Mechanism of clotting

Guided by:Dr. Arundeep Singh

Head of the departmentDept. of Conservative Dentistry

and Endodontics

Mechanism of Clotting

Presented by: Dr. Mohana Pratima

MDS 1st Year Dept of Conservative Dentistry and

Endodontics

Guided By: Dr Dax AbrahamDr. Ravjot Ahuja

CONTENTS• INTRODUCTION TO BLOOD CELLS• MECHANISM OF BLOOD COAGULATION• APPLIED ASPECTS• ORAL CONSEDERATIONS

INTRODUCTION:

• Blood is a connective tissue in fluid form.

• It is considered as the fluid of life because it carries oxygen from lungs to all parts of body and carbon dioxide from all parts of the body to lungs.

• Also called fluid of Growth and also fluid of health

K Sembulingam Essentials Of Medical Physiology

Properties of blood:• Color: Red in color. Arterial blood- scarlet Venous blood-purple red because of more

carbon dioxide.• Volume: in normal adult avg volume is 5L. In new born

volume is 450ml. In females slightly less and is about 4.5L.• Reaction and Ph: slightly alkaline and ph is 7.4 in normal

condition.• Viscosity: 5times more viscous than water. Due to RBC

cells and Plasma proteins.


• COMPOSITION OF BLOOD:

• Blood cells• Plasma• Serum


BLOOD CELLSRed blood cells or erythrocytes

White blood cells or leukocytes

Platelets or thrombocytes


Red blood cells: • Ranges between 4 and 5.5 millions/cu.• In adult males it is 5millions/cu mm• And in adult females is 4.5 Million/cu mm • Are the non nucleated formed elements in the blood.• Also known as Erythrocytes.• The red color is due to coloring pigment called Hemoglobin. K Sembulingam Essentials Of Medical Physiology

Functions• Transport of oxygen from lungs to the tissues.• Transport of carbon dioxide from the tissues to

the lungs.• Buffering action in blood.• In blood group determination


• White blood cells: Are the colorless and the nucleated formed elements of blood.

• Compared to RBC’s WBC’s are larger in size and lesser in number.

• Classifications• Granulocytes: Neutrophils: Eosinophils: Basophils:• Agranulocytes: Monocytes: Lymphocytes:


• Neutrophils

• Eosinophils

• Basophils

• Monocytes

• Lymphocytes

• 50 to 70

• 2 to 4

• 0 to1

• 2 to 6

• 20 to 30

• 3000to6000

• 150 to 450

• 0 to 100

• 200 to 600

• 1500 to 2700


Neutrophils

Eosinophils

Basophils

Monocytes

Lymphocytes

First line of defense against the invading microorganisms. Wander freely all over the body through tissues.

Provide defense to the body by acting the parasitic infections and Allergic conditions like asthma. Are responsible for detoxification,Disintegration, and removal of foreign proteins.

Important role in healing process

Motile and phagocytic in nature. First line defense along Neutrophils

Responsible for development of immunity.


Platelets: Are the formed elements of the blood. Small colorless, non-nucleated and moderately refractive bodies.

Normal count: Is 2,50,000. It ranges between 2,00,000 and 4,00,000/cu mm of blood.


Functions:• Role in blood clotting• Role in clot retraction• Role in prevention of blood loss(hemostasis)• Repair of ruptured blood vessel• Defense mechanism


PLASMA

Solids(7-8%) Water:92-93% Gases

Organic substances

Inorganic substances

OxygenCarbon dioxide

Nitrogen


Organic substances Inorganic substances

I. Plasma proteinsII. Amino AcidsIII. CarbohydrateIV. FatsV. Internal secretionsVI.EnzymesVII.Non protein

nitrogenous substances

VIII.Antibodies

1. Sodium2. Calcium3. Potassium4. Magnesium5. Bicarbonate6. Chloride7. Phosphate8. Iodide9. Iron10.copper


• In coagulation system• Defense mechanism of body• Transport mechanism• Maintenance of osmotic pressure in blood.• Regulation of acid base balance.• Viscosity of blood• Erythrocyte sedimentation rate• Suspension stability of BBC’s• Production of Trephone substances• As reserve protein.


• Platelet rich plasma:• PRP is a blood plasma that has been enriched with platelets. As

concentrated source of autologous platelets, PRP contains several growth factors and cytokines that stimulate healing of bone and soft tissues.

Clinical applications include:Tendinitis, cardiac muscle injury, Bone repair and regeneration, Oral

surgery.

SERUM• Clear straw colored fluid that is left after blood

is clotted.• When the blood is collected in a container, it

clots.• In this process, the fibrinogen is converted into fibrin and the blood cells are trapped in this fibrin forming the clot.• So fibrinogen is absent in serum.• Serum= Plasma-Fibrinogen.


FUNCTIONS OF BLOOD:

• Nutrient function• Respiratory function• Excretory function• Transport of hormones and enzymes• Regulation of water balance• Regulation of acid balance• Body temperature• Storage function• Defense function


COAGULATION OF BLOOD

• Definition: As the process in which the blood looses its fluidity and becomes a jelly like mass few minutes after it is shed out or collected in a container.


FACTORS INVOLVED IN BLOOD CLOTTING:

• Factor I: Fibrinogen• Factor II: Prothrombin• Factor III: Thromboplastin• Factor IV: Calcium• Factor V: Labile factor• Factor VI: Prescence has not been proved• Factor VII: Stable Factor• Factor VIII: Antihemophilic • Factor IX: Christmas factor• Factor X: Stuart factor• Factor XI: Plasma Thromboplastin antecedent• Factor XII: Hagan factor• Factor XIII: Fibrin stabilizing factor


Sequence of clotting mechanism: Enzyme cascade theory::• Most of the clotting factors in the form of enzymes.• Normally all the factors are present in the form of

inactive proenzyme.• This theory explains how various reactions involved in

the conversation of proenzymes to active enzymes take place in form of cascade.

• Cascade refers to a process that occurs through a series of steps, each step initiating the next, until the final step is reached.


Stages of blood clotting : 1. Formation of prothrombin activator 2. Conversion of prothrombin into thrombin 3. Conversion of fibrinogen into fibrin


Stage 2 positive feedback Prothrombin Thrombin

Extrinsic pathway Tissue Trauma + Tissue Thromboplastin

Glycoprotein Phospholipids

Xa X

Stage 1 Intrinsic pathwayEndothelial damage + collagen exposure kallikrein HMWKinogenXII XIIa Platelets HMWXI XIa calciumIX IXa Phospholipid VIII,calciumX Xa V + Thrombin

Prothrombin activator

CalciumV+Thrombin

Stage3 Fibrinogen a Fibronogen Polymerisation Loose strands of fibrin

XIII Calcium Fibrin tight blood clot

Positive feedback


HEMOSTASISDefined as arrest or stoppage of bleeding.Stages:Vasoconstriction.Formation of platelet plug.Coagulation of blood.


Blood clot

Blood clot• Defined as the mass of coagulated

blood which contains RBC’s WBC’s and platelets entrapped in fibrin meshwork.

• RBC’s and WBC’s are not necessary for clotting process. However when clot is formed these cells are trapped in it along with platelets.

• The trapped RBC’s are responsible for the red color of the clot.

• The external blood clot is also called scab. It adheres to the opening of damaged blood vessel and prevents blood loss.


Clot retraction:• After the formation, the blood clot starts contracting. And

after about 30-45 minutes, a straw colored fluid called serum oozes out of the clot.

• This process is called Clot retraction. • The contractile proteins namely, actin, myosin, thrombosthenin are responsible for clot retraction.


Fibrinolysis:• Lysis of blood clot inside the blood vessel is called

fibrinolysis.• Helps to remove the clot from the lumen of the blood

vessel.• This process requires a substance called plasmin or

fibrinolysin. Plasmin formation:• Formed from inactivated glycoprotein called

plasminogen.• Synthesized in liver and is Incorporated with other

proteins in the bloodclot.


• Plasminogen is converted into plasmin by Plasminogen activator (t-PA), lysosomal enzymes and thrombin.

• The t-PA is inhibited a substance called t-PA inhibitor. And also by factors V and VIII.

• Besides t-PA, there is another Plasminogen activator called urokinase Plasminogen activator (u-PA).


• Sequence of events involved in the activation of Plasminogen

• During intravascular clotting the endothelium of the blood vessel secretes a thrombin binding protein called Thrombomodulin.


Damaged tissue and endothelium Lysosomal enzymes Thrombomodulin + Thrombin

Thrombomodulin-thrombin complex

Protein C Activated protein C Protein S

Inactivation of V and VIII Inactivation of t-PA inhibitor

Activation of t-PA thrombin u-PA

Plasminogen Plasmin Lyses of clot(fibrin)


Anticlotting mechanism in the body:• Under physiological conditions, intravascular clotting

does not occur. Because of some physiochemical factors in the body:

• Physical factors:• i. Continuous circulation of blood.• ii. Smooth endothelium lining of the blood.• Chemical factors:• Prescence of natural anticoagulant heparin that is

produced by the liver.• All the clotting factors are in inactive state.• Inactivation of factor V and VIII prevents clot formation.


Anticoagulants• The substances, which

prevent or postpone coagulation of blood, are called anticoagulants.

• Three types:• Used to prevent blood

clotting inside the body, i.e. in vivo

• Used to prevent clotting of the blood that is collected from the body i.e. in vitro

• Used to prevent clotting both i.e. in vivo and in vitro


Heparin:• Naturally produced anticoagulant in the body.

• It is produced by mast cells which are abundant in liver and lungs. Basophiles also secrete heparin.

• Heparin is a conjugated polysaccharide. Commercial heparin is produced from liver and other organs of animals.

• Available in liquid form or dry form as sodium, calcium, ammonium, or lithium salts.


Mechanism of action:• Prevents blood clotting by its antithrombin activity.

• Combines with antithrombin III and removes from circulation.

• Activates antithrombin III

• Inactivates other factors like IX, X, XI, XII.


HEPARIN

SUPRESSES THROMBIN ACTION

INACTIVATES FACTORS IX, X, XI XII

ACTIVATES ANTITHROMBIN III

REMOVES THROMBIN

NO BLOOD CLOTTING


Uses of heparin:As an anticoagulant both in vivo and in vitro.Clinical useIntravenous injection of heparin(0.5-1 mg/kg body weight)

postpones clotting for 3-4 hours. So widely used in clinical practice.

i. To prevent intravascular blood clotting surgery.ii. During dialysis when blood is passed through artificial

kidney.iii. During cardiac surgery, which involves passing blood

through heart lung machine.iv. Anticoagulant to preserve the blood transfusion


In laboratory:• Used as anticoagulant

in vitro while collecting blood for various investigations.

• About 0.1-0.2 mg is sufficient for 1ml of blood.

• Effective for 8-12 hours.

• Most expensive anticoagulant

Initial condition

Effective clotting

Thrombus formation

Low dose heparin

High dose heparin


• Coumarin derivatives• Dicoumoral and Warfarin

Mechanism of action:

• Prevents blood clotting by inhibiting the action of Vitamin K

• Essential for formation of various clotting factors namely VII, IX, X.


Uses:• Oral anticoagulants in clinical practice (in vivo)


EDTA:• Ethylenediaminetetra acetic acid (EDTA) is a strong

anticoagulant. Available in two forms:• Disodium salts(Na2EDTA)• Tripotassium salt(K3EDTA) Mechanism of action:• Prevents clotting by removing calcium. Uses:• I.V in case of lead poising.• In-vitro 0.5-2.0 mg of EDTA per ml of blood sufficient to

preserve the blood for at least 6hours.• In refrigerator it can prevent blood for up to 24 hours


Oxalate Compounds:• Prevents clotting by forming calcium oxalate. Thus these

compound of reduce calcium level.• Earlier sodium and potassium oxalates were used.• Nowadays mixture of ammonium oxalate and potassium

oxalate in ratio of 3:2 were used.• Each salt is an anticoagulant by itself.• Potassium oxalate causes shrinkage of RBC’s.• Ammonium oxalate causes swelling of RBC’s.


Mechanism of action:• Combines with calcium and forms insoluble calcium

oxalate.• Thus it removes calcium from blood and lack of calcium

prevents coagulation. Uses:• In vitro anticoagulant.• 2mg of mixture is necessary for 1ml of blood.• Oxalate is poisonous so it cannot be used in vivo


Citrates:• Sodium, ammonium and potassium citrates are used as

anticoagulants.

• Mechanism of action:

• Combines with calcium in blood to form insoluble calcium citrate.

• Like oxalate, citrate also removes calcium from blood and lack of calcium prevents coagulation.


Uses:• To store blood in blood banks availabl in two forms:

• Acid citrate dextrose(ACD) – 1part of ACD with 4 parts of blood.

• Citrate phosphate dextrose(CPD) – 1 part of CPD with 4 parts of blood.

• Used in laboratory in vitro. Formol-citrate solution (Dacie’s solution) is used for RBC and platelet counts.


Other substances which prevent blood clotting:

• Peptone, proteins, from venom of copperhead snake and hirudin (from leach) are the known coagulants.


Physical method to prevent blood clotting:• 1. Cold:• Reducing the temperature to about 5 c postpones

coagulation of blood.

• 2. Collecting blood in a container with smooth surface:• Like silicon coated container prevents clotting. This

inhibits the activation of factor XII and platelets.• So formation of prothrombin activator is prevented.


Procoagulants• Or hemostatic agents are the substances , which

accelerate the process of blood coagulation. • Procoagulants are:• Thrombin: Sprayed upon bleeding surface to arrest

bleeding by hastening blood clotting.• Snake venom: Venom of snakes contains proteolytic

enzymes which enhance blood clotting by activating the clotting factors.


Extracts of lungs and thymus• Obtained from lungs and thymus has Thromboplastin,

which causes rapid blood coagulation.

Sodium or calcium alginate:• Enhance blood clotting by activating hegman factor.

Oxidized cellulose:• Clotting by activating hegman factor.


Tests for clotting • Bleeding time• Clotting time • Prothrombin time• Partial prothrombin time• Thrombin time.


Bleeding time:• Time interval from oozing of blood after a cut or injury

till arrest of bleeding. • Determined by Duke method using blotting paper or

filter paper method. • Its normal duration is 3-6 min • Prolonged in purpura


Clotting time:• Time interval from oozing of blood after cut or injury till

the clot formation. • Usually determined by capillary tube method.• Normal duration is 3-8 minutes• Prolonged in Hemophilia.


Prothrombin time:• Time taken by blood to clot after adding tissue Thromboplastin to it. • Blood is collected and oxalated so that, the calcium is precipitated and

prothrombin is not converted into thrombin.• Large quantity of tissue thromboplastin with calcium is added.• Tissue thromoplastin activates prothrombin and blood clotting occurs.• During this procedure, the time taken by blood to clot after adding tissue

Thromboplastin is determined.• Normal duration is 12 seconds • Prolonged in prothrombin Deficiency and other factors like factor I, V, VII and X.• Normal in hemophilia


PARTIAL PROTHROMBIN TIME:• Is the time taken for blood to clot after adding

phospholipid and calcium to blood.• It is also called activated prothrombin time.• Done to investigate bleeding disorders and to detect the

Prescence of heparin in patients treated with heparin.• Carried out by observing clotting time after adding

phospholipid, surface activator and calcium to patients.• Phospholipid is platelet substitute and surface activator

is Kaolin.• Normal duration is 30-50 sec.• Prolonged in heparin therapy deficiency of factors II, V,

VIII, IX, X, XI, XIIK Sembulingam Essentials Of Medical Physiology

THROMBIN TIME:• Time taken for the blood to clot after adding thrombin to

it.• Done to investigate the presence of heparin in plasma or

to detect fibrinogen abnormalities.• Involves the observation of clotting time after adding

thrombin to patients plasma.• Normal duration is 12-20 sec.• Prolonged in heparin therapy and during dysfibrinogenimia.


APPLIED

PHYSIOLOGY

• HAEMORRHAGIC DIATHESES DUE TO PLATELET DISORDERS.

• Disorders of platelets produce bleeding disoreders by one of the following 2 mechanisms.

i. Due to reduction in the number of platelets ii. Due to defective platelets

Harsh Mohan Essential Pathology for Dental Students

THROMBOCYTOPENIAS:• Reduction in the peripheral blood platelet count below the lower limit of

normal i.e. 150,000/ul.• Associated with abnormal bleeding.

May result from 4 main groups of causes:• Impaired platelet production. General bone marrow failure Selective suppression of platelet production.• Accelerated platelet destruction Immunological thrombocytopenias Increased consumption.• Splenic sequestration. Splenomegaly• Dilutional loss. Massive transfusion of old stored blood to bleeding patients


Drug-induced thrombocytopenia• Many commanly used drugs cause

thrombocytopenia by depressing megakaryocyte production.

• Drugs include: Chemotherapeutic agents(antimetabolites,

anthracyclines), certain antibiotics (sulfonamides, rifampacin,pencillins), drugs used in cardiovascular disesases (digitoxin, thiazide diuretics), heparin and excessive consumption of ethanol.


• Disorders of platelet functions: Herediatry disorders: Defective platelet adhesion. Defective platelet aggregation. Disorders of platelet release reaction. Aquired disorders: Aspirin therapy: Others:


COAGULATION DISORDERS • Are the diseases characterized by prolonged bleeding or

clotting time.• Disorders are of three types. i. Hemophilia ii. Purpura iii. von Willebrand disease. iv. Vitamin K defeciency. v. Coagulation disorders in liver diseases. vi. Fibrinolytic defects.


HEMOPHILIA.• Group of sex linked inherited disorders featured by

prolonged clotting time.• Usually affects males, females being the carriers.• Damage of skin while falling or extraction of tooth cause excess bleeding for few weeks.• Easy bruising and hemorrhage in muscles and joints are also common.


CAUSES• Due to lack of formation of

prothrombin activator.• Bleeding time and prothrombin time

are normal.• Function of prothrombin time is

effected due to deficiency of factor VIII, IX, or XI.

Types of hemophilia: Hemophilia A or classic hemophilia:• Due to the deficiency of factor VIII.

85% of people are affected. Hemophilia B or Christmas Factor

IX: • It is due to the deficiency of factor IX.

15% are affected. Hemophilia C or factor XI

deficiency: • Due to deficiency of factor XI. It is a

very rare disorder.


SYMPTOMS:• Spontaneous bleeding. • Prolonged bleeding due to cuts, tooth extraction and

surgery.• Hemorrhage in gastrointestinal and urinary tract.• Bleeding in joints followed by swelling and pain.• Appearance of blood and urine. TREATMENT :• Replacing the missing clotting factor.


PURPURA:• Characterized by prolonged bleeding time.• Characteristic feature is spontaneous bleeding under skin

from ruptured capillaries.• Causes small tiny hemorrhagic spots in many areas of

the body.• These spots under the skin are called purpuric spots.• Blood also sometimes collects in large areas beneath the

skin which are called Ecchymoses. • But clotting time is normal


• Types and causes:• Depending upon causes classified as i. Thrombocytopenic purpura:• Due to deficiency of platelets. • In bone marrow disease platelet production is affected

leading to deficiency of platelets. ii. Idiopathic thrombocytopenic purpura:• Due to some unknown cause called idiopathic

thrombocytopenic purpura.• Platelet is count is decreased due to development of

antibodies against platelets


• iii. It is due to structural or functional abnormality of platelets.

• Platelet count is normal. • Normal clotting time, normal or prolonged bleeding

time but defective clot retraction.


von Willebrand disease:

• Characterized by excess bleeding disorder even with a mild injury.

• Due to inherited deficiency of von willebrand factor.

• Responsible for adherence of platelets to endothelium of blood vessels during hemostasis after an injury.

• This deficiency suppresses platelet adhesion and also causes deficiency of factor VIII.

• This results in excess bleeding that occurs during platelet dysfunction.


• TypeI. Most common characterized by mild to moderate decrease in plasma vWF.

• TypeII. Much less common and is characterized by normal or near normal levels of vWF which is functionally defective.

• TypeIII. Extremely rare and most severe form of disease. Bleeding episodes are treated by

Cryoprecipitates.


VITAMIN K DEFICIENCY:• Is a fat soluble vitamin which plays important role in hemostasis as

a co-factor in the formation of 6 prothrombin complex proteins synthesised in the liver: factor II, VII, IX, X. protein C and S.

• Vitamin K deficiency may present in new born or in subsequent childhood or adult life.

• NEONATAL vitamin K deficiency.• Vitamin K deficiency in children and adult.


COAGULATION DISORDERS IN LIVER DISEASE:• Liver also produces inhibitors of coagulation such as antithrombin III and

protein C and S and plays a role in the clearance of activated factors and fibrinolytic enzymes.

• The major causes of bleeding in liver disease are : I. Anatomic lesion: Portal hypertension Peptic ulceration Gastritis II. Hepatic dysfunction: Impaired hepatic synthesis of coagulation factors. Impaired hepatic synthesis of coagulation inhibitors. Impaired absorption and metabolism of vitamin K. III. Complications of therapy: Massive transfusion Infusion of activated coagulation proteins. Following heparin therapy


THROMBOSIS:• Thrombosis or intravascular blood clotting refers to

coagulation of blood inside the blood vessel. Causes of thrombosis:• Injury to blood vessel.• Roughened endothelial lining.• Sluggishness of blood flow.• Agglutination of RBC’s.• Toxic thrombosis.• Congenital absence of protein C.


COMPLICATIONS OF THROMBOSIS• Thrombus: The solid mass of platelets, red cells and/0r clot, which

obstructs the blood vessel is called Thrombus.• This thrombus formed due to agglutination of RBC is

called agglutinative thrombus.• Embolism and embolus:• Process in which the thrombus or part of it is detached

and carried in bloodstream and occludes the small blood vessels results in arrests of blood flow to any organ or region of the body.

• Common in lungs, brain or heart.



ISCHEMIA:• Insufficient blood supply to an organ or area of body by

the obstruction of blood vessels is called ischemia.

• Results in tissue damage because of hypoxia.

• Also causes discomfort, pain, and tissue death.

• Death of body tissue is called necrosis.


NECROSIS AND INFRACTION:

• Necrosis in general term refers to tissue death caused by loss of blood supply, injury, infection, inflammation, physical agents or chemical substances.

• Infraction means the tissue death due to loss of blood supply.

• Loss of blood supply is usually caused occlusion of an artery by thrombus or embolus and sometimes by atherosclerosis.

• Infraction commonly occurs in heart, brain, lungs, kidneys and spleen.


DISSEMINATED INTRAVASCULAR COAGULATION:

• Also termed as defibrination syndrome or consumption coagulopathy.

• Etiology:• Massive tissue injury.• Infections• Widespread edothelial damage• MiscellaniousClinical features: 2main features of DIC: Bleeding as the most common manifestation and Organ

damage due to ischemia caused by effects of wide spread intravascular thrombosis such as kidney and brain.


Oral

Considerations

ORAL HEALTH CONSIDERATIONS• Platelet deficiency and vascular wall disorders result in

extravasations of blood into connective tissues of the skin and mucosa creating pinpoint hemmorages called petechiae and larger patches called Ecchymoses.

• Hemarthrosis is a common complications in hemophiliac’s.• An acute TMJ arthrosis associated with FIX deficiency was

resolved with factor replacement.

Burket’s Oral Medicine

Dental management:• Dental modifications required for patients with bleeding disorders

depend on both the type and invasiveness of dental procedure and the type and severity of the bleeding disorder.

• Less modification is needed for patients with mild- coagulopathies in dental procedures.

• When significant bleeding is expected, the goal of management is to preoperatively restore the hemostatic system.

• For reversible coagulopathies the best to remove the causative agents or primarily treat the illness.

• For irreversible coagulopathies the treatment is missing or defective element may be replaced from exogenous source to allow control of bleeding.


• PLATELET DISORDERS:• When medical management is unable to

restore the platelet level of 50,000/mm3 required for surgical hemostasis , platelet transfusions must be required prior to dental extractions or other oral surgical procedures.

• Six units of platelets are commanly expected to infuse at a time.

• Local hemostatic methods are also important .

• The thromosthenic patients needing dental extractions may be succesfully treated with microfibrillar collagen and antifibrinolytic drugs.

• If using of aspirin, avoidance of aspirin is recommended, when possible for 1 week prior to extensive oral procedures

• Adjunctive local hemostatic agents are useful in preventing post operative oozing when aspirin therapy is in use at the time of minor surgical procedures.


• Adjunctive local hemostatic agents are useful in preventing post operative oozing when aspirin therapy is in use at the time of minor surgical procedures.

• When extensive surgery is emergently indicated DDAVP can be used to decrease the aspirin induced prolongation of the BT or to treat aspirin related postoperative oozing.


• HEMOPHILIAS A and B and vWD:• To make certain preoperative factors levels of at least 40 to 50% of

normal activity have been obtained, transfusion recommendations generally aim for replacement of missing coagulation factors to levels of 50-100%.

• Postsurgical bleeding occurs due to fibrinolysis it commonly starts 3 to 5 days after surgery and can be easily controlled by local measures and use of antifibrinolytics. Continuous oozing from unstable fibrinous clots require removal and repacking of the extraction socket with hemostatic agents.

• Gingival or dental bleeding unresponsive to antifibrinolytics require 20-30% of clotting FVIII or FIX.

• Higher hemostatic factor levels are needed with large wound cavities like extraction of multiple or multi rooted teeth, gingival inflammation, bleeding, tooth mobility, or apical lesions


• Fibrin sealants or fibrin glue has been used effectively as an adjunct with adhesive and hemostatic effects to control bleeding at wound or surgical sites.

Preventive and periodontal therapies:• Periodontal probing and suprgingival scaling can be routinely

done.• Subgingival scaling rarely warrents replacement therapy.• Severly inflammed and swollen tissues are best treated initially by

chlorhexidine oral rinses or by gross debridement with hand instruments to allow gingival shrinkage.

• Deep subgingival and root plannning performed by quadrent to reduce potential bleeding

• Locally applied pressure and antifibrinolytic mouth rinses are usually succesful

• Periodontal packing material aids hemostasis and protects the surgical site.


• Restorative and prosthodontic therpy:

• Rubber dam isolation is advised ti minimize the risk of laceration soft tissue in operative field and to avoid creating ecchymoses and hematomes.

• Care is taken to select tooth clamp. Matrices, wedges and hemostatic gingival retraction cord are used with caution to protect soft tissues.

• Endodnotic therapy:• Is often the treatment of choice for

patient with severe bleeding.• Generally no contraindications for root

canal treatment, provided that instrument does not extend beyond the apex.

• Application of epinephrine intrapulpally to apical area is succesful in providing hemostasis.


Pediatric dental therapy:• Administration of factor concentrate and extraction of decidious

teeth with curretage may be neccesary for patient comfort and hemorrhage control.

• Hemorrhage control is obtained by guage pressure and seepage generally stops by 12 hours.

• Pulpotomies can be performed without excessive pulpal bleeding. • Topical fluoride applications and pit and fissure sealants decrease

the need for extensive therapy.

Orthodontic therapy:• Avoid mucosal lacerations,• Minor cuts usually respond to local pressure.


• PATIENTS ON ANTICOAGULANTS:• It is generally held that non surgical dental treatment can be

successfully accomplished without alterations of the anticoagulant regimen that INR is not grossly above the therapeutic range and trauma is minimized.

• The AHA recommends that patients undergoing dental procedures, Tranexamic acid or EACA mouth wash can be applied without interrupting anticoagulant therapy.

• ACCP recommends i.) for patients going dental procedures who are not considered to

be at high risk of bleeding, ACCP recommends Warfarin therapy not to be discontinued. In patients high risk for bleeding Warfarin can be discontinued.

ii.) in whom local bleeding must be controlled, Tranexamic acid or EACA mouth wash must be administered without interrupting anticoagulant therapy.


• For surgical procedures, physician consultation is advised in order to determine the patients most recent INR level and the best treatment approach based on patients relative hemorrhagic risks.


Dental treatment Suboptimal INR rangeOf anticoagulants

Nor mal target INR rangeOf anticoagulants

Anticoagul-ants Out of range

<1.5 1.5<2.0 2.0<2.5 2.5<3.0 3.0<3.5 >3.5

Examination, radiographs,impressions, orthodontics

Simple restorative dentistry, supragingival prophylaxis

Complex restorative dentistry, scaling and root planning, endodontics

Caution:probably safe

Simple extractions, curettage, gingivoplasty, biopsy

Probably:safe

Caution:Localmeasures

Caution:Localmeasures

Hospitalprocedure


Dental treatmentSuboptimal INR range Normal INR range Out of

range<1.5 1.5<2.0 2.0<2.5 2.5<3.0 <3.0 to 3.5 >3.5

Multiple extraction, removal of single bony impaction

Gingivectomy, apicectomy, minor periodontal flap, placement of single implant

Probably:safe

Caution:Probablysafe


Full mouth or arch extractions


Caution:Local measures

Extensive flap surgery, extraction of multiple bony impactions, multiple implant placement


Open fracture reduction, orthognathic surgery.

Hospital procedure


• PRP• The first step of the treatment plan was

to complete the root canal therapy obturation was done on the day of surgery. The surgical protocol included a routine medical history followed by blood investigations. The surgical procedure included reflection of a full thickness mucoperiosteal flap by sulcular incision and two relieving vertical incisions. Debridement of tissues at the defect site was followed by irrigation with sterile saline solution. Root planing was performed on the root surface under the apical portion of the root. No root resection was done.

Bony cavity filled with Platelet-Rich plasma gel

Journal of Conservative Dentistry | Apr-Jun 2011 | Vol 14 | Issue 2

• Wound closure was obtained with a 3-0 black silk suture. • Analgesics (Combiflam {ibuprofen 400 mg + paracetamol 325 mg}

twice a day)• Antibiotics (Amoxycillin 500 mg twice a day) and 0.2%

Chlorhexidine mouthwash was prescribed for five days post surgically.

• The sutures were removed after seven days. The patients were reviewed at regular intervals of one week, and one, three, six, nine, and twelve months.



• Essentials of medical physiology-5th edition

• Harsh Mohan Essential pathology for dental students-3rd edition

• Burket’s oral medicine-11th edition

• Journal of Operative Dentistry-Apr-June2011, Vol14, Issue 2

Science

Mechanism of clotting