Medical History
The patient’s medical history revealed high blood pressure diagnosed five years ago and takes clonidine 0.2 mg twice daily (b.i.d). She has hypothyroidism diagnosed 10 years ago and takes levothyroxine 0.88 mcg once a day. Also she has been taking omeprazole, a proton pump inhibitor, 20 mg orally once a day for seven years. She is postmenopausal. The patient is compliant with her medication and her vital signs were within normal limits.
Height: 5′2″
Weight: 100 lbs
BMI: 18.3
Dental History
Patient has not had a dental exam or prophylaxis in five years. She brushes daily with a soft toothbrush and uses an interdental brush. She had full mouth periodontal surgery over 10 years ago. She noticed that her tongue is red, feels funny, and burns after eating certain foods. She is concerned about her periodontal health.
Social History
Patient has been a vegetarian for seven years. She drinks one glass of red wine daily. She purchases her produce at the local farm market and cooks for herself. She does not eat any processed food or animal products. Her diet consists mainly of plant based foods and some grains. She does not take any vitamin supplements. Due to limited finances, she has a very restricted budget.
Her oral symptoms have impacted her social life because she finds it difficult to eat and talk. She finds that her attention span has diminished and has been feeling fatigued. She was a member of a bridge group but has not attended in the last month.
Dental Examination
Extraoral exam revealed no significant findings. Intraorally the patient presents with the appearance of a red enlarged tongue, denuded papilla on dorsum of tongue, and pale oral mucosa. Generalized moderate biofilm, slight supra, and subgingival calculus with bleeding upon probing posteriorly on all quadrants. Generalized maxillary and mandibular probing depths of 3–4 mm with generalized 1–2 mm recession. Class I malocclusion with slight mandibular anterior crowding.
Dental Hygiene Diagnosis
| Problems | Related to Risks and Etiology |
| Increased caries and periodontal diseases | Dental neglect |
| Significant xerostomia, orthostatic hypotension | Clonidine |
| Glossitis with papillary atrophy | Proton pump inhibitor >seven years |
| Vitamin deficiency, low BMI, fatigue | Plant‐based diet |
| Cervical abrasion, root caries, and root sensitivity | Loss of clinical attachment from periodontal surgery |
| Increased caries and periodontal diseases | Generalized moderate biofilm, slight supra and subgingival calculus with bleeding upon probing posteriorly on all quadrants |
| Differential diagnosis of Vitamin B12 deficiency | Medication and diet |
| Noncompliance with medication | Hypertension |
Planned Interventions
| Planned Interventions (to arrest or control disease and regenerate, restore or maintain health) |
||
| Clinical | Education/Counseling | Oral Hygiene Instruction |
| Take blood pressure at every visit; monitor chair position for orthostatic hypotension Periodontal maintenance Topical anesthetic as needed for sensitivity 5% NaF fluoride varnish to prevent root caries Air polish with glycine powder Initial exam, radiographs, and study models Referral to primary care physician for complete physical exam and blood tests (to rule out systemic disease) |
Importance of regular dental visits Increased risk for caries and reoccurrence of periodontal disease Nutritional counseling, journaling for dietary analysis Educate and motivate about the importance of healthy lifestyle Educate and motivate on the importance of biofilm management |
Modified Stillman’s brushing technique Interdental cleaning with interproximal brushes Recommend use of fluoride toothpaste Recommend frequent sips of water during the day or salivary substitute to minimize xerostomia |
Progress Notes
Patient arrived early for her appointment but was seen at the appointed time. A complete medical, social, and dental history was taken. Initial exam, FMS, dental, and periodontal exams were performed. Patient agreed to a periodontal maintenance procedure and air polishing with glycine powder. Biofilm management was explained and tailored to her needs. A seven‐day nutrient dietary assessment journal was explained and given to the patient. Patient was instructed to return in one week for dietary analysis and counseling. Patient was advised to see primary care physician for a differential diagnosis of Vitamin B12 deficiency.
Discussion
Pathophysiology and Differential Diagnosis of Vitamin B Deficiency
The appearance of a red, denuded tongue and diminished attention span may be symptoms of a Vitamin B deficiency (Field et al. 1995). The B complex vitamins are water‐soluble and include: Thiamin (B1), Riboflavin (B2), Niacin (B3), Pantothenic acid (B5), Pyridoxine (B6), Biotin (B8), Folate (B9), Cobalamin (B12), and Choline (B13). Since the body cannot synthesize water‐soluble vitamins, dietary consumption of meat, fish, eggs, and dairy products is necessary. Specifically, glossitis, cognitive impairment and other neurological manifestations are cited in the literature as symptoms of a B12 or cobalamin deficiency (Field et al. 1995; Andres 2004; Pontes et al. 2009; Hoffbrand et al. 2010; Goosen 2016).
Vitamin B12 or cobalamin, is necessary for sound deoxyribonucleic acid (DNA) metabolism in cells of tissues that are constantly reproducing, such as skin, blood, and the lining of the gastrointestinal tract (Peckenpaugh 2010). For example, B12 acts as a coenzyme in DNA biosynthesis for developing blood cells in the bone marrow (hematopoiesis) (Goosen 2016). Impaired DNA cripples cell division, which allows immature cells to become enlarged and often multinucleated resulting in megaloblastic anemia (ineffective hematopoiesis) (Stabler 2013). These enlarged cells are ineffective in carrying oxygen to the peripheral tissues resulting in anemia, from the Greek anaimia or “without blood” and a disruption in homeostasis (Goosen 2016).
Additional clinical manifestations of Vitamin B12 deficiency and oxygen deficit includes “demyelination of the cervical and thoracic dorsal and lateral columns of the spinal cord,” (Stabler 2013) fatigue, jaundice, paresthesia, memory loss, and peripheral nervous system interferences (walking) (Pontes et al. 2009; Stabler 2013; Goosen 2016). Abnormal epithelial cell proliferation interferes with keratinization and causes smoothing of the tongue, which would appear red and inflamed, along with reduced taste and a burning sensation (Pontes et al. 2009).
In this case, a referral to a primary care physician is indicated for a differential diagnosis. The physician will conduct blood tests to determine whether the deficiency is due to inadequate diet, food‐cobalamin malabsorption in the stomach, or lack of intrinsic factor (IF), otherwise known as pernicious anemia (Andres 2004).
Once consumed, cobalamin passes through a series of “hand‐offs” (Figure 3.4.1) as it makes its way through the digestive system to the liver where cobalamin is stored (Andres 2004). Aśok Antony describes the process as an “odyssey … [whereby] cobalamin is accompanied by several chaperones that sequentially bind, sequester, and thereby ensure that cobalamin does not participate in side reactions. This ensures its fitness for service [sic] for critical enzymes” (Antony 2016). Though, failure or damage to any function or process along the way can cause a deficiency.
Figure 3.4.1: Cobalamin metabolism and corresponding causes of deficiency. Causes of cobalamin deficiency are shown in blue. The metabolic pathway starts when (1) dietary cobalamin (Cbl), obtained through animal foods, enters the stomach bound to animal proteins (P). (2) Pepsin and HCL in the stomach sever the animal protein, releasing free cobalamin. Most of the free cobalamin is then bound to R‐protein (R), which is released from the parietal and salivary cells. IF is also secreted in the stomach, but its binding to cobalamin is weak in the presence of gastric and salivary R‐protein. (3) In the duodenum, dietary cobalamin bound to R‐protein is joined by cobalamin–R‐protein complexes that have been secreted in the bile. Pancreatic enzymes degrade both biliary and dietary cobalamin–R‐protein complexes, releasing free cobalamin. (4) The cobalamin then binds with IF. The cobalamin–IF complex remains undisturbed until the distal 80 cm of the ileum, where (5) it attaches to mucosal cell receptors (cubilin) and the cobalamin is bound to transport proteins known as transcobalamin I, II and III (TCI, TCII, and TCIII). TCII, although it represents only a small fraction (about 10%) of the transcobalamins, is the most important because it is able to deliver cobalamin to all cells in the body. The cobalamin is subsequently transported systemically via the portal system. (6) Within each cell, the TCII–cobalamin complex is taken up by means of endocytosis and the cobalamin is liberated and then converted enzymatically into its two coenzyme forms, methylcobalamin and adenosylcobalamin.
Dietary Deficiency
Dietary deficiency in healthy adults is less than 5%, while studies conducted with the elderly reveal up to a 50% incidence of cobalamin deficiency (Andres 2004). Plants do not synthesize B12, and strict vegetarians, who do not supplement with B12, are susceptible for a dietary B12 deficiency (Goosen 2016).
Food‐Cobalamin Malabsorption
Cobalamin is initially bound to the animal protein as it enters the mouth and forms a bolus when chewed and swallowed. Absorption of cobalamin begins in the stomach where pepsin and hydrochloric acid (HCl) are released to break apart the cobalamin from the animal protein (Andres 2004; Antony 2016; Goosen 2016). Malabsorption of cobalamin can occur if the release of pepsin and HCL are impaired resulting in gastric atrophy, thus failing to break apart cobalamin from the protein (hypoclorhydria or achlorhydria) (Andres 2004; Goosen 2016). Reasons for impairment and subsequent food‐cobalamin malabsorption include, an overgrowth of Helicobacter pylori (H. pylori) and ulcerations of the stomach lining; as well as long‐term use of antacids, and medications used to treat gastric reflux (GERD), such as H2 receptor agonists (Zantac, Pepcid) and proton pump inhibitors (Prilosec, Nexium) that interfere with production of HCL and pepsin (Andres 2004; Goosen 2016). Andres writes that “food‐cobalamin malabsorption is caused primarily by gastric atrophy … in 40% of patients older than 80” (Andres 2004).
Lack of Intrinsic Factor
Free cobalamin is next picked up by a protein released by the salivary glands –“haptocorrin, also known as R protein or transcobalamin” (Antony 2016; Goosen 2016) and is carried through the stomach to the lower part of the stomach or duodenum. In the duodenum, pancreatic enzymes weaken this transport mechanism in order to allow for the freed cobalamin to bind with IF that is produced by the parietal cells in the stomach. Intrinsic factor is a glycoprotein with only one important function, and that is to carry cobalamin through the lower regions of the stomach – the jejunum to the ileum (Figure 3.4.2) where it is absorbed into the circulatory system (Andres 2004; Antony 2016). Lack of IF is considered an autoimmune disease that is associated with the presence of anti‐intrinsic factor antibodies and chronic atrophic gastritis that results in the (Andres 2004; Antony 2016) “destruction of gastric parietal cells” (Stabler 2013) that produce IF. These combined symptoms present a cobalamin deficiency disease known as pernicious anemia (PA). Other autoimmune diseases such as hyperthyroidism (Graves disease), hypothyroidism (Hashimoto thyroiditis), Type 1 diabetes mellitus, and vitiligo are also associated with pernicious anemia (Andres 2004; Stabler 2013). Serious illnesses that require gastrectomy or cancer, may also affect production of IF (Andres 2004; Goosen 2016). Stabler writes about the prevalence of pernicious anemia as, “The most frequent cause of severe vitamin B12 deficiency … that ranges from 50 to 4000 cases per 100 000 persons. All age groups are affected … with a median age of 70–80 years” (Stabler 2013).
Figure 3.4.2: The small intestine connects the stomach and the colon. It includes the duodenum, jejunum, and ileum.
Management of Vitamin B12 Deficiency in the Dental Office
The liver stores an abundant amount of cobalamin, and a deficiency may take two to five years to develop (Field et al. 1995, Pontes et al. 2009). Symptoms are most frequently observed in the elderly population and strict vegetarians. Oral and peri‐oral manifestations, such as glossitis, angular cheilitis (Figure 3.4.3 and 3.4.4), and candidiasis, are frequently observed prior to other more significant symptoms of a vitamin B12 deficiency (Pontes et al. 2009).
Figure 3.4.3: Angular cheilitis and depapillation of the tongue in a patient with pernicious anemia.
Source: Ibsen, 1992. Reproduced with permission of Elsevier.
Figure 3.4.4: The mucosa becomes atrophic in pernicious anemia and easily ulcerated. Note ulcer on left lateral aspect of the tongue.
Source: Ibsen, 1992. Reproduced with permission of Elsevier.
This patient’s oral symptoms, along with a history of hypothyroidism, strict vegetarianism, and fatigue may all be related to a vitamin B12 deficiency. Patient discussion would include a referral to her primary care physician for blood tests to determine the cause of her symptoms. A physician would need to determine first, that the anemia is present. This is usually done by evaluating the complete blood count (CBC). Once anemia is confirmed, the physician would need to identify the anatomic location and cause for the deficiency and rule out any underlying disease (Antony 2016).
Dietary counseling would include the role of vitamin B12 in cell maintenance and homeostasis. In most instances, dietary deficiency can be alleviated with vitamin supplements or parenteral injections.
Take‐Home Hints
- An average nonvegetarian Western diet contains 5–7 mcg per day of cobalamin, which adequately sustains normal cobalamin equilibrium.
- A vegetarian diet supplies between 0.25 and 0.5 mcg per day of cobalamin, so most vegetarians do not receive adequate dietary cobalamin and are at risk for cobalamin deficiency.
- The recommended daily allowance is 2.4 mcg for men and nonpregnant women, 2.6 mcg for pregnant women, 2.8 mcg for lactating women, and 1.5–2 mcg for children aged 9–18.
- When placing radiographic holders or sensors be careful of patient’s sensitivity due to the condition of the oral mucosa.
- Vitamin B12 is found naturally only in foods of animal origin, such as liver, meats, and milk. Some cereals are fortified with Vitamin B12.
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