ANEMIAS

Some important concepts

Anemia is defined as a reduction in the oxygen-carrying capacity of the blood

and usually is related to a decrease in number of circulating red blood cells (RBC)
or to an abnormality in the hemoglobin (Hb) contained within the RBCs
Iron deficiency

Decreased production of RBCs Pernicious anemia (vit B12 )

Folate deficiency

Anemia
Blood loss  Usually chronic blood loss

Increased rate of destruction of RBCs  Hemolytic anemia

Some important concepts

 Represents the % of packed RBC’s in

whole blood

M
F
41-50 36-45

Normal Values:
Men 41.5-50.4%
Women 35.9-44.6%
Classification of anemia by pathogenesis
Blood Loss Anemias
Hemolytic anemias
Bone Marrow

Destruction of RBCs Chronic

Factory Spleen Peripheral

Materials

Hypoproliferative anemias

“Formula” Disorders of Hemoglobin

 Classification of anemia by pathogenesis

Blood loss anemia Iron deficiency anemia

Plummer-Vinson Syndrome

Hemolytic anemias Glucose 6 phosphate dehydrogenase

Deficiency (G-6-PD deficiency)
Drug Induced
Immune mediated
Disorders of hemoglobin Sickle cell anemia
Thalassemia

Hypoproliferative anemias Vitamin B12 Deficiency

Pernicious anemia
Folic acid deficiency
Aplastic anemia
Blood loss anemias

Iron deficiency anemia

-Most common of all anemias

-30% of the world population

-In U.S. 5-11% of women and 2% of men

-Southeast Asia  High prevalence: Cultural background

-Causes:Chronic blood loss

Malabsorption syndrome  “Pica”

Celiac disease

Helicobacter Pylori
Blood loss anemias

Iron deficiency anemia

Diagnosis:

•Low hemoglobin level

•Microcytic – hypochromic cells in a peripheral blood smear
•Decrease mean corpuscular value (hemoglobin)

•Low serum iron level

•Markedly reduced serum ferritin level
•High serum iron-binding capacity
•GOLD STANDARD  Iron stores in bone marrow
Blood loss anemias

Iron deficiency anemia

peripheral blood smear

Low number of RBCs, pale and small in size

 Some important concepts

 Food
 Liver, meat, green vegetables, legumes,
nuts, egg yolk whole grain or enriched
breads, cereals
 Supplements
 Vitamins
▪ Elemental iron in iron supplements
 Ferrous fumarate 33%
Ferrous gluconate 11.6%
Ferrous
Ferrous SO4 20%
Ferrous sulfate, dessicated 30%

Iron interferes with absorption of: tetracyclines, quinolones, levothyroxine, pencillamine, levodopa. Wait 2 hrs
between drugs.
Hemolytic anemias

 G6 PD deficiency anemia
 Due to a deficiency of an enzyme in the hexose
monophosphate shunt pathway
 Found in 400 M persons worldwide
 11% of African Americans (has an association with SCA)
 Very prominent in persons of Mediterranean origin
 Blockage of this pathway allows accumulation of
oxidants in the RBCs with altered cell
membranes and resulting hemolysis
 Hemolytic episodes can be triggered by infection,
drugs and foods (fava beans)
 Aspirin, dapsone, ascorbic acid, vitamin K
Disorders of the hemoglobin

•SCA falls under a broad entity of diseases known as hemoglobinopathies

•Main Problem: Abnormal hemoglobin

•SCA: autosomal recessive disorder and is characterized by an abnormality in

the B-chain of the hemoglobin and an abnormal RBC (trait vs disease)

•Mainly affects persons of African or Afro-Caribbean descent

•When the red blood cell is subjected to a low oxygen tension the hemoglobin will
form a sickle-shaped crystal within the erythrocyte

Sickling may also be precipitated by infection, dehydration, hypoxia, acidosis

and results in painful “crises” due to infarcts caused by stasis of blood flow
(spleen, bones, joints, brian, kidneys, lungs, eyes and skin)
Disorders of the hemoglobin

When the red blood cell is subjected to a

low oxygen tension the hemoglobin will
form a sickle-shaped crystal within the
erythrocyte
 Disorders of the hemoglobin

•Sickle cell trait

Normal adult hemoglobin molecule is made of 2 alpha and 2 beta chains:

Hemoglobin A

In patients with SCA the normal molecule is substituted for 75-100% hemoglobin S
(substitution of the a.a.)

In patients with the sickle cell trait  20-35% of the hemoglobin is S, the rest
is normal  hemoglobin A

Patients with the “trait: usually have a normal life with mild symptoms,
except under ABNORMAL low oxygen conditions
Disorders of hemoglobin

 Thalassemias
 Due to a genetic defect in either the α- or
β-globin chain of hemoglobin resulting in
diminished survival of RBCs
 Common in persons of Mediterranean,
African and Southeast Asian ancestry
 β-thalassemia treated with blood
transfusion, folic acid supplement and
ascorbic acid, and possibly splenectomy
Hypoproliferative anemias

Vitamin B12 deficiency

•Vitamin B12 deficiency along with folic acid deficiency falls under the
group: MEGALOBLASTIC ANEMIAS

•Foods of animal origin are the primary dietary sources of Vitamin B12

•Vitamin B12 deficiency takes 2 to 5 years to develop  storage

•Cobalamin is necessary for DNA synthesis and a deficiency prevents

the normal cell duplication in the bone marrow

•Production of large erythrocytes

•Vitamin B12 deficiency seen in  Malabsorption

 Strict vegetarians.
Hypoproliferative anemias

Pernicious Anemia

Pernicious Anemia (PA) is the most common cause of Vitamin B12

-Pernicious
deficiency and is associated with chronic atrophic gastritis.

Other conditions than can lead to vitamin B12 deficiency: gastrectomy

-Other

-PA develops because atrophic changes in the gastric mucosa results

in lack of intrinsic factor production, which is necessary for the absorption
of Vitamin B12 from the gut
Hypoproliferative anemias

Pernicious Anemia

-In 85% of the patients serum antibodies to the gastric parietal cells are
noted

-Additionally in 50% of patients, serum antibodies to intrinsic factor

have been noted

-Other autoimmune conditions: Grave’s, Hashimoto, Addison

-Diagnosis: Shilling test: small amount of radioactive Vitamin B12 orally 

after 24 hours: amount of radioactive Vit. B12 in the urine (7-30%)
Physical and Oral Manifestations

Iron deficiency anemia

•Pallor

- Oral mucosa: Soft palate, tongue and sublingual tissues

- Conjunctiva

•Jaundice is usually not evident

•“Spoon-shaped fingernails”  Koilonychia

•Atrophic tongue

•Glossodynia

•Burning Mouth Disorders

 Physical and Oral Manifestations

Plummer-Vinson Syndrome

•Type of Iron deficiency characterized by dysphagia and microcytic hypochromic anemia

•Sore depapillated tongue

•Xerostomia

•Angular stomatitis

•Koilonychia

•Atrophic changes are not limited to the oral cavity  pharynx, upper GI

•Pallor fatigue, dyspnea

•DYSPHAGIA  Muscular degeneration of the esophagus

•Important: Increased prevalence of oral and pharyngeal carcinoma

Physical and Oral Manifestations

Glucose 6-phosphate dehydrogenase deficiency

• Most common manifestation : JAUNDICE

• Jaundice: sclera, palate and floor of the mouth

•Radiographic changes: Increase in the trabeculation of the bone (more radiolucent)

Hyperplasia of the erythroid elements of the bone marrow

Physical and Oral Manifestations
Sickle cell anemia

•Marked underdevelopment

•Majority of the patients die before 40 years of age

•Hemolytic anemia  Pallor

Jaundice
Congestive Heart Failure
Strokes
Pain crisis
Small Infarcts

Increased risk for developing infections with:

- S. pneumoniae
- H. influenza
- Salmonella
- E. Coli
 Physical and Oral Manifestations
Sickle cell anemia

•Hypoplasia of the dentition

•Delayed eruption

•Increased bone trabeculation

•Dense lamina dura

•Skull film: thick cortex  classical appearance “hair on end”

•Areas of bone sclerosis in periapical films

•Sometimes paresthesia of mental nerve

Physical and Oral Manifestations
Sickle cell anemia
Thick Cortex

classical appearance “hair on end”

Physical and Oral Manifestations

Thalassemia

•Bone marrow expansion  Ineffective erythropoiesis

•Bimaxillary protrusion

•Spacing of the teeth

•Marked open bite

•Prominent malar bones

•Thin cortical bone

•Discoloration of the teeth  Iron deposit

Physical and Oral Manifestations

Folic Acid deficiency anemia

-Pharyngitis

-Ulcerative Stomatitis

-Angular cheilitis

-Difference with pernicious anemia: No neurological symptoms

Physical and Oral Manifestations

Vitamin B12 deficiency / pernicious anemia

•In children Vitamin B12 deficiency often presents with non-specific symptoms

•Neurological symptoms: paresthesia, sensory deficit, loss of reflexes, hypotonia

seizures, dementia

•Abnormal skin pigmentation

•Systolic murmurs

•Glossodynia

•Atrophic tongue

•Tongue hypotonic (advance stage)

•Erythema and macular lesions in the dorsum of the tongue

•Dysphagia and taste aberrations

•BMD: Burning mouth Disorder

Dental Management of Patients with

Anemia
Dental Management of Patients with Anemia

General issues:
Patients with severe anemia may not tolerate blood loss or hypoxia
Patients with anemia may not tolerate certain drugs
Patients with anemia may not handle infection well

1. CBC with differential in who patient presents with sign and symptoms
of anemia

1. Consultation with primary MD if low hematocrit or hemoglobin is found

2. Assessment of the severity of the anemia in conjunction with the patient MD

3. Possible blood transfusion prior to treatment if anemia is severe

4. Avoidance of elective treatment in patient who are in “crisis”

Dental Management of Patients with Anemia
Sickle cell anemia

Cautious use of nitrous oxide analgesia in patient with sickle cell anemia;
ensure good oxygenation at all times

Avoid respiratory depressants

Avoid aspirin in large doses (to avoid acidosis); acetaminophen or codeine

are better choices

Consider prophylactic antibiotics for surgical procedures

Aggressive management of infections

G-6-PD Deficiency
Avoid the use of aspirin
The end