ORAL SURGERY

LECTURE 3 ‫احمد فاضل ابراهيم القيسي‬.‫د‬.‫م‬.‫ا‬

Bleeding disorder
A number of procedures that are performed in dentistry may cause bleeding. Under
normal circumstances, these procedures can be performed with little risk; however,
patients whose ability to control bleeding is altered by congenital defects in
coagulation factors, platelets, or blood vessels may be in grave danger unless the
dentist identifies the problem before performing any dental procedure. In most cases,
after a patient with a congenital bleeding problem has been identified, steps can be
taken to greatly reduce the risks associated with dental procedures.
Hemophilia A:
The hemostatic abnormality in hemophilia A is caused by a deficiency or a defect of
factor VIII. Factor VIII circulates in plasma bound to Von Willebrand factor (vWF).
Unbound factor VIII is destroyed. Factor VIII was thought to be produced by
endothelial cells and not by the liver, as most coagulation factors are. However,
when disease was corrected by transplantation in several liver transplant recipients
with hemophilia, it became clear that liver parenchymal cells also produce factor
VIII.
Hemophilia A is inherited as an X-linked recessive trait. The defective gene is
located on the X chromosome. An affected man will not transmit the disease to his
sons; however, all of his daughters will be carriers of the trait because they inherit
his X chromosome. A female carrier will transmit the disorder to half of her sons
and the carrier state to half of her daughters. Severity of bleeding varies from kindred
to kindred. Within a given kindred, the clinical severity of the disorder is constant;
for example, relatives of people with severe hemophilia are likely to be affected
severely. The mutation rate for the responsible gene is unusually high (up to 30%),
which explains why a rare condition such as hemophilia A does not die out after
several generations. Because of the high mutation rate of the responsible gene, a
negative family history is of limited value in excluding the possibility of hemophilia
A. The assay of factor VIII activity can be used to identify female carriers of the
trait. About 35% of carriers will show a decrease in factor VIII (≈50% of normal
factor VIII levels). Other carriers may have normal levels of factor VIII.
Immunoassays for vWF can greatly improve the detection rate among carriers of
hemophilia A. Polymorphic DNA probes are now available that are capable of
detecting 90% of affected families and 96% or more of carriers. Hemophilia A can
manifest in women. This occurs in a mating between an affected male and a female
carrier. Half of the daughters of such a mating would inherit two abnormal X
chromosomes—one from the affected father and one from the carrier mother. These
daughters would have homozygous hemophilia. In addition, hemophilia may occur
in a minority of heterozygous carriers. Normal homeostasis requires at least 30%
factor VIII activity. Symptomatic patients usually have factor VIII levels below 5%.
Those with factor VIII levels between 5% and 30% have a mild form of the disease.
Patients with levels between 1% and 5% have moderate disease, and severe forms
of the disease occur when the level is less than 1% of normal. About 60% of cases
of hemophilia are severe.
HEMOPHILIA B
In hemophilia B (Christmas disease), factor IX is deficient or defective.
Hemophilia B is inherited as an X-linked recessive trait (F9 gene). Factor IX levels
below 10% have been reported in a few women. Similar to hemophilia A, the
disorder manifests primarily in males. Severe disease, in which affected patients
have less than 1% of normal amounts of factor IX, is less common than in
hemophilia A. Clinical manifestations of the two disorders are identical. Screening
laboratory test results are similar for both diseases. Specific factor assays for factor
IX establishes the diagnosis. Purified factor IX products are recommended for the
treatment of minor and major bleeding. Recombinant factor IX is now available for
clinical use.
Von Willebrand's disease
The most common inherited bleeding disorder is von Willebrand disease,
which is caused by an inherited defect involving platelet adhesion. The cause of
platelet dysfunction in von Willebrand disease is a deficiency or a qualitative defect
in vWF.
The disease has several variants, depending on the severity of genetic expression.
Most of the variants are transmitted as autosomal dominant traits (types 1 and 2).
These variants of the disease tend to result in mild to moderate clinical bleeding
problems. Type 1 is the most common form of von Willebrand disease. It accounts
for about 70% to 80% of the cases. The greater the deficiency of vWF in type 1
disease, the more likely it is that signs and symptoms of hemophilia A will be found.
Type 2 A is responsible for 15% to 20% of cases. The other variants of the disease
are uncommon. Type 3, which is rare, is transmitted as an autosomal recessive trait
that leads to severe deficiency of vWF and FVIII.
Variants of von Willebrand disease with a significant reduction in vWF or with a
vWF that is unable to bind factor VIII may show signs and symptoms of hemophilia
A, in addition to those associated with defective platelet adhesion.
in mild cases, bleeding occurs only after surgery or trauma. In the more severe
cases—type 2N and type 3—spontaneous epistaxis or oral mucosal bleeding may be
noted.
Thrombocytopenia:
It occurs when the platelet count that falls below the lower limit of normal, i.e.,
150000/microliter (for adults). risks associated with thrombocytopenia range from
no risk at all to bleeding risks and thrombosis. The correlation of severity of
thrombocytopenia and bleeding risk is uncertain. Spontaneous bleeding can occur
with a platelet count under 10000/microliter and surgical bleeding with counts below
50000/microL. Thrombocytopenia is associated with risk of thrombosis in
conditions like heparin-induced thrombocytopenia (HIT), antiphospholipid antibody
syndrome (APS), disseminated intravascular coagulation (DIC), thrombotic
microangiopathy (TMA), paroxysmal nocturnal hemoglobinuria (PNH).

Infiltration and block injections of local anesthesia can be provided in patients with
platelet counts above 30,000/µL. Also, most routine dental procedures can be
performed. If the platelet count is below this level, routine dental treatment involving
minor tissue injury should be delayed. For urgent or emergency dental needs, platelet
replacement is indicated. If the platelet count is above 50,000/µL, extractions and
dentoalveolar surgery can be performed. For more advanced surgery, the platelet
count should be 80,000/µL and 100,000/µL or higher. Patients with platelet counts
below these levels will need platelet replacement before undergoing the planned
procedures.
Common causes of thrombocytopenia:
1- Primary immune thrombocytopenia (primary ITP). An autoimmune
condition where antibodies are produced against platelets resulting in
platelet destruction.
2- Drug-induced immune thrombocytopenia:
o Heparin-induced thrombocytopenia (HIT) - in this condition, anti-
platelet antibodies activate platelets resulting in thrombosis (both
arterial and venous)
o Quinine
o Sulfonamides, ampicillin, vancomycin, piperacillin
o Acetaminophen, ibuprofen, naproxen
o Cimetidine
3- Drug-induced non-immune thrombocytopenia. Drugs like valproic acid,
daptomycin, linezolid cause thrombocytopenia by dose-dependent
suppression of platelet production.
4- Infections:
o Viral: HIV, hepatitis C, Ebstein-Barr virus, parvovirus, mumps,
varicella, rubella, Zika viral infections can cause thrombocytopenia.
o Sepsis causes bone marrow suppression.
o Helicobacter pylori
o Malaria
5- Hypersplenism due to chronic liver disease
6- Chronic alcohol abuse
7- Nutrient deficiencies (folate, vitamin B12, copper)
8- Autoimmune disorders like systemic lupus erythematosus, rheumatoid
arthritis associated with secondary ITP
9- Pregnancy. Mild thrombocytopenia presents in gestational
thrombocytopenia; moderate-severe thrombocytopenia can occur in
preeclampsia and HELLP (hemolysis, elevated liver enzymes, low platelet
count) syndrome
10- Aplastic anemia
11- Inherited thrombocytopenia. Often seen in children, rare in adults
o Von Willebrand disease type 2
o Alport syndrome
o Fanconi syndrome.
o Bernard–Soulier syndrome
 Dental management of the patient with bleeding disorders
1- Patient Evaluation and Risk Assessment
• Evaluate and determine whether a bleeding disorder (e.g., hemophilia) exists.
• Obtain medical consultation if undiagnosed, poorly controlled, or if uncertain.
Screen patients with bleeding history or clinical signs of a bleeding disorder with
PT, PTT, TT, and platelet count.

2- Drugs
Analgesics Avoid aspirin, aspirin-containing compounds, and other NSAIDs;
acetaminophen with or without codeine is suggested for most patients.
Antibiotics Not indicated unless acute infection is present.
Anesthesia Avoid block anesthetic injections in patients not on desmopressin,
aminocaproic acid, or factor concentrates.
Anxiety No issues
Allergy Patients placed on factor VIII replacement need to be observed for signs
and symptoms of allergy.
3- Bleeding
These patients are at great risk of bleeding from invasive dental procedures.
Special precautions must be taken before invasive procedures. Patients with mild
to moderate hemophilia can be managed using desmopressin and aminocaproic
acid for many dental procedures. Factor VIII replacement is needed for patients
with more severe hemophilia. Patients who are low responders for inhibitors
(antibody response to factor VIII) require higher doses of factor VIII. Patients
who are high responders are most difficult to manage and require activated
factor VII, porcine factor VIII, steroids, or other special preparations such as
prothrombin complex concentrates or activated prothrombin complex
concentrations.
4- Consultation
The patient’s hematologist must be consulted before any invasive dental
procedures are performed. The severity of disease must be established. The
presence of inhibitors and level of response to factor VIII need to be
determined. Determine if the patient can be managed with desmopressin and
aminocaproic acid. Establish the type and dosage of factor replacement needed
for invasive dental procedures or surgery. Determine if the patient can be
managed in the dental office or will require hospitalization.
5- Devices
Splints: may be constructed before multiple extractions or surgical procedures
in patients with severe hemophilia.
Drugs: Avoid all drugs that may cause bleeding, such as aspirin and other
NSAIDs, certain herbal medications, and over-the-counter drugs containing
aspirin.

6- Emergencies
Excessive bleeding may occur after invasive dental procedures or surgery.
Systemic and local means may be required to control the bleeding. Allergic
reactions may occur in patients receiving factor replacement.
7- Follow-up
Patients should be seen and examined for signs of allergy or bleeding within
24 to 48 hours after surgical procedures
 Blood dyscrasias
Disorders of the RBCs
1- Anemia
Anemia is the reduction in the oxygen carrying capacity of the blood, it is associated
with the decreased number of circulating RBCs or abnormalities in the Hemoglobin
(Hb) contained in the RBCs, which is the oxygen carrying molecule of the
erythrocytes, it is also responsible for the transport of CO2. Hb is a heterogeneous
group of proteins consisting of 4 globin chains and 4 haem (heme) groups. In anemia
Hb level is below 12 g/dl in adult female and below 13 g/dl in adult male. Anemia
is not a disease but rather a feature or symptom that results from many underlying
causes.

Types of anemia:
• Deficiency anemias: Iron deficiency anemia; it is caused by blood loss, poor iron
intake, poor iron absorption or increased demands for iron. It is more common in
women than in men due to blood loss during menstruation and pregnancy. Vitamin
B12 (cobalamin) deficiency, Folate (Folic acid) deficiency and Pernicious anemia;
(Vit. B12 and folic acid are needed for RBCs formation and growth within the bone
marrow. Vit B12 is bound to gastric intrinsic factor secreted by the parietal cells
and absorbed in the terminal ileum, deficiency of the intrinsic factor causes
Pernicious anemia).
• Hemolytic anemias: Hemoglobinopathies; these are inherited abnormalities of the
Hb formation like Sickle cell anemia and Thalassemia. Inherited abnormal function
or structure of erythrocytes; Erythrocyte metabolic defects as in Glucose-6-
Phosphate Dehydrogenase deficiency (G6PD). And Erythrocyte membrane defects
as in Spherocytosis, Ovalocytosis and Stomatocytosis. Damage to erythrocytes;
which could be autoimmune, drug induced or infective. Worldwide Malaria is the
most common cause of hemolytic anemia.
• Other anemias: Aplastic anemia; it is a pancytopenia with a non-functioning bone
marrow, many cases are idiopathic but possible causes include: Chemical like
Benzene, drugs, hepatitis virus, irradiation and graft versus host disease.
 Anemia caused by bone marrow infiltration by abnormal cells; like in Leukemia and
Multiple Myloma.
Anemia associated with systemic diseases; like in chronic inflammation and
connective tissue diseases such as Rheumatoid Arthritis, Liver disease,
Hypothyroidism, Hypopituitarism, Hypoadrenocorticism, Uremia and HIV
infections.
Oral manifestations
Pale mucosa, oral ulcerations, angular cheilitis, glossitis and loss of papillae
with atrophic changes in the oral mucosa.
patients with iron deficiency anemia may develop Plummer-Vinson syndrome
and burning mouth symptoms.
patients with hemolytic anemia, there may be oral evidence of jaundice due to
excessive red cells destruction, the trabecular pattern of bone may be affected
due to hyperplasia of marrow elements so radiographs show enlarged marrow
spaces and osteoporosis, the trabeculae between the teeth appear horizontal
(stepladder).
Skull radiographs show hair on end appearance due to the new bone formation
on the outer table of the skull. Vaso-occlusive events can lead to osteomyelitis,
necrosis and peripheral neuropathy. Dental hypoplasia and delayed eruption of
teeth often occur.

Dental management

1- Identification of the conditions associated with anemia through obtaining

careful history, the questions should include history of dietary intake,
malnutrition, alcohol or drug use, history of blood loss especially for women
during menstruation and pregnancy. The clinician should also identify signs
and symptoms of anemia and can also order some screening tests, if the
results of one of the tests or more are abnormal, the patient should be
referred for medical evaluation and treatment.
2- the clinician should ensure that the patient's underlying condition is under
therapeutic control before proceeding with routine dental care. Patients with
signs and symptoms of anemia and Hb level below 11 g/dl with abnormal
heart rate or reduced oxygen saturation (below 91% in oximetry) are
considered unstable and routine dental treatment should be deferred.
3- Local anesthesia (LA) is satisfactory for pain control, conscious sedation
can be given only if there is supplemental oxygen, elective operations under
general anesthesia (GA) are not carried out when Hb level is below 10 g/dl.
4- In patients with G6PD deficiency, certain drugs should be avoided since
they can cause hemolysis, such as Sulfonamides (Sulfamethoxazole),
Aspirin, Chloramphenicol and to a lesser extent Penicillin, Strepromycin
and Isoniazide. Also, dental infections should be avoided and if they occur,
they should be treated effectively.
5- In patients with Sickle cell anemia, routine dental care can be provided for
stable patients during non-crisis period, appointments should be short and
the procedures should be not complicated, oral infections should be avoided,
LA without vasoconstrictor for routine dental care is used while for surgical
procedures LA with vasoconstrictor 1:100000 can be used. Barbiturates and
strong narcotics should be avoided and Diazepam used when sedation is
needed, prophylactic Antibiotics for surgical procedures are used, liberal
use of Salicylates should be avoided and pain control can be achieved with
acetaminophen (Paracetamol) and Codeine. In general infection,
dehydration, hypoxia, acidosis and cold should be avoided in patients with
Sickle cell anemia because the can precipitate acute crisis.

2- Polycythemia
It is an expansion mainly in the red cell population, it may be primary and
idiopathic associated with normal erythropoietin level (Polycythemia Rubra
Vera) PRV. It can also be secondary to tumors that release erythropoietin
hormone. PRV is a disease of elderly and of smokers, it has a slight male
predilection. Diagnosis of Polycythemia is made when Hb level is above 16.5
g/dl and hematocrit 48% in women and when Hb is above 18.5 g/dl and
hematocrit 52% in men.
Dental management
• LA regional blocks should be avoided if possible.
• Conscious sedation can be given.
• GA is allowed.
• Susceptibility to thrombosis and hemorrhage should be considered.
• Cytotoxic chemotherapy may cause oral complications that require
management.
WBCs Disorders
1- Leukemia
Is cancer of the WBCs that affects the bone marrow and circulating blood. It
involves exponential proliferation of lymphoid or myloid cells. Leukemias is
classified by the clinical course into: acute and chronic, and by the cell of origin
into: lymphoid or myloid (non-lymphoid). In acute leukemia there is a rapidly
progressive disease that result from accumulation of immature, functionless
WBCs in the bone marrow and blood, it is more common than chronic
leukemia. While in the chronic leukemia there is slower onset and the cells are
more mature. There are 4 types of leukemia with many subtypes:
1. Acute Lymphoblastic Leukemia ALL, it is the most common type in
children.
2. Acute Mylogenous Leukemia AML, the most common type in adults.
3. Chronic Lymphocytic Leukemia CLL, the second most common type in
adults.
4. Chronic Myloid Leukemia CML.

Oral manifestations
Are more common in acute leukemia than in chronic leukemia, they include:
• Localized or generalized gingival enlargement, caused by infiltration of
immature WBCs, it occurs in about 35% of acute leukemias and 10% of the
chronic leukemias.
• The gingiva bleeds easily, sometimes spontaneously oral hygiene measures
and chemotherapy may cause resolution.
• Oral ulcerations.
• Recurrent oral infections, due to the immature WBCs and as a complication
of chemotherapy.
• Localized mass of leukemic cells in the gingiva and other site of the oral
cavity, it is termed Chloroma (Granulocytic Sarcoma).
• Pallor of oral mucosa.
• LAP.

2- Lymphoma
Lymphoma is a solid malignant tumor that originate in the lymph nodes or
extranodal lymphoid tissues in any part of the body. Lymphoma comprises
Hodgkin's lymphoma or disease and non-Hodgkin's lymphoma NHL. NHL is
more common than the Hodgkin's type.
 1. Hodgkin's disease; it is a neoplasm of B lymphocytes; it contains a
characteristic tumor cell (Reed Sternberg cell). The cause is unknown but
EBV may be implicated. It presents as a painless enlargement of non-
tender lymph nodes involving head and neck, axillary, mediastinal or
groin lymph nodes. Fever, night sweats, fatigue and weight loss may be
experienced by the patient. The diagnosis is based on nodal biopsy and
bone marrow aspirate. Medical management requires staging on the basis
of history, physical examination, lab. Findings and imaging.
2. Non-Hodgkin's lymphoma; a large group of lymphoproliferative disorders
of either B lymphocytes (more than 80% of the cases) or T lymphocytes
origin. There are many types of NHL. The cause is unknown but some
genetic factors and chromosomal abnormalities in addition to other
environmental factors such as infection with EBV, irradiation and drugs
were implicated as possible causative factors. The clinical presentation
includes; LAP, fever, weight loss, abdominal or chest pain and extranodal
tumors. The diagnosis is based on biopsy of the lymph nodes or extranodal
tumor. Proper staging is required which consists of blood investigation,
imaging and bone marrow biopsy.
Oral manifestations
• Cervical LAP.
• Intraoral tumors that may involve Waldeyer's ring (named after the German
anatomist Heinrich Wilhelm Gottfried von Waldeyer Hartz), salivary glands,
mandible, palate, gingiva or floor of the mouth.
• Oral ulcerations.
• Oral complications secondary to treatment include; burning mouth symptoms,
xerostomia, infections, trismus, impaired craniomandibular growth and
osteoradionecrosis.

Burkitt's Lymphoma
It is an aggressive type of B cell NHL. It is the most common lymphoma of
children. Types of Burkitt's lymphoma:
1. the endemic or African type.
2. non-endemic type, occurs in western societies.
 3. recently described type associated with HIV infected individuals.

Oral manifestations
Include; tumors of the maxilla or mandible that cause bone destruction,
mobility of the teeth, pain and paresthesia. On radiograph it appears as an
osteolytic lesion with poorly demarcated margins.

Multiple Myeloma
It is a lymphoproliferative disorder that results from overproduction of cloned
malignant plasma cells resulting in bony lesions involving the skeletal system.

Oral manifestations
• Painful bony lesions, that appear as osteolytic punched out lesions which may
be associated with cortical bone expansion.
• Extramedullary plasma cell tumor.
• Deposition of Amyloid in soft tissues like tongue.
• Osteonecrosis of the bone associated with Bisphosphonates treatment; it
usually appears after surgery especially tooth extraction as a painful, non-
healing socket. Treatment is directed to limiting the progression of necrosis
through debridement, irrigation with antiseptics and antibiotics.

To minimize the likelihood of developing necrosis:

• Early treatment of any source of odontogenic infection preferably before
starting treatment with Bisphosphonates.
• Non-surgical approaches are to be preferred.
• If extraction is required it should be as conservative as possible.
• The risk of necrosis should be discussed with the patient.

Dental management of WBCs Dyscrasias

• The clinician attempts to identify and recognize the presence of WBCs
disorders through obtaining a thorough history about the signs and symptoms of
these disorders, such as easy bruising or bleeding tendency, also family history
of WBCs disorders.
• Thorough extraoral and intraoral examination of the head and neck, oral cavity
and oropharynx to identify any abnormalities that are suggestive of WBCs
disorders. Screening blood investigations may be needed and if the results are
abnormal, the patient is referred for further evaluation and routine dental care
can be deferred.
Dental management of patients with diagnosed Leukemia, Lymphoma and
Multiple Myloma It involves the three phases of the medical therapy:
3. Pretreatment assessment and preparation of the patient: Full knowledge of the
patient's condition is required, the aim of this phase is to prevent oral infections,
all potential sources of infection must be eliminated through restorative,
periodontal and surgical treatment preferably 3 weeks prior to medical treatment.
Oral hygiene measures should be encouraged. When extraction is planned it
should be as conservative as possible avoiding any hemostatic packing agents
and attaining primary closure.
Prophylactic antibiotic is recommended before oral surgical procedure, 2 g oral
Penicillin 1 hour before the procedure, 500 mg 4 times daily for 1 week.
Patients with platelet count below 50.000/mm³ should not undergo oral surgical
procedures unless correction by transfusion is carried out.
4. Oral health care during medical treatment: during treatment the patient is
susceptible to many oral complications that require care:
• Mucositis; appear 7-10 days after initiation of treatment and resolve after it.
The non-keratinized mucosa is more severely affected. Oral hygiene measures
should be maintained to minimize infection, antiseptic and antimicrobial mouth
washes e.g. Chlorhexidin are recommended, topical anesthetics and systemic
analgesics can be given.
• Neutropenia and Infection; neutropenia leads to gingival inflammation, oral
ulceration and infection which can be severe but with minimal clinical signs.
Unusual bacterial infections, fungal and viral infections occur in patients with
Leukemia, Lymphoma and Multiple Myloma on chemotherapy and require
treatment. When oral infections develop, a specimen of the exudate should be
sent for culture and antibiotic sensitivity tests.
• Bleeding; thrombocytopenia may case submucosal hemorrhage and sometimes
spontaneous gingival bleeding, oral hygiene measures should be improved, when
bleeding occurs local hemostatic measures should be used first like using
pressure, gelatin sponge with thrombin or the use of oral antifibrinolytic agents.
If these measures fail transfusion may be needed.
• Graft versus host disease; it occurs after bone marrow transplantation when
immunologically active donor T cells react against host tissues, it can be acute
(within 2-3 weeks) causing rash, mucosal ulcerations, increased liver enzymes
and diarrhea. Or it could be chronic (3-12 months) producing features like
Sjögren syndrome, scleroderma, lichenoid changes, xerostomia, mucositis,
dysphagia and damage to liver. It can be prevented by corticosteroids and
immunosuppressive drugs.
• Adverse effects of drugs; such as gingival overgrowth with patients taking
Cyclosporine.
• Disturbance of growth and development; due to treatment with chemotherapy
and radiotherapy during childhood leading to micrognathia, malocclusion and
teeth abnormalities.

3. Posttreatment management: patients in remission state can have routine dental

care while patients with poor prognosis should receive emergency care only.
When invasive procedures are planned (e.g. oral surgery), platelet count and
bleeding time should be investigated, the patient's physician should be consulted.
In patients with surgically removed spleen, prophylactic antibiotic is needed,
since they are at risk of bacterial infections, especially in the first 6 months after
splenectomy. In patients with acute symptoms, routine dental care should be
deferred. LA regional block should be avoided if possible, in patients with
bleeding tendency. Conscious sedation can be given and GA is allowed.