 for preventing and treating proliferative diseases associated Related U.S. Application Data with aberrant receptor tyrosine kinase (RTK) activity. The (60) Provisional application No. 61/751.217, filed on Jan. therapeutic indications described herein more specifically 10, 2013, provisional application No. 61/889,887, relate to the non-selective inhibition of RTKs associated with filed on Oct. 11, 2013. vascular and pulmonary disorders. Patent Application Publication Dec. 10, 2015 Sheet 1 of 26 US 2015/0353527 A1 FIG. 1A $: 8:3 $38: Coacentration (nM) FG, B C s C am u was e D 9 9 A. Concentration (nM) Patent Application Publication Dec. 10, 2015 Sheet 2 of 26 US 2015/0353527 A1 F.G. 1 C Concentration (in M) F.G. 1D c C R sa spagh d g e d A. :::::: Concentration (in M) Patent Application Publication Dec.
    [Show full text]
  • Actinomycosis Israeli, 129, 352, 391 Types Of, 691 Addison's Disease, Premature Ovarian Failure In, 742
    Index Abattoirs, tumor surveys on animals from, 823, Abruptio placentae, etiology of, 667 828 Abscess( es) Abdomen from endometritis, 249 ectopic pregnancy in, 6 5 1 in leiomyomata, 305 endometriosis of, 405 ovarian, 352, 387, 388-391 enlargement of, from intravenous tuboovarian, 347, 349, 360, 388-390 leiomyomatosis, 309 Acantholysis, of vulva, 26 Abdominal ostium, 6 Acatalasemia, prenatal diagnosis of, 714 Abortion, 691-697 Accessory ovary, 366 actinomycosis following, 129 Acetic acid, use in cervical colposcopy, 166-167 as choriocarcinoma precursor, 708 "Acetic acid test," in colposcopy, 167 criminal, 695 N-Aceryl-a-D-glucosamidase, in prenatal diagnosis, definition of, 691 718 of ectopic pregnancy, 650-653 Acid lipase, in prenatal diagnosis, 718 endometrial biopsy for, 246-247 Acid phosphatase in endometrial epithelium, 238, endometritis following, 250-252, 254 240 fetal abnormalities in, 655 in prenatal diagnosis, 716 habitual, 694-695 Acridine orange fluorescence test, for cervical from herpesvirus infections, 128 neoplasia, 168 of hydatidiform mole, 699-700 Acrochordon, of vulva, 31 induced, 695-697 Actinomycin D from leiomyomata, 300, 737 in therapy of missed, 695, 702 choriocarcinoma, 709 tissue studies of, 789-794 dysgerminomas, 53 7 monosomy X and, 433 endodermal sinus tumors, 545 after radiation for cervical cancer, 188 Actinomycosis, 25 spontaneous, 691-694 of cervix, 129, 130 pathologic ova in, 702 of endometrium, 257 preceding choriocarcinoma, 705 of fallopian tube, 352 tissue studies of, 789-794 of ovary, 390, 391 threatened,
    [Show full text]
  • MOLECULAR GENETIC MECHANISMS of ONTOGENESIS. DISORDERS of ONTOGENESIS and THEIR PLACE in HUMAN PATHOLOGY Plan 1
    Topic: MOLECULAR GENETIC MECHANISMS OF ONTOGENESIS. DISORDERS OF ONTOGENESIS AND THEIR PLACE IN HUMAN PATHOLOGY Plan 1. Ontogenesis, its periodization. 2. Embryonic development, its stages. Provisional organs. 3. Molecular and cellular mechanisms of differentiation. 4. Differentiation of embryonic leaves and tissues. Embryonic induction. 5. Critical periods of human embryonic development. Teratogenic environmental factors. 6. Congenital malformations, their modern classification: hereditary, exogenous, multifactorial; embryopathy and fetopathy; phylogenetically determined and non- phylogenetic. 7. Postembryonic human development and its periodization. Neurohumoral regulation of growth and development. 8. Aging as a stage of ontogenesis. Theories of aging. The concept of gerontology and geriatrics. 9. Clinical and biological death. Recommended literature: 1. Medical Biology : text-book / Bazhora Yu. I., Bylyk R. Ye., Chesnokova M. M. et al. 2nd ed., revised and updated. Vinnytsia : Nova Knyha, 2019. 448 p. 2. Organismic level of life organisation. Bases of human genetics. Training text-book on Medical biology (module II) for students of medical and stomatological faculties / Dubinin S.I., Ovcharenko O.V., Vatsenko A.V. et al. Poltava, 2014. 78 p. 3. Lazarev K.L. Medical Biology: Text-book. Second edition. – Simferopol: IAD CSMU, 2003. 592 p. 4. Medical biology: The study guide of the practical classes course / O.V. Romanenko, O.V. Golovchenko, M.G. Kravchuk, V.M. Grinkevych. Edited by O.V. Romanenko. – K.: Medicine, 2008. 304 p. 5. Bekish O.-Y.L. Medical biology: Textbook for students of higher educational establishments. Vitebsk: VSMU Press, 2003. 346 p. 6. Green N.P., Stout G.W., Taylor D.I. Biological Science. Cambridge, 1994. 7. Kimball, John W.
    [Show full text]
  • Benacka, MD, Phd Department of Pathophysiology Faculty of Medicine, UPJS, Slovakia
    Academic lectures for students GENERAL of medical schools – 3rd Year PATHOPHYSIOLOGY updated 2004 - 201 5 NEOPLASMS 1 CLINICAL PATHOLOGY R. A. Benacka, MD, PhD Department of Pathophysiology Faculty of Medicine, UPJS, Slovakia Templates, figures and tables herein might be adapted from various printed or electornic resources and serve strictly for educational purposes and pro bono of mankind Epidemiology Incidency of neoplasms Mortality of neoplasms Age related types of tumours Neoplasms - history Evidences of bone tumors were found in prehistoric remains of homo sapiens and predestors. Description of disease found in early writings from India, Egypt, Babylonia, and Greece . Hippocrates distinguished benign from malignant growths; introduced the term karkinos (in Latin cancer ) presumably because a cancer adheres to any part that it seizes upon in an obstinate manner like the crab. Hippocrates described in detail cancer of the breast , and in the 2nd century AD, Paul of Aegina commented on its frequency. Over the decades paleoarchaeologists have made about 200 possible cancer sightings dating to prehistoric times. The Karkinos was giant crab which oldest known case of metastasizing prostate cancer was found came to the aid of the hydra in in Scythian burial mound in the Russian region of Tuva. battle against Hérakles Terminology comes form greek and latin words: Neoplasia - the process of "new growth," and a new growth is called a neoplasm. Tumor - originally applied to the swelling caused by inflammation. Neoplasms also may induce swellings. Non- neoplastic usage of tumor has passed; the term is now equated with neoplasm. Oncology (Greek oncos = tumor) - the study of tumors. Cancer is the common term for all malignant tumors.
    [Show full text]
  • DR. RUCHIKA GUPTA Designation: Scientist C Tel: 012-2446920 E-Mail
    Name: DR. RUCHIKA GUPTA Designation: Scientist C Tel: 012-2446920 E-mail: [email protected], [email protected] Educational Qualifications: 2000 M.B.B.S., Lady Hardinge Medical College, University of Delhi, Delhi 2005 M.D. (Pathology), Maulana Azad Medical College, University of Delhi, Delhi Professional Experience: Scientist C (Apr 2015 till date) National Institute of Cancer Prevention & Research, Noida Assistant Professor & Head (May 2010 – Feb 2015) Chacha Nehru Bal Chikitsalaya, Geeta Colony, Delhi Senior Research Associate (June 2008-May 2010) All India Institute of Medical Sciences, New Delhi Senior Resident (Jan 2006-June 2008) All India Institute of Medical Sciences, New Delhi Senior Resident (Jun 2005-Jan 2006) Maulana Azad Medical College, Delhi Awards/ Honors: Dr VR Khanolkar Prize for best published research paper entitled " Focal segmental glomerulosclerosis in idiopathic membranous glomerulonephritis: a clinico-pathological and stereological study ", IAPM, Hyderabad, 2010. Best Oral Paper Prize for the paper entitled “Risk factors for calcineurin inhibitor toxicity in pediatric idiopathic steroid resistant nephrotic syndrome: an analysis of clinical and histopathological features” presented at the XXV Annual Conference of the Delhi Chapter of IAPM in April 2010. Dr R P Mathur Memorial Award for "Best III Year Outgoing Junior Resident" in Department of Pathology, 2004, MAMC, New Delhi. Prize for proficiency in Surgery, 2000-01, LHMC, New Delhi. Publications 1. Arora P, Chakravarty P, Khanna D, Gupta R. Cutis laxa autosomal recessive type II or wrinkly skin syndrome? Indian Dermatol Online J 2016;7:440-2. 2. Mahana S, Tomar R, Agrawal R, Saksena R, Manchanda V, Gupta R. Tuberculous lymphadenitis: Comparison of cytomorphology, Ziehl-Neelsen staining, and rapid mycobacterial culture at a pediatric superspecialty hospital.
    [Show full text]
  • The Reserve Cell in the Uterine Cervix
    The Reserve Cell in the Uterine Cervix aspects of development, differentiation and diagnosis The Reserve Cell in the Uterine Cervix aspects of development, differentiation and diagnosis De reservecel in de cervix uteri detectie, differentiatie en diagnose. Proefschrift ter verkrijging van de graad van doctor aan de Erasmus Universiteit Rotterdam op gezag van de rector magnificus Prof. Dr. S.W.J. Lamberts en volgens besluit van het College voor Promoties. De openbare verdediging zal plaatsvinden op 3 december 2008 om 15.45 uur door Johanna Elisabeth Martens geboren te Haarlem Promotiecommissie Promotoren: Prof. dr. Th.J.M. Helmerhorst Prof. dr. F.C.S. Ramaekers Overige leden: Prof. dr. C.W. Burger Prof. dr. C.J.L.M. Meijer Prof. dr. J.W. Oosterhuis Copromotoren: Dr. F.M.M. Smedts Dr. A.H.N. Hopman Voor Rudolph Klein-bastaard van Muyden Contents Chapter 1 General introduction 9 Chapter 2 Reserve cells in human uterine cervical epithelium are 27 derived from Müllerian epithelium at midgestational age. International Journal of Gynecological Pathology 2007 26(4):463-468 Chapter 3 Cytokeratin 17 and p63 are markers of the progenitor cell of 45 the human uterine cervical epithelium, a putative HPV target cell. Based on: Anticancer Research 2004 24:771-775 Chapter 4 Distribution pattern and markerprofile disclose two 61 subpopulations of reserve cells in the endocervical canal. Submitted Chapter 5 Glutathione S-transferase p is expressed in (pre) neoplastic 79 lesions of the human uterine cervix irrespective of their degree of severity Based on: Anticancer Research 1997 17:4305-4309 Chapter 6 Can Cytokeratin 8 and 17 immunohistochemistry be of 95 diagnostic value in cervical cytology? A feasibility study.
    [Show full text]
  • Curriculum.Pdf
    st 126BMODULE 1 Semester Hours/Semester L P ECTS Molecules, Cells, Tissues (including Histology, 1st Embryology, Molecular Biology, Genetics, 89 43 13.5 Chemistry, Biochemistry, Physiology) 3rd (Ι) Biostatistics 18 12 3.0 3rd (Ι) Informatics (score grading not required) 12 1.0 3rd (Ι) Foreign language terminology 24 3.0 Introduction to the Veterinary Science (score 3rd (Ι) 3 grading not required) Animal Science Ι (including General Animal 4th (I) Husbandry, Welfare & Animal behaviour, 31 30 6.0 Ecology and Protection of the Environment) Total 165 97 26.5 Instructors of 1st Semester Modules Angelopoulou Katerina Κ.Α. Arsenos George G.Α. Banos George G.B. Batzios Christos C.B. Botsoglou Nikolaos N.B. Dori Ioanna I.D. Flaskos John J.F. Fortomaris Paschalis P.F. Georgiadis Marios Μ.G. Kamarianos Athanasios Α.Κ. Karamanlis Xanthippos X.Κ. Lavrentiadou Sofia S.L. Stamataris Constantinos C.S. Tserveni‐Gousi Angeliki A.T. ‐ G Valergakis George G.V. 9 1st Module ‐ 1st Semester 127BMolecules, Cells, Tissues Learning objectives This module aims to introduce students to the principles of chemistry, cellular and molecular biology, genetics, biochemistry, histology and embryology. The learning objectives include the understanding of the following concepts: • chemical bonds, stereochemistry, aqueous solutions, acids/bases, thermodynamics • cell structure and function • structure and function of biomolecules • transport via cell membranes and second messenger systems • flow of genetic information and heredity • histology of basic tissues • cell and body metabolism • embryological development and organogenesis 1st Section 128BA. Organization of the cell 1st hour The cell. Cytoplasm [Ι.D.] 2nd hour Structure of cell membrane.
    [Show full text]
  • AAM See Aggressive Angiomyxoma (AAM) Abdominal Endometriosis
    Index A – histology of maternal response 1023, 1024 – of the skin 87 AAM see aggressive angiomyxoma (AAM) – maternal response 1023 – of the urethra 96 abdominal endometriosis 661 – neonatal infection 1027 – to the vulva, metastatic 89 abdominal pain 540 – pathogenesis 1022 – of primary peritoneal origin 638 abdominal scar–related endometriosis 659 – preterm birth (PTB) 1026 – of the vulva, primary 81 ablation, effects on endometrium 351 acute fatty liver of pregnancy (AFLP) 1063 – signet–ring cell 629 abnormal mitotic figure (AMF) 214, 219 acute on chronic transfusion, TTTS 1017 – well–differentiated 367 – in SIL 215 acute twin–twin transfusion syndrome – with diffuse peritoneal involvement 638 abortion 1064 (TTTS) 1016 adenocarcinoma in situ (AIS) 219, 278 abscess, tubo–ovarian 544 acute villitis, histology 1025 – of the cervix 227 absent ovary 581 acyclovir 10 – of the cervix, clinical features 227 ACA see acute chorioamnionitis (ACA) 1022 Addison’s disease, and autoimmune – of the cervix, differential diagnosis 229 acantholysis 30, 31 oophoritis 613 – of the cervix, TBS terminology 239 acantholytic disease of the vulva, localized 29 adenoacanthoma (AA) 413 – clinical behavior 232 acantholytic squamous cell carcinoma of the adenocarcinoma 83, 657 – colonic type 228 vulva 78 – arising in mesonephric duct remnants 147 – distribution in the cervix 228 – histology 78 – endocervical type 240 – endocervical glands 228 acanthosis 23, 39, 134, 137, 210 – endometrial type 240 – endocervical type 228 acanthosis nigricans (AN) 597, 840 – high–grade,
    [Show full text]
  • Pathological and Regenerative Plant Anatomy
    PATHOLOGICAL AND REGENERATIVE PLANT ANATOMY by Professor Dr. Siegfried Fink Freiburg (Breisgau) With 1091 figures 1999 GEBRÜDER BORNTRAEGER • BERLIN • STUTTGART Contents 1. Introduction 1 2. Structural Forms of Pathological and Regenerative Changes 6 2.1 Pathological and Regenerative Changes at the Organelle Level 6 2.1.1 Plasma Membrane 8 2.1.2 Cytosol 13 2.1.3 Cytoskeleton 13 2.1.4 Nucleus 16 2.1.5 Mitochondria 22 2.1.6 Plastids 27 .7 Microbodies 42 Endoplasmic Reticulum 44 2.1.9 Ribosomes 44 2.1.10 Dictyosomes 45 2.1.11 Vacuole 46 2.1.12 Cell Wall 48 2.2 Pathological and Regenerative Changes at the Cell Level 93 2.2.1 Embryonal Cell 96 2.2.2 Mature Cell : . 96 2.2.3 Cell Malformation 96 2.2.4 Hypotrophy 97 2.2.5 Hypertrophy 99 2.2.6 Cell Division 105 2.2.7 Positional Changes 108 2.2.8 Metabolie Changes 111 2.2.8.1 Gene Activation 111 2.2.8.2 Changes in Enzyme Activities 112 2.2.8.3 Changes in Primary Metabolites 114 2.2.8.4 Changes in Secondary Metabolites 116 2.2.9 Compartmentation 124 2.2.10 Plasmolysis 135 2.2.11 Cytorrhysis 141 2.2.12 Cavitation 142 2.2.13 Cytorrhexis ... 143 2.2.14 Cytolysis 143 2.2.15 Cell Death 145 2.2.16 Regeneration 152 2.2.17 Active Exchange 154 2.2.18 Passive Withdrawal 160 2.2.19 Apoplastic Interchanges 161 2.2.20 Haustorial Interchanges 171 2.2.21 Intracellular Associations 184 2.2.22 Symplastic Interchanges 196 VIII Contents 2.2.23 Gene Transfer 202 2.2.24 Cell Fusion 213 2.3 Pathological and Regenerative Changes at the Tissue Level 215 2.3.1 Meristematic Tissue 218 2.3.2 Mature Tissue -.-.- 219 2.3.3 Target Cells .
    [Show full text]
  • Prof. Ivan Dinev, Dsc, Phd, DVM Faculty of Veterinary Medicine Trakia University Stara Zagora, Bulgaria
    VETERINARY PATHOLOGY A COLOUR ATLAS prof. Ivan Dinev, DSc, PhD, DVM Faculty of Veterinary Medicine Trakia University Stara Zagora, Bulgaria First edition CEVA ANIMAL HEALTH BULGARIA LTD 2020 1 VETERINARY PATHOLOGY A Colour Atlas © Ivan Dinev Ivanov 2020 All rights reserved: This book is protected by the copyright law. The reproduction, imitation or distribution of the book, in whole or in part, in any format (electronic, photocopies etc.) without the prior consent, in writing, of copyright holders is strictly prohibited. First edition, 2020 This edition is composed and published in Bulgaria Graphic design and printing: 2M PRINT LTD ISBN: 978-954-9411-41-6 2 TABLE OF CONTENTS Preface 5 Acknowledgements 6 1. Gastrointestinal tract pathology 7 1.1. Upper gastrointestinal tract pathology 8 1.2. Stomach and forestomach pathology 19 1.3. Intestinal tract pathology 30 1.4. Hepatites and hepatoses 54 1.5. Peritonites 78 2. Respiratory tract pathology 81 2.1. Upper respiratory tract pathology 82 2.2. Lower respiratory tract pathology 89 3. Pathology of cardiovascular and haematopoietic systems 112 3.1. Pericardites 113 3.2. Endocardites 119 3.3. Infarctions 125 3.4. Other cardiovascular disorders 129 3.5. Pathology of the haematopoietic system 138 3.5.1. Lymph node pathology 138 3.5.2. Spleen pathology 144 3.5.3. Bone marrow pathology 149 3.5.4. Thymus gland pathology 150 4. Pathology of nervous and endocrine systems 151 5. Pathology of musculoskeletal and integumentary systems 164 5.1. Skin lesions 165 5.2. Musculoskeletal lesions 179 5.3. Skin and musculoskeletal neoplasms 189 5.4.
    [Show full text]
  • Cell Injury, Adaptation, Apoptosis and Necrosis
    MINISTRY OF HEALTH CARE OF REPUBLIC BELARUS ESTABLISHMENT OF EDUCATION GOMEL STATE MEDICAL UNIVERSITY Department of pathologic anatomy with the course of the forensic medicine CELL INJURY, ADAPTATION, APOPTOSIS AND NECROSIS Laboratory manual of 3-ed year’s students Gomel GSMU 2008 УДК 611.018.1:616-002.4=20 ББК 52.51 П 42 Авторы: С. Н. Нимер, О. А. Голубев, Л. А. Мартемьянова, Р. В. Дорошенко Рецензент: заведующий лабораторией клинических исследований ГУ «Республиканский научно-практический центр радиационной медицины и экологии человека», кандидат медицинских наук, доцент Э. А. Надыров Повреждение клетки, адаптация, апоптоз и некроз: учеб.-метод. П 42 пособие по патологической анатомии для студентов 3 курса факуль- тета по подготовке специалистов для зарубежных стран = Cell injury, adaptation, apoptosis and necrosis: laboratory manual of 3-ed year’s students / С. Н. Нимер [и др.]. — Гомель: учреждение образования «Гомельский государственный медицинский университет», 2008. — 20 с. ISBN 978-985-506-201-2 В пособии материал распределен на апоптоз, некроз и компенсаторные и приспособительные реакции, а также патоморфологические фотографии для данного раздела, постановка вопросов соответствует клиническому направлению кафедры . Утверждено и рекомендовано к изданию Центральным учебным научно- методическим советом учреждения образования «Гомельский государственный медицинский университет» 19 сентября 2008 г., протокол № 9. УДК 611.018.1:616-002.4=20 ББК 52.51 ISBN 978-985-506-201-2 © Учреждения образования «Гомельский государственный медицинский университет», 2008 URGENCY OF THE THEME Apoptoses — genetically programmed death of cells in the living organism. The dominant role of apoptoses — establishment of the homeostatic equilibrium between the processes of proliferation and loss of cells. Differences in apoptoses from the necrosis: 1.
    [Show full text]
  • 46. Metaplasia, Pseudometaplasia Regeneration
    46. Metaplasia, pseudometaplasia Regeneration • resorption, remotion, replacement • perfect regeneration restitutio ad integrum (regeneratio) • imperfect regeneration restitutio cum defectu REPARATION Direct forms of repair – Hypotypia • original cells, but not the original structure – Heteromorphosis • instead of original cells other (not connective tissue) type of cells – Hyperregeneration, hypermorphosis • fill the area, but continue proliferation – Repair • Organisation, Demarcation Indirect forms of repair • Accomodation (adaptation) after irrevocable, permanent dysfunction – Atrophy – Hypertrophy (increase in size) – Hyperplasia (increase in number) – Metaplasia (change in the tissue type) – Transformation • certain changes in internal architecture Metaplasia • special case of defective healing – one type of differentiated tissue is replaced by another type of differentiated tissue • limited possibility of changing • only two types of tissue – epithelial tissue to epithelial tissue – connective tissue to connective tissue • NO OTHER POSSIBILITIES! Forms of metaplasia • direct metaplasia (occurrence not proved yet) – differentiated cells undergo transformation • indirect metaplasia – multipotens cells replace the degenerated tissue – differentiate in a different way (columnar epithelium simple epithelium = basal cell metaplasia) – prosoplasia (more differentiated) – anaplasia (less differentiated) Cartilagenous and osseous metaplasia (*) of the dura matter of the spinal cord Causes of metaplasia • every kind of cell damage, but…
    [Show full text]