Hema Duddukuri

1st year pg
Dept. of Periodontics
PMVIDS
 CONTENTS
 Introduction
 Properties of Blood
 Functions of Blood
 Composition of Blood
 Hematopoiesis
 Formed elements
 Coagulation
 Mechanism of clotting
 Bleeding disorders
 Applied Physiology
 Conclusion
 INTRODUCTION

 Blood: Specialized connective tissue.

 Fluid of life

 Fluid of growth

 Fluid of health

 Circulated around the body through blood vessels

by the pumping action of heart.

 PROPERTIES OF BLOOD
Color:
• Arterial blood - scarlet red.
• Venous blood - purple red.
• Anemia- watery and pale.
Volume:
• Adult - 5 L.
• Newborn baby - 450 ml.
• Females - 4.5 L.
• About 8% of the body weight.
Reaction & pH:
• Slightly alkaline – pH: 7.4
• Due to presence of alkaline phosphates and bicarbonates.
 Specific gravity:
• Total blood: 1.052 to 1.061
• Blood cells: 1.092 to 1.101
• Plasma: 1.022 to 1.026

 Viscosity:
• 5 times more viscous than water.

 Osmotic pressure/ Oncotic pressure:

• Depends upon its colloid and crystalloid contents.
• Measures about 25-30 mm/Hg.
• 75% of the colloid osmotic pressure is due to
serum albumin.
 FUNCTIONS OF BLOOD
Nutritive function:

Glucose, Vitamins,
G.I.T Amino Acids.. BODY

Respiratory:
Excretory:

Transport of hormone and enzymes:

Homeostasis:

Defensive function:

Storage function:
Hematopoiesis
 COMPOSITION OF BLOOD
Blood contains the blood cells - formed elements and
the liquid portion - plasma.
SERUM:
• Clear straw-colored fluid that oozes from blood clot.
• Differs principally from plasma by the absence of
fibrinogen and other coagulation factors.
FORMED ELEMENTS
RED BLOOD
CELLS
 Non-nucleated formed elements in blood
 Red in color due to the pigment-hemoglobin

 Hemoglobin:

• Chromoprotein forming 95% of dry weight of RBC.

• Function: carry the respiratory gases & acts as a buffer.
• Molecular weight: 68,000.
• Normal Hb content:
o At birth : 25 g/dL

o After 1 year : 17 g/dL

o From puberty onwards : 14 to 16 g/dL

 Morphology of RBC:
Shape: Disc shape & biconcave
Size:

Structure:
Lack nucleus, mitochondria, golgi apparatus and insulin
receptors.
Special cytoskeleton made up of actin, spectrin and ankyrin
Lack of spectrin results in Hereditary Spherocytosis.
 Properties:
• Rouleaux formation:

• Packed Cell Volume

(Hematocrit):

• Suspension stability:
 Life span: 120 days.
Determined by: Radioisotope method.
 Fate of RBC:
Functions
of
RBC
 Size

Physiologic Pathologic

Microcytes Macrocytes Anisocytes

• Iron-deficiency
anemia. • Megaloblastic Pernicious
• Prolonged anemia anemia
Venous RBC forced • Decreased
> breathing. osmotic
Arterial RBC • Increased pressure in
osmotic blood.
pressure in
blood.
 Shape

Shape of RBCs is altered in many conditions including

different types of anemia.
1. Crenation: Shrinkage as in hypertonic conditions.
2. Spherocytosis: Globular form as in hypotonic conditions.
3. Elliptocytosis: Elliptical shape as in certain types of anemia.
4. Sickle cell: Crescentic shape as in sickle cell anemia.
5.Poikilocytosis: Unusual shapes due to deformed cell membrane.
The shape will be of flask, hammer or any other unusual shape.
 Number

Increase Decrease

Physiologic Pathologic Physiologic Pathologic

Polycythemia
• At birth: 8-10 • High
10:Polycythemia
million/mm3 barometric
vera (>14 million/mm ) 3
pressures
• High altitudes Myeloproliferative
• Sleep
Anemia
• Excersice disorders
• Emotional • Pregnancy
20:in some pathologic conditions
conditions Emphysema • Females (in
• After meals Congenital Heart reproductive
• Increased Disease stage)
CO Phosphorous &
environmental
Arsenic poisoning
temperature Repeated Mild
hemorrhages
 ANEMIA

 Anemia is the blood disorder, characterized by the reduction in:

1. Red blood cell (RBC) count
2. Hemoglobin content
3. Packed cell volume (PVC).

 Anemia is classified by two methods:

1. Morphological classification
2. Etiological classification.
Morphologic classification of anemia
Etiologic classification of anemia
Thalassemia
 Anemia & Periodontal Health
 Studies:
Lainson et al (1968): anemia as a systemic cause of periodontitis.
Chawla et al (1971): anemia to be an etiologic factor of periodontitis
Siegel et al (1945): decrease in RBC secondary to the presence of periodontal
disease.
Hutter et al (2001): periodontitis patients have lower hematocrit, RBC, Hb, &
higher ESR
Gokhale et al (2010):chronic periodontitis associated with decreased RBC & Hb.
Pradeep et al (2011): NSPT improved the RBC parameters.
 Possible mechanism:
 WHITE
BLOOD CELLS
• Colorless and nucleated formed elements of blood.
• Greek word leukos = white.
• NORMAL WHITE BLOOD CELL COUNT
1. Total WBC count (TC): 4,000 to 11,000/cu mm of
blood.
2. Differential WBC count (DC):
 WHITE BLOOD CELLS

AGRANULOCYTES GRANULOCYTES
 Substances secreted by WBCs

Proteases Eosinophil
Heparin Interleukin-1
Myeloperoxidases peroxidase.
Histamine Colony
Elastases Major basic
Bradykinin stimulation
Metalloproteinase protein.
Serotonin factor.
Defensins Eosinophil
Proteases Platelet-
Cathelicidins cationic protein.
Myeloperoxidase activating
NADPH oxidase Eosinophil-
s factor.
Platelet-activating derived
factor Interleukin-4 neurotoxin.
Interleukin-4 & 5
Functions of WBC:
 Lifespan:
• Not constant.
• It depends upon the demand in the body and
their function.
• Lifespan of these cells may be as short as half a
day or it may be as long as 3 to 6 months.
 Physiologic variations in WBC
o Age: 20,000 per cu mm in infants
10,000 to 15,000 per cu mm in children.
In adults - 4,000 to 11,000 per cu mm of blood.
o Sex: Slightly more in males than in females.
o Diurnal variation: Minimum in early morning
Maximum in the afternoon.
o Exercise: Increases slightly.
o Sleep: Decreases.
o Emotional conditions like anxiety: Increases.
o Pregnancy: Increases.
o Menstruation: Increases.
o Parturition: Increases.
Pathologic variations in WBC

Neutrophils
Eosionophils

Basophils
Monocytes

Lymphocytes
PLATELETS
 Small colorless, non-nucleated and moderately refractive bodies.
 Considered to be the fragments of cytoplasm
 Size of Platelets:
Diameter : 2.5 μ (2 to 4 μ)
Volume : 7.5 cu μ (7 to 8 cu μ).
 Shape:
•Several shapes – spherical/rod , oval/disc
others: comma, cigar, dumbbell,…
 Structure & Composition
Platelet is constituted by:
1. Cell membrane or surface membrane
2. Microtubules
3. Cytoplasm.
 PROPERTIES OF PLATELETS

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

1. Adhesiveness
2. Aggregation
3. Agglutination.
 FUNCTIONS OF PLATELETS

 Activated platelets immediately release many substances.

 This process is known as platelet release reaction.
 Functions of platelets are carried out by these substances.

1. ROLE IN BLOOD CLOTTING

2. ROLE IN CLOT RETRACTION

3. ROLE IN PREVENTION OF BLOOD LOSS

4. ROLE IN REPAIR OF RUPTURED BLOOD VESSEL

5. ROLE IN DEFENSE MECHANISM

 ACTIVATORS AND INHIBITORS OF PLATELETS

ACTIVATORS OF
PLATELETS:
INHIBITORS OF PLATELETS:
•Collagen
•Nitric oxide
•Von Willebrand factor
•Clotting factors: II, IX, X, XI,
•Thromboxane A2
XII
•Platelet-activating factor
•Prostacyclin
•Thrombin
•Nucleotidases
•ADP
•Calcium ions
•P-selectin
•Convulxin
 LIFE SPAN AND FATE OF
PLATELETSN

• Lifespan: 8 and 11 days.

• Platelets are destroyed by tissue macrophage system in
spleen.
• Splenomegaly: decreases platelet count and
• Splenectomy: increases platelet count.
 PLATELET DISORDERS

Thrombocytopenia Thrombocytosis Thrombocythemia Glanzmann’s

thrombasthenia:
Acute infections
Acute leukemia Allergic Carcinoma Inherited disorder
Aplastic and conditions Chronic leukemia associated with
Pernicious anemia Asphyxia Hodgkin’s disease. structural or
Chickenpox Hemorrhage functional
Smallpox Bone fractures abnormalities in
Splenomegaly Surgical platelets.
Scarlet fever operations
Typhoid Splenectomy
Tuberculosis Rheumatic fever
Purpura Trauma
Gaucher’s disease.
COAGULATION
 Hemostasis:
Hemostasis is defined as arrest or stoppage of bleeding.
 Coagulation:
The process by which blood changes from a liquid to a gel,
forming a blood clot, resulting in hemostasis.
 Clot: Blood clot is defined as the mass of coagulated blood which
contains RBCs, WBCs and platelets entrapped in fibrin
meshwork.
STAGES OF HEMOSTASIS:
When a blood vessel is injured, the injury initiates a series of
reactions, resulting in hemostasis. It occurs in three stages.
1. Vasoconstriction.
2. Platelet plug formation.
3. Coagulation of blood.
 MECHANISM OF CLOTTING

• 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.
• Thirteen clotting factors are identified.
 SEQUENCE OF CLOTTING MECHANISM

ENZYME CASCADE THEORY:

Enzyme cascade theory explains how various reactions,

involved in the conversion of proenzymes to active enzymes
take place in the form of a cascade, occurring in 3 stages:

1.Formation of prothrombin activator

2.Conversion of prothrombin into thrombin
3.Conversion of fibrinogen into fibrin.
 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.
 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.
2. Chemical Factors – Natural Anticoagulants
i. Presence of natural anticoagulant called heparin produced by
liver.
ii. Production of thrombomodulin by endothelium
iii. All the clotting factors are in inactive state.
 ANTICOAGULANTS

Substances which prevent or postpone coagulation of blood are

called anticoagulants.
Anticoagulants are of three types:
1. Anticoagulants used to prevent blood clotting inside the
body, i.e. in vivo.
2. Anticoagulants used to prevent clotting of blood that is
collected from the body, i.e. in vitro.
3. Anticoagulants used to prevent blood clotting both in
vivo and in vitro.
 In Vitro
In Vitro & In Vivo
Heparin
Calcium Complexing Heparin

Agents: Sodium Citratre Dextran Sulphate

Sodium Oxalate Ancord

EDTA
 PROCOAGULANTS

• Procoagulants or hemostatic agents are the substances

which accelerate the process of blood coagulation.
• Procoagulants are:
 Thrombin
 Snake venom
 Sodium/Calcium alginate
 Oxidized cellulose
 MANAGEMENT OF BLEEDING
• Bleeding due to surgical procedures can be managed through following
ways:
a) Pressure
b) Hemostat
c) Ligation
d) Cauterization
e) Cryosurgery
f) Use of hemostatic agents:
 Adrenaline
 Thrombin
 Oxidized cellulose
 Gelatin sponge
 Bone wax
 Microfibrillar collagen
 BLEEDING DISORDERS

Bleeding disorders are the conditions characterized by

prolonged bleeding time or clotting time.
Bleeding disorders are of Four types:
1. Vessel wall disorders
2. Platelet disorders
3. Coagulation disorders
4. Fibrinolytic disorders
CONGENITAL COAGULOPATHIES ACQUIRED COAGULOPATHIES

Hemophilia A
Hemophilia B Anti-coagulant Disease related:
Factor 9 deficiency related :
Factor 12 deficiency Liver
Factor 10 deficiency Heparin Vitamin k
Factor 5 deficiency Coumarin deficiency
Factor 13 & 1 deficiency derivatives Disseminated
von Williebrand’s Intravascular
disease Coagulation
Fibrinolytic disorders:

Disorders of the fibrinolytic system can lead to

hemorrhage when clot breakdown is enhanced, or
excessive clotting and thrombosis when clot
breakdown mechanisms are retarded.

 Disseminated Intravascular Coagulation

 Thrombosis
PERIODONTAL MANIFESTATIONS OF BLOOD DYSCRASIAS
Anemia:
 Marked pallor of gingiva
 Increased susceptibility to infections
 Generalized osteoporosis of jaws
 Periodontal infections may precipitate sickle cell crisis.

 Thrombocytopenia:
 Spontaneous bleeding
 Petechiae
 Swollen, soft and friable gingivae
 Bleeding is difficult to control
 Abnormal changes in gingiva in response to local irritation.
 Dramatical alleviation of these changes on removal of the local
irritant.
Leukocyte disorders:
 Neutropenia:
Severe destruction of periodontium & Increased susceptibility to
infections.
 Agranulocytosis:
Gingival hemorrhage, Necrosis and Fetid odor
 Cyclic neutropenia:
Recurrent exacerbations of periodontal infections.
Generalized Aggressive Periodontitis
 Lazy Leukocyte Syndrome:
Susceptible to aggressive periodontitis, with destruction of bone
and early tooth loss.
 Leukocyte Adhesion Deficiency:
Extremely acute inflammation with proliferation of gingival tissues
and rapid bone destruction.
Leukemia:
 Gingiva is bluish red-cyanotic, spongelike and friable.

 Bleeds easily.

 Gingival enlargement due to leukemic cell infiltrate

 Acute gingival ulcerations with pseudomembrane formation

mimicking NUG
 Increased susceptibility to infections.
 DIAGNOSIS OF BLOOD DYSCRASIAS
Patients with a h/o bleeding problems should be diagnosed carefully
in order to minimize the risks associated with the disease and treat
accordingly.
This can be done with a proper history taking, clinical examination
and lab. Investigations.
Lab. Investigations should measure the hemostatic, coagulation and
lytic phases of the clotting mechanism.
These tests include:
 Bleeding time (BT)
 Clotting time (CT)
 Tourniquet test
 Complete blood cell count (CBP)
 Prothrombin time (PT) - INR
 Activated Partial thromboplastin time (APTT)
 MANAGEMENT

The treatment planning should include:

Physician consultation

Blood investigations

Conservative, nonsurgical periodontal treatment,

whenever possible.
Oral hygiene instructions and frequent maintenance

visits.
THERAPEUTIC APPLICATIONS OF BLOOD & ITS PRODUCTS

• Platelet Rich Plasma:

• Pure PRP (P-PRP)
• Leukocyte rich PRP (L-PRP)
• Platelet Rich Fibrin:
• Pure PRF (P-PRF)
• Leukocyte rich PRF (L-PRF)
• Injectable PRF (I PRF)
• Advanced PRF (A PRF)
• Titanium tubes PRF (T PRF)
 CONCLUSION
• Blood and coagulation plays an essential role in the maintenance
of a healthy periodontium. Consequently, disorders involving
them can have a profound effect on the it.
• It is the responsibility of the clinician to identify the patients
medical problem and formulate a proper treatment plan, as failure
to do this will result in serious complications.
• In order to achieve this, one must be familiar with current
understanding of various medical disorders, their management
and the recommendations provided by the concerned authorities
from time to time.
 REFERENCES
Essential of Medical Physiology. 6th Ed. K. Sembulingam.

Carranza’s Clinical Periodontology. 2nd South Asia Edition.

Medical Physiology-A Cellular and Molecular Approach

Updated second edition. Walter F. Boron.

Textbook of Medical Physiology. 13th Ed. Guyton & Hall.

Ganong’s Review of Medical Physiology. 25th Ed. Kim E.

Barrett.
Textbook Of Oral And Maxillofacial Surgery. 2nd Ed.

Chitra Chakravarthy.
Medical Physiology. Principle of Clinical Medicine. 4th Ed.

Roadney A. Rhodes.
Gokhale S, Sumanth S, Padhye A. Evaluation Of Blood

Parameters In Patients With Chronic Periodontitis For

Signs Of Anemia. J Periodontol2010;81:1202-1206.
Bleeding And Clotting Disorders Lauren L. Patton, DDS

Bleeding Disorders And Periodontology. Philip

Vassilopoulos & Kent Palcanis. Periodontology 2000, Vol.
44, 2007, 211–223.