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Bleeding disorders /certified fixed orthodontic courses by Indian dental academy
1. BLEEDING DISORDERS
INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education
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2. INDEX
- PLATELETS:
FORMATION
MORPHOLOGY
FUNCTIONS
-HAEMOSTASIS:
VASCULAR SPASM
PLATELET PLUG FORMATION
COAGULATION
INHIBITORS OF COAGULATION
www.indiandentalacademy.com HAEMOSTASIS
DRUGS USED FOR OPPOSING
3. - THE LABORATORY TESTS FOR DIAGNOSIS OF
BLEEDING DISORDERS
- BLEEDING DISORDERS
- PERIODONTAL TREATMENT OF BLEEDING
DISORDERS
- REFERENCES
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4. PLATELETS
• INTRODUCTION:
Platelets are tiny cells that congregate around
ruptures in bloodvessels to provide backbone of
clot.the platelets essentially form a temporary plug
to stop bleeding.active platelets also stimulate the
action of other coagulation proteins.
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5. • FORMATION OF PLATELETS
MYELOID STEM CELLS
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6. • Factors controlling thrombopoiesis:
1.Interleukins(IL): IL-3,IL-6,IL-11,colony stimulating
factors stimulate thrombopoiesis.
2.thrombopoietin(TPO): Produced by liver & kidney.It
helps the megakaryocyte to produce the platelets
rapidly.
3.TGFBeta: when excessive thrombopoiesis it is
released from platelets and depress the platelet
production.
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7. • The life span of platelet is – 7 to 12 days
Most of the platelets are destroyed in
spleen.
• The normal platelet count is
150000 – 400000 / ul of blood
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8. MORPHOLOGY
• SHAPE – disc shape ( inactive platelet)
spherical (active platelet)
• SIZE - 2-4 um in diameter
• Platelets exist in red bone marrow,blood &spleen
• Platelets have plasma membane , cytosol & no
nucleus.
• Plamamembrane has 2 layers
Outer glycocalyx layer:contains glycoproteins
Inner lipoprotein layer:contains phospholipids
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10. • The cytosol consists of
1.Granules:
-Alpha granules contain fibronectin, factor V, factor
VII, PF4, PDGF.
-Dense granules contain ADP, ATP, histamine&
Calcium
2.Tubules:
-Open tubules: Communicate with extracellular
fluid(ECF). During activation,ca++ from ECF enter
the inside of platelets via these tubules
-Dense tubules: donot communicate with the
exterior.They store ca++.
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20. * 3.Blood clotting:
• Within the vessels blood is in liquid form.when it is
drawn from body it thickens and forms a gel.
• The gel separates from the liquid.This straw colored
liquid is called serum & the gel is called clot.
• The process of gel formation – clotting or
coagulation.
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21. • Definition :
Blood clotting is an complex cascade of
enzymatic reactions in which each clotting factor
activates many molecules of the next one in a fixed
sequence.finally a large quantity of product (clot) is
formed.
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22. • THE FACTORS INVOLVED IN CLOTTING:
-Clotting factors (CF)
-Ca++
-Enzymes synthesized by hepatocytes
-Molecules associated with platelets
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24. * Clotting can be divided into 3 stages.
• 1.Formation of prothrombinase by 2 pathways.
Extrinsic pathway
Intrinsic pathway
• 2.Prothrombinase converts prothrombin into
thrombin.
• 3.Thrombin converts fibrinogen into soluble
fibrin.Fibrinwww.indiandentalacademy.com
forms the clot.
27. Thrombin has 2 +ve feedback mechanisms
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28. Clot retraction
• Clot retraction is the consolidation or tightening of the
fibrin clot.As the clot retracts it pulls the edges of the
damaged vessel close together.Fibroblasts from ruptured
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area &new epithelial cells repair the vessel lining.
30. • Intra vascular clotting
*Clotting in an undamaged bloodvessels –
thrombosis.
*The clot – thrombus.
*A blood clot,bubble of air,fat from broken bones or
a piece of debris transported by the blood stream
-embolus
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31. Inhibitors of coagulation
• Circulatory anti coagulants
• The fibrinolytic mechanism
• Tissue factor pathway inhibitor (TFPI)
• Thrombomodulin
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32. • Role of Vitamin k
• Role of VWF
• Role of liver
• Role of bloodvessels
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37. • TFPI :
After the onset of coagulation mechanism,
TFPI begins to be formed and inhibits the intrinsic
pathway.
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38. • Role of vitamin K :
Vitamin K is required for synthesis of
factors II,VII,IX&X
Source of vitamin K:vegetables
Vitamin k is synthesized by intestinal
bacterial flora.
*Vitamin K deficiency:
-Vitamin K free nutrition
-Antibiotics like cephalosporins
-Newborns
-Obstructive jaundice
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39. • Role of blood vessels:
-The subendothelium is highly thrombogenic.
-The contact of blood with subendothelium triggers
the formation of XIIa.
-Vascular endothelium synthesize PGI2 (prostacyclin)
opposes the action of TXA2 thus prevents the
platelet activation.
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40. • Role of liver:
-Liver synthesizes prothrombin, fibrinogen, factors
V,VII,IX,X & XI.Thus the liver failure causes
failure of clot formation.
-Liver also synthesizes antithrombin III, heparin,
proteinsC & S.Thus liver failure also can cause
excessive clotting.
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41. • Role of VWF:
- Synthesized by megakaryocytes & vascular endothelium.It
acts as a bridge between platelet & denuded endothelium.
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42. * The drugs used for opposing haemostasis:
• 1.Anti thromboitics
• 2.Anti coagulants
• 3.Thrombolytic drugs
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43. * 1.Anti thrombotics
• Eg:Aspirin
• Aspirin inhibits vasoconstriction & platelet
aggregation by blocking synthesis of TXA2.
• It reduces the chance of thrombus formation.
• Indications :
-Transient ischaemic attacks
-Myocardial infarction
-Angina pectoris
-Blockage of peripheral arteries
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44. * 2.Anti coagulants:
• In vivo:
-Heparin :potentiates the action of anti thrombinIII
-Vitamin K antagonists :eg-warfarin
Blocks the synthesis of CF II,VII,IX,X.
-Indications: Deep venous thrombosis
Myocardial infarction
Pulmonary embolism
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45. • In vitro: To prevent clotting in donated blood,
blood banks and laboratories often add a substance
which prevents coagulation by removing the
ionized calcium of blood citrate.
-Eg :
EDTA
CPD
Oxalates.
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46. • 3.Thrombolytic drugs: These are injected into the
body to dissolve clots that have already formed to
restore circulation.
-The mechanism of action: activate plasminogen.
-Eg: Streptokinase
Tissue plasminogen activator
Urokinase
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47. * The common laboratory tests for diagnosis of
bleeding disorders:
• 1.Bleeding time(BT)
• 2.Clotting time(CT)
• 3.Prothrombin time(PT)
• 4.Partial thromboplastin time(PTT)
• 5.Platelet count
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49. I) BLEEDING DISORDERS CAUSED BY VESSEL
WALL ABNORMALITIES
• Called non thrombocytopenic purpura.
• They induce small haemorrhages such as petchiae
and purpura in the skin,mucous
membranes,particularly in gingivae.
• The platelet count,BT,CT,PTT are normal.
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50. CAUSES:
* 1.Infections: Meningococcemia
Septicaemia
Infective endocarditis.
Rickettsia
Measles
* 2.Drug reactions:The vascular injury is mediated by
drug induced Abs and deposition of immune
complexes in vessel walls leading to
hypersensitivity vasculitis.
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51. • 3.Scurvy & Ehlers - Danlos Syndrome:
-Impaired formation of collagens causes
microvascular bleeding.
-Cushings syndrome-Protein wasting effects of
excessive corticosteroid production cause loss of
perivascular supporting tissues.
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52. • 4.Amyloid infiltration of blood vessels:
Systemic amyloidosis associated with
perivascular deposition of amyloid and consequent
weakening blood vessel walls.
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53. 5.Henoch-Schonlein purpura: (senile purpura)
- Systemic hypersensitivity disease characterized
by a purpuric rash, ployarthralgia,acute
glomerulonephritis
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54. * 6.Heriditary haemorrhagic telangiectasia:
• is an autosomal dominant disorder
characterized by dilated,tortuous blood vessels that
have thin walls and hence bleed readily.most
commonly occurs under the mucous membranes of
the nose,tongue,mouth,eyes,GIT.
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55. • II.BLEEDING DISORDERS DUE TO FAULT OF
PLATELETS:
A.Related to reduced platelet number
(thrombocytopenic purpura)
B.Related to defect in platelet function
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56. A.Related to reduced platelet number:
(Thrombocytopenic purpura)
• Platelet count is < 100000/ul.
• post traumatic bleeding is aggravated-when platelet
count is 20000-50000/ul.
• BT is prolonged.
• PT,PTT – normal.
• The common sites involved are:
-skin
-Mucous membrane of GIT &
genito urinary tract
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57. CAUSES:
1.Decreased production of platelets
- Generalized diseases of bonemarrow
a) Aplastic anaemia
b) Leukaemia
- Selective impairment of platelet production
a) Drug induced : Alcohol,thiazides,cytotoxicdrugs.
b) Infections: measles,HIV.
- Infective Megakaryopoiesis
a) Megaloblastic anaemia
b) Myelodisplastic syndrome
c) Paroxysmal nocturnal haemoglobinuria.
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58. 2.Sequestration:
- Spleen normally sequesters
30-40% of platelets.
-In case of hypersplenism or
splenomegaly it sequesters 90% of all platelets.
-Treatment: splenectomy
3.Dilutional:
-Massive transfusions may produce
thrombocytopenia.Blood stored for longer than
24hrs contains virtually no viable
platelets.Thus,plasma volume &RBC are
reconstitued by transfusion,but the number of
circulating platelets is reduced.
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62. PRIMARY ITP: CHRONIC:
• Most common
• Cause:the formation of auto Abs against platelet membrane
glycoproteins,most often IIb-IIIa or Ib-IX
• Prevalence: F:M=3:1
• Age : <40yrs
• C/F: -Insidious in onset.
-Bleeding into skin,mucousal surface
-Petechiae prominent in the dependent areas where the
capillary pressure is high.Petechiae become confluent &
give rise to ecchymosis.
-Long history of easy bruising ,epitaxis,bleeding gums.
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63. • The disease may be manifested first by malena,haematuria
and increased menstrual flow.
• Subarachnoid haemorrhage & intracerebral haemorrhage
very rarely seen.
• Diagnosis:
-Decreased platelet count
-Normal or Megakaryocytes in bone marrow.
-Prolonged BT
* Treatment:Glucocorticoids & splenectomy
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64. ACUTE ITP:
• Occurs in children
• M:F=1:1
• C/F:
-Abrupt in onset
-The interval between infection & onset is 2wks
-Usually selflimited and resolves spontaneously within
6months.
-20% of children may develop chronic ITP.
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*Treatment:corticosteroid therapy
65. Secondary ITP:
• Drug induced:Heparin
Quinidine
Sulfa compounds
-Heparin induced : occurs in 5% of cases receiving
heparin.
Two types: TypeI-occurs rapidly after onset of
therapy
TypeII-5-14 days after onset of
therapy. www.indiandentalacademy.com
66. • HIV associated thrombocytopenia:
CD4, the receptor for HIV on T cells demonstrated
on megakaryocytes,making it possible for these cells
to be infected by HIV.Infected megakaryocytes
undergo apoptosis causing impaired platelet
production.
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68. • B.Bleeding disorders related to defective platelet
function:
1.Congenital
2.Acquired
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69. 1.Congenital
• On the basis of specific functional abnormality
a)Defect in platelet adhesion to sub endothelial
matrix.eg:Bernard-Soulier syndrome.
Platelet membrane glycoprotein is a receptor for
VWF and is essential for platelet adhesion.
b)Defect in platelet aggregation
Eg:Glanzmann’s thrombasthenia.
Platelets fail to aggregate in response to
ADP,collagen,thrombin,fail to form glycoprotein
complex which forms bridges between platelets.
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70. c)Disorders of platelet secretion:
Eg: storage pool disorders.
-Characterized by normal initial aggregation with
collagen ADP, but the secretion of
TXA2,prostaglandins, & granule bound ADP are
impaired.
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72. • III)BLEEDING DISORDERS RELATED TO
ABNORMALITIES IN CLOTTING FACTORS:
(FAULT IN SECONDARY HAEMOSTASIS)
-The Bleeding is manifested by large post traumatic
ecchymosis or haematomas
-Prolonged BT
-Bleeding into GIT,UT & joints.
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73. • Two types
1.Congenital:deficiency of fac VIII-haemophilia A
deficiency of fac IX- haemophilia B
2.Acquired: DIC
VitaminK deficiency
Liver disorders
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74. • Haemophilia A :
-Most common heriditary disorder.
-Caused by reduction in amount or activity of fac VIII.
-It is inherited as an X-linked recessive trait.
-Occurs in males & homozygous females.
-30% of pts-no family history.caused by new
mutations.
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75. -The severity correlates with the level of fac VIII
activity.
• <1% of normal activity – severe
• 2-5% of normal activity- moderate
• 6-50% of normal activity- mild
-C/F:Easy bruising & massive haemorrhage after
truama or operative procedures.spontaneous
haemorrhages occurs in regions of body normallly
subject to trauma,particularly in joints(haem
arthroses)
-Normal BT,platelet count & PT but prolonged PTT.
-Treatment:Recombinant fac VIII
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76. • Haemophilia B (Christmas disease):
-It is inherited as an X linked recessive trait.
-Caused by a wide sprectrum of mutations involving-
the fac IX gene.
-Clinically indistinguishable from haemophilia A.
-14% of pts fac IX is present but non functional.
-Prolonged PTT,normal PT& BT.
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-Treatment: Recombinant fac IX.
77. • VONWILLEBRAND DISEASE
• Caused by an inherited defect in involving platelet adhesion.
• C/F:Spontaneous bleeding from mucous
membranes,excessive bleeding from wounds,menorrhagia.
• Prolonged BT,normal platelet count.
• Types:Type1
Type2
Type3
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78. Type 1&3 are associated with a reduced quantity of
circulating VWF.
• Type1:mild&autosomal dominant.
• Type3:severe&autosomal recessive
haemarthroses is common
Severe deficiency of VWF has a marked effect on
stability of fac VIII.
• Type 2 is characterized by qualitative defects in
VWF.
-Because of mutations the VWF is abnormal.
C/F:mild to www.indiandentalacademy.com
moderate bleeding.
79. • Patients with Vonwillebrands disease have a
compound defect involving platelet function &
coagulation pathway.
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80. * Acquired haemophilia
• Disseminated intravascular clotting:
• It occurs as a secondary complication in a vareity of
diseases.
• It results from pathologic activation of the extrinsic and/or
intrinsic pathways or impairment of clot inhibiting
influences.
• The mechanisms trigger DIC
- release of TF into the circulation
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- wide spread of injury to endothilial cells.
81. Release of TF into the circulation
Causes
Obstetrics complications.
- retained dead foetus
- septic abortion
- amniotic fluid embolism
- toximia
neoplasms - adenocarcinoma, leukemia
infections – gm-ve species,
malaria,
histoplasmosis
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aspergillosis
86. PERIODONTAL TREATMENT OF
HAEMORRHAGIC DISORDES
• Identification of the pt via the health history,clinical
examination and lab tests.
1.H/O bleeding after previous surgery or trauma.
2.Past & present drug history.
3.H/O bleeding problems among relatives.
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4.Illness associated with potential bleeding problems.
88. • LABORATORY TESTS :
BT
CT
PT
PTT
Complete bloodcell count
Torniquet test
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89. * Haemophilia A:
• To prevent surgical haemorrhage fac VIII levels of atleast
30% are needed.
• Parentral 1-deamino-8-D-arginine vasopressin (DDAVP)
can be used to raise fac VIII levels in mild to moderate
haemophilia.
• In severe case preoperative infusion of fac VIII or
cryoprecipitate form is recommended.
• Advantage of DDAVP:Avoids the risk of viral disease
transmission from fac VIII infusion.
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90. * Haemophilia B:
• To prevent surgical haemorrhage fac VIII levels of
atleast 30%-50% are needed.
• Purified prothrombin complex concentrates or fac
IX concentrates can be used to raise fac IX levels .
• Mild-DDAVP before periodontal surgery or
toothextraction.
• Severe-preoperative infusion of
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cryoprecipitate form.
91. • Probing scaling and prophylaxis – without medical
modification.
• More invasive treatment such as block local
anesthesia,root planning or surgery – prior physician
consultation.
• Local haemostatic measures:to enhance clot
formation.
Pressure packs
Electro cautery
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Splints&dressings
92. • Anti haemostatic agents:may be placed over surgical sites or
extraction sockets.
-Oxidized cellulose
-Gel foam
-Surgicel
-Avitene
-Purified bovine collagen.
• Anti fibrinolytic agents:
-Epsilon-aminocaproic acid(EACA)-systemically
-Amicar systemically
-Tranexamic acid-systemically, also available in a
mouthrinse.
-100mg / kg – preoperatively
continued towww.indiandentalacademy.comat a dose 50mg/kg
8-10 days postoperatively
qid.
93. • TREATMENT OF LIVER DISEASES OPPOSING
HAEMOSTASIS
-physician consultation
-Lab tests
-Conservative,non surgical periodontal therapy
-If surgery is required may require hospitalization
-Platelet count should be >80000/mm3
-PT <2.5
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94. * TREATMENT IN PTS TAKING ANTI COAGULANT
THERAPY
• The effectiveness of anticoagulant therapy is
monitored by PT.
• The recommended INR-2to3.
-INR < 3- infiltration anesthesia,scaling &
rootplaning.
-INR < 2-block anesthesia, minor surgery & simple
extractions.
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-INR <1.5-complex surgeries,multiple extractions.
95. • Physician consultation to determine the degree of
required anticoagulation & dicontinuation of the
drug until the desired PT is achieved.May be
discontinued for 2-3 days.
• The pts taking aspirin <325 mg / day – discontinued
for atleast 7-10 days before periodontal therapy in
consultation with physician.
• NSAIDS like ibuprofen – the effect is
transitory,lasting only a short time after the last drug
dose. www.indiandentalacademy.com
96. *Thrombocytopenic purpura
• Removal of local irritants to reduce the inflammation & to
avoid the aggressive therapy.
• Oral hygiene instructions & frequent recall visits.
• Platelet count < 60000/mm3-scaling &rootplaning is safe.
• Platelet count >80000/mm3-surgical procedures safely can
be performed.
• Platelet transfusion may be required before surgery.
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• Atraumatic surgical techniques&local haemostatic measures
97. * Non thrombocytopenic purpura
• Surgical therapy should be avoided unless
qualitative & quantitative platelet problems are
resolved.
• Local haemostatic pressure&atraumatic technique
should be applied.
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98. REFERENCES
1.Concise medical physiology-Choudhuri
2.Principles of anatomy&physiology-Tortora
3.Pathologic basis of disease-Robbins
4.Clinical periodontology-Carranza
5.Management of dental pts with bleeding
disorders:Review and Update
(Oral surg Oral med Oral pathol 1988;66:297-303.
6.Haematology text book-Martin & Peter
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