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BLEEDING DISORDERS AND PERIODONTOLOGY

PHILIP VASSILOPOULOS & KENT PALCANIS Periodontology 2000, Vol. 44, 2007

INTRODUCTION
Unexpected clinical bleeding Most common complication. Two forms - During surgery Several days after the procedure. Controlling the hemorrhage and stabilization of the patients clinical status.

WHY IMPORTANT FOR A DENTIST ?


Periodontitis An inflammatory disease. Treatment approach Nonsurgical / Surgical. Increased incidence in the medically compromised group of patients. Polypharmacia and medical conditions Increases the concern towards bleeding disorders and periodontitis.

PREVALENCE OF BLEEDING DISORDERS


Coagulation factor abnormalities - most common inherited bleeding disorders.

Von Willebrand disease, Hemophilia A and Hemophilia B 9597% of all coagulation Deficiencies.
Von Willebrand disease Most frequently inherited bleeding disorder, 0.82% of the general population, however is often undiagnosed.

Hemophilia A - Most common of the inherited coagulopathies, (one per 5,000 male births). Other rare coagulation factor deficiencies : factor I (fibrinogen), factor II (prothrombin), factor VII (proconvertin), factor X (Stuart-Prower) factor XI (plasma thromboplastin antecedent). Also included are Disorders due to platelet deficiency Eg Thrombocytopenia.

BASIC PHYSIOLOGY OF HEMOSTASIS


Hemostasis - Primary or secondary / A four phase process. Primary hemostasis A platelet plug formation Duration - 23 seconds Predominant mechanism of blood loss stoppage in capillaries and small-diameter vessels. Secondary hemostasis Fibrin synthesis and its deposition Provides stabilization of the hemostatic clot Several minutes to complete.

Four-phase process
A) Vascular phase : Immediately afret disruption of blood vessels. Contraction of smooth muscles to reduce the lumen. Close situation of endothelial cells Reduction in blood loss.

Pressure by extracellularly accumulated blood Reduced blood loss.

B) Platelet phase : Derived from Megakaryocyte, 2-4 in size, 150,000400,000/ l, circulate in the periphery of the vascular lumen. Characterized by - platelet adhesion, activation, secretion and aggregation Adherence of platelets to subendothelial connective tissue glycoprotein receptors located in the platelet membrane. (Predominant role of GP Ib-IX-V and GP Ia-IIa, as well as GP VI).

Von Willebrand factor - A bridge between GP Ib-IX-V and underlying collagen. Activation of platelets Aggregation of platelets (1st wave) Secretion by platelets 2nd wave. Hemostatic plug organisation (Binding of GP IIb-IIIa PAR with Fibrinogen) Granules include : Alpha garnules & Dense granules. Also Glycogen particles, Mitochondria and lysosomes.

C) COAGUALATION PHASE : A complex series of protelytic reactions on the activated platelet membrane.

Variety of enzymes, cofactors and contact factors Thrombin formation and conversion of fibrinogen to fibrin.
Two inter-related pathways (intrinsic and extrinsic) merge into the common pathway Prothrombinase complex Prothombinase complex - activated factor X, activated factor V, phospholipid membrane and calcium ions.

Extrinsic/ tissue dependent pathway :


Activates factor VII, Acts faster, Produces little amount of thrombin, Regulated by tissue factor inhibitor, Triggers intrinsic pathway (main production of thrombin).

Intrinsic pathway :
Contact factors prekallikrein, high-molecular-weight kininogen and factor XII complex activates factor XI.

Prothombinase from both the pathways


THROMBIN

Thrombin.

coagulation activation V, VII, VIII, XI, XIII

FIBRIN CLOT PROTECTION (Thrombin


activated fibrinolysis inhibitor)

PLATELET AGGREGATION

FIBRIN FORMATION

Platelet clot fibrin stabilising factor

Fibrin clot

D) Fibrinolytic phase :
Initiates disintegration of the hemostatic plug and the tissue repair process. PLASMINOGEN Tissue plasminogen acivator Urinary plasminogen activator PLASMIN Plasminogen activator inhibitor Fibrin clot a 2 antiplasmin

Fibrin peptides

HEMOSTASIS

Vascular
1. Smooth cells contraction 2. Extravascular

pressure

Platelet 1. Adhesion 2. Activation 3. Secretion 4. Aggregation

Coagulation Pathways 1. Tissue factor dependent 2. Intrinsic

Fibrinolytic 1. Lysis of fibrin network into peptides 2. Fibrinogen deactivation

CLASSIFICATION AND DEFINITION


Hematological conditions characterized by a functional impairment in the hemostatic process.

Bleeding disorders

Inherited/hereditary

Acquired

Inherited bleeding disorders


Vascular disorders : Associated with syndromes, Characterized by blood vessel developmental abnormalities. Eg. Hereditary hemorrhagic telangiectacia, or OslerWeberRendu syndrome (malformed blood vessels)

EhlersDanlos syndrome (defects in the subendothelial and perivascular connective tissue)

Platelet disorders
Clsssified as : Quantitative Eg. congenital thrombocytopenia (platelet count is <150,000/ l)

Qalitative disorders can be :


Platelet receptor defect Eg BernardSoulier syndrome Platelet secretory defect / Storage pool defects absent or deficient granules. Eg. WiscottAldrich syndrome.

Coagulation disorders
A) Von Willebrand disease :

Qualitative or quantitative deficiency of von Willebrand factor.


Role in platelet aggregation.

Binds to coagulation factor VIII and makes it more resistant to the degradation process.

B) Hemophilia A : A recessive X chromosome- linked coagulation factor VIII disorder. 3 types Severe form coagulation factor activity is <1%, Moderate ranges (15%) Mild range (549%)

C) Hemophilia B/Christmas disease : Deficiency in factor IX

Fibrinolytic disorders :

Rare incidence.
Deficiency of plasminogen activator or a2antiplasmin.

Acquired bleeding disorders


Vascular disorders : Associated with diseases affecting the epithelium and connective tissue of blood vessels. Eg. Scurvy Platelet disorders: Quantitative and qualitative disorders, Causes - decreased platelet production, increased platelet destruction, and increased sequestration, primarily anemia, leukemia and medication-induced infection.

Coagulation disorders

Hepatic failure - hepatitis B and C, cirrhosis or alcohol abuse persistent decrease of coagulation factors.
Patients on anticoagulants Oral / parenteral. Caumarin (oral) - vitamin K-dependent factors II, VII, IX, and X. Fractionated and unfractionated heparin - Enhances the action of antithrombin III. Patients on aspirin or aspirin-containing compounds or long term antibiotics.

Others : ADP receptor inhibitors Eg. Clopidogrel bisulfate Fibrinogen receptor (GP IIbIIIa) inhibitors Eg. tirofiban, abciximab

Fibrinolytic disorders Liver disease can reduce the metabolization of certain fibrinolytic activators.

Streptokinase - to destroy the formed clot in thromboembolic disorders, create the potential for fibrinolysis.
Prostate carcinoma - Associated with increased plasmin levels and fibrinolysis.

MEDICAL DIAGNOSIS
History - nature of hemorrhagic disease, whether inherited or acquired. Physical examination Multiple and small-in-size mucocutaneous hemorrhagic lesions, such as petechiae and ecchymoses/ dissecting hematomas. Superficial cuts leading to profuse bleeding. Laboratory evaluation Adjunct in establishment of diagnosis. Screening tests - Partial thromboplastin time - 25 to 35 seconds Prothrombin time - 11 to 15 seconds Platelet count - 150,000400,000/ l.

MANAGEMENT OF PERIODONTAL PATIENTS WITH BLEEDING DISORDERS

PRE-OPERATIVE PRECAUTIONS
A detailed medical history Family history, Previous bleeding episode, Current illnesses, such as hepatic and renal failure, medications including anticoagulation agents. Consultation with the primary care physician and a hematologist. Nature and severity of the disorder, the degree of invasive dental procedures outlines treatment needs.

Management in diseases :

Chronic renal failure - Managed the day after dialysis, heparin will be cleared from the system.
Lack of vitamin K eg. malabsorption syndrome, vitamin K supplement before the dental appointment. Liver failure - Platelet transfusion.

Anticoagulation agents Serious thromboembolic events reported after the interruption. Risk of thromembolic episode more likely and severe than bleeding. The decision be based on International normalized ratio (INR)value, Invasiveness and extent of dental procedure, Current illnesses and medications. Unfractionated heparin can be interrupted 46 hours before the surgical procedure, Aspirin stopped atleast for 3 days, upto 7 days. Anticoagulation treatment is resumed 1218 hours after the dental procedure.

INR : A key component 3.5 - Periodontal surgical procedures carried out in dental office. >3.5 - Adjustment in anticoagulant dose. Therapeutic levels for most medical conditions - 2.5 to 3.5. Values normalized to 3.5 by minor adjustments involving the reduction, but not the discontinuation, of coumarin. Takes up to 4 days for INR values to return to normal.

Preventive care :
Regular dental visits,
Frequent professional tooth cleanings,

Oral hygiene reinforcement,


Fluoride supplements and mouthrinses, A low-sugar diet Annual radiographic examination. Preventing and arresting diseases in the initial stages reduced risk of bleeding.

INTRAOPERATIVE MEASURES
Inherited coagulopathies
Managed systemically with replacement of coagulation factors.

IV infusion of deficient, or missing, factor -1 hour before the procedure to achieve level 30% above the normal plasma concentration (50% of the normal amount when regional block anesthesia is administered).
Mild and moderate cases - Desmopressin or 1-desamino-8-D arginine vasopressin can be useful. It induces the release of factor VIII/vonWillebrand Factor from platelets and endothelialcells.

Acquired bleeding disorders

Local hemostatic measures. Eg. use of local antifibrinolytic mouthwash, such as tranexamic acid or epsilon aminocaproic acid during scaling procedure.
Regional block anesthesia must be avoided. Local infiltration anesthesia with the use of vasoconstrictive agent, (Lidocaine 2% with 1:100,000 epinephrine / Articaine 4% with 1:100,000 Epinephrine.) Handling of soft tissues -Conservative flap design and minimizing flap elevation Curettage of the extraction sockets and removal of all granulation tissue.

LOCAL HEMOSTATIC AGENTS - Enhance clot stabilization Includes : Absorbable gelatin Absorbable collagen Microfibrillar collagen and collagen dressings Oxidized regenerated Cellulose Thrombin Tranexamic acid & epsilon-aminocaproic acid Fibrin glue (thrombin, fibrinogen, fibronectin and aprotinin.) Platelet-rich plasma

Collagen, gelatin and cellulose products scaffold for adhesion of platelets. Thrombin converts fibrinogen fibrin fibrin clot.

Tranexamic acid & epsilon-aminocaproic acid - inhibits plasminogen action and reduces the fibrinolytic activity. Aprotinin delays the degradation of the hemostatic clot.

OTHER MEASURES : Bite on a moistened gauze, or gauze soaked with the hemostatic agent, for 30 minutes. Electrocautery and laser - Control bleeding in the soft tissues. Bone burnishing and bone wax - Hard tissues.

POSTOPERATIVE MEASURES
Good care of the surgical area. Rinsing is prohibited on the day of surgery.

Liquids and a high-protein diet are recommended.


The use of antifibrinolytic mouthwash is recommended. eg10 ml of 4.85%tranexamic acid solution, four times a day, for 2 minutes. Prescribing antibiotics and analgesic medications (Drug interaction should be carefully avoided).

CURRENT CONCEPTS AND NEW APPROACHES


Management of patients with bleeding disorders - safe in a dental office with thorough knowledge of bleeding disorders. Communication and close co-operation with the medical care professional and hematologist, is essential. Low-molecularweight heparin - A less expensive and easier alternative for patients on anticoagulation

Single coagulopathies - Antifibrinolytic mouthwashes, localized pressure applied to surgical flaps, and a collagen sponge placed into extraction sockets are good measures.

CONCLUSION
A detailed medical history, following the principles of hemostasis and exercising rational clinical judgment, contribute to the effective dental treatment of patients with bleeding disorders.