Dental Considerations of Children with Anemias - An Overview

Review Article

J Dent & Oral Disord. 2019; 5(2): 1113.

Dental Considerations of Children with Anemias - An Overview

Nirmala SVSG* and Saikrishna D

¹Department of Paedodontics & Preventive Dentistry, Narayana Dental College & Hospital, India

²Department of Oral & Maxillofacial Surgery, India

*Corresponding author: Nirmala SVSG, Department of Paedodontics & Preventive Dentistry, Narayana Dental College & Hospital, Nellore, India

Received: June 03, 2019; Accepted: July 15, 2019; Published: July 22, 2019

Abstract

Anaemia affects one-fourth of the world’s population and iron deficiency is the predominant cause. It affects both the genders but more frequently seen in females than males. It is associated with chronic fatigue, impaired cognitive function, and diminished well-being. Anaemic disorders associated with orofacial signs and symptoms include iron deficiency anaemia, megaloblastic anaemia, sickle cell anaemia, and aplastic anaemia. The manifestations include conjunctiva and facial pallor, atrophic glossitis, angular stomatitis, dysphagia, magenta tongue, midfacial overgrowth, osteoclerosis, osteomyelitis and paraesthesia/anaesthesia of the mental nerve. Orofacial petechiae, conjunctivae haemorrhage, nose-bleeding, spontaneous and post-traumatic gingival haemorrhage and prolonged post-extraction bleeding are common orofacial manifestations. Dental management of patients of aplastic anaemia requires inter disciplinary care with the consultation of the treating dentist with haematologist. This article provides aetiology, clinical features, investigations, diagnosis and treatment of different types of anaemia.

Keywords: Anemia; Children; Dental management; Oral health

Introduction

Anaemia is a term used to define a decrease in the oxygen carrying capacity of blood characterized by a decrease in the number of red blood cells, haemoglobin, and haematocrit result from blood loss (iron deficiency anaemia), decreased red cell production (Aplastic anaemia) or increased red cell destruction (Haemolytic anaemia) [1].

The World Health Organization defines anaemia as a level of Hb below 13.0 g/dL in male adults, below 12.0 g/dL in female adults who are not pregnant, and below 11.0 g/dL in pregnant women. 47 Hb levels may vary across age and race, 48 so care must be taken, particularly in the interpretation of borderline values [2].

Classification

Anaemia can be classified morphologically, etiologically and based on Reticulocyte Production Index (RTI) (kinetic classification).

Morphological classification

It is based on measurement of red blood cells. “There are three types of anaemias depending on RBC size (Table 1).

Table 1: Showing morphological classification.





  

    
1

    
Microcytic hypochromic

    
Characterized by low mean    corpuscular volume (MCV) and mean corpuscular haemoglobin (MCH). e.g.    iron deficiency anaemia, thalassemia

  

  

    
2

    
Normocytic normochromic

    
Characterized by normal MCV and    MCH, e.g. acute blood loss, marrow infiltration, haemolysis (occasionally    macrocytic) and chromic disease (occasionally microcytic hypochromic).

  

  

    
3

    
Macrocytic

    
Characterised by raised MCV,    eg. megaloblastic anaemia

  










Table 1: Showing morphological classification.

Etiological classification: It is based on the cause of anaemia and can be classified as per etiology as represented in (Table 2).

Table 2: Showing etiological classification.





  

    
Due to destruction of RBC, e.g.    haemolytic anaemia

  

  

    
Due to bleeding

  

  

    
Dilution of RBC by increased    plasma level of hypersplenism

  

  

    
Failure of RBC production by    the bone marrow

  

  

    
    
      
  • Nutritional deficiency, e.g. Iron, Vitamin BIZ and Folate
    • 
    

  

  

    
    
      
  • Ineffective red cell formation, e.g. chronic inflammation, thalassemia    and renal disease
    • 
    

  

  

    
    
      
  • Reduced bone marrow erythroid cells, e.g. aplastic anaemia, bone    marrow infiltration in case of leukaemia or malignancy
    • 
    

  










Table 2: Showing etiological classification.

Based on the Reticulocyte Index (RPI) anaemias are classified as 2 types (Table 3).

Table 3: Showing reticulocyte index classification.





  

    
1

    
Hypo proliferative (RPI <    2.5)

    
i.e. anaemias caused by    decreased RBC production due to deficiency of nutrients or systemic disease

  

  

    
2

    
Haemolytic (RPI > 2.5)

    
Which can be congenital or    acquired.

  










Table 3: Showing reticulocyte index classification.

Iron deficiency anemia

Iron deficiency is the predominant cause of anaemia across countries and in both sexes, with women more commonly afflicted [1]. The prevalence of anaemia increases with age3 and in the hospital setting. Anaemia decreases the capacity for work and increases health care costs. Iron deficiency is also associated with Restless Legs Syndrome (RLS), diminished quality of life, fatigue, impaired cognitive function, and infertility, all of which may occur in the absence of anaemia and may be reversed with iron therapy.

Iron deficiency is the predominant cause of anaemia across countries and in both sexes with women more commonly afflicted [1-3]. Prevalence of anaemia increases with age3 and in the hospital setting. anaemia decreases the capacity for work and increases health care costs [4,5] iron deficiency is also associated with restless legs syndrome rls diminished quality of life fatigue impaired cognitive function and infertility all of which may occur in the absence of anaemia and may be reversed with iron therapy [1-3]. Clinical and oral manifestations 5 are shown in (Tables 4-6).

Table 4: Showing clinical manifeastations.





  

    
Clinical Manifestations

  

  

    
    
      
  • Headaches
    • 
    

  

  

    
    
      
  • Lack of concentration
    • 
    

  

  

    
    
      
  • Feeling weak and tired more often
    • 
    

  

  

    
    
      
  • Koilonychia, glossitis/dysphagia (not common in developed world).
    • 
    

  










Table 4: Showing clinical manifeastations.

Table 5: Showing oral manifestations.





  

    
Oral manifestations

  

  

    
Angular stomatitis manifested as painful fissures at the corner of the    mouth.

  

  

    
Angular cheilitis manifested as scaling of the lips and corner of the    mouth, usually associated with fungal infection.

  

  

    
General pallor of lips mucosa

  

  

    
Erythematous mucositis

  

  

    
Burning mouth syndrome

  

  

    
Plummer-Vinson syndrome

  

  

    
Atrophic glossitis can be described as flattening of tongue papillae    leading to smooth red tongue appearance resembling migratory glossitis

  

  

    
Tongue appears to be erythematous, atrophic, non-indurated and big in    size, they do not change their position

  

  

    
Decreased healing response

  










Table 5: Showing oral manifestations.

Table 6: Simple Scheme for the estimation of total iron need.





  

    
Degree    of Iron Deficiency 

    
Hemoglobin    Level g/dL 

    
Dose    for Body Weight <70 kg, mg 

    
Dose    for Body Weight =70 kg, mg 

  

  

    
No    anaemia 

    
Normal 

    
500 

    
1000 

  

  

    
Moderate 

    
10-12    (Women) 

    
1000 

    
1500 

  

  

    
10-13    (Men) 

  

  

    
Severe 

    
10-Jul 

    
1500 

    
2000 

  

  

    
Critical 

    
>7 

    
2000 

    
2500 

  










Table 6: Simple Scheme for the estimation of total iron need.

Investigations: Haematocrit shows microcytic and hypochromic RBC.

MCV: MCV less than 95 pm is suggestive of Iron Deficiency Anaemia (IDA).

Ferritin: Ferritin less than or equal to 45 mg/mL is suggestive of IDA. If ferritin is between 46 mg/mL and 99 mg/mL, the Serum Transferrin Receptor (TfR) is assessed. Increased TfR confirms iron deficiency anaemia.

Modified from Evstatiev R, et al, with permission [7].

Management [6]

1. Oral iron therapy is the first line of treatment. Hb level of lg/dL should increase every 2-3 weeks on iron therapy; however, it may take up to 4 months for iron stores to become normal.

2. Iron sulfate 300 mg provides 60 mg of element iron, whereas 325 mg of iron gluconate provides 36 mg of element iron.

3. Gastrointestinal absorption of element iron is increased with acidic environment, which is achieved by giving ascorbic acid in conjunction of iron therapy.

4. Blood transfusion should be considered if patient complains of fatigue or dyspnoea on exertion and in cardiac patient with Hb less than 10 g per dL.

Aplastic anaemia

It is a severe and frequently fatal hematologic disorder characterized by hypoplastic bone marrow and peripheral pancytopenia. Aplastic anaemia is a sporadic, noncontagious and possibly life threatening disorder formed by destruction of pluripotent stem cells in the bone marrow with an annual incidence of 2 to 6/1,000,000 [1]. Liable on affected cell lines, aplastic anaemia is linked with not only fatigue, but also bleeding due to thrombocytopenia and recurrent infections owing to neutropenia [8]. The diagnosis ‘aplastic anaemia’ is established by hypocellularity of the bone marrow and the remaining cells are morphologically unaffected without malignant infiltration.

It is classified as acquired or congenital. The congenital type is rare and frequently related with Fanconi’s anaemia and dyskeratosis congenita. In more than 50% of acquired cases of aplastic anaemia, the exact cause is unidentified. Probable causes for the onset of aplastic anaemia comprise T-cell mediated auto-immune disease, iatrogenic agents, viral infection and pregnancy [1].

It is more common in Asian population than in the United States and Europe with about 6000–7000 new cases reported yearly global. It can be seen at any age but is most classically make out in children aged 2-5 years, young adults between 20 and 25 years.

A pancytopenia is identified when two of three principles are met: a neutrophil count of less than 0.5 · 109 cells/L, a platelet count less than 20 · 109 cells/L and a reticulocyte count less than 1%. When the neutrophil count is less than 0.2, the disease is then described as severe [1].

Oral manifestations are common in patients with aplastic anaemia and are directly associated with pancytopenia. These manifestations include petechial hemorrhages, gingival swelling and spontaneous bleeding, ulceration, pallor and severe periodontal disease.

Gingival bleeding is another collective manifestation concomitant with reduced platelet level seen in aplastic anaemia patients [7]. Oral traumatic and petechial haemorrhagic lesions have been related with the diminished platelet level. It was designates the risk factors linked with oral manifestations of aplastic anaemia and proposes that the level of thrombocytopenia is not essentially suggestive of the degree of petechial haemorrhage [16,17] (Table 7).

Table 7: Showing causes and clinical features of Aplastic Anaemia.





  

    
Causes

    
Oral manifestations

  

  

    
Failure In production of    erythrocytes

    
Gingival haemorrhage

  

  

    
Acquired

    
Mucosal pallor

  

  

    
    
      
  • Idiopathic, Autoimmune
    • 
    

    
Petechial spots

  

  

    
    
      
  • Drugs: Cytotoxic
    • 
    

    
Oral ulceration and infection

  

  

    
    
      
  • Idiosyncratic
    • 
    

    
Neutropenia there is a lack of    resistance to infection

  

  

    
    
      
  • Lnfectlous -- hepatitis
    • 
    

    
candidiasis and viral    infection,

  

  

    
    
      
  • Pregnancy
    • 
    

    
  

  

    
    
      
  • Paroxysmal, nocturnal
    • 
    

    
  

  

    
    
      
  • hemoglobinuria
    • 
    

    
  

  

    
CongenitaI/famillal

    
  

  

    
    
      
  • Fanconi's anemia
    • 
    

    
  

  

    
    
      
  • Dyskeratosis congenital
    • 
    

    
 

  

  

    
    
      
  • Black fan-Diamond anemia
    • 
    

    
  










Table 7: Showing causes and clinical features of Aplastic Anaemia.

Management [13-15]

1. Treatment is given with parenteral vitamin B 12 cncbl a daily dose. The transfusion is only required in special cases like when Hb goes below 15% of normal or if a patient is in heart failure.

2. Dental management of patients of aplastic anaemia requires interdisciplinary care with the consultation of the treating dentist with haematologist.

3. It is advisable to perform dental treatment on the day of platelet transfusion.

4. To reduce the risk of uncontrolled bleeding during major dental treatments, the patients should take antifibrinolytics. These agents may decrease bleeding, particularly oral mucosal bleeding, in patients with thrombocytopenia by stabilization of thrombi.

5. Jones et al have reported a case of idiopathic aplastic anaemia which was treated with a combination of modalities including early platelet transfusion, oral hygiene instruction, dental prophylaxis and systemic aminocaproic acid.

6. Patients with aplastic anaemia are more susceptible to infection; therefore, dental treatment should be postponed until the patient’s white blood cell count rises to a normal level.

7. Prior to the dental procedure consider prescribing antibacterial mouthwash and oral antibiotics.

8. If necessary, consultation with a haematologist.

Megaloblastic anemia

It is the type of anaemia produced by disorders of DNA synthesis of erythrocyte precursors in bone marrow. Megaloblastic red blood cells are larger than the normal red blood cells and contain more cytoplasm in relation to the nucleus.

Aetiology: Megaloblastic anaemia can arise due to any of the following causes:

Folate deficiency: It can occur in case of decreased intake, poor nutrition, old age, alcoholism, haemodialysis, premature infants, spinal cord injury, small intestine disease, and tropical and no tropical sprue.

Increased requirement: Increased requirement corresponds with pregnancy, increased cell turnover. Chronic haemolytic anaemia and cobalamin deficiency. Impaired absorption: It can occur in cases of pernicious anaemia, gastrectomy, Zollinger-Ellison syndrome and pancreatic insufficiency.

Drugs: Antimetabolites, anticonvulsants, oral contraceptives, etc.

In-born errors and decreased intake [18].

Clinical features and oral manifestations are given in (Table 8).

Table 8: Showing clinical features and oral manifestations.





  

    
Oral manifestations

    
Clinical features

  

  

    
Painful atrophic changes of    entire oral mucosa

    
Weakness

  

  

    
Glossitis

    
Palpitation

  

  

    
Recurrent aphthous ulcer

    
Light-headedness

  

  

    
Burning mouth syndrome

    
Loss of appetite

  

  

    
Ulcerative gingivitis

    
Shortness of breath

  

  

    
Stomatitis

    
Diarrhoea

  

  

    
Bleeding gingivae

    
Peripheral numbness.

  

  

    
Denuded tongue

    
Smooth or tender tongue

  

  

    
Glossodynia

    
  

  

    
Delayed wound healing

    
  

  

    
Oral paraesthesia

    
  

  

    
Loss of taste and Xerostornia

    
  

  

    
Bone loss

    
  










Table 8: Showing clinical features and oral manifestations.

Management

1. Treatment is given with parenteral Vitamin B12 (CnCBl) a daily doses.

2. Transfusion is only required in special cases like when Hb goes below 15% of normal or if patient is in heart failure.

Sickle cell anemia

Introduction: Linus Pauling actually identified haemoglobin S as the abnormal haemoglobin associated with Sickle Cell Anaemia. Sickle cell anaemia is a genetic disease that primarily affects the black population. This anaemia is due to a homozygous state of the abnormal haemoglobin S. An alteration occurs on the DNA molecule involving the substitution of the amino acid valine for glutamic acid at the sixth position on the beta polypeptide chain (Rose and Kaye 1983). This biochemical variation on the DNA molecule creates a physiological change that causes sickle-shaped red blood cells to be produced. The sickle-shaped cells are the result of the haemoglobin S being deoxygenated. With a decrease in affinity of oxygen to an abnormal haemoglobin, deoxygenation will occur, again producing more sickle-shaped cells. This leads to obstruction or microvasculature erythrostasis, causing vasocclusion and extensive organ damage. It is a cyclic process [19,20].

Sickle cell anaemia may be diagnosed in the sixteenth week of gestation, but manifestations normally do not appear until the sixth month after birth. Newer techniques for hemoglobin electrophoresis can be used to diagnose the abnormal hemoglobin at birth. Painful episodes or ”crises“ characteristic of this disease are vasocclusion, sequestration, aplastic, and to a lesser degree, hyperhemolysis.

Many factors can precipitate a sickle cell crisis, including acidosis, hypoxia, hypothermia, hypotension, stress, hypovolemia, dehydration, fever, and infection [21].

Incidence: Approximately one of every 500 black children in the United States has SCA. The homozygous state of this chronic hemolytic anaemia typifies the most devastating effect [22]. Persons with the sickle cell trait occasionally may show manifestations of the disease in hypoxic states caused by exposure to high altitudes or shock [23]. These patients are usually without Symptoms; however, it has been reported that systemic diseases, dehydration, infection, and hypoxia are some of the etiological factors of sickle cell Anaemia due to haemolysis, aplastic crisis, impaired growth and skeletal deformities are general features.

Clinical features and oral manifestations are given below (Table 9) [24].

Table 9: Showing clinical features and oral manifestations.





  

    
Clinical features

    
Oral manifestations

  

  

    
Shortness of breath

    
Mucosa pallor

  

  

    
Headaches

    
Accentuated incremental line

  

  

    
Dizziness Coldness of hand and    feet

    
Developmental defects occurring    due to hypomineralization of enamel along with delayed eruption of teeth

  

  

    
Sudden pain throughout the body

    
Pulp stones or calcification of    pulp, pulpal pain may be due to tissue infarction and thrombosis

  

  

    
Jaundice

    
Hypercementosis

  

  

    
    
Dental caries

  

  

    
    
Malocclusion, midline diastema

  

  

    
    
Midfacial overgrowth due to    marrow hyperplasia , Thickening of skull, Osteoporotic changes in jaw

  

  

    
    
Step ladder appearance of    alveolar bone

  

  

    
    
Coarse trabecular pattern    between the root apices and

  










Table 9: Showing clinical features and oral manifestations.

Dizziness Coldness of hand and feet.

Developmental defects occurring due to hypomineralization of enamel along with delayed eruption of teeth

Sudden pain throughout the body Pulp stones or calcification of pulp, pulpal pain may be due to tissue infarction and thrombosis.

Radiographic changes are associated with sickle cell anaemia. There are a generalized radiolucency and loss of trabeculae with prominent lamina dura, caused by increased erythropoietic demands that result in the expansion of the marrow spaces. Bone growth may be decreased in the mandible, resulting in retrusion, and the teeth may be hypomineralized. Occasionally, patients with sickle cell anaemia have infarcts in the jaw, which may be mistaken for a toothache or osteomyelitis [22,25,26]. The patients experience dental pain with the absence of pathology (Table 10).

Table 10: Showing radiographic features of sickle cell anaemia.





  

    
Increased radiolucency of the    jaw

  

  

    
Coarse trabecular pattern and    decreased number of trabecular

  

  

    
'Thin inferior border of the    mandible

  

  

    
Distinct areas of osteoporosis.

  

  

    
Generalized osteoporosis

  

  

    
Step ladder effect due to    horizontal rows of trabeculation and Retrusive maxilla

  

  

    
Dense lamina dura due to hyperplastic    marrow.

  










Table 10: Showing radiographic features of sickle cell anaemia.

Radiographic Features are shown in (Table 10).

Many patients with sickle cell anaemia have defective spleen function or undergo a splenectomy, which leaves them more vulnerable to infection because immunoglobulin production is decreased and phagocytosis of foreign antigens is thus impaired. Most patients with sickle cell anaemia are taking low-dose daily prophylactic antibiotics, and the need for additional antibiotics for dental procedures is debatable. Some authors have recommended the use of antibiotics for all dental procedures, whereas others recommend the administration of additional antibiotics when there is an obvious dental or periodontal infection. The selection of an antibiotic is usually similar to that in cases of a heart defect [27-30].

Dental Management [31-35]

1. Dental appointments should be short to reduce possible stress on the patient.

2. The importance of an aggressive preventive program cannot be understated, and such a program should have the goal of maintaining excellent oral health and lessening the possibility of oral infection.

3. Dental treatment should not be initiated during a sickle cell crisis. If emergency treatment is necessary during a crisis, the only treatment that will make the patient more comfortable should be provided.

4. Patients with sickle cell anaemia may have skeletal changes that make orthodontic treatment beneficial.

5. Special care must be taken to avoid tissue irritation, which may induce bacteraemia, and the disease process may compromise the proposed treatment.

6. Careful monitoring is a necessity when proposing elective orthodontic treatment in patients with sickle cell anaemia.

7. The restoration of teeth, including pulpotomies, is preferable to extraction.

8. Polypectomy in a nonvital tooth is reasonable if the practitioner is fairly confident that the tooth can remain non infected. if the tooth is likely to persist as a focus of infection, then extraction is indicated.

9. The use of general anaesthesia for dental procedures must be approached cautiously in consultation with the haematologist and anaesthesiologist.

10. Previously, the standard protocol was to perform a direct transfusion (immediate introduction of whole blood or blood components) or an exchange transfusion (repetitive withdrawal of small amounts of blood and replacement with donor blood until a large portion of the patient blood has been exchanged) before general anaesthesia.

11. The goal of the transfusion is to increase the patient’s haemoglobin level to higher than 10 g/dL and to decrease the haemoglobin 8 levels below 40%. Transfusions do not provide complete protection against venous complications, but they may temporarily improve the patient’s condition and reduce the hazards of surgery.

12. The current thinking is to weigh the risks associated with transfusion prior to anaesthesia induction.

13. Suggested guidelines for performing a prophylactic transfusion before general anaesthesia have been proposed. Patients with a haemoglobin level of less than 7 g/dL and a hematocrit of less than 20% may require a transfusion.

14. Pediatric patients are usually less likely to have posttransfusion complications than are adults. A high frequency of hospitalizations is indicative of more severe anaemia, and such patients may require transfusion before surgery.

15. Minor surgeries may not require a transfusion.

16. Local anaesthetic is the preferred anaesthetic for those patients as according to Malamud and these patients belong to ASA Ill categories. The use of local anaesthetic does not affect the oxygenation of the blood molecule.

17. Oral sedation can also be used as an anxiolytic agent.

18. The use of local anaesthetic does not affect the oxygenation of the blood molecule.

19. Oral sedation can also be used as an anxiolytic agent.

For cases to be considered under general anaesthesia: [36,37]

1. Proper/adequate haemoglobin levels to be activated 15 days prior to the procedure through transfusion to prevent sickle cell anaemia crisis.

2. Optimum level to be maintained for children is 1012 g/dL. Prophylactic antibiotic to be given before the procedure in order to avoid infection.

3. Blood transfusion is used to manage acute manifestations of the disease such as aplastic crises, splenic sequestration, etc.

4. Hydroxyurea is a cytotoxic drug, which is commonly used in treatment of leukaemia and polycythaemia Vera. But it also has property to increase fetal haemoglobin and fetal haemoglobin prevents sickling of cells.

5. The only cure of sickle cell disease is hematopoietic stem cell disease [38].

Conclusion

Hematologic diseases are a major health problem and have a greater significance to the practice of dentistry. Children with anaemias frequently exhibit oral manifestations of the condition. Prevention, early diagnosis and proper treatment of oral complications are essential to diminish morbidity and avoid a possible outcome. Oral lesions can be the first manifestation of these anaemias; consequently, dentists should be aware of these manifestations so that an early diagnosis of the disease can be made in children. Hence, their quality of life is improved.

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Citation:Nirmala SVSG and Saikrishna D. Dental Considerations of Children with Anemias - An Overview. J Dent & Oral Disord. 2019; 5(2): 1113.