M.

G IN
ORAL
MEDICINE

2013-2014
Hematologic Diseases
18 Pages

M.G IN ORAL MEDICINE | Hematologic Disease

1 Hematologic Disease
Hematologic
Disease
Red Blood Cell
Disorders
Polycythemia
Erythrocytosis
Absolute
Primary
Secondary
Relative
Anemia
Etiology
Blood Loss
Decreased
Production
Increased
Destruction
Size
Microcytic
Normocytic
Macrocytic
Conc. of Hb
Hypochromic
Normochromic
White Blood
Cell Disorder
Quantitative
Disorder
Qualitative
Disorder

Hematologic Diseases




















Red blood cell disorder
A) Polycythemia = Erythrocytosis
Erythrocytosis describes conditions with an increase in circulating red blood cells (RBCs),
characterized by a consistently raised hematocrit (HCT)
It is classified into
a) Absolute Erythrocytosis (true increases in red cell)
b) Relative Erythrocytosis (normal red cell, reduced plasma volume)
Absolute Erythrocytosis are usually subdivided:
a) Primary: excessive proliferation of erythroid elements independently of extrinsic
influences or by responding inadequately to them. (e.g. polycythemia Vera)
b) Secondary: increased erythropoietin production to compensate for hypoxia, (may be
caused by lowered oxygen tension as; High altitude, Heart disease, Pulmonary
disease).







M.G IN ORAL MEDICINE | Hematologic Disease

2 Hematologic Disease
Primary (Polycythemia Vera)
It is a rare disorder, of unknown etiology (may be genetic)
RBCs increase 6-12million/mm
3

Peak incidence in the sixth decade

Clinical Manifestations
o May be asymptomatic
o Patient angry face appearance.
Skin: purplish red (face, neck, ears, hands, feet.
Superficial veins: dark, distended.
o headache
o dizziness
o tinnitus
o Spleenomegaly

Oral Manifestations:
o Purplish red oral mucosa, gingiva & tongue.
o Tongue as if painted crystal violet
o Varicositis in the ventral tongue
o Erythematous, edematous gingiva.
o Petechiae, ecchymosis of oral mucosa.

Prognosis:
o The patient blood is characterized by high viscosity which increase the tendency for
thrombosis
o Transformation to acute myeloid leukemia.

Treatment:
o Treatment of blood hyperviscosity by
Phlebotomy (to remove RBCs)
Chemotherapy
Radioactive phosphorus (32P)
Myelosuppressive therapy (Hydroxyurea, -interferon)
o low-dose aspirin therapy as prophylaxis of thrombotic complications
o Bone marrow transplantation

Oral considerations:
o Complete blood count is essential before treatment
o Reduce hemoglobin level below 16g/dl and hematocrit below 2%
o Control of hemorrhage after dental surgery should be considered.











M.G IN ORAL MEDICINE | Hematologic Disease

3 Hematologic Disease
Anemia
Etiology
Blood Loss
Iron Deficiency
anemia
Plummer Vinson
Syndrome
Decreased
Production
Pernicious
anemia
Folic acid def.
Aplastic anemia
Increased
Destruction
Intracorpuscular
Defect
Extracorpuscular
Defect
Enviromental
factor
Size
Microcytic Normocytic Macrocytic
Conc. of Hb
Hypochromic Normochromic
B) Anemia
Decrease in the normal amount of the circulating RBCs & reduction in Hemoglobin (Hb)
concentration














1) Blood loss
a. Iron Deficiency Anemia
Microcytic, Hypochromic
It is a microcytic hypochromic anemia due to inadequate supply of iron for normal
hemoglobin synthesis in developing erythroid cells in the bone marrow.

Cause:
1. Chronic blood loss
from GIT: from hemorrhoids, peptic ulcers, esophageal varices, or carcinoma
from menstrual cycle and uterine bleed
2. Impaired iron absorption (gastrectomy, metabolic syndrome).
3. Inadequate iron intake.
4. Increased iron requirement (e.g. pregnancy; added iron demands of the fetus)










M.G IN ORAL MEDICINE | Hematologic Disease

4 Hematologic Disease
Clinical Features:
1. General:
o Pallor (of skin & palpebral conjunctiva), Fatigue, dyspnea,
palpitation, tachycardia.
2. Cutaneous:
o Nails: pale, brittle, split, spoon shaped (Koilonychia).
3. Oral Manifestations:
o Glossitis with different degrees of atrophy of fungiform and filliform papillae
o Erythernatous mucositis
o Recurrent aphthous stomatitis
o Pale oral mucosa
o Angular cheilitis
o Oral candidiasis
o Burning mouth for several months to 1 years duration.

Lab. Findings:
o RBCs (3 - 4 million/mm3).
o Hb conc.
o MCV decreased
o MCH
o MCHC
o Serum Fe.
o TIBC increased Increase

Treatment:
o Eliminate cause.
o Ferrous sulfate administered at 325 mg (60 mg iron) orally three times daily
o Parental iron (in cases of iron malabsorption or partial gastrectomy).
o High protein diet.

Dental considerations:
o Physician consultation prior to surgical treatment is recommended.
o When the hemoglobin is less than 8 g/dl, general anesthesia should be avoided and the
potential for clinical bleeding and faulty wound healing should he recognized.
o Narcotic use should be avoided for those with severe anemia,
o Dentists should be aware that anemia places a patient at increased risk for ischemic
heart disease.














Decrease

M.G IN ORAL MEDICINE | Hematologic Disease

5 Hematologic Disease
b. Plummer-Vinson Syndrome
(Patterson-Kelly Syndrome)
(Sideropenic dyspliagia)
Microcytic, Hypochromic.

It is a rare syndrome with the classic triad
1. Anemia
Pallor (of skin & palpebral conjunctiva), Fatigue, dyspnea, palpitation,
tachycardia
Nails: pale, brittle, split, spoon shaped (Koilonychia).
2. Glossitis
Smooth, Red, Painful atrophic tongue
It is associated by angular cheilitis
3. Dysphagia
Patient complains of food sticking in the throat
The dysphagia may be intermittent or progressive over years, is usually
painless and limited to solids, and sometimes is associated with weight loss.
It results from esophageal muscular degeneration and stenosis or webs of
the esophageal mucosa
Relative degrees of achlorhydria are usually present
Complications:
o Oral, pharyngeal or esophageal carcinoma.

Mechanism:
o Mucosal atrophy due to depletion of iron.

Treatment:
o Ferrous sulphate 200mg 3 times /day.
o Glossitis improves within 3 weeks.
o Angular cheilitis improves at slower rate.
o In cases of significant obstruction of the esophageal lumen by esophageal webs/
strictures with persistent dysphagia mechanical dilation of the web may be required.
o patient should be followed closely since there is an increased risk of squamous
carcinoma of the pharynx and esophagus


2) Decreased RBCs Production
Megaloblastic Anemias
Macrocytic Normochromic.

A group of disorder chiefly affects cells of rapid turnover; (hematopoitic cells, epithelial cells,
GIT mucosa, and oral mucosa]
Deficiency of vit B 12 and folic acid deficiency are the major causes of Megaloblastic anemia.






M.G IN ORAL MEDICINE | Hematologic Disease

6 Hematologic Disease

a. Pernicious Anemia

Megaloblastic or pernicious anemia is an autoimmune disease resulting from autoantibodies
directed against intrinsic factor (a substance needed to absorb vitamin B12 from the
gastrointestinal tract) and gastric parietal cells.
Vitamin B12 is necessary for the formation of RBCs.

Clinical Features:
o General:
Pallor (of skin & palpebral conjunctiva), Fatigue, dyspnea, palpitation, tachycardia
Nails: pale, brittle, split, spoon shaped (Koilonychia).
o Neurologic: tingling sensation fingers, toes numbness, incoordination.
o Psychiatric ;Irritability, personality changes, Mild memory impairment, dementia,
Depression
o Cardiac: Possible increased risk of myocardial infarction and stroke

Oral manifestations:
o Tongue: sore, fiery red, burning sensation in the tongue, lips, buccal mucosa, and other
mucosal sites.
o The tongue and mucosa may be smooth or patchy areas of erythema.
o dysphagia and taste disturbance may be present
o Aphthous like ulcers

Laboratory Findings
o RBCs
o Platelets
o Increased MCV
o MCHC Normal.
o Megaloblastic marrow changes
o Serum B 12 decreased (N. 200-600 pg/mi).
o Circulating antibodies against Intrinsic factor.
o Schilling test +ve
o Achlorhydria.

Treatment:
o weekly intra- muscular injections of vitamin B12 or large oral doses
o It should be continued for the rest of the patients life
o It corrects the hematologic changes but only arrest not correct the neurologic changes.

b. Folic acid deficiency anemia
Cause:
o Inadequate intake (diet devoid of leafy vegetables).
o Increased demand in pregnancy
o Intestinal malabsorption.
o Drugs: barbiturates, phenytoin, oral contraceptives.

Clinical Features:
o As pernicious anemia. No neurologic symptoms

Abnormally large.

M.G IN ORAL MEDICINE | Hematologic Disease

7 Hematologic Disease
Oral manifestations:
o Severe angular cheilitis.
o Glossitis.
o Recurrent aphthae
o Severe ulcerative stomatitis and pharyngitis

Lab. Findings:
o MCV increased
o MCHC
o Serum B12
o Schilling test -ve
o Serum folate decreased
o (Folic acid N. value: S-20 g/ml).

Treatment:
Oral folic acid tablets 1- 5mg/day

c. Aplastic Anemia
Pancytopenia (bone marrow aplasia)
Normocytic normochromic

Aplastic anemia (AA) is a rare blood dyscrasia in which peripheral blood pancytopenia results
from reduced or absent blood cell production in the bone.

Cause:
o Idiopathic.
o 2ry Bone Marrow toxicity Due to:
Viruses
Radiation
Toxins
Drugs (as sulfonamides, anti-rheumatic & chloramphenicol).
Chemicals as paint solvents, benzol.


Clinical Features:
o Anemia: General manifestations of anemia.
o Leukopenia: Increased susceptibility to infection. (Candidiasis and viral infection,)
o Thrombocytopenia: Purpura and bleeding, epistaxis or gingival bleeding.

Oral manifestations:
o Pallor, gingival bleeding, Petechiae & ecchymosis.
o Ulcers as in neutropenia, surrounded by little erythema.
o Advanced cases resemble acute leukemia.







Normal


M.G IN ORAL MEDICINE | Hematologic Disease

8 Hematologic Disease
Lab. Findings:
o MCV
o MCHC
o Hb
o RBCs
o Platelets
o WBCs

Treatment:
o Eliminate cause.
o Supportive therapy with blood transfusions to correct anemia and thrombocytopenia
o immunosuppression (with antithymocyte globulins and cyclosporine) is effective at
restoring blood cell production in the majority of patient










3) Increased destruction of RBCs
(Hemolytic Anemia)

The normal RBC life span is 90 to 120 days in the circulation. Hemolytic diseases result in
anemia if the bone marrow is not able to replenish adequately the prematurely destroyed
RBCs.


Accelerated destruction of RBCs can be caused by:
1. Intra corpuscular defect
o a molecular defect inside the red cell
o two types
Hemoglobinopathies ex) sickle cell anemia and thalassemia
Enzymopathy: ex) glucose -6- phosphatase dehydrogenase deficiency
2. extra corpuscular defect
o an abnormality in membrane structure and function
3. Environmental factor
o Such as an autoimmune hemolytic disease, infection, hyperspleenism.









Normal
Decrease

Fanconi anemia
o Fanconi anemia is inherited aplastic anemia that manifest in children
o Fanconi anemia is associated with brown skin pigmentation
o hypoplasia of kidney and spleen
o mental and sexual retardation


M.G IN ORAL MEDICINE | Hematologic Disease

9 Hematologic Disease
Intra corpuscular defect
a. Hemoglobinopathies
Hemoglobin molecule consists
2

2
globin chains (amino acid) bound to a single Heme.
Defects in globin portion of Hb so RBC carry abnormal Hb which will lead to hemolysis










Sickle Cell Disease/Sickle Cell Anemia
Normocytic, Normochromic.
It is a hereditary hemolytic anemia.
Characterized by a hemoglobin gene mutation, consisting of replacement of glutamic acid by
valine in chain globin.
As a result, the erythrocytes have their normal biconcave discoid shape distorted, generally
presenting a sickle-like shape, which reduces both their plasticity and lifetime from the normal
120 days average down to 14 days.
The Hb forms a sickle cell shaped crystal (HgS).
sickling is reversible although repeated sickling cause the cell to lose their flexibility and remain
deformed
This result in the underlying anemia and hypertrophic bone marrow.



Sickling is precipitated by:
o Hypoxia (high altitude, general anesthesia)
o Viral and bacterial infection
o Dehydration.
o Acidosis.

Sickling can lead to:
o Hemolysis (destruction of sickle cell) with features of
anemia
o Increased viscosity and clumping of cells in the microcirculation leading to ischemia,
thrombosis and infarction.
o The disease is hereditary and manifest itself as the sickle cell trait or sickle cell anemia

Sickle cell trait (HbAS)
o Heterozygous (one -chain abnormal).
o 20 - 40 % of Hb is HbS, rest is HbA
o Asymptomatic, normal life
o Sickling caused by: reduced 0
2
tension (general anesthesia, high altitude).


Note:
Adult hemoglobin (HbA) is composed of
2

2

Fetal hemoglobin (HbF) is composed of
2

2

Normal adult Hb is HbA.
At birth 80% Hb is HbF.
At 6 months HbF <5%.
Adult life HbF is < 1%.


M.G IN ORAL MEDICINE | Hematologic Disease

10 Hematologic Disease
Sickle cell anemia (HbSS)
o Occurs mainly in blacks.
o 2 chains are abnormal (Homozygous).
o 75% Hb is HbS remainder is HbF.
o Appears by 3 months of life.

Clinical manifestation:
o This disease characterized by periods of latency interrupted by periods of acute crisis.
o The patient shows marked under development
o Manifestations of anemia and hemolysis (pallor, fatigue, dyspnea and jaundice, Cardiac
failure may develop)
o Manifestation following stasis of blood and vasoocclusion (splenic infarction, leg ulcers,
bone pain, stroke)
o Aplastic crisis may develop from infection or hypersensitivity reaction which results in bone
marrow suppression

Oral manifestations:
o Oral mucosa pale, yellow tinge.
o Delayed teeth eruption.
o Enamel hypoplasia.
o Increased overbite and overjet (maxillary overgrowth)
o Susceptible osteomyelitis.
o vasoocclusion and interruption of the blood supply can result in
anesthesia of the inferior alveolar nerve
pulpal necrosis
facial pain or sensory changes in the distribution of the inferior alveolar nerve

Radiographic changes:
o It affect Jaw bones, skull, vertebrae, long bones:
a) Osteoporosis:
2ry to bone marrow hyperplasia to compensate short life span of RBCs.
b) Osteosclerosis:
2ry to thrombosis acts nidus for calcification.

o Lateral skull view:
Marked thickening of the diploe with trabeculae running perpendicular to outer and
inner table and thin cortex give the characteristic (hair on end) pattern.

o Jaw bones: osteoporosis & Osteosclerosis.

o Alveolar bone:
Trabecular pattern horizontal rows between roots --> step ladder appearance.
Lamina dura: dense, distinct, intact,


Lab Findings:
o Hb -->decreased
o Normocytic, Normochromic.
o Sickling test +ve.
o Hb electrophoresis.


M.G IN ORAL MEDICINE | Hematologic Disease

11 Hematologic Disease
Treatment:
o Only symptomatic treatment
o The precipitating factors for sickling should be avoided.
o Acute attack require (IV fluid, oxygen, antibiotics and analgesics and anti-inflammatory to
manage acute pain of vasoocclusive attacks)
o use of folic acid dietary supplement
o Blood transfusion indicated during aplastic crisis

Dental Considerations:
o Avoid dental procedures during crisis.
o Local anesthesia recommended no vasoconstrictor.
o General anesthesia is hazardous.
o Infection treated immediately.
o Surgery carried out under antibiotic cover.
o Poor wound healing
o Management of pain that may be due to: osteomyelitis, infarction, odontalgia

Thalassemia
Microcytic hypochromic
Thalassemia is a genetic disorder of hemoglobin synthesis characterized by a disturbance of
either alpha or beta hemoglobin chain production.
As a result RBCs are microcytic hypochromic.
It is classified into
o Alpha Thalassemia.
o Beta Thalassemia
Thalassemia minor (trait)
thalassemia major (coolys anemia)

Thalassemia minor (trait) ()
Heterozygous, usually asymptomatic.
Aggravated by: pregnancy, illness.
Resembles iron deficiency anemia.
No therapy

Thalassemia major (Homozygous) ()
Cooleys anemia (Mediterranean)
Clinical Features:
1- Severe Anemia:
o Ashen gray skin color (due to combination of pallor, jaundice and hemosiderosis)
o irritability, weakness, dyspnea,
o sore painful tongue (decreased folate)
o patient may present with Hepatospleenomegaly (due to extramedullary hemopoiesis)

2- Iron overload (Hemosiderosis):
o Patients survival depends on repeated blood transfusion which results in iron overload.
o Iron deposits causes functional abnormalities in various organs and tissues: heart, liver,
pancreas, skin.
o Parotid gland - painful swelling.


M.G IN ORAL MEDICINE | Hematologic Disease

12 Hematologic Disease
3- Dentofacial changes:
o Large head, mongoloid features frontal bossing
o (prominent bone short nose, depressed nasal bridge)
o Maxilla - enlarged maxillary overbite
o Mandibular prominence
o Forward drifting and spacing of teeth

Radiographic changes:
A. Lateral skull view:
o Thickening of the diploe, Hair on end appearance
B. Alveolar bone:
o Decreased density, loss trabecular detail and thinning of the
cortical bone.
o Rarefactions between roots of teeth which will lead to Chicken
wire appearance.

Oral manifestations:
o Marked development of maxilla > B.M expansion.
o Open bite, spacing & drifting of teeth.
o Oral mucosa pale (esp,, Hard & soft palate).
o Sore painful tongue (decreased folate).
o Painful swelling of parotid gland-iron deposits.
o Delayed dental development
o Short roots
o Discoloration of enamel and dentine due to iron deposition.

Diagnosis & Lab. Findings:
o Clinical appearance (Mongoloid face).
o Blood film, (microcytic, hypochromic).
o Decreased Hb and increased serum iron.
o Decreased serum folate due to utilization for erythropoiesis.
o Hb electrophoresis: 90% HbF & rest HbA2

Treatment
o Regular blood transfusion
o iron chelation by continuous injection of(deferoxamine) to resolve the iron overload,
o Treatment of complications and possible infections


Glucose -6- phosphatase dehydrogenase deficiency
it is an hereditary enzyme defect that causes episodic hemolysis because of a reduced
capacity of RBCs to deal with oxidative stresses.
patients are more likely to manifest neonatal jaundice
risk of developing acute hemolytic anemia in response to: fava beans, viral or bacterial
infections, and drugs.






M.G IN ORAL MEDICINE | Hematologic Disease

13 Hematologic Disease
White Blood Cell Disorder
A) Quantitative Leukocyte Disorder

1. Granulocytosis
Increase in number of WBCs
Neutrophilia (an excess of neutrophils) is more common.
Causes of Neutrophilia are varied and include acute infections, acute myocardial infarction,
rheumatic fever, and hypersensitivity reactions, neoplastic diseases.

2. Agranulocytosis (granulocytopenia/Neutropenia)
Mostly due to decrease in neutrophils (no neutrophils found in peripheral circulation).

Etiology:
o Idiopathic.
o Secondary: drugs, viral infection, antibody-mediated destruction, myelosuppression &
irradiation.

Clinical Features:
o Fever, chills, fatigue.
o Mucosal ulcers, acute pharyngitis.
o Infection (characteristic feature) in the mouth, GIT, urinary tract, skin.
o Regional lymphadenopathy

Oral Features:
o Painful necrotizing ulcers: Gingiva, tongue & palate.
o Ulcers: large, deep, irregular, necrotic, no inflammatory reaction at margins.
o 2ry fusospirochetal infection foul odor.

Treatment:
o Eliminate the cause.
o Dental Management:
Parenteral antibiotics.
Topical antibiotics
Chlorhexidine mouth wash.
Topical anesthesia for painful ulcers.
No dental surgery performed.

3. Cyclic neutropenia
Cyclic neutropenia is a rare hematologic disorder, characterized by repetitive episodes of
fever, mouth ulcers, and infections attributable to recurrent severe neutropenia.
Neutropenia recurs with a regular periodicity of 21 days, persists for 3 to 5 days.
Infectious events are usually less severe than in severe chronic Neutropenia.
It is an aitosom3-cIominant disease caused by a gene mutation
It can during the first few years of life.





M.G IN ORAL MEDICINE | Hematologic Disease

14 Hematologic Disease
Clinical and Oral Manifestations
o Periodic oscillations of neutrophil counts associated with fever and mouth ulcers,
lymphadenopathy, and infections.
o Patient is healthy between neutropenic episodes

Dental considerations:
o Most common 2 manifestation=oral mucosal ulcers and periodontal disease
o Early management of infections and maintained good oral hygiene.
o Recall patient every 2-4 months

B) Qualitative disorder
1. Leukemia
Neoplastic proliferations of WBC, Abnormal increase in number of circulating immature
WBCs.
The malignant cells replace and turn off the normal marrow elements causing anemia,
thrombocytopenia, and deficiency of normal functioning leukocytes.

Etiology:
o Genetic factors play a role.
o Individuals with down syndrome have increased incidence with leukemia.
o Exposure to radiation with high dose, certain chemicals and drugs.

Leukemia is classified into


Acute leukemia
Acute leukemia occur at any age
ALL is commonly found in children
AML is more frequently in adults
The signs and symptoms results from either bone marrow suppression or infiltration of
leukemic cells into other organs
Gingival hyperplasia secondary to leukemia cell infiltration may be a first sign
Leukemia
Acute
Lymphocytic
Leukemia
(ALL)
Myoloid Leukemia
(AML)
Chronic
Lymphocytic
Leukemia
Mylocytic
Leukemia

M.G IN ORAL MEDICINE | Hematologic Disease

15 Hematologic Disease

Clinical manifestations:
o Anemia: fatigue, malaise, pallor,
o Thrombocytopenia: mucosal bleeding, Petechiae.
o Decrease leukocytic function: fever, local infections (infection of lung, urinary tract
skin...), Lymphadenopathy
o Localized tumors consisting of leukemic cell infiltrate.
o Chemotherapy-induced mucositis and infection, including herpes simplex ulcers and oral
candidiasis, are commonly observed complications of leukemia in the oral cavity

Oral Manifestations:
o Pallor of oral mucosa,
o Atrophy of tongue coating
o Oral & gingival bleeding Petechiae & ecchymosis
o Gingival Enlargement
o Oral ulceration -->Ulcers large, deep irregular, No
inflammatory halo
o Ulceration due Chemotherapy
o Infection(Viral, Bacterial, Fungal)
o Foul odor due to Spirochetal infection.

Oral Health Considerations
o Prechemotherapy dental assessment, maintenance of oral hygiene, and management of
periodontal infection to prevent oral and systemic complications during treatment.
o Symptomatic treatment for oral ulcers & candidiasis.
o Analgesic pain.
o Antifungal antiviral for oral lesions
o Drainage of abscessed tooth
o No surgery except emergency patient hospitalized
o Spontaneous gingival bleeding remove gross local factors, place subgingivally under
pressure absorbable gelatin saturated + thrombin

Chronic leukemia
Characterized by the presence of large number of well differentiated cells in the bone
marrow.
This distinguish chronic leukemia from acute leukemia in which immature cells predominate
and the untreated clinical course leads to death in months
less pronounced marrow failure than acute leukemia

Chronic mylocytic leukemia
Disorder resulting in myeloid marrow hyperplasia.
less pronounced marrow failure than acute leukemia have an indolent course that usually
lasts several years
Clinical manifestation
o No symptoms are noted for 3 to 5 years in which patients have no symptoms followed
by an accelerated phase and blast crisis, resembling acute leukemia [fever, weakness,
fatigue, anorexia, weight loss, Spleenomegaly; anemia, and infection)
o Oral presentations are not common, resemble acute leukemia but are less severe,


M.G IN ORAL MEDICINE | Hematologic Disease

16 Hematologic Disease
Chronic lymphocytic leukemia
More than 90%of cases involve the B lymphocytes and 5% of cases account for T-
lymphocytes
B lymphocytes do not carry out their normal immunologic function and do not differentiate
into normal immunologic producing plasma cells when exposed to antigen

Clinical manifestations
o asymptomatic phase last for years
o can be detected by routine hematology before any or when patients present with [fever,
night sweats, weight loss, fatigue),
o bone marrow infiltration causes anemia and thrombocytopenia
o Leukemic cell infiltrate effects of other tissues as skin mucosa, liver and spleen.
o Oral manifestations at presentation of CII are infrequent less severe than acute
leukemia, and generally related to bleeding.
o The oral lesion incidence rate increases once chemotherapy is initiated for treatment.

Multiple myeloma
It is a plasma cell neoplasm that is characterized by a bone marrow plasmacytosis.

Clinical Manifestations
o Symptoms include fatigue, weakness, weight loss, bone pain, and recurrent infections.
o This disease is characterized by a high capacity to induce focal osteolytic bone lesions,
diffuse osteopenia, and pathologic fractures.
o This result from increased osteoclast formation, osteoblast inhibition induced by mm
cells.

Oral Manifestations
o Patients can manifest soft tissue masses of the jaws.
o Punched-out lesions in the skull from the focal proliferation of plasma cells inside the
bone marrow, ranging from asymptomatic osteolytic lesions to pathologic fracture.

Lymphoma
Classification
o Hodgkins Disease
o Non- Hodgkins Lymphoma

Hodgkins disease
Malignant neoplasm of lymphoid tissue.
Etiology unknown.
Asymptomatic.
Enlarged cervical LNs.
Discrete rubbery not tender.

Clinical Features:
o LNs enlarged causing pressure on organs or ducts.
o Retroperitoneal LNs --> urinary obstruction.
o Mediastinal LNs -->Dysphagia, chest pain, cough, and dyspnea.
o BM invasion, invasion of spleen, liver, lung & spinal cord.
o night sweats, fever, and weight loss

M.G IN ORAL MEDICINE | Hematologic Disease

17 Hematologic Disease
o Hodgkins disease rarely presents as an extra nodal mass in the head and neck region.

Oral Health Considerations
o Patients who receive radiation in fields involving the cervical nodes will invariably have
their submandibular and sublingual salivary glands in the field and are at risk for
temporary, and occasionally permanent, xerostomia.

Non-Hodgkins Lymphoma
Malignant neoplasms, arise from lymph nodes.
Nodular or diffuse.
Mainly B-cell origin.
Poor prognosis.
Clinical manifestations
Slowly progressive, usually painless peripheral lymphadenopathy,
Extranodal involvement of the GIT, skin, bone marrow, sinuses, thyroid, or central nervous
system.
Systemic constitutional symptoms such as fever, chills, night sweats, and weight loss occur

Oral manifestations:
o Hodgkins disease rarely affects mouth.
o It may cause soft tissue swelling in pharynx, palate, tongue, gingiva or lips



-THE END-