3.blood and its current concepts in coagulation

Dr.M.Aminah
MDS-I ,
Department of paedodontics and Preventive Dentistry.
2
Dr.M.AMINAH
Post Graduate
Dept. of Pediatrics and Preventive Dentistry

 Introduction
 Blood : properties , composition , function.
 Plasma proteins
 RBC
 Blood index
 Hemoglobin
 Blood group
 WBC
 Platelets : structure ,development ,function disorder
 Hemostasis and blood coagulation
Event in Hemostasis
Mechanism (old as well current concept)
Intravascular anti coagulant
Bleeding condition
Anti coagulant
Local hemostasis measured
Laboratory evaluation
 Blood transfusion
3

4
Blood is “that part of extracellular fluid consisting of plasma,
red blood cells, white blood cells, and platelets that is circulated
by the heart through the arteries and veins carrying oxygen and
nutrients to and waste materials away from all the body tissues”.
The role of blood in internal environmental is “homeostasis”

 Colour - Red
 Forms 6-8 % of total body weight.
 Average adult volume:
Males – 5 Litres
Females – 4.5Litres
New born 450 ml
 pH = 7.4
 Specific Gravity = 1.052 – 1.061
 Viscosity = 3 – 5 times more viscous than water.
5
K Sembulingam Essentials of Medical Physiology-6rd edition.

Plasma:
solids: 7-8%
organic substances
inorganic substances
Water: 92-93%
Gases:
Organic Inorganic
Plasma protein Na
Amino acids Ca
Carbohydrate K
Fat Mg
Hormones Hco3
Enzymes Cl
Antibodies Fe, cu
7

9
Functio
ns
Respiratory
Excretory
Homeostasis
Defense
Maintenance
of body
temperature
Transport
Storage
Acid-base
regulation
Nutritional

Normal values of the plasma proteins are:
Total proteins : 7.3 g/dL (6.4 to 8.3 g/dL)
Serum albumin : 4.7 g/dL
Serum globulin : 2.3 g/dL
Fibrinogen : 0.3 g/dL
10

 Coagulation of blood
 Defense mechanism of body
 Transport mechanism
 Maintenance of osmotic pressure in blood
 Regulation of acid-base balance
 Viscosity of blood
 Role in erythrocyte sedimentation rate
 Role as reserve proteins
11

12
Guyton and Hall Text book of medical physiology 12th edition 2011.

 Also known as erythrocytes.
 Most abundant cells of the blood.
 transport hemoglobin, which in turn carries oxygen from
the lungs to the tissues.
13

 Shape: Biconcave discs
 Size: 7.2 micrometers
 Thickness: 2.2 micrometers at the thickest point and 1
micrometer or less in the center.
 The average volume: 85 to 90 cubic micrometers.
 Normal value
Male : 5-6 million/mm3
Female : 4.5-5.5 million/mm3
Infant : 6-7 million/mm3
14
Ganong Review of Medical Physiology-23rd Edition.

 I. U Life:
• 3rd week-3rd month -- yolk sac
• 3rd month-5th month -- liver
• 5th month onwards -- RBM
 Post-natal : Red Bone Marrow
15

Relative rates of red blood cell
production in the bone marrow of
different bones at different ages
Genesis of Blood Cells
16
Ganong Review of Medical Physiology-23rd Edition.

 Regulation of Red Blood Cell Production
Role of Erythropoietin
17

Requirement for Vitamin B12
(Cyanocobalamin) and Folic Acid.
 Both of these are essential for the synthesis of DNA, because
each in a different way is required for the formation of thymidine
triphosphate, one of the essential building blocks of DNA.
 Therefore, lack of either vitamin B12 or folic acid causes abnormal
and diminished DNA and, consequently, failure of nuclear
maturation and cell division.
18

 Average life span -- about 120 days.
 Spleen -- Graveyard of red blood cells.
 Daily 10% red blood cells, which are
senile, get destroyed in normal young
healthy adults.
19

 Transport the oxygen from
the lung to the tissue.
 Transport the carbon
dioxide from the tissue to
the lung.
 Buffering action in blood.
 In blood group
determination.
20

IN NUMBER
IN SIZE
IN SHAPE
21

PHYSIOLOGICAL VARIATIONS
 Increase in count--Physiological Polycythemia
• Age
• Sex
• High altitude
• Muscular exercise
• After meal
 Decrease in count
• High barometric pressure
• sleep
22

PATHOLOGICAL VARIATIONS
Decrease in no. – ANAEMIA
Increase in no. - POLYCYTHAEMIA
23

Microcytes
• Iron deficiency anemia
Macrocytes
• Megaloblastic anemia
Anisocytes
• Pernicious anemia
24

1. Crenation: Shrinkage -- hypertonic condition.
2. Spherocytosis: Globular – hypotonic
condition.
4. Sickle cell: Crescentic -- sickle cell anemia.
5. Poikilocytosis: unusual shapes due to
deformed cell membrane.
25

 Anemia is defined as an abnormal reduction in the
number of circulating red blood cells, the quantity of
hemoglobin and the volume of packed cell in a given
unit of blood.
 Types:
 Pernicious anemia
 Aplastic anemia
 Thalassemia
 Sickle cell anemia
 Erythroblastosis fetalis
 Iron deficiency anemia
26

Effects of Anemia on Function of the
Circulatory System:
 one of the major effects of anemia is greatly
increased cardiac output, as well as increased
pumping workload on the heart.
 acute cardiac failure.
Guyton and Hall Text book of medical physiolog 12th edition 2011.
27

28
Title The impact of sickle cell disease on oral health-related quality of life.
Author Ralstrom E, da Fonseca MA, Rhodes M, Amini H
Journal Pediatr Dent. 2014 Jan-Feb;36(1):24-8.
Level of
evidence
III
Aim The purpose of this study was to characterize the impact of sickle cell disease (SCD) on oral
health and examine its impact on quality of life
Method Fifty-four study subjects were recruited from the sickle cell clinic and 52 control subjects from the
adolescent medicine clinic at Nationwide Children's Hospital, Columbus, Ohio. A dental exam was
performed to determine each participant's caries burden. The Child Oral Health Impact Profile
survey was used to assess their oral health-related quality of life
Result Most subjects in both the SCD and control groups rated their overall health and oral health as
"good" or "excellent." There was no statistically significant difference in OHRQoL between these
groups. Additionally, no significant relationship was found between white blood cell count,
medication intake, or the number of sickle cell crises as related to the caries burden. Statistically
significant differences were detected in caries burden between the control group and the sickle cell
hemoglobin C disease (HbSC) group (P<.02) and between the sickle cell anemia and HbSC
subjects (P=.04)
Conclusion Adolescents with sickle cell hemoglobin C disease had fewer caries than with sickle cell anemia or controls, though
the cause of this finding is not clear.

POLYCYTHAEMIA / ERYTHROCYTOSIS
Means increase in RBC count., usually
with a corresponding increase in Hb level.
TYPES:
Primary polycythaemia / Polycythaemia
Vera
Secondary polycythaemia
29

 Importance – Help in diagnosis & typing of Anaemias.
 Different Blood Indices
Packed Cell Volume
Mean Corpuscular Volume (MCV)
Mean Corpuscular Hemoglobin (MCH)
Mean Corpuscular Hemoglobin Concentration (MCHC)
30

Packed cell volume (PCV) is the proportion
of blood occupied by RBCs expressed in
percentage.
It is the volume of red blood cells packed
at the bottom of the hematocrit tube when
the blood is centrifuged at the speed of
3000 RPM for 30 mins.
In males = 40 to 45 %
In Females = 38 to 42 %
31

Significance of determining PCV :-
 Diagnosis and extent of anemia
 Diagnosis and extent of polycythemia
 Determination and extent of dehydration and recovery
from that
 Decision of blood transfusion
Variation in PCV
 Increases in polycythemia and dehydration
 Decreases in anemia, and pregnancy
32

 It is average volume of a single red blood cell and it
is expressed in cubic micron.
 Normal MCV is 90 cu micron (78 – 90 Cu micron)
MCV = volume of packed cell in ml per liter of blood
red cells in million per cu. mm
More in pernicious anemia and megaloblastic anemia
Less in iron deficiency anemia
33

 It is the quantity of hemoglobin present in one
red blood cell.
 It is expressed in Pico gram (Pg)
Hb (gm) /litre of blood
Red cell count in millon /cu.mm
It decreases in pernicious anemia and
megaloblastic anemia.
34

 This is the concentration of hemoglobin in
one red blood cell.
 Amount of hemoglobin expressed in relation
to the volume of one red blood cell.
 Expressed in percentage
 Normal value is 30%
Hb % in 100ml of blood X 100
volume of p.c in 100ml
increases in iron deficiency anemia
35

 The red, oxygen
carrying pigment in
the RBCs is
hemoglobin. It
consists of the
protein globin
(polvpeptide)
united with the
pigment haem
(heme).
36

• Haem
It is an iron containing porphyrin.
The iron in haem is in the
ferrous (Fe2+) form.
Each Fe2+ combines loosely
and reversibly with one
molecule of oxygen.
37

Globin:
• It is a protein built from 4
polypeptide chains, two alpha and
two beta chains.
• Therefore, the normal adult
haemoglobin (HbA) is written as
HbA (alpha2 beta2).
• Of two alpha chains each
contains 141 amino-acids and
of two beta-chains each contains
146 amino-acids.
38

 Transport of oxygen from lungs to the tissues.
 Transport of CO2 from the tissues to the lungs.
 It acts as an excellent acid-base buffer, being a protein.
It is responsible for 70% buffering power
of whole blood.
Types :
39K Sembulingam Essentials of Medical Physiology-6rd edition.

Stage of life Value
At Birth 25 gm%
After 3rd Month 20 gm%
After 1 year 17 gm%
In adult Males 15 gm%
In Adult Female 14.5 gm%
40

 Synthesis of hemoglobin begins
in the proerythroblasts and
continues even into the
reticulocyte stage of the red
blood cells.
 Therefore, when reticulocytes
leave the bone marrow and pass
into the blood stream, they
continue to form minute
quantities of hemoglobin for
another day or so until they
become mature erythrocytes.
41

 Genetic Mutation Structural Variation
In
polypeptide chain
Abnormal hemoglobin can be :
 Hemoglobinopathies:
 Hemoglobin S (can be inherited from the parent)
 Hemoglobin C (problem with a gene called beta globin)
 Hemoglobin E (low MCV and very abnormal red blood
cells (target cells).
 Hemoglobin M
Hemoglobin in thelassemia and related disorders
42

Carboxy hemoglobin (1-3%)
Methemoglobin (0.6-2.5%)
Sulfemoglobin (<1%)
43

44

45
Title Association between iron status, iron deficiency anaemia, and severe early childhood
caries: a case-control study.
Author Schroth RJ1, Levi J, Kliewer E, Friel J, Moffatt ME
Journal BMC Pediatr. 2013 Feb 7;13:22.
Level of
evidence
III
Background Severe tooth decay is known to affect the health and well-being of young children. However, little
is known about the influence of Severe Early Childhood Caries (S-ECC) on childhood nutritional
status. The purpose of this study was to contrast ferritin and haemoglobin levels between
preschoolers with S-ECC and caries-free controls
Method Children were recruited as part of a larger case-control study examining differences in nutritional
status between those with and without S-ECC. Preschoolers with S-ECC were recruited on the
day of their dental surgery, while caries-free controls were recruited from the community. Parents
completed a questionnaire and the child underwent venipuncture. The study was approved by the
University's Health Research Ethics Board. Statistics included descriptive, bivariate and logistic
regression analyses. A p value ≤ .05 was significant. A total of 266 children were recruited; 144
with S-ECC and 122 caries-free
Result The mean age was 40.8 ± 14.1 months. The mean ferritin concentration for all children was 29.6 ±
17.9 μg/L while the mean haemoglobin level was 115.1 ± 10.1 g/L. Children with S-ECC were
significantly more likely to have low ferritin (p=.033) and low haemoglobin levels (p>.001). Logistic
regression analyses revealed that children with S-ECC were nearly twice as likely to have low
ferritin levels and were over six times more likely to have iron deficiency anaemia than caries-free
controls.
Conclusion Children with S-ECC appear to be at significantly greater odds of having low ferritin status compared with caries-
free children and also appear to have significantly lower haemoglobin levels than the caries-free control group.
Children with S-ECC also appear to be at significantly greater odds for iron deficiency anaemia than cavity-free

46
Discovered in 1901.
Alexander S. Wiener
Australian scientist Karl
Landsteiner

 Blood groups are determined by the presence of
antigen in RBC membrane.
 When blood from two individuals is mixed, some
times clumping of RBCs occurs. This clumping
is because of immunological reactions.
47

Landsteiner’s law
 If a particular antigen is present in the RBCs,
corresponding antibody must be absent in
the serum.
 If a particular antigen is absent in the RBCs,
the corresponding antibody must be present
in the serum.
Landsteiner discovered two blood systems
-ABO system
-Rh system
48

ABO system
Based on presence or absence of antigen A and
antigen B, blood is divided in to four groups:
1. ‘A’ group
2. ‘B’ group
3. ‘AB’ group (AB Rh D positive : univ. recipients)
4. ‘O’ group ( ‘O’ negative : univ. donor)
49

Antigen and antibody present in ABO
blood groups:
Group Antigen in RBC Antibody in
serum
A A Anti B
B B Anti A
AB A and B No antibody
O No antigen Anti A and Anti B
50

The blood typing is done on the basis of
agglutination.
To determine the blood group of a person,
a suspension of his RBC and testing anti-
serum are required.
Antiserum A, contains anti A.
Antiserum B contains anti B.
51

Signs and symptoms
Nonhemolytic reaction
Fever
Difficulty in breathing
itching
Hemolytic reaction
Acute:
Fever
Chills
Increase heart rate
Low blood pressure
Nausea
Vomiting
Chest pain
Back pain
Delayed:
Jaundice
Cardiac shock
Renal Shutdown
52

 The antigen was discovered by Landsteiner
and Wiener.
 There are many Rh antigen but only the D is
more antigentic in human.
 The persons having D antigen are called Rh
positive and those without D antigen are
called Rh negative
53

54

Due to excessive hemolysis severe
complications develop
1. Severe anemia
2. Hydrops fetalis
3. Kernicterus.
55

 Also called the HH group.
 They do not express the H
antigen.
 Hence cannot form A antigens or
B antigens on their RBC’s.
 Thus they can donate blood to
anybody with ABO grouping but
cant receive from any other.
56
Dr.Y.M.Bhende in 1952

 Microcytic hypochromic
 Normocytic normochromic
 Macrocytic normochromic
57

Iron deficiency anemia
58
Smooth, bald,burning
tongue
Pallor of lips
Denudation of filliform
papilla

Pernicious anemia
• Beefy red tongue
• Xerostomia
• Ulcerative gingivitis
• Angular cheilitis
• Sore and burning tongue
• Paraesthesia of the
mental nerve
59

 Sickle cell anemia
• Orofacial pain
• Step ladder defect of the
alveolar bone in radiograph
• Pulpal necrosis
• Enamel hypomineralisation
• Prominent maxilla with
severe malocclusion
• Gingival enlargement
• Buccal mucosal pallor
60

Thalassaemia
• Enlargement of the maxilla
• Bossing of the skull
• Prominent malar eminences
• Increased overjet with
spaced maxillary teeth
• Other degrees of malocclusion
61

62
White blood cells are colorless cell which
circulates in the blood and body fluids
and is involved in counteracting foreign
substances and disease.

 WBC count:
Avg : 7000/ cc.mm (4000-11000)
Infants : 20,000/ cc.mm
Children : 10,000- 15,000/ cc.mm
63

Neutrophils : 2-5 days
Eosinophils: 7-12 days
Basophils: 12-15 days
Monocytes: 2-5 days
Lymphocytes: 1 days
66

 SIZE : 10-14 microns in diameter
 NUCLEUS :
Multilobed (1-6 lobes), that is why also called
Polymorphonuclear Leucocyte which is purplish.
 CYTOPLASM : Slight bluish in colour,
granular.
 GRANULES :'fine' sand like Particles:- called
'pinpoint' granules with 'neutrophilic' nature
containing varieties of enzymes which can 'lyse'
any type of substance, the granules are thus
regarded as lysosomes.
67
Textbook of Physiology – 4th Edition by Chaudary

69
Function:
 Plays vital role in nonspecific cellular immunity
system which is against pathogenic microorganism,
such as bacteria, virus, parasite, etc.
Clinical relation:
 Number of neutrophil greatly
increases in
 Neutropenia reduces the body's
ability to fight off bacterial
infections seen in typhoid and viral diseases.
Inflammatory condition
Acute hemolysis
Metabolic disorder
Infection of foreign protein
Poison by insect venom
After acute hemorrhage

It is mainly the neutrophils and tissue macrophages that attack and
destroy invading bacteria, viruses, and other injurious agents.
Diapediasis
Move Through Tissue
Spaces by Ameboid
Motion.
Attracted to Inflamed
Tissue Areas by
Chemotaxis
70

Phagocytosis
71
Text book of medical pathology 6th edition by Harsh Mohan.

 Size: 10-14 microns in diameter
 Nucleus:
• purple color. Usually bilobed, the two lobes are
connected with chromatin thread thus
producing 'spectacle' appearance.
 Cytoplasm:
• acidophilic, therefore, appears light pink in
colour,granular.
72

Granules:
(i) Coarse; stains bright red with acidic dye.
(ii) They contain:
a) Eosinophil peroxidase – Destroys worms
bacteria and tumor cells
b) Major basic protein – Destroys parasites
c) Eosinophil cationic protein – Major
destroyer of worms and parasites.
73

 Functions :
• Mild Phagocytosis because less motile than
neutrophils.
• Eosinophils collect at the sites of allergic reactions.
• Eosinophils attack parasites that are too large to be
engulfed by phagocytosis
• Eosinophil granules release chemicals which are toxic
to larvae of parasites.
74

Eosinophilia: i.e. increase in eosinophils
 Causes
• Allergic conditions e.g. bronchial asthma
• Parasitic infestation
• Skin diseases
Eosinopenia : i.e. decrease in eosinophils
• Seen after injection of ACTH or corticosteroids
75

0.5% of the WBC's
- Release histamine and heparin
- Important in Allergic Reactions
- Heparin helps clear fat from blood
76

 Size : 10 – 14 microns in diameter
 Nucleus : As in eosinophils.
 Cytoplasm : Slight basophilic, therefore, appears blue;
granular.
 Granules:
• (i) Coarse; stains purple or blue with basic
(methylene blue) dye.
• (ii) Granules are plenty in number and overcrowd the
nucleus resulting in obscure boundary of the
nucleus.
• (iii)Contain histamine and heparin
77

Functions:
• i) Mild phagocytosis
• ii) Liberates heparin which acts as anticogulant and
keeps the blood in fluid state in the body.
• iii) Proteases and myeloperoxidase: these enzymes
exaggerate the inflammatory responses.
• iv) cytokine: IL-4 accelerates inflammatory response
78

 Basophilia : i.e. increase in basophils.
Causes
 Chickenpox
 Smallpox
 Tuberculosis
 Influenza
 Basopenia : i.e. decrease in basophils.
Causes
 After administration of glucocorticoids.
 Drug induced reactions.
79

25-33 % of the WBC's
B-lymphocytes:
Produce Antibodies
T-lymphocytes:
Directly destroy virus-
invaded cells and cancer
cells
80

 They are of two types:
• Large lymphocytes: 10-14 microns in diameter:
precursor of small lymphocytes.
• Small lymphocytes : 7-10 microns in diameter;
responsible for antibody production.
 Both large and small lymphocytes have the same
structure.
81

 Nucleus:
• Single; very big; purple in colour.
• Shape: round, oval or indented.
• Central in position and occupies whole of the cell
leaving marginal cytoplasm at one end of it or all
around it.
• Nuclear chromatin is coarse and lumpy (shapeless).
83

 Cytoplasm :
• Pale blue
• Scanty, its amount is always less than the amount of
the nucleus
 Functions:
• Produce antibodies, immune substances, specially in
delayed hypersensitivity
85

 Lymphocytosis i.e. increase in lymphocytes.
Causes
 1. In children lymphocytes (60%) are more than
neutrophils (40%), called Relative Lymphocytosis.
 Chronic infections e.g. tuberculosis (TB).
 Lymphatic leukaemia.
 Viral infections.
 Lymphopenia i.e. decrease in lymphocytes.
Causes
 Hypoplastic bone marrow
 AIDS (acquired immuno deficiency syndrome)
86

2-6 % of the WBC's.
 Exit blood (diapedesis) to become macrophages
 Phagocytic = defend against viruses and bacteria
87

 Size: 10-18 microns in diameter with
irregular cell outline.
 Nucleus:
• Single, Pale staining.
• Round or indented (kidney shaped).
• Eccentric in position i.e. present on
one side of the cell.
• Nuclear chromatin is finely reticular.
 Cytoplasm:
• Usually pale blue; clear.
88

Monocytosis: increase in monocytes.
Causes
 Tuberculosis
 Syphilis
 Some leukemia's.
Monocytopenia: decrease in monocytes.
Cause:
 Hypoplastic bone marrow.
89

 The total combination of monocytes, mobile
macrophages, fixed tissue macrophages, and a few
specialized endothelial cells in the bone marrow,
spleen, and lymph nodes is called the
reticuloendothelial system.
 The macrophages are called by different name at
different sites,
90
 Tissue Macrophages in the Skin
 Macrophages in the Lymph Nodes
 Alveolar Macrophages in the Lungs
 Kupffer Cells in the Liver Sinusoids
 Macrophages of the Spleen and Bone Marrow

91
Shape : Biconvex disk like, diameter about 2~4 µm
Complicated structure : Under the electronic microscope, there are α-
granule, dense body, lysin peroxide enzyme,
opening tubular system, dense tubular system,
canaliculus, etc.
Dense body : It contains ADP, ATP, 5-HT, Ca2+,epinephrine,etc.

Average: 2.59 lacs/ cumm (range: 1.5 to 4 lacs/ cumm)
 The circulating platelets represent approx. 60-75% of the
platelet pool of the body, the remaining are mostly in the
spleen.
 Therefore, spleen acts as a reservoir of platelets.
 Life span: 8-12 days.
 Destruction: mainly in the spleen. In hypersplenism
(overactivity of spleen), the platelets may almost disappear
from circulation
93

Variations:
 Thrombocytosis i.e. increase in platelet count.
Causes:
• after administration of epinephrine due to splenic contraction.
• after trauma e.g. surgery, injury, child birth etc.
• splenectomy (removal of spleen)
• stress - causes increased epinephrine release resulting in
spleen contraction.
• Hemorrhage
• Allergic Condition
94

 Thrombocytopenia i.e. decrease in platelet count.
Causes:
• Bone marrow depression.
• splenomegaly
• Viral infection e.g. dengue fever (particularly attacks platelets).
• Aplastic and pernicious anemia
• Acute infections
• Typhoid
• Tuberculosis
 Thrombocytopenia leads to purpura which is associated with
bleeding disorders
95

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
96

2. ROLE IN CLOT RETRACTION
 In the blood clot, blood cells including platelets are in
between the fibrin threads.
 Cytoplasm of platelets contains the contractile proteins,
namely actin, myosin and thrombosthenin, which are
responsible for clot retraction.
97

3. ROLE IN PREVENTION OF BLOOD
LOSS (HEMOSTASIS)
 secrete 5-HT constriction of blood vessels.
 Due to the adhesive property,
the platelets seal the damage
in blood vessels like capillaries.
 By formation of temporary plug.
98

4. ROLE IN REPAIR OF RUPTURED
BLOOD VESSEL
 Platelet-derived growth factor
(PDGF) formed in cytoplasm of
platelets is useful for the repair
of the endothelium and other
structures of the ruptured
blood vessels.
99

100
The activated platelets:
1. change the shape i.e. put out pseudopodia
2. discharge their granule contents, and
3. stick to each other, called platelet aggregation

Purpura:
 Purplish discoloration of the skin and mucous
membranes due to the spontaneous extravasation of
blood and it self as a symptoms rather then a disease
entity.
 Nonthrombocytopenic purpura
 Thrombocytopenic purpura
1. primary
2. secondary
101
Shafer”s textbook of oral pathology 6th edition

Thrombocytasthenia:
 Thrombocytasthenia is a variety of disease
characterized by a qualitative defect in blood platelets.
Thrombocythemia:
 increase in the number of circulating blood platelets.
Shafer”s textbook of oral pathology 6th edition
102

10
3
Title Gingival inflammation and platelet count in patients with leukemia:
preliminary results
Author Patrícia Daniela Melchiors Angst,Danilo Antônio Milbradt Dutra, Carlos Heitor Cunha Moreira,
Karla Zanini Kantorski
Journal Braz Oral Res. 2011 Nov-Dec;25(6):544-9
Level of
evidence
III
aim The aim of this cross-sectional study was to assess the correlation between the Gingival Index and
Bleeding on Probing with the platelet count in patients with leukemia.
Method Two trained and calibrated examiners evaluated the Plaque Index, Gingival Index (GI), Probing
depth, Bleeding on Probing (BOP), and Clinical Attachment Loss. Hematologic data were collected
from a blood test performed on the same day as the periodontal examination. Thirty-seven patients
(26 males), aged between 15 and 80 years (mean age 41.7 ± 18.31) were
evaluated.
Result Correlation between platelet count and BOP (p > 0.05), or between platelet count and
GI (p > 0.05), were both weak and not statistically significant.
Conclusion It can be concluded from the preliminary results that the low platelet count was not
correlated with the higher prevalence of gingival and periodontal bleeding in patients
with leukemia.

10
4
Title Platelet Concentrate Versus Platelet Transfusion
Author Nadia Cocero¹, Laura Bergamasco2, Marco Mozzati3
Journal (Int Dent Res 2012;2(2):33-36
Level of
evidence
III
aim Surgical treatment of patients with severe thrombocytopaenia (<50,000 platelets/ L) is a major
problem for dentists due to an increased risk of bleeding. To reduce post-extraction haemorrhage,
we tested a new approach using a platelet concentrate and compared its outcomes with those of
routine platelet transfusion.
Method Sixty-six patients with a platelet count between 29,000 and 46,000/ L were included in the study.
Each patient was to undergo at least two sessions for the extraction of teeth; in one session the
patients received a platelet transfusion before the extraction and in the other the post-alveolar
sockets were treated with Plasma Rich in Growth Factors (PRGF). Patients were evaluated after
0.4, 1, 3 and 7 days to assess bleeding and haematoma.
Result Patients treated with PRGF consistently exhibited a statistically significant reduction in post-
extraction bleeding, hematoma and need for re-intervention. There is ample evidence that
application of PRGF in the post-alveolar socket markedly reduced the risk of haemorrhage and
associated complications in all patients.
Conclusion PRGF concentrate is recommended for the treatment of thrombocytopaenic patients due to its
remarkable ability to stimulate healing while greatly reducing side effects, such as bleeding and
haematoma.

Hemostasis prevention of blood loss
Mechanisms:
(1) Vascular constriction
(2) Formation of a platelet plug
(3) Formation of a blood clot
(4) Eventual growth of fibrous tissue
107
Events in Hemostasis:

Vascular Constriction:
The contraction results from:
(1) local myogenic spasm
(2) local autacoid factors from the traumatized
tissues and blood platelets
(3) nervous reflexes.
108

109Guyton and Hall Text book of medical physiology 12th edition 2011
Platelets come in contact with a damaged
vascular surface
change their shape, begin to swell, assume
irregular forms with numerous irradiating
pseudopods protruding from their surfaces.
contractile proteins contract forcefully and
cause the release of granules
they become sticky and adhere to
collagen in the tissue and the protein
called von
Willebrand factor leaks into
traumatized tissue from the plasma.

110
they secrete large quantities of ADP; and their enzymes form
thromboxane A2.
The ADP and thromboxane in turn act on nearby platelets to activate
them as well, and the stickiness of these additional platelets causes
them to adhere to the original activated platelets.

• The platelet-plugging mechanism
is extremely important for closing
minute ruptures in every small
blood vessels that occur many
thousands of times daily.
111

 The clot begins to develop in 15 to 20 seconds if
the trauma to the vascular wall has been severe,
and in 1 to 2 minutes if the trauma has been
minor.
 Activator substances from the traumatized
vascular wall, from platelets, and from blood
proteins adhering to the traumatized vascular
wall initiate the clotting process
112
Guyton and Hall Text book of medical physiology 12th edition 2011

 PHYSICAL EVENTS:
113

Basic Theory. More than 50 important
substances that cause or affect blood
coagulation have been found in the blood
and in the tissues.
some that promote coagulation, called
procoagulants, and others that inhibit
coagulation, called anticoagulants
114Guyton and Hall Text book of medical physiolog 12th edition 2011

115Guyton and Hall Text book of medical physiology 12th edition 2011

Prothrombin activator is generally
considered to be formed in two ways:
(1) by the extrinsic
 pathway that begins with trauma to the vascular
wall and surrounding tissues.
(2) by the intrinsic
 pathway that begins in the blood itself.
116

Guyton and Hall Text book of medical physiology 12th edition 2011 117

when blood is removed from a person, it can be
prevented from clotting by reducing the calcium
ion concentration
• By deionizing the calcium by causing it to react
with substances such as citrate ion
• By precipitating the calcium with substances such
as oxalate ion.
119
Calcium ions are required for promotion or acceleration of all the blood clotting
reactions.

 After blood vessels rupture, clotting occurs by both
pathways simultaneously.
 Extrinsic pathway can be explosive,once initiated clotting
can occur in as little as 15 seconds.
 The intrinsic pathway is much slower to proceed usually
requiring 1 to 6 minutes to cause clotting.
120

122
It is now widely agreed that the principal initiating pathway of
coagulation is the so-called extrinsic pathway due to the action of
tissue factor and Factor VII.
Although the “intrinsic pathway” is no longer felt to be the initiator of
coagulation, recent evidence suggests that Factor XIa may constitute
an important amplification pathway of the coagulation system in vivo.
It is hoped that detection and characterization of platelet antigens,
including adhesion molecules such as P-selectin. will enable further
understanding of the platelet's role in pathological coagulation and
inflammation.
The endothelium is also intricately involved and recent work has
determined the importance of endothelial produced factors such as
endothelium-derived relaxation factor, endothelin, and
thrombomodulin.

*
• Finally, with the meteoric rise in molecular genetic
technology, specific genetic abnormalities in a number
of plasma proteins has been elucidated, with marked
implications on the understanding of the coagulation
process.
*
• For example. the mutation on the gene for Factor V,
leading to Arg506 replacement with Gln. produces
activated protein C resistance with a concomitant
increased risk of venous thrombosis.
12
3

Lysis of blood clot inside the blood vessel
is called fibrinolysis.
This occurs by a substance Fibrinolysin /
plasmin
Significance – allows reopening of the
affected blood vessel and prevents the
development of infarction.
125

Tissue plasminogen activator
Plasminogen Plasmin
dissolves the clot by digesting fibrin
(Action)
126

Endothelial Surface Factors:
- smoothness of the endothelial cell surface.
- layer of glycocalyx on the endothelium.
- thrombomodulin
 Antithrombin action of fibrin and Antithrombin III
 Heparin
127

 Fluoride supplements may be used
 Three exposures of sugar per day is the recommended
maximum.
 Toothbrush should have medium texture bristles
 Artificial sweeteners can be used as an alternative to sugars
in food and drinks. Examples are aspartame, sorbitol,
acesulfamate, etc.
 Regular dental visits, usually every 6 months, will help
identify problems early, reinforce prevention, and emphasize
the importance of reducing the intake of food and drink
containing high levels of sugar or acid.
128

Vitamin K deficiency:
 Vitamin K is necessary for liver to form five of the
important clotting factors: prothrombin, Factor VII, Factor
IX, Factor X, and protein C.
 In the absence of vitamin K, subsequent insufficiency of
these coagulation factors in the blood can lead to serious
bleeding tendencies.
129

 Hemophilia:
This is characterized by prolonged coagulation time and
hemorrhagic tendency.
Type: Hemophilia A
Hemophilia B
Hemophilia C
 Von Willebrand’s Disease
 Parahemophilia
 Hypofibrinogenemia
 Fibrin-stabilizing factor deficiency
 Thrombocytopenia
130

 Factor VIII must be replaced with porcine Factor VIII or recombinant Factor VIII
to a level adequate to ensure hemostasis if bleeding starts or is expected.
 The bleeding tendency can be aggravated by NSAIDs. Safer alternatives for pain
control are acetaminophen, codeine and Cox-2 inhibitors.
 Local anesthetic regional blocks, lingual infiltrations or injections into the floor of
the mouth must not be used in the absence of Factor VIII replacement because
of the risk of hemorrhage hazarding the airway and being life-threatening.
 If FVIII replacement therapy has been given, regional LA can be used provided
the FVIII level is maintained above 30%.
 Infiltrations, intraligamentary, intraosseous or intrapulpal injections are still safer.
131

 There is a risk of bleeding with the use of matrix bands or wooden
wedges. This can be controlled by local means or the application of topical
agents.
 Formaldehyde-derived substances may also be used in cases where
there is persistent bleeding or even before the pulpectomy.
 Use a 10% solution of tranexamic acid or EACA to dampen the swab
or as a mouthwash if the bleeding is difficult to stop.
 Desmopressin and tranexamic acid are primary alternatives.
 Mild hemophiliacs requiring surgeries can be managed usually without
factor replacements.
 Tranexamic acid as a mouthwash in anticoagulant is an alternative
method to discontinue anticoagulant therapy in children. 132

 Patient and Methods: 58 dental extractions in 15 patients during 19 interventions were
performed.
 Replacement therapy with recombinant and plasma-derived factor VIII and IX was
applied systematically in combination with antifibrinolytic treatment and local
haemostatic measures.
 The following data were recorded: type of surgery, applied local haemostatic
measures, general substitution, systemic antifibrinolytic agents and occurrence of
postoperative bleeding complications.
 Results: Two patients presented postoperative bleeding. One had secondary bleeding
requiring additional injection of factor concentrates. The other one presented epistaxis
which was managed conservatively with a nasal tamponade.
 Conclusions: Excellent haemostasis is achievable after dental extractions in
patients with Haemophilia A and B by following a protocol using defined pre- and
postoperative doses of factor concentrates in combination with haemostatic
measures
133

Thromboembolic Conditions in the Human Being:
1)Thrombus and emboli
2)Disseminated Intravascular Coagulation
3)Femoral Venous Thrombosis and Massive
pulmonary embolism
134

In some thrombo-embolic conditions, it is desirable to delay the
coagulation process. Various anticoagulants have been developed
for this purpose.
Heparin as an Intravenous Anticoagulant:
 Injection of relatively small quantities, about 0.5 to 1 mg/kg of
body weight, causes the blood-clotting time to increase from a
normal of about 6 minutes to 30 or more minutes.
 The action of heparin lasts about 1.5 to 4 hours. The injected
heparin is destroyed by an enzyme in the blood known as
heparinase.
135

Coumarins as Anticoagulants:
 When a coumarin, such as warfarin, is given to a patient,
the plasma levels of prothrombin and Factors VII, IX, and
X, all formed by the liver, begin to fall, indicating that
warfarin has a potent depressant effect on liver formation
of these compounds.
 Warfarin causes this effect by competing with vitamin K.
136
Normal coagulation usually returns 1 to 3 days after
discontinuing coumarin therapy.

Siliconized containers
Heparin
Various substances that decrease the
concentration of calcium ions
Deionizing the blood calcium
sodium, ammonium, or potassium citrate
137

Thermal agents:
• Cautery
• Cryosurgery
• Electrosurgery
• Argon- beam coagulator
Textbook of oral and maxillofacial surgery by Nelima Anil Malik 2nd edition
138
Mechanical methods :
Pressure
Use of hemostats
Suture and ligation

Chemical method:
Local agents:
 Monsel’s solution & tannic acid
 Bone wax
 Thombin
 Gelfoam
 Oxycel
 Fibrin glue
 Adrenaline
Textbook of oral and maxillofacial surgery by Nelima Anil Malik 2nd edition
139
Systemic agent:
 Whole blood
 Fresh frozen plasma
 Cryoprecipitate
 Ethamsylate

 Bleeding Time (BT)
 Clotting Time (CT)
 Prothrombin Time (PT)
 Partial thromboplastin Time (PTT)
 Thrombin Time (TT)
141

BLEEDING TIME : Provides assessment of
platelet count & function
Prolonged BT:-
► Congenital & acquired disorder of platelet function
► Von Willebrand disease
► Thrombocytopenia
► Purpura
Normal value:-
3-6 Minutes
142

Prolonged in Hemophilia.
Method
Capillary Glass Method
Normal Clotting Time:
4-9 Min.
143

Measures Effectiveness of the Extrinsic Pathway
Prolonged PT:-
 Deficiency of Prothrombin
 Disseminated Intravascular Coagulation
 Vit. K deficiency
Normal value :
 10-15 SECS
144
Guyton and Hall Text book of medical physiology
12th edition 2011

Measures Effectiveness of the Intrinsic Pathway
Measures coagulation disorders.
Prolonged PTT-
► Factor III deficiency
► Increases in Hemophilia
► Anticoagulation with heparin
NORMAL VALUE
 25-40 SECS
145

Is a measure of the rate of conversion of fibrinogen to fibrin
Prolonged TT
► Contamination with heparin
► Acquired (DIC, liver disease)
NORMAL VALUE
9-13 SECS
146

 WHOLE BLOOD TRANSFUSION
Loss of whole blood due to,
• Accidental injuries
• During and after major surgery
 PACKED CELL TRANSFUSION :
• Patients with severe anemia, Hb concentration < 4 gms%
 LEUKOCYTE TRANSFUSION :
• Patients with decreased immunity (increased susceptibility
for infections) or
• Patients suffering from agranulocytosis.
147
A manual on clinical surgery by S Das 10th Edition

 PLATELET TRANSFUSION
• Disorders due to Thrombocytopenia.
 TRANSFUSION OF COAGULATION FACTORS
• Factors VIII or AHG -- hemophilic patient
• Factor IX -- patient suffering from Christmas
disease.
• Factors obtained in concentrated form from fresh
plasma (human) by way of cryoprecipitation.
148

 Refers to the transfusion of an individuals own
blood which has been withdrawn and stored.
 It is done under the following situations:
• For elective surgery, a self pre-donation is a norm in
some hospitals;
• During surgery, the cell saver machine when used
sucks up blood from the wound, recycles it, and
returns it to the patients body;
• Some sports persons are known to use autologous
transfusion a few days before an important event to
enhance performance.
149

Precautions
while
Blood transfusion
BEFORE
No
communicable
diseases
Matching ABO &
Rh compatibility
DURING
Volume overload
Metabolic
side effects
AFTER
Observation for
delayed effects

A manual on clinical surgery by S Das 10th Edition
Can be of different types:
• Transfusion reactions
• Transmission of diseases
• Reaction caused by massive transfusion
• Complication of IV fluid administration
151

 Transfusion reactions:
• Incompatibility
• Allergic reactions
• Sensitization to leukocytes & platelets
 Transmission of diseases:
• Serum hepatitis
• AIDS
• Bacterial infections
152

Reaction due to massive transfusion :
• Acid-base imbalance
• Hyperkalemia
• Hypothermia
Complication of general IV fluid
administration:
• Thrombo embolism
• Air embolism
153

 Guyton and Hall Text book of medical physiolog 12th
edition 2011.
 Ganong Review of Medical Physiology-23rd Edition.
 K Sembulingam Essentials of Medical Physiology-6rd
edition.
 Textbook of oral and maxillofacial surgery by Nelima Anil
Malik 2nd edition.
 Textbook of Physiology – 4th Edition by Chaudary
 Text book of medical pathology 6th edition by Harsh
Mohan.
 Shafer”s textbook of oral pathology 6th edition.
 A manual on clinical surgery by S Das 10th Edition.
154

 Ralstrom E, da Fonseca MA, Rhodes M, Amini H. The impact of sickle cell
disease on oral health-related quality of life. Pediatr Dent. 2014 Jan-
Feb;36(1):24-8
 Schroth RJ1, Levi J, Kliewer E, Friel J, Moffatt ME. Association between
iron status, iron deficiency anaemia, and severe early childhood caries: a
case-control study. BMC Pediatr. 2013 Feb 7;13:22.
 Hegde AM1, Joshi S, Rai K, Shetty S.Evaluation of oral hygiene status,
salivary characteristics and dental caries experience in acute lymphoblastic
leukemic (ALL) children. J Clin Pediatr Dent. 2011 Spring;35(3):319-23.
 Cocero N, Pucci F, Messina M, Pollio B, Mozzati M, Bergamasco L.
Autologous plasma rich in growth factors in the prevention of severe
bleeding after teeth extractions in patients with bleeding disorders: a
controlled comparison with fibrin glue. Blood Transfus. 2014 Oct 29:1-8.
doi: 10.2450/2014.0124-14
 Nadia Cocero, Laura Bergamasco, Marco Mozzati. Platelet Concentrate
Versus Platelet Transfusion. Int Dent Res 2012;2(2):33-36
155

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