03/09/2011 Oral Manifestations of Vitamin B12 Deficiency: A Case Report

Resident: J. Hencler
Date: 03/09/2011

Article title: Oral Manifestations of Vitamin B12 Deficiency: A Case Report
Author: Pontes, Neto, Ferreira, Fonseca, Vallinoto, Pontes, Pinto Jr
Journal: JCDA Sept 2009, Vol. 75, No. 7

Major topic: B12 deficiency and megaloblastic anemia

Type of Article: Case report

Main Purpose: Report a case of megaloblastic anemia in which oral manifestations were significant.

Background:
Megaloblastic anemias are a subgroup of macrocytic anemias caused by impaired DNA synthesis that results in macrocytic RBCs, abnormalities in leukocytes and platelets, and epithelial changes, particularly in the rapidly dividing epithelial cells of the mouth and GI tract. The most common causes of megaloblastic anemias are cobalamin (vitamin B12) and folate (vitamin B9) deficiency. Clinically, megaloblastic anemia progresses slowly (takes 2-5 years to develop) and symptoms include weakness, fatigue, shortness of breath, and neurologic abnormalities. Oral signs and symptoms including glossitis, angular chelitis, recurrent oral ulcer, oral candidiasis, diffuse erythematous mucositis, and pale oral mucosa, offer the dentist an opportunity to diagnosis of this condition.

Findings:
41 year old female with cc of difficulty in eating certain types of food (banana and tomato) because of a burning sensation and the presence of red stains on her cheek and tongue. She has been a strict vegetarian for 2.5 years and had not consumed milk, cheese, fish, meat or eggs during that time. Clinical evaluation and patient reports include paleness and dry lips, disturbance of taste, fatigue after simple daily activities, paresthesia of structures innervated by mandibular division of the trigeminal nerve, and disturbance of memory and slowing mental faculty. Oral exam revealed pale oral mucosa, glossitis with papillary atrophy and multiple areas of painful erythema on the dorsal surface and lateral borders of the tongue and buccal mucosa. Hematologic tests were done and a diagnosis of megaloblastic anemia was made. Treatment comprised doses of B12 (1000mg/wk) and intramuscular hydroxocobalamin and 1mg folic acid daily. After 14 days, the lesions had healed and all symptoms disappeared.

Key points in the article discussion:
Vitamin B12 is only found in bacteria, eggs, and foods of animal origin. Most B12 is stored in the liver. Megaloblastic anemia occurs when the body’s stores fall below 0.1mg. B12 or B9 deficiency are the most important cofactors necessary for normal maturation of all cells and B12 is necessary for DNA synthesis, as it’s deficiency prevents cell division in the bone marrow. When either of these factors is deficient, RBCs become large erythroblasts with nuclear or cytoplasmic asynchrony. A wide range of oral signs and symptoms may appear in anemic patients as a result of basic changes in the metabolism of oral epithelial cells. Abnormalities in cell structure and keratinization pattern of the oral epithelium can lead to a beefy, red, and inflamed tongue with erythematous macular lesions on the dorsal and border surfaces. Differential diagnosis of patients with similar signs and symptoms include iron deficiency, diabetes, allergy, autoimmune disease, physical and chemical injury, atrophic candidiasis, and anemia of chronic disease. Although B12 deficiency is almost always associated with strict vegetarians, the condition can also result from gastrectomy, bacterial overgrowth in small intestine, diverticulitis, celiac disease, Crohn’s disease, alcoholism, HIV, and certain medications. Careful investigation of clinical history and clinical exam will often lead to the cause of megaloblastic anemia.

Summary of conclusions:
Megaloblastic anemia has a complex pathogenesis. As oral lesions are among the most common initial symptoms, the dentist has a responsibility alongside medical specialists to contribute to the diagnosis.

Assessment of article:
Interesting case report, but on a 40 year old vegan. Not really our patient population. The article was well written and included a very detailed discussion on the pathogenesis, oral signs and symptoms, diagnosis, and treatment of megaloblastic anemia (B12 deficiency). I found it interesting that this patient had paresthesia of CN V3 innervated structures. So asked myself…self, what is the mechanism behind such an unfortunate nuerological deficit. The mechanism is not fully elucidated but may be due to impaired synthesis of myelin phospholipids or from a deficit of succinyl-CoA that leads to the generation of odd chained fatty acids which may get incorporated into the myelin and cause the neurological syndrome of Vitamin B12 deficiency. Good shtuff.