Coagulation factors are proteins in the blood that work together to help form blood clots. Some coagulation factor deficiencies can cause bleeding disorders like hemophilia. For dental procedures in patients with coagulation issues, replacement of deficient factors or use of antifibrinolytic drugs is often needed before, during, and after treatment to reduce bleeding risks. Local anesthetic techniques that minimize trauma are preferred. Proper factor level monitoring and hemostatic support tailored to the specific condition can allow for many routine dental treatments to be completed safely.

1. COAGULATION FACTORS
AND
DENTAL PROCEDURES
N.Narmadha

2. INTRODUCTION:
• Coagulants promote coagulation - haemorrhagic states.
• Haemostasis and blood coagulation - complex interactions
between the injured vessel wall , platelets and coagulation
factors.
COAGULATION DEFINITION:
Coagulation or clotting is defined as the process in which blood
loses its fluidity and becomes a jelly like mass few minutes after
which its is shed out.
The process by which blood clots
to form solid masses or clots.

3. Bleeding time:
Time interval from oozing of blood after a cut or injury till
arrest of bleeding.
Clotting time:
Time interval from oozing of blood after a cut or injury till the
formation of clot.
Prothrombin time:
Time taken by blood to clot after adding tissue thromboplastin
to it.
Thrombin time:
Time between the addition of the thrombin and the clot
formation .

4. PROTHROMBINTIME
CLOTTINGTIME
BLEEDINGTIME

8. COAGULATION FACTORS:
Coagulation of blood - activation of a group of substances - clotting
factors.
SYNTHESIS:
Liver.
vWF -endothelial cells & platelets
LOCATION:
Plasma (zymogen).
Tissue factor - does not circulate in blood.
Partial proteolysis - activate the next factor.

9. Factor I - Fibrinogen
Factor II - Prothrombin
Factor III - Tissue Thromboplastin/Tissue Factor
Factor IV - Calcium Ions
Factor V - Labile Factor/Pro Accelarin/Accelerator Globulin
Factor VII - Stable Factor.
Factor VIII- Anti hemophilic Factor/AH Globulin
Factor IX - Christmas Factor /Plasma Thromboplastin Component
Factor X - Stuart –Prower Factor.
Factor XI - Plasma Thromboplastin Antecedent
Factor XII –Haegman Factor/Contact Factor.
Factor XIII –Fibrin Satabilising Factor(fibrinase).

10. FACTOR METABOLISM FUNCTION DISORDERS
I FIBRIN
Forms mesh around
the wound leading
to blood clot
Afibrinogenemia
Hypofibrogenemia
Hyperfibrinogenemia
II THROMBIN
-Convert fibrinogen
to fibrin.
-Activate factors I,V,
VII,VIII,XI &XIII
Hemmoraghic diathesis
Dysprothrombinemia
Hypoprothrombenimia
III -Initiates extrinsic
pathway.
-High affinity
receptor for VII.
-Acts as cofactor
V Acts as cofactor Parahemophilia
Myocardial infarction
Deep vein thrombosis

11. FACTOR METABOLISM FUNCTION
DISORDERS
VII
Acts as cofactor (IX, X)
Epitaxis,Menorrhagia
Hematomas,Hemarthrosis
Cerebral hemmorhages
VIII Cofactor for X Hemophilia A.
IX Cofactor for X Hemophilia B
X Xa
Bleeding diathesis
Hemorhages.Epitaxis
GI bleeds,hemarthrosis
XI Hemophilia c
XII XIIa Activates factor XI
&prekallikrein.
XIII XIIIa Lifelong bleeding
diathesis,intercranial
bleeding and death.

12. ROLE OF COAGULATION SYSTEM:
• Conversion of plasma fibrinogen into solid mass of fibrin .
• Involved in both haemostatic process and thrombus formation.
• Complex interactions between the vascular endothelium , platelets,
coagulation factors, natural anticoagulants & fibrinolytic enzymes.
• Dysfunction - haemorrhage or thrombosis.

13. STAGES OF NORMAL HAEMOSTASIS (Davidson)
STAGE I :Pre injury conditions
STAGE II :VASOCONSTRICTION.
Early hemostatic response , platelets adhere ,coagulation is activated.
STAGE III: Fibrin clot formation,platelets become activated and
aggregate.
STAGE IV: Limiting clot formation.
STAGE V: Fibrinolysis

14. PATHWAYS OF COAGULATION MECHANISM :
Blood substances
Prothrombin activator.
Blood clotting
Occurs through two pathways.
1.Intrinsic pathway
2.Extrinsic pathway.

16. APPLIED PHYSIOLOGY:
COAGULATION DISORDERS:
Inherited Acquired
A) CONGENITAL
􀂂 Hemophilia A
􀂂 Hemophilia B or Christmas disease (factor IX deficiency)
􀂂 Von Willebrand disease (alteration of factor VIII)
􀂂 Fibrinogen alterations
􀂂 Prothrombin (factor II) deficiency
􀂂 Factor V,VII,X,XI,XII deficiency

17. 􀂂 Combined deficiency of vitamin K-dependent factors (VII, IX,X)
􀂂 Combined deficiency of factors V and VIII
􀂂 Combined deficiency of factors VII and VIII
􀂂 Combined deficiency of factors II, VII, IX and X, and C protein.
B) ACQUIRED
􀂂 Liver diseases
􀂂 Vitamin K deficiency:
􀂂 Acquired anticoagulants
􀂂 Disseminated intravascular coagulation (DIC)
􀂂 Primary fibrinogenolysis
􀂂 Anticoagulant drugs.

18. HAEMOPHILIA (Bleeder’s disease, Disease of the hapsburg ,
The disease of kings):
Definition: It is a hereditary blood disorder characterised by a
deficiency in the activation of coagulation factor VIII, IX, XI
in plasma with normal vWF.
Etiology:
• Sex linked inherited disorder. .
• Severe hemophilia A, –inversion mutation- on long arm of the
X chromosome in bands q28.
• Hemophilia B-partial or total deletions - on long arm of the X
chromosome in bands q27 .
• Hemophilia C-mutation on chromosome 4.

19. S.NO TYPES CLOTTING FACTOR
DEFICIENCY
I HEMOPHILIA A VIII
2 HEMOPHILIA B IX
3 HEMOPHILIA C XI
CLASSIFICATION FACTOR
ACTIVITY(% )
CAUSES OF
HEMORRHAGE
Mild > 5 Major trauma or surgery
moderate 1-5 Mild to moderate trauma
severe <1 Spontaneous
hemarthrois,soft tissue
bleeding.

20. CLINICAL FEATURES:
• PREVALANCE- Males, females
are carriers.
• Persistent bleeding,
• Haemmorhage into subcutaneous
tissues , internal organs,
joint –hematomas.
• Spontaneous cyclic remissions
and exacerbations .
• Petechia usually do not occur .
• Hemophilia C- absence of bleeding into joints
and mucles and occurrence in either genders.

21. ORAL MANIFESTATIONS:
• Common finding-Hemmorhage.
• Massive and prolonged gingival hemmorhage.
• Even physiologic process of tooth eruption and exfoliation occurs
with severe prolonged hemmorhage.
• Mandibular ‘pseudotumor’.

22. DIAGNOSIS:
• Clinical history.
• Family history - bleeding response to minor traumatism ,or dental
manipulations
• Definitive diagnosis - quantitation of pro coagulant activity of
VIII(REDUCED).
• DNA analysis - detect carriers and establish prenatal diagnosis.
LABORATARY FINDINGS:
• Coagulation time
• activated partial thromboplastin time
• Normal - bleeding time ,prothrombin time, platelet aggregation.

23. MANAGEMENT:
• Protect from traumatic injuries.
• Minor operation considered as major one and
performed in hospital.
• Preoperative transfusion of whole blood .
• Administration of antihemophilic factor concentrate .
• Antifibrinolytic agents and desmopressin (DDAVP).
• Replacement therapy.
• Gene therapy.

24. Desmopressin (DDAVP):
synthetic vasopressin analog
endothelial cells
FVIII and vWF
platelet adhesion.
• Dose - 0.3-0.4 μg/kg iv infusion - 30 minutes / subcutaneous
injection.
• Inhalatory route - 300 μg in adults & 150 μg in children.
Antifibrinolytic agents:
Routes - oral, intravenous or topical .
EACA -300 mg/kg/day in fractions every 4-6 hours;
AMCHA 30 mg/kg/day in 2-3 daily doses.

25. DENTAL CONSIDERATIONS:
• Mild to moderate hemophilia- noninvasive treatments -
antifibrinolytic coverage.
• Oral cleaning procedures ,minor surgery - DDAVP.
• Severe hemophilia - factor VIII .IX,XI replacement .

26. • Anesthetic block / IM inj - not carried if (FVIII < 50% ).
Preceded by replacement therapy.
• Infiltrating pericemental and intrabony injections - preferred .
PROGNOSIS:
• Now able to lead a normal life with few restrictions.
• Prognosis is variable , many affected persons die during childhood.

27. VON WILLEBRAND’S DIESEASE:
(pseudohemophilia ,vascular hemophilia,vascular purpura)
Most common hereditary hemorrhagic disorder in humans and is
characterized by a prolonged bleeding time with low FVIII titers
ETIOLOGY :
• vWF deficit or dysfunction.
• Inherited defect in the quality and quantity of vWF.
• Mutation, insertion,deletion at the vWF locus on a gene on
chromosome 12p .

28. CLASSIFICATION:
Type 1:Partial quantitative decrease of normal vWF and factor VIII.
Type 2:Qualitative defects of vWF . Autosomal dominant or recessive.
Type 3:Marked deficiencies of both vWF & factor VIII in plasma.
Common in consanguineous marriage.

29. CLINICAL FEATURE:
• Positive family history.
• Minor trauma -Excessive bleeding,
• Mucosal membrane bleeding -gingival hemorrhage, epistaxis.
• Hemarthrosis and musculoskeletal bleeding - more severe forms.
• Spontaneous nosebleeds & cutaneous ecchymoses .
ORAL MANIFESTATIONS:
• Gingival bleeding either spontaneous or only after brushing of the
teeth.

30. LABORATORY FINDINGS:
Normal -platelet count, clotting time, serum fibrinogen,prothrombin
time.
Prolonged –bleeding time(over 300 min,several min,one hour)

31. DIAGNOSIS:
• Coagulation tests.
TREATMENT:
• DDAVP - autologous secretion of vWF and FVIII .
• DDAVP - via IV infusion ,subcutaneous or nasal route .
• Replacement therapy:
• Antifibrinolytic drugs (EACA and AMCHA) via the iv,oral or
topical routes.
• Estrogens effective for menorrhagia.

32. ACQUIRED DISORDERS
LIVER DISEASE:
coagulation factors production, exception of FVIII and FvW -
endothelial cells.
DENTAL CONSIDERATIONS:
Pre-operative management:
• Vitamin k injection-iv 10 mg for 3 days.
• Fresh frozen plasma – immediately before surgery and at frequent
intervals during surgery
• RD- 10-15 ml/kg

33. • Cryoprecipitate- infusion of <100
mg/dl in a dose of one bag of
cryoprecipitate per 10 kg of body
weight.
• Intranasal desmopressin -300mcg.
• Anti fibrinolytics: traneximic acid -
10mg/kg loading dose and repeated
3-4 /day for a total of 2-8 days.
• Recombinant factor VII a-40 mcg/kg

34. Intra operative management:
Anesthetic management:
Inhalational anesthetic agents:isoflurane,desflurane,sevoflurane and
Propofol are prefered
Muscle relaxant –atracurium,cisatracurium.

35. VITAMIN K DEFICIENCY:
Factors II,VII, IX and X are produced in the liver cells.
The most common causes of vitamin K deficiency are:
• Intestinal malabsorption
• Inadequate dietary intake
• liver diseases
• prolonged antibiotic use (which eliminates the intestinal flora - a
natural source of vitamin K2),
• insufficient ingestion of the vitamin (12).
• Management:
• Parentral administration of vitamin k rapidly restores vitakin k in
liver.

36. • DISSEMINATED INTRAVASCULAR COAGULATION (DIC):
• It is an acquired consumption coagulation disorder resulting from
prolonged activation of the coagulation system.
• Result of underlying pathology.
• Clinical problem of DIC - bleeding due to depletion (consumption)
of the coagulation factors .

37. ANTICOAGULANT DRUGS:
Provided with unfractionated or standard heparin, low molecular
weight heparin (LMWH) and oral anticoagulants (coumarins).
DENTAL CONSIDERATIONS:
• SH countered by administering its antagonist, protamine sulfate,
iv 1 mg/100 IU of heparin .
• Dialyzed patients SH has a half-life( 1-2 hours) ,suffices to carry
out dental treatment .
• LMWH - dental care without changes in medication .
postoperative bleeding - controlled by local measures.

38. • If heavier bleeding - treatment suspended for a day, with dental
treatment taking place the day after.
• No need to modify anticoagulant therapy provided the INR is 4 or
lower, since bleeding be controlled with local measures.

40. DENTAL PROCEDURES:
Hemophilia:
Severity of hemophilia - correlates with factor VIII level of the plasma.
Normal plasma contains 1 unit of factor VIII per ml (100%).
Management:
Factor VIII replacement achieved by porcine factor VIII or
recombinant factor VIII.
1 unit factor VIII conc./ kg of body weight raises factor VIII by 2%

41. • Average 70kg individual require infusion of 3500 units to raise the
factor level from less than 1% to 100%.
Dose to infused (units) = Weight x increment needed(u/dl) /2.
• Mild hemophiliacs - cover for surgery requires maintanance of
normal factor VIII levels (1 week),followed by reduced dosage
during convalascence.
• Achieved by repeated bolus injections every 12 hours or by
continuos infusion.

42. Adjunct therapy:
• 50 mg/kg body weight EACA orally as 25% oral rinse every
six hours -7-10 days.
• Tranexamic acid 10 times more potent than EACA .
Pain management:
• Safer drugs -acetaminophen,codeine,cox-2 inhibitors.
Anesthetic management:
• Regional LA -if VIII (30%)
• Infiltrations, intraligamentary,intraosseus or intrapulpal injections are
still safer.
• Buccal infiltration used without any factor replacement.

43. Restorative procedures:
• Metal matrix bands & wooden wedges –risk of bleeding.
• Cotton rolls wetted before removal.
• High speed vaccum aspirators and saliva ejectors cause hemotomas-
minimized by resting on gauze swab.
Endodontics:
• Avoiding instrumentation through the periapex is of prime
importance.
• Sodium hypochlorite – irrigation followed by calcium hydroxide
paste.
• persistent bleeding –formaldehyde derived substances.

44. Rubber dam isolation:
Surgical endodontics:
Mild hemophiliacs managed without factor replacement.
Desmopressin:
Slow iv infusion - 20 min -0.3-0.5 µg/kg
30-60 min prior to surgery – 3 fold increase in VIII activity (9.4 h)
Intranasal ly- 1.5 mg/ml.
Tranexamic acid:
Systemic-1g(30 mg/kg) orally qid , 1hour preoperatively.
Infusions-10mg/kg in 20ml normal saline over 20 min.
Then 1g tds orally – 5days.
Children:20mg/kg.

45. Periodontal treatment:
Supragingival scaling
Treatment over several visits to prevent excessive blood loss.
Chlorhexidine gluconate mouth wash used.
Subgingival scaling can be performed.
Prosthodontic treatment:
Dentures given.
Orthodontic treatment:
Can be carried out .

46. Surgical procedures:
• Rubber band extraction is performed.
• 1-3 tooth can extracted with factor replacement.
Dental extraction:
Factor VIII dose in units= weight in kg x 25 given 1h preoperatively .
For maxillofacial surgery:
Weight in kg x 50 given 1h preoperatively.

47. OPERATION FACTOR VIII
LEVEL
REQUIRED
PREOPERATIV
ELY GIVEN
POATOPERATI
VE SHEDULE
Dental
extraction,dentoalv
eolar,periodontal
surgery
Min-50% at
operation
Factor VIII iv
Tranexamic acid
1g iv (or orally
24h pre op)
Soft diet ;
10 days –
tranexamic acid
1gqid .if bleeding
continues,repeat
the dose of VIII
Maxillofacial
surgery
100% at operation.
50%
postoperatively
Factor VIII( iv) Soft diet.
twice daily (iv) –
VIII -7-10 days.

48. METHODS OF ACHIEVING HAEMOSTASIS:
1.MECHANICAL METHODS:
Pressure
Hemostat
Sutures and ligation
2.Chemical methods:
Adrenaline
Thrombin
Surgicel
Surgicel fibrillar
Oxycel
Gelatin sponge:gelfoam/surgifoam
Microfibrillar collagen(avitene)
Fibrous glue
Styptics and astringents
Alginic acid.
Natural collagen sponge
Fibrin sponge
Bone wax
Ostene-new water soluble hemostatic agent.
3.Thermal agents

49. INVESTIGATIONS :

50. Thank you