1

THROMBOCYTES (PLATELETS)

PRESENTED BY: Dr. Shraddha Patil

(1st year PG)
GUIDED BY: Dr. Rashmi Jayanna
Dr. Swapnil Mhatre
Dr. Priyanka Razdan

Contents:
•Introduction
•Structure and composition
•Thrombopoiesis
•Properties of platelets
•Functions of platelet
•Lifespan and fate of platelets
•Hemostasis
3
• Coagulation of blood
• Fibrinolysis
• Test for blood clotting
• Platelet disorders
• Review of literature
• References
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Introduction:
 Platelets = small plate,
 Thrombo = lump or clot , cytes = cells
 Smallest blood cell
 Size: 2.5 µ (2 to 4 µ)in diameter
 Volume: 7.5 cu µ (7 to 8 cu µ)
 Shape: spherical, oval, or rounded granulated bodies
 Colour: colorless
 Leshman’s staining: faint blue cytoplasm with reddish-purple granules
 Nucleus: Absent
 5
Structure and Composition

 Platelet is constituted by:

1. Cell membrane or surface membrane
2. Microtubules
3. Cytoplasm
 6
Cell membrane:

 6 nm thick.
 Open canalicular system form by extensive
invagination of cell membrane which is a delicate
tunnel system through which the platelet granules
extrude their contents.
 Contains lipids in the form of phospholipids,
cholesterol and glycolipids, carbohydrates such as
glycocalyx, and glycoproteins and proteins.
 Of these substances, glycoproteins and phospholipids
are functionally important
 7

 Glycoproteins
• Prevent the adherence of platelets to normal endothelium.
• But accelerate the adherence of platelets to collagen and damaged endothelium in
ruptured blood vessels.
• Form the receptors for adenosine diphosphate (ADP) and thrombin.

 Phospholipids
• Accelerate the clotting reactions.
• Form the precursors of thromboxane A2 and other prostaglandin-related substances.
 8
Microtubules:

 Form a ring around cytoplasm below the cell

membrane.
 Made up of polymerized proteins called tubulin.
 These tubules provide structural support for the
inactivated platelets to maintain the disk-like shape.
 9
Cytoplasm:

 Contains the cellular organelles, Golgi apparatus,

endoplasmic reticulum, mitochondria, microtubule,
microvessels, filaments and granules.
 Also contains some chemical substances such as
proteins, enzymes, hormonal substances, etc.
 10

 Proteins:
1. Contractile proteins:
• Actin and myosin: Responsible for the contraction of platelets.
• Thrombosthenin: Responsible for clot retraction.
2. Von Willebrand factor:
• Responsible for adherence of platelets and regulation of plasma level of factor VIII.
3. Fibrin-stabilizing factor:
• A clotting factor.
 11

4. Platelet-derived growth factor (PDGF):

• Responsible for repair of damaged blood vessels and wound healing.
• It is a potent mytogen (chemical agent that promotes mitosis) for smooth muscle
fibers of blood vessels.
5. Platelet-activating factor (PAF):
• Causes aggregation of platelets during the injury of blood vessels, resulting in
the prevention of excess loss of blood.
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6. Vitronectin (serum spreading factor):

• Promotes adhesion of platelets and spreading of tissue cells in culture.
7. Thrombospondin:
• Inhibits angiogenesis (formation of new blood vessels from pre-existing vessels)

 Enzymes:
1. Adenosine triphosphatase (ATPase)
2. Enzymes necessary for the synthesis of prostaglandins
 13

 Hormonal Substances:
1. Adrenaline
2. 5-hydroxytryptamine (5-HT; serotonin)
3. Histamine.
 Other Chemical Substances:
1. Glycogen
2. Substances like blood group antigens
3. Inorganic substances such as calcium, copper, magnesium, and iron.
 14

 Platelet Granules:
Granules present in the cytoplasm of platelets are of two types:

Alpha granules Dense granules

-Clotting factors: Fibrinogen, V, and XIII -Nucleotides
-Platelet-derived growth factor -Serotonin
-Vascular endothelial growth factor -Phospholipid
-Basic fibroblast growth factor -Calcium Lysosomes
 15
Normal count :

 2,50,000/cu mm of blood.

 It ranges between 2,00,000 and 4,00,000/cu mm of blood.

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Thrombopoiesis:

 Megakaryocytopoiesis / Development of Platelets

 Platelets are formed in the bone marrow.
 By a process of fragmentation of the cytoplasm of megakaryocytes.
 Megakaryocyte progenitor cells formed by the trilineage myeloid stem cells in
the bone marrow.
 Platelet production is under the control of thrombopoietin.
 The stages in platelet production are: megakaryoblast, promegakaryocyte,
megakaryocyte, and discoid platelets.
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PROMEGAKARYOCYTE:

 A megakaryoblast undergoes endo-reduplication of nuclear

chromatin i.e. nuclear chromatin replicates repeatedly in multiples
of two without division of the cell.
 A large cell containing up to 32 times the normal diploid content of
nuclear DNA (polyploidy) is formed when further nuclear
replication ceases and cytoplasm becomes granular.
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MEGAKARYOBLAST:

 The earliest precursor of platelets in the bone

marrow.
 It arises from hematopoietic stem cell through a
process of differentiation.
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MEGAKARYOCYTE:

 A mature megakaryocyte is a large cell.

 30-90 μm in diameter.
 4-16 nuclear lobes having coarsely clumped chromatin.
 The cytoplasm is abundant, light blue in color, and contains red-purple granules.
 Platelets are formed from pseudopods of megakaryocyte cytoplasm which get
detached into the bloodstream.
 Each megakaryocyte may form up to 4000 platelets.
 The formation of platelets from the stem cell takes about 10 days.
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PLATELETS:

 About 70% of platelets are in circulation while the remaining 30%

are sequestered in the spleen.
 Newly-formed platelets spend 24-36 hours in the spleen before
being released into circulation.
 Factors such as stress, epinephrine, and exercise stimulate platelet
production.
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Properties of platelets:

 Platelets have three important properties (3 ‘A’s):

1. Adhesiveness
2. Aggregation
3. Agglutination.
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ADHESIVENESS:

 Property of sticking to a rough surface.

 During injury of blood vessel, endothelium is damaged and the subendothelial
collagen is exposed.
 While coming in contact with collagen, platelets are activated and adhere to collagen.
 Adhesion of platelets involves interaction between von Willebrand factor secreted by
damaged endothelium and a receptor protein called glycoprotein Ib situated on the
surface of platelet membrane.
 Other factors which accelerate adhesiveness are collagen, thrombin, ADP,
Thromboxane A2, calcium ions, and P-selectin.
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AGGREGATION (GROUPING OF PLATELETS):

 Grouping of platelets.
 Adhesion is followed by activation of more platelets by substances
released from dense granules of platelets.
 During activation, the platelets change their shape with elongation
of long filamentous pseudopodia which are called processes or
filopodia.
 Filopodia help the platelets aggregate together.
 Activation and aggregation of platelets are accelerated by ADP,
thromboxane A2, and platelet-activating factor.
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AGGLUTINATION:

 Clumping together of platelets.

 Aggregated platelets are agglutinated by the actions of some
platelet agglutinins and platelet-activating factor.
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Functions of platelet:

1. Role in blood clotting -

Platelets are responsible for the formation of intrinsic prothrombin activator. This
substance is responsible for the onset of blood clotting.

2. Role in clot retraction –

In the blood clot, blood cells including platelets are entrapped in between the fibrin
threads.
The cytoplasm of platelets contains contractile proteins, namely actin, myosin, and
thrombosthenin, which are responsible for clot retraction.
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3. Role in repair of ruptured blood vessels –

Platelet-derived growth factor (PDGF) formed in the cytoplasm of platelets is useful
for the repair of the endothelium and other structures of the ruptured blood vessels.

4. Role in defense mechanism –

By the property of agglutination, platelets encircle the foreign bodies and destroy
them.
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5. Role in prevention of blood loss (HEMOSTASIS)-

Platelets accelerate the hemostasis by three ways:
i. Platelets secrete 5-HT, which causes the constriction of blood vessels.
ii. Due to the adhesive property, the platelets seal the damage in blood vessels like
capillaries.
iii. By formation of temporary plug, the platelets seal the damage in blood vessels.
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LIFESPAN AND FATE OF PLATELETS:

 Average lifespan of platelets is 10 days.

 It varies between 8 and 11 days.
 Platelets are destroyed by tissue macrophage system in spleen.
 So, splenomegaly (enlargement of spleen) decreases platelet count
and splenectomy (removal of spleen) increases platelet count.
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HEMOSTASIS:

 Arrest or stoppage of bleeding.

 STAGES OF HEMOSTASIS:
1. Vasoconstriction
2. Platelet plug formation
3. Coagulation of blood.
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VASOCONSTRICTION

 Immediately after injury, the blood vessel

constricts and decreases the loss of blood from
damaged portion.
 Usually, arterioles and small arteries constrict.
 Vasoconstriction is purely a local phenomenon.
 When the blood vessels are cut, the endothelium is
damaged and the collagen is exposed.
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 Platelets adhere to this collagen and get activated. The activated platelets
secrete serotonin and other vasoconstrictor substances which cause
constriction of the blood vessels.
 Adherence of platelets to the collagen is accelerated by von Willebrand
factor.
 This factor acts as a bridge between a specific glycoprotein present on
the surface of platelet and collagen fibrils.
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PLATELET PLUG FORMATION

 Platelets get adhered to the collagen of ruptured blood vessels and secrete adenosine
diphosphate (ADP) and thromboxane A2.
 These two substances attract more and more platelets and activate them.
 All these platelets aggregate together and form a loose temporary platelet plug or
temporary hemostatic plug, which closes the ruptured vessel and prevents further blood
loss.
 Platelet aggregation is accelerated by platelet­activating factor(PAF).
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COAGULATION OF BLOOD

 During this process, the fibrinogen is converted into fibrin.

 Fibrin threads get attached to the loose platelet plug, which blocks the
ruptured part of blood vessels and prevents further blood loss completely.
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Coagulation of Blood:

• The process in which blood loses its fluidity and becomes a jelly-like
mass a few minutes after it is shed out or collected in a container.

• Coagulation of blood occurs through a series of reactions due to the

activation of a group of substances.

• Substances necessary for clotting are called clotting factors.

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 13 clotting factors are identified:

• Factor I Fibrinogen
• Factor II Prothrombin
• Factor III Thromboplastin (Tissue factor)
• Factor IV Calcium
• Factor V Labile factor (Proaccelerin or accelerator globulin)
• Factor VI Presence has not been proved
• Factor VII Stable factor
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• Factor VIII Antihemophilic factor (Antihemophilic globulin)

• Factor IX Christmas factor
• Factor X Stuart-Prower factor
• Factor XI Plasma thromboplastin antecedent
• Factor XII Hageman factor (Contact factor)
• Factor XIII Fibrin-stabilizing factor (Fibrinase).
 39
Stages of Blood Clotting:

 In general, blood clotting occurs in three stages:

1. Formation of prothrombin activator

2. Conversion of prothrombin into thrombin
3. Conversion of fibrinogen into fibrin.
 STAGE 2: CONVERSION OF
PROTHROMBIN INTO
THROMBIN
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PROTHROMBIN ACTIVATOR
STAGE 1: FORMATION OF
STAGE 3: CONVERSION OF
FIBRINOGEN INTO FIBRIN
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BLOOD CLOT

 Blood clot is defined as the mass of coagulated blood which contains RBCs,
WBCs and platelets entrapped in fibrin meshwork.
 RBCs and WBCs are not necessary for clotting process.
 However, when clot is formed, these cells are trapped in it along with platelets.
 The trapped RBCs are responsible for the red color of the clot.
 The external blood clot is also called scab. It adheres to the opening of damaged
blood vessel and prevents blood loss.
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CLOT RETRACTION

 The process involving the contraction of blood clot and oozing of serum is
called clot retraction.
 Within a few minutes after the formation the blood clot starts contracting.
 And after about 30 to 45 minutes, the straw-colored serum oozes out of the
clot.
 Contractile proteins( actin, myosin, and thrombosthenin) in the cytoplasm
of platelets are responsible for clot retraction.
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FIBRINOLYSIS:

 Lysis of blood clot inside the blood vessel is called fibrinolysis.

 It helps to remove the clot from lumen of the blood vessel.
 This process requires a substance called plasmin or fibrinolysin.
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Why circulating blood does not clot ?

ANTICLOTTING MECHANISM IN THE BODY:

 Under physiological conditions, intravascular clotting does not
occur.
 It is because of the presence of some physicochemical factors in
the body.
1. Physical Factors
i. Continuous circulation of blood.
ii. Smooth endothelial lining of the blood vessels.
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2. Chemical Factors – Natural Anticoagulants

i. Presence of natural anticoagulant called heparin that is produced by
the liver.
ii. Production of thrombomodulin by endothelium of the blood
vessels (except in brain capillaries).
iii. All the clotting factors are in inactive state.
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TESTS FOR BLOOD CLOTTING

 Used to diagnose blood disorders.

 Also used to monitor the patients treated with anticoagulant drugs such
as heparin and warfarin.
1. Bleeding time
2. Clotting time
3. Prothrombin time
4. Partial prothrombin time
5. International normalized ratio
6. Thrombin time
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1. Bleeding time

 Time interval from oozing of blood after a cut or

injury to the arrest of bleeding.
 Usually, it is determined by Duke method using
blotting paper or filter paper method.
 Its normal duration is 3 to 6 minutes.
 It is prolonged in purpura.
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2. Clotting time

 Time interval from oozing of blood after a

cut or injury till the formation of clot.
 It is usually determined by capillary tube
method.
 Its normal duration is 3 to 8 minutes.
 It is prolonged in hemophilia.
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3. Prothrombin time

 Time taken by blood to clot after adding tissue thromboplastin to

it.
 Tissue thromboplastin activates prothrombin and blood clotting
occurs.
 Time taken by blood to clot after adding tissue thromboplastin is
determined.
 Normal duration of prothrombin time is 10 to 12 seconds.
 It is prolonged in deficiency of prothrombin and other factors like
factors I, V, VII, and X. However, it is normal in hemophilia.
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4. Partial prothrombin time (PPT) or activated
prothrombin time (APTT)

 Time taken for the blood to clot after adding an

activator such as phospholipid, along with
calcium to it.
 Normal duration of time is 30 to 45 seconds.
 It is prolonged in heparin or warfarin therapy
(since heparin and warfarin inhibit clotting) and
deficiency or inhibition of factors II, V, VIII, IX,
X, XI and XII.
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5. International normalized ratio(INR)

 International normalized ratio (INR) is the rating of a

patient’s prothrombin time when compared to an
average.
 It measures the extrinsic clotting pathway system.
 Useful in monitoring impact of anticoagulant drugs
such as warfarin and to adjust the dosage of
anticoagulants.
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 Blood takes longer time to clot if INR is higher.

 Normal INR is about 1.
 In patients taking anticoagulant therapy for atrial fibrillation, INR should
be between 2 and 3.
 For patients with heart valve disorders, INR should be between 3 and 4.
 But, INR greater than 4 indicates that blood is clotting too slowly and
there is a risk of uncontrolled blood clotting.
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6. Thrombin time

 Time taken for the blood to clot after adding thrombin to it.
 It is done to investigate the presence of heparin in plasma or to
detect fibrinogen abnormalities.
 This test involves observation of clotting time after adding
thrombin to patient’s plasma.
 Normal duration of is 12 to 20 seconds.
 It is prolonged in heparin therapy and during
dysfibrinogenimia (abnormal function of fibrinogen with
normal fibrinogen level).
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PLATELET DISORDERS :

 Platelet disorders occur because of pathological variation in platelet count

and dysfunction of platelets.
 Platelet disorders are:
1. Thrombocytopenia
2. Thrombocythemia (Thrombocytosis )
3. Glanzmann’s thrombasthenia
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1. Thrombocytopenia:

 Decrease in platelet count below 1,50,000

cells/cumm is called thrombocytopenia.
 It leads to thrombocytopenic purpura.
 Bleeding from many small venules or
capillaries.
 Small punctate hemorrhages occur
throughout the body tissue as small,
purplish spots called thrombocytopenic
purpura.
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 Thrombocytopenia occurs in the following conditions:

i. Acute infections vi. Splenomegaly
ii. Acute leukaemia vii. Scarlet fever
iii. Aplastic and pernicious anemia viii. Typhoid
iv. Chickenpox
ix. Tuberculosis
v. Smallpox
x. Purpura
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 Management:
• Fresh whole blood transfusion that contains a large number of
platelets.
• Splenectomy
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2. Thrombocythemia (Thrombocytosis)

 Increase in platelet count is called thrombocytosis.

 Two forms are recognized: primary or essential
thrombocythemia (ET) and secondary thrombocythemia
(ST)
 ET is a myeloproliferative/myeloneoplastic condition of
unknown etiology.
 ST is an overproduction of platelets in response to other
diseases
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 ST, also referred to as thrombocytosis, is an increase in the number of

thrombocytes to a level between 4,50,000 and 10,00,000 cells/cumm.
 Thrombocytosis occurs in the following conditions:
i. Allergic conditions
v. Splenectomy
ii. Hemorrhage
vi. Rheumatic fever
iii. Bone fractures
vii. Trauma
iv. Surgical operations
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 Clinical features:
• Increased clotting experienced by these patients, most clots develop in the
brain, hands, and feet.
• A chronic headache
• Dizziness
• Chest pain
• Tingling in the hands and feet
• Epistaxis
• Easy bruising
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• Bleeding from gums (gingival bleeding), and other parts of the GI tract.
• Excessive and prolonged bleeding occurs after dental extractions.
 Treatment.
• ST does not require any special treatment and managing the underlying
condition resolves the thrombocythemia.
• ET in most cases can be managed adequately with daily aspirin.
• Administration of platelet-lowering drugs such as hydroxyurea.
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3. Glanzmann’s Thrombasthenia

 Glanzmann’s thrombasthenia is an inherited hemorrhagic disorder.

 Caused by structural or functional abnormality of platelets.
 Caused by a deficiency of the platelet integrin alpha IIb beta3.
 It leads to thrombasthenic purpura.
 However, the platelet count is normal.
 It is characterized by normal clotting time, and normal or prolonged
bleeding time but defective clot retraction.
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 Signs and symptoms

• Easy bruising.
• Nosebleeds (Epistaxis)
• Bleeding from the gums.
• Gastrointestinal bleeding.
• Postpartum bleeding.
• Increased postoperative bleeding.
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 Management :
• Transfusion of fresh platelets or platelet concentrates.
• Other treatments can be used to control minor bleeding include
-Compression,
-Gelatin sponge,
-Antifibrinolytic agents such as tranexamic acid or topical thrombin
-YAG laser.
 CASE REPORT
67
Dental consideration in management of
Glanzmann’s Thrombasthenia

 International journal of clinical pediatric dentistry January-April 2010; 3(1): 51-56

 Diana n. Mehata, Rupender Bhatia
 In the present case the liver clot was dislodged and the socket was packed with
"Calgigraf Ag-Foam", with the following composition: Silver alginate, calcium
alginate, and maltodextrin wound dressing. To aid in the retention of this dressing,
a nonfunctional, passive, acrylic removable splint which also served as space
maintainer was fabricated.
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BLEEDING DISORDERS:

 Bleeding disorders are the conditions characterized by prolonged

bleeding time or clotting time.
 Bleeding disorders are of three types:
1. Hemophilia.
2. Purpura.
3. Von Willebrand disease.
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1. Hemophilia:

 Sex-linked inherited blood disorders.

 Characterized by prolonged clotting time,
bleeding time is normal.
 Usually, it affects the males, with the females
being the carriers.
 A group of genetic disorders resulting in a
deficiency of one of the coagulation pathway
factors.
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 Symptoms and signs:

• Spontaneous bleeding.
• Prolonged bleeding due to cuts, tooth extraction and surgery.
• Hemorrhage in gastrointestinal and urinary tracts.
• Bleeding in joints followed by swelling and pain
• Appearance of blood in urine.
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 Types of hemophilia : Depending upon the deficiency of the factor involved,

hemophilia is classified into three types:
 i. Hemophilia A or classic hemophilia: Due to the deficiency of factor VIII.
85% of people with hemophilia are affected by hemophilia A.
 ii. Hemophilia B or Christmas disease: Due to the deficiency of factor IX. 15%
of people with hemophilia are affected by hemophilia B.
 iii. Hemophilia C or factor XI deficiency: Due to the deficiency of factor XI. It
is a very rare bleeding disorder.
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 Investigations:
• Clinical history is suggestive.
• Screening tests include-
1. Prolonged partial thromboplastin test (prolonged),
2. Bleeding time (normal),
3. Platelet count (normal)
4. specific tests for missing factors (Factor VIII assay).
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 Management :
• Effective therapy for classical hemophilia involves replacement of missing
clotting factor.
• Cryoprecipitate derived from blood.
• Current treatment goals include prophylactic maintenance of clotting factor
levels at or above 1% to minimize bleeding episodes and joint damage.
• The affected persons should be protected from traumatic injuries.
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• Hemophiliacs should be monitored and counseled to maintain excellent oral

health.
• Extractions and other treatment can be safely carried out under local anesthesia
using infiltration, intrapapillary and intraligamentary injections are often done
under factor cover (20– 40%).
• Dental extraction or surgical procedures carried out within the oral cavity
should be done with a plan for hemostasis management, in consultation with the
hematologist.
• Tranexamic acid or epsilonaminocaproic acid (EACA) can be used after dental
procedures to reduce the need for replacement therapy
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• Local treatments must be considered to treat the hemorrhage. Like,

• Direct pressure on the area using a damp gauze swab, maintained
for at least 15 minutes
• Sutures to close the wound,
• Application of local hemostatic agents,
• Antibiotics, especially in gingival bleeding due to poor oral
hygiene,
• Use of tranexamic acid as a mouthwash.
 Review article
77
Hemophilia A: Dental considerations and
management

 Shastry, et al
 Journal of International Society of Preventive and Community Dentistry in
December 2014

 Restorative treatment and endodontic treatment:

• Endodontic therapy is preferred over extraction whenever possible, as
endodontic treatment generally has a low risk of bleeding in patients with
hemophilia A.
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• Working length of the root canal is calculated precisely to ensure that the instruments do
not pass through the apex of the root canal during root canal treatment.
• There is a risk of bleeding with the use of matrix bands, rubber dam, or wooden wedges
during restorative treatment, which can be controlled by local means or the application
of topical agents.
• A rubber dam should be used to prevent soft tissue lacerations.
• Surgical endodontics requires factor VIII replacement up to 50–75% depending on the
type of surgery and the severity of hemophilia.
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 Local anesthesia
• There are no restrictions with respect to the type of local anesthesia used, those with
vasoconstrictors may provide additional local hemostasis.
• The intraligamental technique or interosseous technique should be considered as a
potential alternative to the nerve blocks.
 Dentures or orthodontic treatment
• Orthodontic treatment or removable prosthesis is not contraindicated in the cases of
hemophilia A.
• These appliances may encourage plaque accumulation, which necessitates vigorous
oral hygiene programs.
• Care must be taken to avoid damage to the gingiva.
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2. Purpura:

 Purpura is a disorder characterized by prolonged bleeding

time. However, the clotting time is normal.
 Characteristic feature of this disease is spontaneous bleeding
under the skin from ruptured capillaries.
 The hemorrhagic spots under the skin are called purpuric
spots (purple colored patch like appearance). That is why this
disease is called purpura.
 Blood also sometimes collects in large areas beneath the skin
which are called ecchymoses.
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 Oral manifestations:
• Thrombocytopenic purpura manifests by the failure of platelet plug
formation and manifests as petechial hemorrhage of the oral
mucosa.
• These oral petechiae are often the first signs of the disease.
• Gingival bleeding occurs in most patients with thrombocytopenic
purpura.
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• Petechiae which appear as numerous, tiny,

grouped clusters of reddish spots only 1 mm or
less in diameter are common on the palate and
other mucosal surfaces .
• Ecchymosis and hematomas that are the more
extensive and severe forms of hemorrhage are
relatively less common.
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 Types and causes of purpura : Purpura is classified into three types

depending upon the causes:

 i. Thrombocytopenic purpura :
• Due to the deficiency of platelets (thrombocytopenia).
• In bone marrow disease, platelet production is affected leading to
the deficiency of platelets.
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 ii. Idiopathic thrombocytopenic purpura :

• Due to some unknown cause is called idiopathic thrombocytopenic purpura.
• It is believed that platelet count decreases due to the development of antibodies
against platelets, which occurs after blood transfusion.
 iii. Thrombasthenic purpura:
• Due to structural or functional abnormality of platelets.
• However, the platelet count is normal.
• It is characterized by normal clotting time, normal or prolonged bleeding time
but defective clot retraction.
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 Treatment :
• Corticosteroids
• Intravenous immunoglobulin therapy (IVIG)
• Splenectomy
• Platelet transfusion
• Noninvasive dental treatment can be carried out with minimal risk of bleeding
at counts ≥50,000 cells/mm3 , but at levels below 50,000 cells/mm3 , bleeding
from invasive procedures may be challenging to manage.
• Invasive procedures are contraindicated without hemostatic cover with platelet
concentrates and IVIG cover at lower counts.
 Review of literature

Dental considerations on the management of 86

Idiopathic Thrombocytopenic Purpura in
children: case report
 VF Rossier et al in Decmber 2015
 concluded that-
• Dental procedures can be performed in patients with platelet counts above 50,000/mm3
• In the need for surgical interventions on a patient whose platelet count is too low, blood
transfusion or previous corticosteroid treatment is necessary.
• The dentist must avoid trauma to the buccal mucosa by carefully puncturing the needles,
adapting orthodontic braces, and avoiding super-activation.
• Prescription of antiplatelet drugs, such as acetylsalicylic acid and ibuprofen, must be
avoided.
• antibiotics prophylaxis can be performed to reduce the risk of postoperative infections.
 87
3. Von Willebrand’s disease:

 An autosomal dominant inherited disorder

 Characterised by defective platelet function and a deficiency
or abnormality of factor VIII.
 Symptoms and signs -
• Include mucocutaneous bleeding and haemarthrosis.
• Gingival bleeding after brushing
• The disease may be discovered after dental extractions
because of prolonged and excessive bleeding.
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 Based on qualitative or quantitative defects in von Willebrand factor, vWD is

categorized into four types-
1. Type 1 vWD (found in 60%–80% of patients):
• A quantitative deficiency of vWF.
• Levels of vWF in the blood range from 20% to 50% of normal.
• The symptoms are usually mild.
2. Type 2 vWD (found in 15%–30% of patients):
• A qualitative deficiency of their vWF.
• Symptoms are mild to moderate.
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3. Type 3 vWD (found in 5%–10% of patients):

• A quantitative deficiency of vWF, but symptoms are typically severe.
• Include spontaneous bleeding episodes, often into their joints and muscles.
4. Acquired vWD:
• An autoimmune disease, such as lupus, heart disease, or some types of
cancer.
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 Investigations:
• Family history
• Bleeding time (normal),
• Platelet count (normal),
• Platelet function tests (poor aggregation adhesion),
• A factor VIII deficiency test is required.
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 Management:
• Administration of factor VIII concentrate.
• Patients scheduled to undergo any surgical procedure (including
dental extractions) can be treated with desmopressin or infusions
of combined factor VIII and vWF.
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REFERENCES:

• John E. Hall, Guyton and Hall Textbook of Medical Physiology, 14th

edition
• B Sivapathasundharam, Shafer's Textbook of Oral Pathology, 9th edition
• K Sembulingam, Prema Sembulingam, Essentials of Physiology for
Dental Students, 3rd edition
• A.K. Jain, Human Physiology For BDS, 5th edition
• Harsh Mohan, Essential Pathology for Dental Students, 5th edition
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 Shastry, et al, Hemophilia A: Dental considerations and management Journal of

International Society of Preventive and Community Dentistry in December
2014
 Diana n. Mehata, rupender bhatia, Dental consideration in management of
glanzmann’s thrombasthenia, international journal of clinical pediatric dentistry
january-april 2010; 3(1): 51-56
 MSD manuals, reactive thrombocytosis (secondary thrombocytopenia).11 nov,
2015.
 VF Rossier et al, Dental considerations on the management of Idiopathic
Thrombocytopenic Purpura in children: case report, December 2015
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