4. PROPERTIES
8% of body weight
Colour : Red
Volume : approximately 5 L
ph : 7.4 ± 0.5
Specific Gravity : 1.052 to 1.061
Viscosity : 5 times more than water
9. 19-9
Plasma
• Liquid part of blood
– Pale yellow made up of 91% water, 9% other
• Colloid: Liquid containing suspended
substances that don’t settle out
– Albumin: Important in regulation of water
movement between tissues and blood
– Globulins: Immune system or transport
molecules
– Fibrinogen: Responsible for formation of blood
clots
10. 19-10
Formed Elements
• Red blood cells (erythrocytes)
• White blood cells (leukocytes)
– Granulocytes
• Neutrophils
• Eosinophils
• Basophils
– Agranulocytes
• Lymphocytes
• Monocytes
• Platelets (thrombocytes)
11. FUNCTIONS OF PLASMA PROTEINS
Coagulation of blood
Immune function
Transport function
Maintain colloidal osmotic pressure
Maintain acid-base balance in the body
Maintain viscosity of blood
Provides stability to blood
12.
13. Red blood cells
Count- 4-5.5millions/cu mm of blood
Shape-disk shaped, biconcave, central portion is thinner and
periphery is thicker
Diameter- 7.5u
Thickness – 2.2u at periphery 1u at the centre.
Rouleaux formation-
Lifespan-about 120 days
14. Erythropoiesis
• It is the process of origin, development
and maturation of erythrocytes
• In the early weeks of embryonic life,
primitive, nucleated red blood cells are
produced in the yolk sac.
• During the middle trimester of
gestation in the liver
• Up to age of 20 years-RBC’S are
produced from red bone marrow of all
bones
• After the age of 20 years-produced
from membranous bone like vertebra,
sternum, ribs, scapula, iliac bones,
skull bones
23. DESTRUCTION OF HEMOGLOBIN
Iron porphyrin globin
Utilisesd for
resynthesis of
Hemoglobin
Stored as ferritin and
hemosiderine
Reutilised for
synthesis of new
Hemoglobin
biliverdin
bilirubin
26. E.S.R
Rate at which the red blood cells settle down
Westergren’s
Wintrobe’s
Male : 3-7 mm/hr
Female : 5-9 mm/hr
27. PACKED CELL VOLUME
Hematocrit value expressed as the percentage of
cellular elements with that of whole blood.
Males : 40-45%
Female : 38-42%
28. Red Cell Indices
1. Packed cell volume (PCV)
2. Mean corpuscular volume (MCV)
PCV x 10/ No. of RBCs per cu. mm.
Normal value – 80 to 90 μ3
3. Mean corpuscular hemoglobin (MCH)
Hb in gm/lt/RBC count
Normal value – 30 pg
4. Mean corpuscular hemoglobin concentration (MCHC)
Hb (in gm%) x 100 / PCV
Normal value – 31 – 35 gm%
Erythrocytes
51. Hemostasis
Haemostasis is prevention of blood loss
Stages of haemostasis-
1) Vasoconstriction
2) Platelet plug formation
3) Coagulation of blood
53. Injury to the blood vessel and damage of endothelium
Exposure of collagen
Adherence of platelets to collagen
Activation of platelets
Secretion of serotonin Secretion of ADP and
thromboxane A2
Formation of
prothrombin activator
Aggregation of
platelets
Formation of
platelet plug
vasoconstriction Blood clotting
stage1 Stage 2 Stage 3
55. Primary hemostasis
Entails platelet plug formation and lasts for 2–3 seconds .
Predominant mechanism in capillaries and small-
diameter vessels
Secondary hemostasis
Associated with fibrin synthesis and its deposition
Provides stabilization of the hemostatic clot
56. CLOTTING FACTORS
FACTORS NAME
I Fibrinogen
II Prothrombin
III Thromboplastin
IV Calcium
V Proaccelerin, Labile factor
VII Stable factor, Proconvertin
VIII Antihaemophilic factor (AHF),
IX Christmas factor
X Stuart – Prower factor
XI Plasma thromboplastin antecedent
XII Hageman factor
XIII Fibrin stabilizing factor
58. Coagulation of blood
Coagulation or clotting is defined as the process in which blood looses its
fluidity and becomes a jelly like mass .
stages
• Formation of prothrombin activator
• Conversion of prothrombin into thrombin
• Conversion of fibrinogen into fibrin
Formation of prothrombin activator occurs through 2 pathways
(1) by the extrinsic pathway that begins with trauma to the vascular wall and
surrounding tissues and
(2) by the intrinsic pathway that begins in the blood it self, initiated by platelets
59. Extrinsic Pathway
Tissue factor dependent pathway
Acts rapidly
Produces a small quantity of thrombin, triggering the
initiation of the intrinsic pathway
60. Intrinsic pathway
Initiated when Factor XII is activated with surface
contact
Occurs more slowly
Common pathway
The steps in clotting after formation of activated factor
X are the same in both pathways.
64. 19-64
• Determined by antigens (agglutinogens) on
surface of RBCs
• Antibodies (agglutinins) can bind to RBC
antigens, resulting in agglutination (clumping)
or hemolysis (rupture) of RBCs
• Groups
– ABO and Rh
Blood Grouping
65. BLOOD GROUPS
ABO System
Rh system
Lewis system
MNS system
P system
Kell system
Duffy system
Lutheran system
68. RhBLOOD GROUP SYSTEM
6 types Of Rh Antigen i.e. Rh Factor
C,D,E,c,d,e
Type D : most prevalent and most antigenic.
If D antigen present : Rh Positive
If D antigen absent : Rh Negative
69. BLEEDING TIME
Duke method
The test is timed from the start of bleeding until bleeding
is completely stopped
Normal – Within 8 mins
71. Increased bleeding time is associated with:
Thrombocytopenic purpura
Auto immune disease
Vascular defects
Coagulation defects
Decreased platelet count
72. PROTHROMBIN TIME
Prothrombin Time (PT)
Increased in deficiency in extrinsic and common
pathway
Normal : 11-14 seconds
PT is prolonged with:
deficiencies of factors II, V, VII, X or fibrinogen
liver disease
Vitamin K deficiency
Warfarin use
73. INTERNATIONAL NORMALIZED RATIO
WHO, 1983
Measure of the extrinsic pathway of coagulation.
Determines the clotting tendency of blood, in the
measure of warfarin dosage, liver damage and vitamin K
status.
Normal range - 0.8-1.2
75. ACTIVATEDPARTIALTHROMBOPLASTIN TIME
aPTT is prolonged only when the factor levels in the
intrinsic and common pathways are < 30%.
The values are altered
Hemophilias A and B
with the use of the anticoagulant heparin.
Normal : 25-40 secs
76. CLOTTING TIME
It measures all stages of coagulation in the intrinsic
system.
Method: Lee & White method, Wright’s capillary tube
method.
Normal range: within 10 minutes
79. POLYCYTHEMIA
Abnormal increase in erythrocyte count in peripheral
blood, usually accompanied by an increase in hemoglobin
and hematocrit
TYPES
Primary
proliferative
Secondary
Apparent
81. ORAL MANIFESTATIONS
A purplish red discoloration of the oral mucosa
Gingiva : red
bleed spontaneously
Petechiae and ecchymoses
Exaggerated Varicosities in the ventral tongue
83. ANEMIA
Abnormal reduction in the number of circulating red
blood cells, the quantity of hemoglobin and the volume
of packed red cells in a given unit of blood.
84. CLASSIFICATION
• Anemia due to blood loss
• Anemia due to impaired red cell
formation
• Anemia due to increased red cell
destruction
Etiologic
classification
• Microcytic, Normocytic,
Macrocytic
• Hypocrhomic, normochromic
Morphologic
classification
85.
86. IRONDEFICIENCY ANEMIA
Iron deficiency anemia : hypochromic microcytic
ETIOLOGY
Chronic blood loss
Inadequate dietary intake
Faulty iron absorption
Increased requirements
88. DENTAL CONSIDERATIONS
Consultation with physician
Complete blood count (CBC) with differential.
Elective oral surgical or periodontal procedures
Hb < 10 g/dL low oxygen tension interactions
between the cellular components of blood decreasing
their ability to clot effectively.
General anaesthesia : not administered unless the
hemoglobin is at least 10 g/dL.
90. HEMOLYTIC ANEMIA
The hemolytic anemias : normocytic,normocromic
Decreased survival of erythrocytes, either episodically
or continuously
Intracorpuscular
defects Extracorpuscular
factors
91. ORAL MANIFESTATIONS
Pallor of oral mucosa
Jaundice : Best seen in the sclera, but the skin, soft
palate, tissues of the floor of the mouth also become
icteric .
Chronic increased erythropoietic activity and marrow
hyperplasia : dental radiographs.
93. ORAL MANIFESTATIONS
Pallor and jaundice
Delayed eruption and hypoplasia of the dentition
Ladderlike pattern “Hair on end” appearence
94. DENTAL CONSIDERATIONS
Elimination of oral sources of infection - infection can
precipitate an aplastic crisis.
Periodontal infections can precipitate sickle cell crisis.
General anaesthesia should be used with caution
96. ORAL MANIFESTATIONS
Bimaxillary protrusion & other occlusal abnormalities -
thalassemia major
Poor spacing of teeth, a marked open bite, prominent
malar bones, saddle nose.
Pneumatization of the maxillary sinuses is delayed.
“Chipmunk facies.”
97. Radiographic changes :
generalized rarefaction of the alveolar bone
thinning of cortical bone
enlarged marrow spaces
coarse trabeculae
Parietal bones- “hair on end” appearance.
98. MEGALOBLASTIC ANEMIAS
Impaired DNA synthesis
Maturation of nucleus delayed relatively to that of
cytoplasm
Vit B12
deficiency/
Pernicious
Anemia
Folic acid
deficiency
Anemia
TYPES
99. PERNICIOUSANEMIA
Decrease maturation of RBC
Decrease absorption of vitamin B12 from ileal mucosa
Decrease binding of vitamin B12
Intrinsic factor secretion decreases
Atrophy of the gastric mucosa(autoimmune)
100. ORAL MANIFESTATIONS
“Beefy red tongue”
Hunter’s / Moeller’s glossitis
Erythematous macular lesions
involving buccal and labial mucosa.
Dysphagia and taste aberrations
Discomfort by denture wearers
Burning mouth sensation due to a neuropathy
102. APLASTIC ANEMIA
Aplastic anemia : normochromic normocytic
Bone marrow failure
Cause is frequently unknown
Term “anemia” : a misnomer
Pancytopenia
103. ORAL MANIFESTATIONS
Pale discoloration of oral mucosa
Increased susceptibility to infections
Bleeding from gingival margin ( Alty 1962, Stamps
1974 )
Severe periodontal destruction ( Stamps 1974 )
104. FANCONIANEMIA
Brown skin pigmentation
Hypoplasia of the kidney and spleen
Absent or hypoplastic thumb or radius
Microcephally
Mental and sexual retardation
Several teeth lost, severe bone loss, pockets > 10mm,
blue red gingiva, bleeding on probing, suppuration
( Opinya et al, 1988)
108. GRANULOCYTOPENIA
Absolute reduction in the number of circulating WBCs
Results from a decrease in neutrophils, and most cases
of granulocytopenia are known as neutropenia.
The degree of neutropenia predicts the risk of serious
bacterial infections.
109. NEUTROPENIA
Normal absolute number of neutrophils in the
peripheral blood : 3000/mm3 - 6000/mm3
Mild
• 1000/mm3 - 2000/ mm3
Moderate
• 500/mm3 - 1000/mm3
Severe
• <500/mm3
110. NEUTROPENIA
Associated with periodontal problems
Cyclic neutropenia
Chronic benign & severe familial neutropenia
Chronic idiopathic neutropenia
Idiopathic Familial
Secondary to
infections
Secondary to
systemic
diseases
Drug induced
111. AGRANULOCYTOSIS
Reduction in the number of circulating granulocytes
Often restricted to a syndrome characterized by
extremely severe neutropenias
fever
malaise
ulceration and necrosis of tissues
112. AGRANULOCYTOSIS
1922 : Werner Schultz : Syndrome of unknown cause
in a middle aged old women
Agranulocytosis
Fulminate form of severe neutropenia : “ Schultz
disease ”
116. ORAL & DENTALCONSIDERATIONS
Fetid odor
Gingival margin may or mat not be involved
Gingival hemorrhage, necrosis, increased salivation
117. ORAL & DENTALCONSIDERATIONS
Oral ulcers, advanced periodontal disease,
pericoronitis, and pulpal infections bacteremia,
septicemia
Topical application of antibacterial mouth rinses
An individualized soft splint : covers palatal lesions
and carries medication
118. ORAL & DENTALCONSIDERATIONS
Combination of topical neomycin, bacitracin, nystatin
Topical anesthetic mouth rinses : A solution containing
5% diphenhydramine hydrochloride with magnesium
hydroxide or kaolin with pectin
119. CYCLIC NEUTROPENIA
Transient severe neutropenia - occurs approximately
every 21 days.
Oral ulceration, rapid periodontal breakdown, alveolar
bone loss ( Rylander and Ericsson 1981 )
Occurrence of aggressive periodontitis with cyclic
neutropenia ( Scully et al,1982 )
120. CHEDIAK-HIGASHISYNDROME
Rare autosomal recessive trait
Partial oculocutaneous albinism
with photophobia and nystagmus,
frequent pyogenic infections,
intermittent febrile episodes.
Presence of abnormal giant granules in the peripheral
circulating leukocytes.
121. PERIODONTAL FEATURES
Severe gingival inflammation ( Gilling and Cladwell
1970, Hamilton and Giansanti 1974 )
Excessive and early periodontal destruction resulting in
premature loss of permanent dentition.
122. LAZY LEUKOCYTE SYNDROME
Defect in leukocyte chemotaxis and random mobility
Marked gingivitis
Susceptibility to aggressive periodontitis
123. LEUKOCYTEADHESION DEFICIENCY
Inability to produce or failure to express cell surface
integrin ( CD 18)
Extremely acute gingival inflammation and
proliferation of gingival tissues with rapid destruction of
bone.
124. PAPILLON LEFEVRE SYNDROME
Hyperkeratotic skin lesions, severe destruction of the
periodontium, calcification of the dura
Periodontal involvement : early inflammatory changes
that lead to bone loss and exfoliation of teeth
By 15 yrs: edentulous except 3rd molars
125. DOWNSYNDROME
High prevalence of periodontal disease
Deep periodontal pockets
Moderate gingivitis
Poor chemotaxis and phagocytosis
126. LEUKEMIA
Malignant neoplasia of WBC precursors characterized
by :
Diffuse replacement of the bone marrow with
proliferating leukemic cells
Abnormal number and forms of immature WBCs in the
circulating blood
Widespread infiltrates in the liver, spleen, lymph nodes
and other body sites
129. PERIODONTIUMIN LEUKEMIA
BLEEDING : Bleeding gingiva early sign
Thrombocytopenia and anemia :
pallor of the mucosa
petechiae
ecchymoses
gingival bleeding
130. PERIODONTIUMIN LEUKEMIA
ORAL ULCERATION AND INFECTION:
Discrete punched out ulcers penetrating deeply into the
submucosa and covered by a firmly attached white slough
Acute gingivitis and lesions resembling necrotizing
ulcerative gingivitis : more frequent in acute leukemias
Acute herpetic gingistomatitis : common infection
131. MANAGEMENTOF PERIODONTALPROBLEMS
Mechanical plaque control with antiplaque agents
where possible
Antimicrobials for acute infections
Drainage and application of topical antimicrobial agent
Gingival hemorrhage : Direct pressure
Absorbable gelatin or collagen sponges, topical
thrombin, placement of microfibrillar collagen held in
place by packing or splints
133. CLASSIFICATION OF BLEEDINGDISORDERS
COAGULATION FACTOR
DEFICIENCIES
Congenital
Haemophilia A & B
von Willebrand’s disease
Other factor deficiencies (rare)
Acquired
Liver disease
Vitamin K deficiency
Warfarin therapy
Disseminated intravascular coagulation
136. A clinicians’ thorough understanding of physiology of
blood, blood dyscrasias, their management and the
various diagnostic tests is essential for treatment planning
as well as avoiding any untoward complications while
treating the patients.
137. REFERENCES
1. Consice medical physiology, Chaudhari, 5th edition
2. Shafer’s text book of oral pathology 5th edition
3. Burkets Oral medicine-10th edition
4. Guyton and hall. Texbook of medical Physiology 11th edition
5. Essentials of medical physiology, K Sembulingam 2nd edition
7. Essential Pathology for Dental Students, Harsh Mohan,4th
edition
138. 8. Anuragh Gupta; Joel B Epestin et al . Bleeding disorders of
Importance in Dental Care and Related Patient Management.
JCDA 2007;73(1):77-83
9. Philip Vassilopoulos & Kent Palcanis. Bleeding disorders and
periodontology Periodontology 2000 2007; 44: 211-223
10. James W. Little, Craig S. Miller et al. Antithrombotic agents:
Implications in dentistry. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 2002; 93: 544- 551
