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Chapter 9

Oral Manifestations of Systemic Diseases

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Outline Endocrine Disorders Blood Disorders Immunodeficiency Oral Manifestations of Therapy for Oral Cancer Effects of Drugs on the Oral Cavity Oral Manifestations of Systemic Diseases

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Oral Manifestations of Systemic Diseases

(pg. 288) Many systemic diseases are reflected in the oral

mucosa, maxilla, and mandible. Mucosal changes may include ulceration or mucosal

bleeding. Immunodeficiency can lead to opportunistic diseases

such as infection and neoplasia. Bone disease can affect the maxilla and mandible. Systemic disease can cause dental and periodontal

changes. Drugs prescribed for a systemic disease can affect oral

tissue.

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Oral Manifestations of Systemic Diseases (cont.)

Local factors may be involved in the manifestation of systemic disease in oral mucosa. The mucosa may be more easily injured due to

a systemic disease, and mild irritation and chronic inflammation may cause lesions that otherwise would not occur.

These may include Endocrine disorders, disorders of red and

white blood cells, disorders of platelets and other bleeding and clotting disorders, and immunodeficiency disorders

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Endocrine Disorders

Hyperpituitarism Hyperthyroidism Hypothyroidism Hyperparathyroidism Diabetes Mellitus Addison Disease

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Endocrine Disorders

(pg. 288) The endocrine system consists of a group

of integrated glands and cells that secrete hormones. The secretion is controlled by feedback

mechanisms. The amount of hormone circulating in blood

triggers factors that control production. Diseases may result from conditions

where too much or too little hormone is produced.

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Hyperpituitarism

(pgs. 288-289) Excess hormone production by the

anterior pituitary gland Caused most often by a benign tumor (pituitary

adenoma) that produces growth hormone Giantism results if it occurs before the closure

of long bones. Acromegaly results when hypersecretion

occurs during adult life.

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Clinical Features and Oral Manifestations of Hyperpituitarism (pgs. 288-289)

Affects both men and women, most commonly during the fourth decade of life Patients experience poor vision, light sensitivity,

enlargement of hands and feet, and an increase in rib size.

Facial changes Enlargement of maxilla and mandible may cause

separation of teeth and malocclusion. Frontal bossing and an enlargement of nasal bones may

lead to deepening of voice. Mucosal changes

May have thickened lips and macroglossia

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Clinical Features and Oral Manifestations of Hyperpituitarism (cont.)

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Diagnosis and Treatment of Hyperpituitarism

Diagnosis involves measurement of growth hormone.

Treatment often includes pituitary gland surgery.

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Hyperthyroidism (Thyrotoxicosis)

(pg. 289) Excess production of thyroid hormone

More common in women than men The most common cause is Graves disease

• Graves disease Appears to be due to an autoimmune disorder in

which a substance is produced that abnormally stimulates the thyroid gland

Other causes include hyperplasia of the gland, benign and malignant tumors of the thyroid, pituitary gland disease, and metastatic tumors.

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Clinical Features of Hyperthyroidism

Rosy complexion, erythema of the palms, excessive sweating, fine hair, softened nails The patient may have exophthalmos. Anxiety, weakness, restlessness, and cardiac

problems may also be associated.

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Oral Manifestations of Hyperthyroidism

May lead to premature exfoliation of deciduous teeth in children and premature eruption of permanent teeth Osteoporosis may affect alveolar bone. Caries and periodontal disease may appear

and develop more rapidly in these patients. Burning tongue also has been reported.

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Treatment of Hyperthyroidism

May include surgery, medications to suppress thyroid activity, or administration of radioactive iodine

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Hypothyroidism

(pg. 289) A decreased output of thyroid hormone

Causes include developmental disturbances, autoimmune disease, iodine deficiency, drugs, and pituitary disease

Cretinism• When it occurs in infancy and childhood

Myxedema• When it occurs in older children and adults

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Hypothyroidism (cont.)

Oral manifestations In infants

• Thickened lips, enlarged tongue, and delayed eruption of teeth

In adults• Enlarged tongue

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Hyperparathyroidism

(pgs. 289-290) Due to excessive secretion of parathyroid

hormone from the parathyroid glands The four parathyroid glands are located near

the thyroid gland. Parathyroid hormone plays a role in

calcium and phosphorous metabolism. Hyperparathyroidism is characterized by

elevated blood levels of calcium (hypercalcemia) and low levels of blood phosphorous (hypophosphatemia).

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Hyperparathyroidism (cont.)

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Hyperparathyroidism (cont.)

May be the result of hyperplasia of parathyroid glands, a benign tumor of one or more parathyroid glands, or a malignant parathyroid tumor Found in middle-aged adults Much more common in women than men

Parathyroid hormone increases the uptake of dietary calcium from the gastrointestinal tract and is able to move calcium from bone to circulating blood when necessary.

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Clinical Featuresof Hyperparathyroidism

Mild cases may be asymptomatic, or may have joint pain or stiffness. Lethargy and coma may occur with severe

disease.

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Oral Manifestations of Hyperparathyroidism

Well-defined unilocular or multilocular radiolucencies Microscopically, they appear to be CGCG

(central giant cell granulomas). Bone may have a mottled appearance.

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Diagnosis and Treatmentof Hyperparathyroidism

Measurement of parathyroid hormone blood levels May include serum calcium and phosphorous

measurements Treatment is directed at correcting the

cause of increased hormone production. Causes may include tumors, renal disease,

and vitamin D deficiency.

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Diabetes Mellitus

(pgs. 290-294) A chronic disorder of carbohydrate

metabolism characterized by abnormally high blood glucose levels These result from a lack of insulin, defective

insulin that does not work to lower blood glucose levels, or increased insulin resistance due to obesity.

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Diabetes Mellitus (cont.)

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Diabetes Mellitus (cont.)

Glucose normally signals beta cells of the pancreas to make insulin. The hormone is then secreted into the

bloodstream to facilitate the uptake of glucose into fat and skeletal muscle.

In the presence of insulin, fat and skeletal muscle cells can use glucose as an energy source.

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Diabetes Mellitus (cont.)

Without insulin, tissue is broken down to provide energy and weight loss occurs. A severe hyperglycemia can lead to diabetic

coma. Ketone can be produced by the breakdown of

fatty acids.• Ketoacidosis lowers the pH of blood.

Phagocytic activity of macrophages is reduced and neutrophil chemotaxis is delayed.

Collagen production is abnormal.

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Types of Diabetes

Insulin-dependent diabetes mellitus Type 1

Non–insulin-dependent diabetes mellitus Type 2

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Insulin-Dependent Diabetes Mellitus

(pgs. 291-292) Thought to be an autoimmune disease

Insulin-producing cells of the pancreas are destroyed.

3% to 5% of all diabetic patients have this type. Can occur at any age, the peak is at 20 Acute onset with polydipsia (excessive

thirst and intake of fluid), polyuria (excessive urination), and polyphagia (excessive appetite)

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Insulin-Dependent Diabetes Mellitus (cont.)

These patients will require insulin their entire lives. The current approach to management of these

patients involves multiple insulin injections and proper diet, exercise, and frequent determination of blood glucose levels.

But multiple injections of insulin can more readily lead to low blood sugar (hypoglycemia) and insulin shock (severe hypoglycemia).

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Insulin-Dependent Diabetes Mellitus (cont.)

New methods of treatment Nasal spray rather than injection Insulin pump

• A backup may be necessary in case the pump fails• Low insulin can lead to ketoacidosis, resulting in

nausea, abdominal cramps, disorientation, and fatigue

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Non–Insulin-Dependent Diabetes Mellitus

(pgs. 292-294) Characterized by insulin resistance

95% of all diabetic patients have this type of diabetes.

Usually occurs in patients 35 to 40 years of age or older

Many of these individuals are obese Obesity probably decreases the number of

receptors for insulin binding in sensitive tissues like fat or muscle.

Diet and weight reduction may control it in some individuals; others require oral hypoglycemic agents.

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Clinical Features of Non–Insulin-Dependent Diabetes Mellitus

(pg. 293) Atherosclerosis, a thickening of the blood vessel

wall from fibrofatty plaques, can lead to impaired circulation, causing impaired oxygenation and nutrition in tissue. This increases the risk of ulceration and gangrene of the

feet, high blood pressure, kidney failure, and stroke. Diabetic retinopathy in the eye can lead to

blindness. The nervous system may be affected. The person may have decreased resistance to

infection.

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Clinical Features of Non–Insulin-Dependent Diabetes Mellitus (cont.)

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Oral Complications of Non–Insulin-Dependent Diabetes Mellitus

(pgs. 293-294) Patients may have an increased prevalence of

oral candidiasis. Mucormycosis, a rare oral fungal infection that affects

the palate and maxillary sinuses, may be seen in uncontrolled or poorly controlled diabetes.

Bilateral asymptomatic parotid gland enlargement may occur. Xerostomia may be associated with uncontrolled

diabetes mellitus. Patients may have an accentuated response to plaque. Patients may have slow wound healing and increased

susceptibility to infection.

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Oral Complications of Non–Insulin-Dependent Diabetes Mellitus (cont.)

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Addison Disease

(pg. 294) Primary adrenal cortical insufficiency

In most cases, the cause of destruction of the adrenal gland is unknown – it may be an autoimmune disease.

It may be due to a tumor or tuberculosis. To compensate, the pituitary gland increases

production of ACTH.

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Addison Disease (cont.)

Clinical features This hormone causes stimulation of

melanocytes. Bronzing of the skin may occur, as well as

melanotic macules on oral mucosa. Treatment

Steroid replacement therapy

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Blood Disorders

Disorders of Red Blood Cells and Hemoglobin

Disorders of White Blood Cells Bleeding Disorders

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Blood Disorders (cont.)

(pg. 294) (Box 9-1) The complete blood count examines red

blood cells, white blood cells, and platelets. It provides information about the number of

each type of cell, the ratio of types, and the appearance of the cells.

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Disorders of Red Blood Cells and Hemoglobin

Anemia Iron Deficiency Anemia Pernicious Anemia Folic Acid and Vitamin B12 Deficiency

Anemia Thalassemia Sickle Cell Anemia Celiac Sprue Aplastic Anemia Polycythemia

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Anemia

(pgs. 294-295) A reduction in the oxygen-carrying

capacity of blood Most often related to a decrease in the number

of circulating red blood cells• Nutritional anemias

A deficiency in a substance required for the normal development of red blood cells, commonly vitamins

• Suppression of bone marrow stem cells

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Anemia (cont.)

Clinical features Pallor of skin and oral mucosa Angular cheilitis Erythema and atrophy of oral mucosa Loss of filiform and fungiform papillae on the

dorsum of the tongue

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Iron Deficiency Anemia

(pg. 295) An insufficient amount of iron is supplied to bone

marrow for red blood cell development. May occur as a result of deficient iron intake, blood loss

from heavy menstrual bleeding or chronic gastrointestinal bleeding, poor iron absorption, or an increased requirement for iron in situations such as pregnancy or infancy

Plummer-Vinson syndrome may result from long standing iron deficiency anemia. Includes dysphagia, atrophy of the upper alimentary

tract, and a predisposition to developing oral cancer

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Clinical Features and Oral Manifestations of Iron Deficiency Anemia

(pg. 295) Often asymptomatic, may have nonspecific

symptoms such as weakness and fatigue In severe cases may see angular cheilitis,

pallor of oral tissue, and an erythematous, smooth, painful tongue

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Clinical Features and Oral Manifestations of Iron Deficiency Anemia (cont.)

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Diagnosis and Treatment of Iron Deficiency Anemia

Laboratory tests show a low hemoglobin content and reduced hematocrit. Red blood cells appear smaller than normal

(microcytic) and light in color (hypochromic) Treatment

Dietary supplements

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Pernicious Anemia

(pgs. 295-296) Probably an autoimmune disorder in most

situations May be caused by removal of the stomach,

gastric cancer, or gastritis Caused by a deficiency in intrinsic factor

Intrinsic factor is secreted by parietal cells in the stomach; it is necessary for absorption of vitamin B12

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Clinical Features and Oral Manifestations of Pernicious Anemia

(pgs. 295-296) Weakness, pallor, and fatigue on exertion

May see nausea, dizziness, diarrhea, abdominal pain, loss of appetite, and weight loss

Angular cheilitis, mucosal pallor, painful atrophic and erythematous mucosa, mucosal ulceration, loss of papillae on the dorsum of the tongue, and burning and painful tongue

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Clinical Features and Oral Manifestations of Pernicious Anemia (cont.)

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Diagnosis and Treatment of Pernicious Anemia

Laboratory tests reveal low serum B12

levels and gastric achlorhydria (lack of hydrochloric acid) Red blood cells have megaloblastic anemia.

• Abnormally large and immature megaloblasts with nuclei

The Schilling test detects an inability to absorb oral vitamin B12

Treatment Injections of vitamin B12

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Folic Acid and Vitamin B12

Deficiency Anemia (pg. 296)

From dietary deficiencies Can occur in association with malnutrition May be found with alcoholism or pregnancy

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Oral Manifestations of Folic Acid and Vitamin B12 Deficiency Anemia

Oral manifestations are indistinguishable from those of pernicious anemia.

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Diagnosis and Treatment of Folic Acid and Vitamin B12 Deficiency Anemia

Based upon laboratory tests – serum assays of folic acid and vitamin B12

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Thalassemia (Mediterranean or Cooley Anemia) (pg. 296)

A group of inherited disorders of hemoglobin synthesis An autosomal dominant inheritance pattern

• The heterozygous form may be mildly symptomatic or asymptomatic.

• The homozygous form is associated with severe hemolytic anemia.

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Clinical Features and Oral Manifestations of Thalassemia (pg. 296)

Yellow skin pallor, fever, malaise, and weakness The face includes prominent cheekbones,

depression of the bridge of the nose, a prominent maxilla, and protrusion or flaring of maxillary anterior teeth.

Radiographs may show a “salt and pepper” pattern. Some trabeculae are prominent, and others

are blurred.

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Treatment of Thalassemia

Experimental May include blood transfusions and

splenectomy Poor prognosis

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Sickle Cell Anemia

(pg. 297) An inherited blood disorder

When someone is heterozygous, it is called sickle cell trait.

When someone is homozygous, they are much more severely affected.

Occurs before age 30 and is more common in women than in men

The red blood cells develop a sickle shape when there is decreased oxygen. This can be triggered by exercise, exertion,

administration of a general anesthetic, pregnancy, or even sleep.

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Clinical Features and Oral Manifestations of Sickle Cell Anemia

(pg. 297) The person has weakness, shortness of

breath, fatigue, joint pain, and nausea. Radiographic

There is a loss of trabeculation, and large, irregular marrow spaces appear.

A “hair-on-end” pattern may be seen in the skull.

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Clinical Features and Oral Manifestations of Sickle Cell Anemia (cont.)

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Diagnosis and Treatment of Sickle Cell Anemia

(pg. 297) The sickle-shaped cells may be seen on a

blood smear. The number of red blood cells is usually low,

as is the hemoglobin content. Treatment is largely supportive, involves

administration of oxygen and IV and oral fluid.

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Diagnosis and Treatment of Sickle Cell Anemia (cont.)

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Celiac Sprue

(pgs. 297-298) A chronic disorder

Sensitivity to wheat gluten Ingestion causes injury to intestinal

mucosa. This injury may cause malabsorption of

nutrients and a resulting anemia.

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Clinical Features and Oral Manifestations of Celiac Sprue

Symptoms include diarrhea, nervousness, and paresthesia. Painful, burning tongue, atrophy of papillae,

and ulceration of oral mucosa

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Diagnosis and Treatment of Celiac Sprue

The patient must avoid wheat gluten. Oral manifestations resolve when the systemic

disease is controlled.

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Aplastic Anemia

(pgs. 298-299) A severe depression of bone marrow

activity causes a decrease in all circulating blood cells. – pancytopenia Primary aplastic anemia – the cause is

unknown Secondary aplastic anemia – a result of a drug

or chemical agent

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Aplastic Anemia (cont.)

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Oral Manifestations of Aplastic Anemia

(pgs. 298-299) Infection, spontaneous bleeding,

petechiae, and purpuric spots

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Diagnosis and Treatment of Aplastic Anemia

(pg. 298) Leukopenia (decrease in white blood cells)

and thrombocytopenia (decrease in platelets) occur.

Primary aplastic anemia is usually progressive and fatal. Secondary aplastic anemia involves removing

the cause.

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Polycythemia

Polycythemia Vera Secondary Polycythemia Relative Polycythemia

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Polycythemia (cont.)

(pg. 298) Characterized by an increase in the

number of circulating red blood cells May be absolute or relative

The three forms of polycythemia are Polycythemia Vera Secondary Polycythemia Relative Polycythemia

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Polycythemia Vera (Primary Polycythemia)

(pg. 298) A neoplastic proliferation of bone marrow

stem cells causes an abnormally high number of circulating red blood cells. Unknown cause More common in men than in women Age of onset usually between 40 and 60 years

of age Clinical features

Headache, dizziness, and itching (pruritus) Thrombi may form.

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Secondary Polycythemia

(pg. 298) The increase in red blood cells is caused

by a physiologic response to decreased oxygen. A decrease in blood oxygen causes an

increase in erythropoietin by the kidneys. May be due to pulmonary disease, heart

disease, living at high altitude, or elevation in carbon monoxide

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Relative Polycythemia

(pg. 298) Caused by a decrease in plasma volume

Causes may include diuretics, vomiting, diarrhea, or excessive sweating.

Most patients are middle-aged white men under physiologic stress, mildly overweight, hypertensive, and heavy smokers.

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Oral Manifestations of Polycythemia

(pg. 299) The oral mucosa may appear deep red to

purple; the gingiva may be edematous and bleed easily. Submucosal petechiae, ecchymosis, and

hematoma formation may be present.

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Diagnosis and Treatment of Polycythemia

(pg. 299) Laboratory testing and measurement of

hemoglobin and hematocrit May include removal of causative factors,

chemotherapy, and phlebotomy

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Disorders of White Blood Cells

Agranulocytosis Cyclic Neutropenia Leukemia

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Disorders of White Blood Cells (cont.)

(pgs. 299-301) Three groups of white blood cells are

found in circulation. Granulocytes

• Neutrophils (PMNs), eosinophils, and basophils

Lymphocytes Monocytes

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Agranulocytosis

(pg. 300) A significant reduction in circulating

neutrophils Leukopenia – an abnormally low white blood

cell count Neutropenia – a reduction in the number of

circulating neutrophils

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Agranulocytosis (cont.)

Can result from a problem in development of neutrophils or accelerated destruction of neutrophils Primary – the cause is unknown, may be an

immunologic disorder Secondary – a result of chemicals or drugs

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Clinical Features and Oral Manifestations of Agranulocytosis (pg. 300)

Sudden onset of fever, chills, jaundice, weakness, and sore throat Oral infection

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Diagnosis and Treatment of Agranulocytosis

(pg. 300) Laboratory testing Marked reduction in WBC count Treatment

Transfusions, antibiotics Removal of the cause for the secondary form

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Cyclic Neutropenia

(pg. 300) A cyclic decrease in the number of

circulating neutrophilic leukocytes Discussed on pages 208-209

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Leukemia

(pgs. 300-301) (Box 9-2) Malignant neoplasms of hematopoietic

stem cells Characterized by an excessive number of

abnormal white blood cells in circulating blood Unknown cause; some are investigating

oncogenic viruses There are many different types

categorized as to whether they are acute or chronic.

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Acute Leukemias

(pgs. 300-301) Characterized by very immature cells and

a rapidly fatal course if not treated Acute lymphoblastic leukemia – involves

immature lymphocytes• Primarily affects children and young adults• Good prognosis

Acute myeloblastic leukemia – involves immature granulocytes

• Primarily affects adolescents and young adults.• Prognosis is not as good.

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Clinical Features of Acute Leukemias

(pg. 301) Weakness, fever, enlargement of lymph

nodes, and bleeding

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Oral Manifestations of Acute Leukemias

Gingival enlargement Oral infection Bleeding gums, petechiae and ecchymosis

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Diagnosis and Treatment of Acute Leukemias

Laboratory findings include elevated white blood cell count, anemia, and low platelet count

Treatment Bone marrow transplant

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Chronic Leukemias

(pg. 301) Slow onset

Primarily affect adults

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Clinical Features and Oral Manifestations of Chronic Leukemias

Easy fatigability, weakness, weight loss, anorexia

Pallor of lips and gingiva, gingival enlargement, petechiae and ecchymosis, gingival bleeding

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Diagnosis and Treatment of Chronic Leukemias

High white blood cell count Treatment

Bone marrow transplant

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Bleeding Disorders

Hemostasis Purpura Hemophilia

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Hemostasis (cont.)

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Hemostasis (cont.)

(pgs. 301-303) (Tables 9-1, 9-2) A cessation of bleeding

Circulating platelets adhere to a damaged surface and aggregate to form a temporary clot.

Fibrin binds the platelets• Fibrin is converted from fibrinogen by a cascade of

circulating proteins.

Defects may be caused by abnormalities of either platelets or coagulation factors. These may be determined with laboratory tests.

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Hemostasis (cont.)

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Platelet Count

(pgs. 301-302) To determine the number of platelets

Normal is 150,000 to 400,000/mm3

• Spontaneous gingival bleeding may occur if the count is less than 20,000/mm3

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Bleeding Time

(pg. 302) The adequacy of platelet function Normal is between 1 and 6 minutes.

Prolonged is greater than 5 or 10 minutes.

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Prothrombin Time (PT)

(pgs. 302-303) The ability to form a clot

Normal is usually between 11 and 16 seconds. INR is the ratio of PT to thromboplastin activity. Values less than 3 are considered normal.

• Patients on anticoagulants may have INR values of 4 to 5.

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Partial Thromboplastin Time (PTT)

(pg. 303) Measures the other way by which clot

formation occurs A normal PTT is usually 25 to 40 seconds.

Prolongation to 45 or 50 seconds may be associated with bleeding problems.

Over 50 seconds may be severe

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Purpura

(pgs. 303-304) A reddish-blue or purplish discoloration of

skin or mucosa from spontaneous extravasation of blood May be due to a defect or deficiency in blood

platelets Blood may ooze from gingival margins.

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Thrombocytopenic Purpura

(pgs. 303-304) A bleeding disorder that results from a

severe reduction in circulating platelets Idiopathic thrombocytopenic purpura

• If the cause is unknown

Immune thrombocytopenia• An autoimmune type of process

Secondary thrombocytopenic purpura• Often associated with drugs

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Clinical and Oral Manifestations of Thrombocytopenic Purpura

Spontaneous purpuric or hemorrhagic lesions on the skin Patients bruise easily, may have blood in urine,

and have frequent nosebleeds.

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Diagnosis and Treatment of Thrombocytopenic Purpura

Laboratory tests show a significant decrease in platelets.

Treatment May include transfusions, corticosteroids, and

splenectomy

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Nonthrombocytopenic Purpura

(pg. 304) Bleeding disorders that can result from

either a defect in capillary walls or disorders of platelet function Vitamin C deficiency and infections or

chemicals and allergy may be the cause of alterations in vascular walls.

Drugs, allergy, and autoimmune disease may cause disorders of platelet function.

Von Willebrand disease is an autosomal dominant disorder of platelet function.

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Oral Manifestations of Nonthrombocytopenic Purpura

Spontaneous gingival bleeding, petechiae, ecchymoses, and hemorrhagic blisters

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Diagnosis and Treatment of Nonthrombocytopenic Purpura

Systemic corticosteroids, splenectomy, and discontinuation of the causative agent

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Hemophilia

(pg. 304) A disorder of blood coagulation

Results in severely prolonged clotting time Due to a deficiency in plasma proteins involved

in coagulation

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Types of Hemophilia

(pg. 304) The two most common types are type A

and type B. Transmitted as X-linked diseases through an

unaffected carrier daughter to a son• Type A

Caused by a deficiency of plasma thromboplastinogen or factor VIII

• Type B Christmas disease Less common, the clotting defect is plasma

thromboplastin or factor IX

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Oral Manifestations of Hemophilia

Spontaneous gingival bleeding, petechiae, and ecchymosis

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Diagnosis and Treatment of Hemophilia

The bleeding time and PT in hemophilia are normal; the PTT is prolonged.

Diagnosis involves identifying the missing factor; treatment involves replacing it.

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Immunodeficiency

(pgs. 304-305) Can involve the different parts of the

immune system either alone or together May involve a deficiency in cell-mediated or

humoral immunity May involve deficiency in phagocytosis

Divided into Primary immunodeficiency of genetic origin Secondary immunodeficiency from another

underlying disorder

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Primary Immunodeficiencies

(pg. 305) Of genetic origin

May involve B cells, T cells, or both Very rare

Bruton disease (X linked congenital agammaglobulinemia)

DiGeorge syndrome (thymic hypoplasia) Severe combined immunodeficiency

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Secondary Immunodeficiencies (Cont.)

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Secondary Immunodeficiencies (Cont.)

(pg. 305) (Table 9-3) Occur as the result of an underlying

disorder May be malnutrition, viral infection, cancer,

renal disease and Hodgkin’s disease May occur with immunosuppressive drugs,

drugs used along with radiation, chemotherapy

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Oral Manifestations of Therapy for Oral Cancer

(pgs. 305-307) Radiation Therapy Chemotherapy

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Oral Manifestations of Therapy for Oral Cancer (cont.)

(pg. 305) Oral cancer can be treated with surgery,

radiation therapy, or chemotherapy, or a combination.

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Radiation Therapy

(pgs. 305-306) The patient often experiences

mucositis during radiation therapy. Mucositis begins about the second

week of therapy and subsides a few weeks after its completion.

It is painful and appears as an erythematous and ulcerated mucosa.

The patients may have difficulty eating, pain on swallowing, and loss of taste.

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(pgs. 305-306) Destruction of major salivary glands may result in

xerostomia The patient is prone to rampant caries and oral

candidiasis. They also are prone to osteoradionecrosis.

Radiation Therapy (cont.)

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Patients should have an oral evaluation before radiation therapy of the head and neck. Potential sources for oral infection and teeth

with a questionable prognosis should be removed.

The hygienist can help with Fluoride application Patient education Frequent follow-up appointments

Radiation Therapy (cont.)

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Chemotherapy

(pgs. 306-307) Drugs used for cancer chemotherapy

affect basal cells of the epithelium. Mucositis and oral ulceration are common

complications. A decrease in all blood cells may occur

Lowered RBC counts can lead to anemia. Lowered WBC counts can lead to infections. Lowered platelets can lead to bleeding

problems.

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Effects of Drugs on the Oral Cavity

(pgs. 307-308) Blood pressure drugs, antianxiety

medications, antipsychotic medications, and antihistamines can cause xerostomia.

Prednisone suppresses the immune system and can lead to candidiasis and oral infections.

Antibiotics may increase risk of candidiasis.

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Effects of Drugs on the Oral Cavity (cont.)

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Effects of Drugs on the Oral Cavity (cont.)

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Effects of Drugs on the Oral Cavity (cont.)

Tetracycline can cause tooth discoloration. Phenytoin and nifedipine can cause

gingival enlargement. Cyclosporine may cause gingival

enlargement.

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Discussion Questions

What oral manifestations of systemic diseases may be observed within the oral cavity?

What disorders of blood cells may be observed within the oral cavity?

What effects may immunodeficiency have upon the oral cavity?

What oral manifestations may be observed during therapy for oral cancer?

What effects of drugs may be observed within the oral cavity?