Ebook Concise oral medicine: Part 1

(BQ) Part 1 book “Concise oral medicine” has contents: Ulcerative and vesiculobullous lesions, red and white lesions, gingival enlargement, tongue lesions, granulomatous diseases and STDs, cross-infection control,… and other contents.

Concise Oral Medicine This Page is Intentionally Left Blank Concise Oral Medicine HR Umarji MDS Professor and Head Department of Oral Medicine and Radiology Government Dental College and Hospital Mumbai CBS Publishers & Distributors Pvt Ltd New Delhi • Bengaluru • Chennai • Kochi • Kolkata • Mumbai • Pune Hyderabad • Nagpur • Patna • Vijayawada Disclaimer Science and technology are constantly changing fields New research and experience broaden the scope of information and knowledge The authors have tried their best in giving information available to them while preparing the material for this book Although, all efforts have been made to ensure optimum accuracy of the material, yet it is quite possible some errors might have been left uncorrected The publisher, the printer and the authors will not be held responsible for any inadvertent errors, omissions or inaccuracies eISBN: 978-93-885-2793-4 Copyright © Authors and Publisher First eBook Edition: 2018 All rights reserved No part of this eBook may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system without permission, in writing, from the authors and the publisher Published by Satish Kumar Jain and produced by Varun Jain for CBS Publishers & Distributors Pvt Ltd Corporate O ice: 204 FIE, Industrial Area, Patparganj, New Delhi-110092 Ph: +91-11-49344934; Fax: +91-11-49344935; Website: www.cbspd.com; www.eduport-global.com; E-mail: eresources@cbspd.com; marketing@eduport-global.com Head O ice: CBS PLAZA, 4819/XI Prahlad Street, 24 Ansari Road, Daryaganj, New Delhi-110002, India Ph: +91-11-23289259, 23266861, 23266867; Fax: 011-23243014; Website: www.cbspd.com; E-mail: publishing@cbspd.com; eduportglobal@gmail.com Branches Bengaluru: Seema House 2975, 17th Cross, K.R Road, Banasankari 2nd Stage, Bengaluru - 560070, Kamataka Ph: +91-80-26771678/79; Fax: +91-80-26771680; E-mail: bangalore@cbspd.com Chennai: No.7, Subbaraya Street Shenoy Nagar Chennai - 600030, Tamil Nadu Ph: +91-44-26680620, 26681266; E-mail: chennai@cbspd.com Kochi: 36/14 Kalluvilakam, Lissie Hospital Road, Kochi - 682018, Kerala Ph: +91-484-4059061-65; Fax: +91-484-4059065; E-mail: kochi@cbspd.com Mumbai: 83-C, 1st floor, Dr E Moses Road, Worli, Mumbai - 400018, Maharashtra Ph: +91-22-24902340 - 41; Fax: +91-22-24902342; E-mail: mumbai@cbspd.com Kolkata: No 6/B, Ground Floor, Rameswar Shaw Road, Kolkata - 700014 Ph: +91-33-22891126 - 28; E-mail: kolkata@cbspd.com Representatives Hyderabad Pune Nagpur Manipal Vijayawada Patna to my wife, Vasu and my daughters Medha and Anagha This Page is Intentionally Left Blank Preface A fter Concise Oral Radiology was well-received by the undergraduate students, I had the temptation of compiling a similar text on oral medicine and for this endeavor I was encouraged and even goaded by many PG students and lecturers The basic motive behind this venture is to present important aspects of oral medicine readily available in various textbooks in a nutshell, to help the exam-going students too hard pressed for time to refer to various books Again I would make no claim regarding the originality of the text in Concise Oral Medicine, on the other hand I may be guilty of ruthlessly cutting down on a lot of information with the primary aim of keeping the text short and simple During my tenure as a student and a teacher, I had the privilege of learning this subject under the erudite guidance of stalwarts of oral medicine in India namely Dr Girish Merchant, Dr Aspi Surveyor, Dr Jakhi, Dr Ani John, Dr Bharati Parekh and Dr RN Mody I will forever remain indebted to these dedicated teachers In fact this text has its roots in the notes made during their lectures Compilation of this book, however, concise, was a challenge to my lazy nature and sceptical attitude and without the active participation of many individuals, it would have been impossible to accomplish this task Dr Eswaran Ramaswamy and Dr Akshay Chaturmohatta spearheaded the venture by compiling the first few chapters Dr Harsha Puri, Dr Amruta Bandal and Dr Ashish Talanje were lecturers in the department and of great help in this venture I relied heavily on the selfless efforts provided by lecturers Dr Suvarna Sawant, Dr Hasan Ali, Dr Prashant Salve, Dr Kavita Amale and postgraduate students Dr Manasi Kajale, Dr Minakshi Hivarkar, Dr Priyanka Verma, Dr Pooja Jain, Dr Ajas Gogri, Dr Deepika Khurana, Dr Sunita Kakade and I express my heartfelt gratitude to all of them and many others whom I might have failed to mention I owe a debt of gratitude to Dr Smriti Khanna, Lecturer, Oral Pathology, for diligent proof reading of a few chapters and Dr Nitin with artistic talent for the line diagrams and also to Mr Ashish Jalamkar and Mr Vikas Jadhav for converting old departmental slides into good quality pictures Dr Shruti Shah was ever helpful and efficiently completed the laborious task of adding the color pictures with legend and overall preparation of the manuscript I am extremely grateful to Dr Nandita Gupta for the preparation of index and Dr Varun Manek for providing constructive criticism which helped in improving the content of the book I consider myself blessed, that I am associated with Government Dental College and Hospital, Mumbai, a great institution which has always encouraged me and almost all the cases presented in this text belong to the patients attending the heavy OPD of GDCH and obtained with courtesy from the ever helpful staff and PG students viii Concise Oral Medicine Dr Sonali Kadam, Associate Professor, has always been co-operative and supportive and I express my gratitude to her for all the help With Dr Jagdish V Tupkari, HOD, Oral Pathology, I have always enjoyed good rapport and benefited immensely by his knowledge, wisdom and wit and willingness to offer a helping hand I will always remain indebted to Dr Mansing G Pawar, Dean, GDCH, for constant support and I always felt encouraged in this institution because of him Mr YN Arjuna and Mr Ramesh Krishnammachari of CBS Publishers always provided all the assistance and it was their enthusiasm which made this text a possibility I also wish to express my gratitude to CBS Publishers & Distributors as without their efforts this book would not have been published HR Umarji Contents Preface Definition and Introduction vii Ulcerative and Vesiculobullous Lesions 17 Red and White Lesions 49 Gingival Enlargement 76 Tongue Lesions 86 Pigmentations 101 Granulomatous Diseases and STDs 113 Cross-Infection Control 133 Bleeding and Clotting Disorders and Hematological Diseases 138 10 Temporomandibular Joint Disorders 163 11 Diseases of Maxillary Sinus 176 12 Salivary Gland Disorders 185 13 Orofacial Pain 199 14 Oral Cancer and Precancerous Lesions 211 15 Immunological Diseases 222 16 Endocrine Disease and Dysfunction 231 17 Management of Medically Compromised Patients and Drug Interactions 244 18 Differential Diagnosis of Miscellaneous Diseases 249 19 Forensic Odontology 256 20 Evidence-Based Dentistry 264 21 Orofacial Syndromes 269 22 Routine Blood Investigations 275 Index 281 148 Concise Oral Medicine Clinical Features • Infection, fever, stomatitis, pharyngitis, and skin abscess occurring during neutropenic episodes • Oral mucosal lesions are large, irregular and scarring similar to major aphthae • Periodontal involvement ranging from marginal gingivitis to advancing periodontal bone loss • Patients with unusual periodontal destruction or severe oral ulcerations should be subjected to total and differential WBC count to rule out the possibility of cyclic neutropenia Treatment • Careful monitoring of patients for infection during neutropenic periods • Hematopoietic growth factor such as G-CSF (Neupogen {filgastrim}, amgen) reduces the number and severity of infectious episodes • Maintenance of oral hygiene LAZY LEUKOCYTE SYNDROME It is caused by a loss of chemotactic function of neutrophils Severe neutropenia results due to inability of cells to migrate from marrow to peripheral blood Phagocytic and bactericidal functions remain intact Clinical Features • Manifestation become apparent at to years of age • Common infections noted are gingivitis, stomatitis, otitis media, and bronchitis Diagnosis • Neutrophil migration tests showing lack of normal response to epinephrine and piromen (Pseudomonas polysaccharide) • Inflammatory stimulation using skin windows will show a little neutrophil migration • Normal phagocytosis and bacteriocidal activity CHEDIAK-HIGASHI SYNDOME It is a congenital, autosomal recessive defect of granule containing cells like granulocytes and melanocytes As a result of this, neutrophils show reduced chemotactic and bactericidal activity, although phagocytosis remains intact Clinical Features • Oculocutaneous albinism milky white to slate gray skin, light coloured eyes, hypopigmentation of hair (peculiar silver colour) Presence of large but fewer melanin granules produces pigment dilution • Bacterial infections of skin and respiratory tract and enterocolitis • Easy bruisability and bleeding • Photophobia • Nystagmus • Peripheral neuropathy and ataxia • Oral cavity shows gingival and periodontal diseases, ulcerations, early loss of teeth • Sinus and oral infections caused by β hemolytic streptococci, S aureus, gramnegative organisms Diagnosis Presence of giant blue granules in cytoplasm of granulocytes on peripheral blood smear, bone marrow aspirate examination—myeloid precursor cells, eosinophils Treatment Symptomatic antibiotics for infection, childhood immunization Bleeding can be avoided by avoiding aspirin For severe bleeding— desmopressin, aminocaproic acid, or platelet transfusion Chemotherapy, corticosteroids, IV immunogloboulins currently hematopoietic stem cell transplant (HSCT) Oral surgical procedure can lead to excessive blood loss hence better plan for hemostasis, patients cannot tolerate bright operatory light advised sunglasses Bleeding and Clotting Disorders and Hematological Diseases LEUKEMIA Gingival enlargements are commonly manifested in Leukemia and hence this topic is described in the chapter on gingival enlargements LYMPHOMA Lymphomas are a group of malignant solid tumours involving the cells of lymphoreticular or immune system such as B lymphocytes, T lymphocytes and monocytes Two major categories: Hodgkin’s lymphoma (HL) Non-Hodgkin’s lymphoma (NHL) Hodgkin’s Lymphoma • Was first described by a British pathologist Thomas Hodgkin in 1832 • Etiology unknown, genetic and environmental factors and EBV play a role Clinical Features Painless enlargement of lymph nodes without any other symptoms of the disease Cervical nodes involvement most common followed by axillary, inguinal, mediastinal Waldeyer’s ring structures also involved • The involved nodes are non-tender and feel rubbery Asymptomatic enlarged lymph nodes common in young patients (histologically lymphocyte predominant/ nodular sclerosis) • In older patients (increased chances of lymphocyte depleted, mixed cellularity histologic pattern), symptoms such as fever, malaise, nightsweats may precede the noticeable lymphadenopathy • In advanced cases, signs and symptoms are due to pressure from enlarging LN: dysphagia—mediastinal LN, ureteral obstruction—retroperitoneal LN • Cyclic spiking of high fever—Pel-Ebstein fever Severe pruritus, more so in young women 149 Diagnosis Can be established with the lymph node biopsy Characteristic Reed-Sternberg cells diagnostic, but the nature of these cells is controversial CT scans can help to study the location size and extent of LN enlargements Whole body radionuclide scans and PET scans to localize the LN Ann Arbor classification is currently used to stage lymphoma and guide the treatment choice Treatment Radiation: IFRT involved field radiation therapy 35 Gy Chemotherapy: ABVD adriamycin (doxorubicin) bleomycin, vinblastine, dacarbazine Non-Hodgkin’s Lymphoma • Arises from B or T lymphocytes • NHL is associated with immunosuppression: HIV infection (100-fold more risk than normal population), medication after organ transplant, Sjögren’s syndrome, celiac disease, rheumatoid arthritis • More common in patients above 40 years, however, can occur at any age • Painless, persistent enlargement of LN, but extranodal lesions more common than in HL • NHL lesions appear in Waldeyer’s ring GI tract: Large abdominal masses Spleen: Splenomegaly Bone marrow: Cytopenia • In the oral cavity, NHL presents as gingival or mucosal tissue enlargements/swellings, intrabony lesions may be mistaken for toothache associated with periodontal infection and extraction of the tooth is followed by rapid growth of NHL from the unhealed socket • If the clinical examination shows mobile tooth surrounded by suspicious growth and radiograph shows irregular bone loss 150 Concise Oral Medicine (unlike the periodontal abscess with the well demarcated bone loss), it is better to subject the patient to biopsy than to extraction • In fact it is now important to include NHL in the differential diagnosis of localized gingival swellings, more so if the patient is immunosuppressed • Ann Arbor classification to stage and to help select treatment plan • Treatment includes chemotherapy cyclophosphamide, doxorubicin, oncovin (vincristine) and prednisolone (CHOP) Addition of rituximab to this regimen helps to improve response and prolongs eventfree survival in elderly patients Radiotherapy IFRT (Involved Field Radiation Therapy) Radioimmunotherapy: NHL cells are radiosensitive and can be targeted by monoclonal antibody Radioimmuno conjugates (Yttrium 90, ibritumomab, tiuxetan and iodine 131 tositumomab) used as a novel therapy for relapse If radiotherapy is delivered to the mandible or maxilla during tooth formation phase there is delayed and ectopic eruption, the roots show malformations and appear blunt, shortened, tapered, V-shaped Burkitt’s Lymphoma • Dennis Burkitt in 1950s described a rapidly growing jaw and abdominal lymphoid tumor, in East African children in areas where malaria was endemic • This tumor is the human cancer most closely linked with a Epstein-Barr virus • It is a rapidly growing extranodal jaw and abdominal tumor, which expands rapidly and may double in size every 1–3 days, making it the fastest growing human cancer • Clinically evident jaw tumor may result in mobility of teeth, pain, swelling of mandible and maxilla and anterior open bite • Radiographically alveolar bone resorption, loss of lamina dura, enlargement of tooth follicle, disappearance of cortex around tooth crypts, displacement of teeth and tooth buds by the enlarging tumor giving rise to ‘floating tooth appearance’ and periosteal reactions—‘sunray spicules’ as bone forms perpendicular to the mandible • Histologically uniform, large, neoplastic cells with abundant cytoplasm, high mitotic rate and numerous macrophages scattered create a characteristic ‘starry sky’ appearance • BL has a dramatic response to chemotherapy, specially cyclophosphamide Other agents used are vincristine, methotrexate and corticosteroids However, surgical debulking and palliative low dose radiotherapy to local tumor site are also considered in treatment planning MULTIPLE MYELOMA Multiple myeloma (MM) is a malignant neoplasm of plasma cells, that is characterized by bone marrow plasmacytosis, production of pathologic M protein (abnormal paraprotein), bone lesions, kidney disease, hyperviscosity and hypercalcemia Third most common hematologic malignancy after leukemia and lymphoma Clinical Features • Fatigue, weakness, weight loss • Bone pain: Most common symptom resulting from osteolysis caused by the accumulating tumor cells or indirectly from the osteoclastactivating factors secreted by the MM cells or by osteoblast inhibition Numbness or paresthesia can also occur • Recurrent infection • Renal failure results from a combination of amyloidosis, hypercalcemia and infiltration of malignant cells • Bleeding in MM results from many causes: – Thrombocytopenia Bleeding and Clotting Disorders and Hematological Diseases – Abnormal platelet function – Clotting defects result from abnormal myeloma protein coating the platelets and interfering the coagulation cascade – Paraprotein-induced factor VIII or X deficiency – Hyperviscosity of blood and tissue fragility associated with amyloidosis • Typical radiographic picture is that of multiple separate punched out radiolucencies in the skull, resulting from the focal proliferation of plasma cells in the bone marrow and mandibular involvement varying from clear cut osteolytic lesion to pathologic fracture Generalized osteoporosis can also occur Diagnosis i From clinical picture of pain, swelling and paresthesia of bone, unexplained mobility of teeth, epulis formation ii Typical punched out radiolucent lesions of skull vault, mandible iii Monoclonal protein in plasma and urine Bence-Jones proteins in urine (also seen in polycythemia vera and leukemia) iv Bone marrow biopsy reveals atypical plasma cells v The tongue may be enlarged and studded with small garnet colored enlargements, biopsy in such cases will show evidence of amyloidosis Treatment Chemotherapy with vincristine, doxorubicin and dexamethasone Radiotherapy, surgery for focal lesions HSCT (usually autologous) improves response and overall disease-free survival Bisphosphonates are specific inhibitors of osteoclastic activity and monthly IV infusion of zoledronic acid/pamidronate have reduced the skeletal complications and are mainstay of myeloma therapy 151 Bisphosphonate-induced osteonecrosis is a serious complication affecting the jaw bones Multidisciplinary approach involving dental specialists, hematologist, physician and surgeon necessary for the management of osteonecrosis Consultation with the hematologist is mandatory to avoid and arrest hemorrhage during and after dental surgery PLATELET DISORDERS Platelet disorders are divided into categories by etiology: Congenital and acquired Into two additional categories by type: Thrombocytopenias: Reduction in number of platelets caused by: • Decreased production in the bone marrow • Increased sequestration in the spleen • Accelerated destruction Thrombocytopathies: Qualitative platelet disorders: defect in platelet reaction • Adhesion • Aggregation • Granule release Thrombocytopenic Purpura Two of the most commonly encountered platelet disorders, idiopathic or immune thrombocytopenic purpura (ITP) and thrombotic thrombocytopenic purpura (TTP), have clinical symptoms including petechiae and purpura over the chest, neck, and limbs— usually more severe on the lower extremities Mucosal bleeding may occur in the oral cavity and gastrointestinal and genitourinary tracts Idiopathic Thrombocytopenic Purpura ITP may be acute and self-limiting (2 to weeks) in children In adults slow onset, persistent, lasting for years and has recurrent exacerbations In severe cases of ITP, oral hematomas and hemorrhagic bullae may be the presenting 152 Concise Oral Medicine clinical sign Most patients with chronic ITP are young women Intracerebral hemorrhage, although rare, is the most common cause of death ITP is assumed to be caused by accelerated antibody-mediated platelet consumption ITP may be a component of other systemic diseases Autoimmune thrombocytopenia like that associated with systemic lupus erythematosus can be severe and require aggressive treatment Immune-mediated thrombocytopenia associated with HIV disease Thrombotic thrombocytopenic purpura catastrophic disease considered fatal in the past ‘Dengue’ a parasitic infection common in mosquito infested area can also cause thrombocytopenia Medications can also reduce absolute numbers of platelets or interfere with their function, resulting in postsurgical haemorrhage Drug-related platelet disorders are reversible within to 10 days of discontinuation of the drug Aspirin prevents platelet aggregation, induces a functional defect in platelets detectable as prolongation of BT Aspirin is commonly used as an inexpensive and effective antiplatelet therapy for thromboembolic protection to reduce the risk of myocardial infarction and stroke Causes Management • • • • Modality determined by the type of defect Thrombocytopenias—platelet transfusion ITP—corticosteroids Chronic ITP—splenectomy Bone marrow transplantation Plasmapheresis to remove circulating isoantibodies is held in reserve for cases of severe thrombasthenia and life-threatening bleeding Metastatic malignancy Pregnancy Mitomycin C High-dose chemotherapy Clinical Features In addition to thrombocytopenia, clinical features of TTP include: • Microangiopathic hemolytic anemia • Fluctuating neurologic abnormalities • Renal dysfunction • Fever • Microvascular infarcts occur in gingival and other mucosal tissues and appear as platelet rich thrombi Thrombocytopenia may be a component of other hematologic disease such as myelodysplastic disorders, aplastic anemia, and leukemia Bone marrow suppression from cytotoxic chemotherapy can result in severe thrombocytopenia Thrombocytopenia and thrombocytopathy in liver diseases are complicated by coagulation defects In renal disease the coagulopathy consists of acquired platelet defect resulting from uremia Alcohol can also induce thrombocytopenia RBC DISEASES Polycythemia Polycythemia may be defined as an abnormal increase in the erythrocyte count in the peripheral blood, usually accompanied by an increase in hemoglobin and hematocrit It is divided into absolute erythrocytosis (a true increase in red cell mass) and relative erythrocytosis (the red cell mass is normal, but the plasma volume is reduced) Relative polycythemia Real/primary polycythemia vera Loss of tissue and intraActual neoplastic vascular fluid proliferation of Diabetic ketoacidosis erythrocytes Postsurgical dehydration Prolonged vomiting or dehydration Rapid diuresis (treatment of CCF) Bleeding and Clotting Disorders and Hematological Diseases 153 Secondary Polycythemia Oral Manifestations It is due to an increase in erythropoietin production to compensate for hypoxia • People who live in high altitudes • Chronic pulmonary disease • Congenital heart disease • Renal disease (hydronephrosis) • Tumours producing erythropoietin-like substance • A purplish-red discoloration of the oral mucosa is visible on the tongue, cheeks, and lips • Purplish-red discolored tongue called as crystal violet tongue • The gingivae are red and may bleed spontaneously • Petechiae and ecchymoses are observed in patients with platelet abnormalities • Varicosities in the ventral tongue, a frequent normal finding, are exaggerated in cases of polycythemia Apparent Polycythemia It is characterized by an increased hemoglobin concentration and packed cell volume but normal RBC mass, due to reduction in plasma volume • Obese men with hypertension and significant social history of smoking and alcohol consumption • Diuretic therapy Polycythemia Vera Polycythemia vera (PV) is a myeloproliferative disorder characterized by excessive proliferation of erythroid elements along with granulocytic and megakaryocytic cells It usually begins after 50 years of age Etiology Acquired genetic changes in the stem cell leading to disturbances of normal cellular growth Clinical Features • Patients with PV develop episodes of thrombosis and hemorrhage in the later stages of the disease • A characteristic clinical picture of ruddy cyanosis is seen on the face and extremities, owing to the presence of deoxygenated blood in cutaneous vessels • Patients complain of headache, dizziness, tinnitus, fullness of the head and face, and pruritus • Splenomegaly • Coronary thrombosis • “Erythromelalgia” may manifest as paresthesias involving the cranial nerves Treatment • The major therapy for PV involves repeated phlebotomy • Myelosuppressive agents to reduce the hematocrit to its upper limit of 50% • Alkylating agents and radioactive phosphorus (32P) have been shown to increase the risk of leukemia and should be avoided • Chemotherapy with agents such as busulfan, chlorambucil, cyclophosphamide, and melphalan may also be beneficial • Treatment with hydroxyurea also decreases the thrombotic complications Oral and Dental Considerations • Dental treatment presents a risk because of the possibility of bleeding or thrombosis • Patients should have a complete blood count prior to treatment • To prevent complications, it is recommended that the hemoglobin be reduced below 16 g/dl and the hematocrit to below 47% • Patients with this disease require special attention to local hemostasis • Preoperative myelosuppressive treatment should be considered prior to dental treatment when the blood counts are not controlled with phlebotomy alone Anemia Anemia is present whenever there is a decrease in the normal amount of circulating hemoglobin 154 Concise Oral Medicine Anemia may result from: • Blood loss, as in common iron deficiency anemia • Increased destruction of red blood cells as in the hemolytic anemias • Decreased production of red cells, as in pernicious and folic acid deficiency anemias, or • Combinations of these three Anemias also may be classified according to their pathophysiologic basis: Size of RBCs: • Microcytic • Normocytic • Macrocytic On the basis of their hemoglobin concentration: • Hypochromic • Normochromic The term “hyperchromic” is seldom used, but it refers to a macrocytic cell with normal hemoglobin concentration that, because of its large size, has an increased hemoglobin content General symptoms of all anemias include: • Pallor of the skin, palpebral conjunctiva, and nailbeds • Dyspnea and easy fatigability, palpitation • Cracked and splits in nails, spoon-shaped nails Iron Deficiency Anemia (Blood Loss Anemia, Hypochromic Microcytic Anemia) It is the most common of all anemias It may result from chronic blood loss, such as occurs in: • Menstrual or menopausal bleeding • Parturition, bleeding hemorrhoids, varices • Bleeding malignant lesion or ulcer in the gastrointestinal tract • Subtotal or complete gastrectomy, or a habit of clay eating • Malabsorption syndromes • Worm infestations like hookworm, tapeworm, etc Clinical features include pallor, dyspnea and fatigue and also palpitation, numbness and tingling in fingers, toes Oral Manifestations • The major oral sign of iron deficiency anemia is pallor of the mucosa • In addition, the oral mucosa become atrophic, with loss of normal keratinization • The tongue may become smooth due to atrophy of the filiform and fungiform papillae, and glossodynia can be a presenting or associated symptom These changes are associated with significant reduction of mean epithelial thickness • Dietary iron deficiency anemia should be suspected in every case of glossitis, glossodynia, angular cheilitis, erythematous mucositis, candidiasis and burning mouth when no other obvious causes are identified • In long-standing cases, esophageal strictures or webs can develop, resulting in dysphagia Diagnosis • Lowered hemoglobin in routine blood counts • RBCs microcytic and hypochromic on peripheral smear • Mean corpuscular hemoglobin, the mean corpuscular hemoglobin concentration, and the mean corpuscular volume are decreased • Serum ferritin levels are markedly reduced