Presented by

Dr. Sourav Bose

1st yr PG
 PREVIOUS YEAR QUESTIONS

• RBC

(MDS Degree examinations March 1994, 2000)

• RBC Morphology & Functions

(MDS Degree examination April/May 07 & 2010)

• Iron deficiency anemia

(MDS Degree examination Sept 2007)

 CONTENTS
 Introduction
 History
 General features
 Erythropoiesis
 Hemoglobin
 ESR & PCV
 RBC Disorders
 Public Health
Significance
 Conclusion
 References
 INTRODUCTION
• RBC - red cells / red blood corpuscles / haematids / erythroid
cells / erythrocytes.

• Derived from Greek erythros for "red" and kytos for

"hollow vessel", with -cyte translated as "cell" in modern
usage.

• Non-nucleated formed elements in the blood.

• It lacks cytoplasmic organelles such as nucleolus, mitochondria
& ribosomes.

• The red color of RBC is due to the presence of Hemoglobin

(90%).
 HISTORICALBACKGROUND
• JAN SWAMMERDAM-1658 - Dutch biologist and
microscopist. He called them ruddy globules
• ANTON VAN LEEUWENHOEK-1674- Discovered
Microscope and established its size.
• OTTO FUNKE 1851 - German physiologist was the first
scientist to successfully crystallize hemoglobin.
• DR. MAX PERUTZ- 1959 - by use of X-ray crystallography
unravelled the structure of hemoglobin.
• MENGHINI-1747- presence of iron in the blood, identified the
red corpuscles as the chief site of iron within the organism.
 GENERAL FEATURES
• Dimensions

• Normal Count

• Composition

• Functions

• Fragility

• Variations

• Fate &
Lifespan
 DIMENSIONS

• Shape: Biconcave

• Size: 7.2um in diameter

• Thickness: 2um at the periphery and 1um at the center

• Volume: 87um3
Advantages of Biconcave Shape of RBCs:

•Greater surface area for exchange of gases.

•Flexibilty of RBC
•Minimal tension when the volume of cell alters.

How is the shape maintained?

 Spectrin

- a contractile protein

- maintains shape and flexibility of RBC

 NORMAL COUNT

• Adults males: 4.5 – 6 million cu mm of blood

• Adult females: 4 – 5.5 million cu mm of blood

• At birth: 6.7 million cu mm of blood

 COMPOSITION
• 62.5% water

• 35% Hemoglobin

• 2.5% :

-Sugar – Glucose

-Lipids – Cephalin, Cholesterol & Lecithin

-Protein – Glutathion : insoluble protein which acts as
a reducing agent and prevents damage of hemoglobin

-Enzymes – Carbonic anhydrase and catalase

-Ions – Na+, K+, Ca2+, PO43-

 FUNCTIONS

• Respiratory

• Acid Base balance (it regulates hydrogen ion conc)

• Blood Group determination( presence of A antigen B

antigen & Rh Factor)
 FRAGILITY AND HEMOLYSIS
• Hemolysis- Breakdown of RBC and liberation of hemoglobin.
• Fragility- Susceptibility of RBC to hemolysis or tendency to
break easily.

• There are 2 types:

1. Osmotic fragility- due to exposure to hypotonic saline.

2. Mechanical fragility- due to mechanical trauma

 VARIATIONS
Physiologic causes of increase count:

• Age

• Gender

• High altitude

• Exercise

• Temperature

• Meal
 Decrease in count:
 High barometric pressure

 Pregnancy

 sleep
Pathological variations:

Increase: Polycythemia

Decrease: Anaemia
 VARIATIONS IN SHAPE

• Crenation: Shrinkage as in hypertonic

solutions.

• Spherocytosis: Globular form as in hypotonic conditions.

 Elliptocytosis: elliptical shape

 Sickle cell: Crescent shape

 Poikilocytosis: Flask, hammer or any other unusual shape.

 VARIATIONS IN SIZE
• Physiological conditions: RBC in venous blood slightly larger
than those in arterial blood.

• Pathological conditions:

1. Microcytes – smaller cells

2. Macrocytes – larger cells

3.Anisocytes – cells of different sizes

 LIFESPAN AND FATE OFRBC

• Lifespan – 120 days

• Site of destruction:
Reticuloendothelial system
 ERYTHROPOIESIS
• The process of origin, development and maturation of erythrocytes.

 Site of erythropoiesis:

• In fetal life: - Mesoblastic stage

- Hepatic stage

- Myeloid stage

• In newborns, children and adults –

are produced from red bone marrow

FIGURE 10.1: Stem cells. L = Lymphocyte, R = Red blood cell, N = Neutrophil, B = Basophil,
E = Eosinophil, M = Monocyte, P = Platelet.
• Factors necessary for erythropoiesis:

1. General factors:

-Erythropoietin

-Thyroxine

-Hypoxia

2. Maturation factors:

-Vitamin B12 (Cyanocobalamin)

-Intrinsic factor of Castle

-Folic acid
 HEMOGLOBIN
• Hb is the iron containing coloring pigment of RBC

• Molecular weight of Hb is 68,000

• Normal value:

-At birth: 25g/dl

-From puberty: 14-16 g/dl

-Adult males: 15g/dl

-Adult females: 14.5g/dl

 STRUCTURE OF HEMOGLOBIN
• Conjugated protein
• Protein part called Globin and iron containing pigment called heme.

• Heme part is called porphyrin and is

formed by 4 pyrole rings

attached with each other by CH4

• Globin is made up of 4
polypeptide chains – 2 alpha and 2 beta

chains.
 Types of Hemoglobin :

• Normal: - Adult Hb ( 2 alpha and 2 beta) HbA

- Fetal Hb ( 2 alpha and 2 gamma) HbF

• Abnormal derivatives:

-Carboxyhemoglobin (1-3 %)

-Methemoglobin (0.6 -2.5 %)

-Sulfhemoglobin (less than 1%)

• Red cells have the property of Rouleaux (piling one on the other)
formation.

• Piled red cells are heavier than the individual ones.

• The rate at which the red cells fall is known as ESR.

• Normal values:
Wintrobe’s method: Males: 0 – 9mm/hr
Females: 0 – 20mm/hr

Westergren’s method: Males: 3 – 7mm/hr

Females: 5 – 9 mm/hr
Rouleaux (piling one on the other)
formation.
Westergren’s method:
• Westergren’s tube is used which is 300 mm long & opened at
both the ends.

• It requires collecting 2 ml of venous blood into a tube

containing 0 .5 ml of sodium citrate. It should be stored no
longer than 2 hours at room temperature
or 6 hours at 4 °C. The blood is drawn into

the tube to the 200 mm mark. The tube is

placed in a rack in a strictly vertical position

for 1 hour at room temperature,

Wintrobe’s method:
• The Wintrobe method is performed similarly except that the
Wintrobe tube is smaller in diameter than the Westergren tube
and only 100 mm long.
• EDTA anticoagulated blood without extra diluent

is drawn into the tube, and the rate of fall of red

blood cells is measured in millimeters after 1 hour.

 PACKED CELL VOLUME
• Hematocrit is the fractional volume of blood that the
erythrocytes occupy

• It is a reliable index of red cell population.

• Normal values : Males – 46%

Females – 42%
 RBCINDICES
• MCV (MEAN CORPUSCULAR VOLUME)
– The average volume of single RBC

PCV per 100ml blood

MCV =  10um3
RBC count (million/cu mm)

Normal range : 78 – 94 um3

 RBC with normal volume are called Normocytes
 RBC with less then normal volume, Microcytes
 RBC with more than normal volume, Macrocytes
• MCH (mean corpuscular hemoglobin)
– The average content of Hb in average RBC.

Hb in gm%
MCH =  10pg
RBC count (million/cu mm)

• Normal range: 28 – 32pg

• MCHC (mean corpuscular hemoglobin concentration)
– Express the average concentration of hemoglobin per unit
volume of RBC.
– It defined as the ratio of the weight of hemoglobin to
volume of RBC.

Hb in gm%
MCHC =  100
PCV per 100ml blood

Normal range: 33 – 38 gm/100ml of cells

 DISORDERS OF RBC
• Anemia
Morphologic classification

Etiologic classification

• Polycythemia
Polycythemia Vera

Relative polycythemia

Secondary polycythemia
 ANEMIA
• Anemia is defined as Hb concentration in blood below the

lower limit of the normal range for the age and sex of the

individual.

• In adults, the lower extreme of normal Hb is taken as 13g/dl

for males and 11.5g/dl for females.

 MORPHOLOGICAL CLASSIFICATION
• Depends upon the size and color of RBC.
• Size of RBC is determined by mean corpuscular volume
(MCV).

• Color is determined by mean corpuscular hemoglobin

concentration (MCHC).

• By this method, the anemia is classified into four types

Hyperchromic Hypochromic Macrocytic Microcytic
 ETIOLOGICAL CLASSIFICATION

• On the basis of etiology, anemia is divided into five types:

1. Hemorrhagic anemia

2. Hemolytic anemia

3. Nutrition deficiency anemia

4. Aplastic anemia

5. Anemia of chronic diseases.

 IRON DEFICIENCY ANEMIA
• Iron deficiency anemia is the most common type of anemia.
• It develops due to inadequate availability of iron for
hemoglobin synthesis.

• RBCs are microcytic and hypochromic.

 • Causes of iron deficiency anemia:
i. Loss of blood
ii. Decreased intake of iron
iii. Poor absorption of iron from intestine
iv.Increased demand for iron in conditions like growth and
pregnancy.
 • Clinical Features of iron deficiency anemia:
1. It occurs in mostly women in 4th and 5th decade of life.
2. Brittle nails,
3. Spoon shaped nails (koilonychias),
4. Brittle hair,
5. Atrophy of papilla in tongue
6. Dysphagia (difficulty in swallowing).
7. Knuckle pigmentation - (pigmentation can be seen on the dorsum of
the hand)
Oral manifestations:

• Pallor of mucosa

• Atrophy of oral mucosa

• Tongue changes – redness, soreness or burning sensation.
Papillae of the anterior two thirds undergo atrophy.

• Angular cheilitis

• Ulcerations

• Slow healing
 Diagnosis:
• Clinical – Koilonychia, angular cheilitis, depapillation of
tongue

• Lab diagnosis – Hb level as low as 4g/100ml. MCV, MCH &

MCHC all are reduced. RBC count slightly reduced or normal.

Management:
• Iron supplement: oral ferrous fumerate or ferrous sulphate

300mg three to four times a day for a period of 6 months

• Parenteral route : single dose of iron sorbitol 1.5mg/kg body

weight daily
Oral Health Considerations ( Burkets 12th edition)
• For dental patients with extremely low Hb levels- physician
consultation

• When Hb is less than 8g/dl, GA should be avoided

• Narcotic use should be limited for those with sever anemia as
there is increased rick of ischemic heart disease.
 PLUMMER VINSON SYNDROME
• Patterson Brown Kelly syndrome / Sideropenic dysphagia
• Characterized by iron deficiency anemia, dysphagia and
esophageal webs or strictures.

Clinical Features:

• Middle aged women- 4th to 7th decade oflife

• Dysphagia, angular cheilitis, sore tongue.

• Patient complains of spasm in throat or food sticking in throat.

• Spoon shaped nails.

Management:

• Correction of anemia

• Dilation of esophagus – to correct dysphagia

 SICKLE CELL ANEMIA
• First described by Herrick in 1910.

• Severe genetic disorder of hemoglobin synthesis.

• Autosomal dominant

• Abnormal hemoglobin, which under low oxygen tension,

results in sickling of the cell.

• In this, α-chains are normal and β-chains are abnormal.

 Diagnosis:
• Newborn screening is an important starting point for simple
public health strategies such as parental education, penicillin
prophylaxis, immunization and utilization of prenatal testing.

• The HbS solubility test can be performed in 5mins

for screening of adult hemoglobinopathies.
• Prenatal testing by DNA analysis of amniotic fluid at 14 to 16
weeks can be done to find out alterations and mutations in
genes.
 Clinical Features: (Burkets 12th edition)
 Acute chest syndrome

 Fever/ sepsis

 Strokes

 Severe anemia

 Chronic leg ulcers

 Hematuria

 Osteomyelitis

 Pain (lower back, knee &hips)

Oral Manifestations:
• Enamel hypomineralization

• Increased overjet and overbite

• Calcified canals

• Pallor of oral mucosa and delayed eruption of teeth.

• Mongoloid facies – with high cheek bones

• SCA is not associated with increased levels of

• gingivitis or periodontitis.*

• *Periodontal Disease in Sickle Cell Disease Subjects by John M. Crawford.

Journal of Periodontology. March 1988, Vol. 59, No. 3, Pages 164-169
 Management:
• Regular monitoring of hematological state

• Blood transfusion – cerebrovascular symptoms in early

childhood , recurrent pulmonary thrombosis

• Mild to moderate anemia - Blood transfusion

• Hydroxyurea (increases featal form of hemoglobin)

• Painful crisis – analgesics

• Incidence of hypoxia and dehydration should be avoided

• Prophylatic antibiotics should be given to prevent

infections.
 DENTAL MANAGEMENT
• Dental treatment - Directed towards palliative therapy during
crisis period
• Preventive dental care – antiseptic mouth rinses , topical fluoride
recommended

• Antibiotic prophylaxis – penicillin is the drug of choice

• Odontogenic and nonodontogenic infection should be
aggressively treated

• Periodontal status - closely monitored

 THALASSEMIA
• Thalassemia is an inherited disorder, characterized by
abnormal hemoglobin.

• It is also known as Cooley’s anemia or Mediterranean

anemia.

• It is more common in Thailand and to some extent in

Mediterranean countries.

• Thalassemia is of two types:

1. α-thalassemia

2. β-thalassemia.
• In normal hemoglobin, number of α and β polypeptide chains is
equal.

• In thalassemia, the production of these chains become

imbalanced because of defective synthesis of globin genes.

• This causes the precipitation of the polypeptide chains in the

immature RBCs, leading to disturbance in erythropoiesis.
 α-Thalassemia
• α -thalassemia occurs in fetal life or infancy.

• In this α-chains are less, absent or abnormal.

• In adults, β-chains are in excess and in children, γ-chains are
in excess.

• This leads to defective erythropoiesis and hemolysis.

• The infants may be stillborn or may die immediately after

birth.
β-Thalassemia (Thalassemia major)
• More common type of thalassemia.
• In β-thalassemia, β-chains are less in number, absent or
abnormal with an excess of α-chains.

• Severity ranges from complete lack of symptoms to

transfusion dependence.

• Cooley’s anemia, or thalassemia major is the name for the

most severe form.
Oral Manifestations:

• Excessive overgrowth of maxilla

• Oral mucosa has a lemon yellow tint because of chronic
jaundice – hard palate and floor of the mouth.

• Chipmunk facies- Saddle nose, prominent malar bone, retracted

upper lip

• Poor healing

• Spacing between teeth

• Discoloration of dentin
 General management (GHOMS )
• Blood transfusion

• Iron chelating agents – desferroxamine

• Folic acid supplements

• Splenectomy – severe cases

 Dental management

• Surgery has been used successfully to treat the facial

deformities

• HIV and HEPATITIS infections are common in transfused

patients

• Prophylactic antibiotics in splenectomy cases

MEGALOBLASTIC (PERNICIOUS) ANEMIA &
VIT B12 (COBALAMIN) ANEMIA
• Occurs due to deficiency of Vit B12 or folic acid or both,
resulting in disordered cell proliferation.

Clinical Features & Oral Manifestations:

• Weakness, anemia, palpitations, diarrhoea

• Paresthesia of finger, toes & also dementia may be observed.

• Burning sensation of tongue, angular cheilitis

• Hunter’s glossitis: Atrophy of filiform and fungiform papillae
leading to smooth fiery red surface of tongue
 Management:
• Blood tranfusion: when Hb level is less than 4g/dl of blood

• Folic acid supplements:

 initial dose - 5 mg orally daily
 maintenance dose - 5 mg orally once a week
• Vit B12 therapy:
 Initial dose – 1000 mcg , intramuscularly 4 to 6 wks
 Maintenance dose – 1000 mcg intramuscularly once every
week
 APLASTIC ANEMIA
• A rare disorder characterized by peripheral blood pancytopenia
associated with bone marrow suppression.

• Occurs due to failure of haematopoietic precursor cells in bone

marrow to produce adequate number of all blood cell types.
 Clinical Features:

• Commonly seen in young adults

• Erythrocyte deficiency: Headaches, pale skin, breathlessness

• Thrombocyte deficiency: Bruising & bleeding. Cerebral
haemorrhages

• Leukocyte deficiency: Bacterial and fungal infections are

common.

• Ankle edema, anginal pain, congestive cardiac failure

 Management:

• Supportive therapy: Antibiotics & transfusion

• Bone marrow transplantation

• Stimulation of haemopoiesis and promote marrow recovery

 Androgenic steroids - oxymetholone

 Corticosteroids –Prednisolone or methyl prednisolone

 Antithymocyte or antilymphocyte globulin combined with
cyclosporine.
 POLYCYTHEMIA
• Abnormal increase in the number of RBCs in the peripheral blood, u
with increase in Hb level.

• Types:

o Polycythemia Vera

o Relative Polycythemia

o Secondary Polycythemia
 POLYCYTHEMIA VERA
• Polycythemia rubra vera / Osler’s disease / Erythremia /
Vaquez’s disease

• Uncontrolled proliferation of erythroid stem cells leading to

excess of erythroid cell mass in the body.

Clinical Features:

• Male predilection – Middle age

• Skin appears flushed, reddened

• Spleen is palpable
 • CLINICAL FEATURES

• GI pain
• Headache
• Parasthesia
• Fatigue
• Weakness
• Visual disturbances
• Tinnitus
 •Oral manifestations:
• Purplish red discoloration

of mucosa

• Glossitis

• Swollen bleeding gingiva

• Petechiae
Management:
• Venesection: done at periodic intervals to remove 500-600ml
of blood. Also called Phlebotomy.

• Radioactive phosphorus: Excellent treatment modality when

the diagnosis is certain.

• Aspirin – given for thrombotic event

 PUBLIC HEALTH SCENARIO
 Globally, anaemia affects 1.62 billion people, which
corresponds to 24.8% of the population.

 The highest prevalence is in preschool-age children

(47.4%), and the lowest prevalence is in men (12.7%).

 However, the population group with the greatest

number of individuals affected is pregnant women
(41.8%).

 In women, anaemia may become the

underlying cause of maternal mortality and
perinatal mortality.
• Nearly 50 per cent of women of reproductive age and 26 per cent
of men in the age group of 15-59 years are anemic.

• Nine out of ten anemia sufferers live in developing countries,

about 2 billion people suffer from anemia and an even larger
number of people present iron deficiency.
Anemia in India
• Infants, Pre-school Children, Adolescents and Women of
Childbearing age, particularly Pregnant Women, are at greatest risk
of developing Iron Deficiency Anaemia.

• The condition has a prevalence rate of 74 percent among pregnant

women in the region ranging from 13.4 percent in Thailand to 87
percent in India.

• According to the NFHS-(III), more than half of women in India

(55%) have anaemia, including 39 % with mild anemia, 15 % with
moderate anemia and 2 percent with severe anaemia.
• The survey further revealed that among the states, Assam is the
worst affected with 72% of married women being anaemic,
followed by Haryana (69.7%) and Jharkhand (68.4%).

*Anaemia ‘a silent killer’ among women in India: Present scenario Kawaljit Kaur . Euro J
Zool Res, 2014, 3 (1):32-36
 CONCLUSION
• Red blood cells play an important role in our health by
carrying fresh oxygen throughout the body.

• Hemoglobin is the protein inside red blood cells that carries

oxygen.

• Most people don't think about their red blood cells unless they
have a disease that affects these cells. Problems with red blood
cells can be caused by illnesses or a lack of iron or vitamins in
the diet. Some diseases of the red blood cells are inherited.
• Anemia is the most common disorder of the blood with it
affecting about a quarter of people globally.

• Anemia goes undetected in many people, and symptoms can be

minor or vague.

• Appropriate dental care improves a patient’s quality of life by

preventing eating difficulties, oral diseases, and esthetic
concerns, and facilitates the management of the disease by the
hematologist.
• Preventive dental care is must for patients with blood cell

disorders of any kind in combinations with appropriate lab

investigations and diagnosis before planning of any treatment.

 REFERENCES
• Essentials of medical physiology by Dr.Sembulingam.

• Medical physiology for dental students by Dr G K Pal

• Essential Pathology for dental students by Harsh Mohan 3rd
edn

• Text book of Oral Medicine Ghom 2nd edn

• Human physiology for B.D.S by Prof. A K Jain 3rd edn

• Burket’s Oral Medicine by Greenberg . Glick . Ship . 12th edn