Platelets are small non-nucleated cell fragments that originate from megakaryocytes in the bone marrow. They have a lifespan of 8-12 days and function to form blood clots to stop bleeding from damaged blood vessels. Platelets adhere to sites of injury in blood vessels and aggregate together to form a platelet plug. They release chemical signals that recruit additional platelets and activate the coagulation cascade to form a stable blood clot. Platelet structure includes a cell membrane, microtubules, and cytoplasm containing granules of proteins and enzymes involved in clotting and wound healing. Common platelet function tests include platelet count, bleeding time, and platelet aggregation assays. Abnormal platelet counts or function can occur in various medical conditions.

1. PLATELETS
PRESENTED BY
DR.SHENPAGA PRIYA.I
I YEAR PG

2. CONTENTS:
INTRODUCTION
FORMATION
LIFE SPAN & FATE OF PLATELETS
STRUCTURE
PROPERTIES
FUNCTIONS OF PLATELETS
PLATELET FUNCTION TESTS
APPLIED ASPECTS
DENTAL COSIDERATIONS

3. Small
Granulated
Non-nucleated
Round or oval-inactive
Spherical or rod shape-active
2 – 4 μ in diameter
1,50,000 – 3,50,000/mm³
INTRODUCTION

4. FORMATION
BONE MARROW
BLOOD STREAM
Each megakaryocyte produces
between 1,000 to 3,000 platelets
during its lifetime.
Formation
of
platelets
from stem
cells takes
10 days

5. LIFE SPAN & FATE OF PLATELETS
Life span – 8-12 days
Avg – 10 days.
Fate – Destroyed by tissue macrophage system in
spleen.
Splenomegaly – reduces platelet count.
Splenectomy – increases platelet count.

6. STRUCTURE
1 .CELL MEMBRANE
2.MICROTUBULE
3.CYTOPLASM

7. It is 6 nm thick and contain
 Carbohydrates(glycocalyx),
 Proteins (Glycoproteins)
 Lipids (phospholipids, cholesterol and glycolipids)
Out of all glycoprotein and phospholipids are
functionally important.
1 .CELL MEMBRANE
STRUCTURE

8. Glycoproteins:
STRUCTURE
Prevents the adherence of platelets to normal endothelium.
Accelerates the adherence of platelets to collagen and
damaged endothelium in ruptured blood vessels.
Forms a receptor for ADP and thrombin.
Phospholipids:
Accelerated clotting reaction.
Form precusors for THROMBAXANE A2 &
PROSTAGLANDINS.

9. 2.MICROTUBULE
• Made up of tublins (proteins)
• It responsible for structural support
for inactivated platelets
STRUCTURE

10. STRUCTURE
3.CYTOPLASM
1. Contractile proteins
Actin
Thrombosthenin
Myosin
Enable activated platelets to change their shape

11. STRUCTURE
2.Golgi apparatus & Endoplasmic reticulum:
Synthesis of enzymes
Calcium store
3.Mitochondria:
Synthesis of ATP and ADP
3.CYTOPLASM

12. STRUCTURE3.CYTOPLASM
4.Lyzosomes:
Containing hydrolytic enzymes.
5.Glycogen granules:
For production of energy anaerobically.

13. 6.Enzyme system:
Synthesize prostaglandins from
phospholipids of the Platelet membrane.
7.Chemical substances:
Calcium ions
Mg- ions.
Adenosine triphosphate (ATP)
Adenosine diphosphate (ADP)
STRUCTURE3.CYTOPLASM

14. STRUCTURE3.CYTOPLASM
8.Types of granules
Alpha
granules
Clotting
factors
Fibrin
stabilizing
factor XIII
Platelet
derived
growth factor
Contain
secreted
proteins
Dense
granules
ATP ADP
Ca++ &
serotonin
contain
non-protein
substances

16. PROPERTIES
ADHESIVENESS :
 Injuty to blood vessel - Vascular Constriction
platelets become stickey and adhere to the collagen
matrix in sub-endothelium.
Factors responsible are collagen, thrombin,
ADP,thromboxane A2, Ca ion& Von-Willebrand Factor.

17. AGGREGATION :
 Property to stick to each other Factors
responsible are ADP & Thromboxane A2.
PROPERTIES

18. AGGLUTINATION :
 Property of clumping together of
platelet
 Its due to platelet Agglutinins.
PROPERTIES

20. 1.ROLE IN HAEMOSTASIS
Haemostasis – spontaneous arrest of bleeding
from injured blood vessel.
Vasoconstriction – by 5HT & other vasoconstrictors
Temporary haemostatic plug – by platelets due to
its property of adhesiveness & aggregation.
 Definite haemostatic plug – also initiated by
platelets.

21. 1.ROLE IN HAEMOSTASIS

22. 2.ROLE IN CLOT FORMATION
 Play role in formation of intrinsic prothrombin activator
 It is responsible for onset of blood clotting.

23. Contraction of contractile proteins-
Actin,
Myosin &
Thrombosthenin.
 Responsible for clot Retraction & wound healing.
3.ROLE IN CLOT RETRACTION

24. Platelet derived growth factor (PDGF) in
cytoplasm of platelet for Repair of
Endothelium.
4.ROLE IN REPAIR OF
INJURED BLOOD VESSELS

25. 5.ROLE IN DEFENCE MECHANISM
Due to the property of agglutination , platelets are
capable of Phagocytosis.
 Mainly in Phagocytosis of carbon particles, viruses &
immune complexes.

26. PLATELET FUNCTION TESTS
 Platelet count- Peripheral blood smear
 Bleeding time- Dukes Method.
 PFA (PLATELETS FUNCTION ASSAY).
 Platelet Aggregation Test (Flow cytometry).

27. Platelet count- Peripheral blood smear
Platelet to be counted in a region
where RBCs & platelets are well
dispersed
Atleast 10 oil immersion fields to be
counted.
Average no of platelets in a field
multiplied by 10000 is the approximate
platelets count.
<8 platelets /OIF = decreased.
 8 to 20 platelets /OIF = adequate.
>20 platelets /OIF = increased.
PLATELET FUNCTION TESTS

28. Bleeding time- Dukes Method
With the Duke method, the patient is
pricked with a special needle or lancet,
preferably on the earlobe or fingertip.
The prick is about 3–4 mm deep. The
patient then wipes the blood every
30 secs with a filter paper.
The test ends when bleeding stops.
 The usual time is about 2-6min.
Other method-IVY METHOD.
PLATELET FUNCTION TESTS

30. PHYSIOLOGICAL VARIATIONS
 Age – Less in infant, reach adult level by 3
months of age.
Sex –No difference but during mensturation
reduced in females.
 Meal – Increases after meal.
 Muscular exercise – Increases.
Altitude – Increases.

31. PATHOLOGICAL VARIATIONS
Thrombocytosis:
 Increase in count more than 4,50,000/mm3
After Splenectomy
After hemorrhage,
Severe injury,
Major operation.

32. Persistence & abnormal increase in platelets
 Myloproliferative Disorders –
Chronic Myeloid Leukemia,
 Polycythemia vera,
Myelofibrosis.
Thrombocythemia:

33. Thrombocytopenia
DECREASED
PLATELETS
PRODUCTION
Decrease in count less than 150,000/mm3
Acute infection
Aplastic
Anemia Acute
leukemia
Bone marrow suppression
chicken Pox
Dengue fever
Malignancy
Drugs-Asprin,Antiplatelet
(Ex.Clopidogrel, Dipyridamole, etc)

34. Thrombotic Thrombocytopenic
Purpura
Idiopathic
Thrombocytopenic Purpura
Splenomegaly
Disseminated
Intravascular
Coagulation
AIDS
DECREASED
PLATELETS
SURVIVAL

35. DENTAL COSIDERATION

36. DENTAL COSIDERATION
Before extraction
Proper history taken from patient:
 Stroke Patient on Anti-platelet drugs- Clopidogrel,
warfarin, heparin etc
Hyperlipedimic patient on Asprin for prevention MI.
Advice to stop drugs for 3 days afterwards extraction
procedure done in patient.
Hemorragic disease:
Proper precaution for stop bleeding before extraction procedure.
Gelatin foam
Adrenalin pack
Electrocautery
Thrombin sponge