Chapter 9

Chapter 9
Oral Manifestations of Systemic

Diseases
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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

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.

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
Endocrine Disorders
Hyperpituitarism
Hyperthyroidism
Hypothyroidism
Hyperparathyroidism
Diabetes Mellitus
Addison Disease
Endocrine Disorders
The endocrine system consists of a group

of integrated glands and cells that secrete
hormones.
(pg. 288)
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.
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.
Clinical Features and Oral

Manifestations of Hyperpituitarism
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
(pgs. 288-289)
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

Clinical Features and Oral Manifestations

of Hyperpituitarism (cont.)
Diagnosis and Treatment of

Hyperpituitarism
Diagnosis involves measurement of

growth hormone.
Treatment often includes pituitary gland
surgery.
10
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.
11
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.
12
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.
13
Treatment of Hyperthyroidism
May include surgery, medications to

suppress thyroid activity, or administration
of radioactive iodine
14
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
15
Hypothyroidism (cont.)
Oral manifestations
In infants
Thickened lips, enlarged tongue, and delayed
eruption of teeth
In adults
Enlarged tongue
16
Hyperparathyroidism
Due to excessive secretion of parathyroid

hormone from the parathyroid glands
(pgs. 289-290)
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).
17
Hyperparathyroidism (cont.)
18
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.
19
Clinical Features
of Hyperparathyroidism
Mild cases may be asymptomatic, or may

have joint pain or stiffness.
Lethargy and coma may occur with severe

disease.
20
Hyperparathyroidism
Well-defined unilocular or multilocular

radiolucencies
Microscopically, they appear to be CGCG

(central giant cell granulomas).
Bone may have a mottled appearance.
21
Diagnosis and Treatment

of 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.
22
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.
23
Diabetes Mellitus (cont.)
24
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.
25
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.
26
Types of Diabetes
Insulin-dependent diabetes mellitus
Type 1
Noninsulin-dependent diabetes mellitus
Type 2
27
Insulin-Dependent Diabetes
Mellitus
Thought to be an autoimmune disease
(pgs. 291-292)
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)
28
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).
29
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
30
NonInsulin-Dependent
Diabetes Mellitus
Characterized by insulin resistance
(pgs. 292-294)
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.
31
Clinical Features of NonInsulinDependent Diabetes Mellitus
Atherosclerosis, a thickening of the blood vessel

wall from fibrofatty plaques, can lead to impaired
circulation, causing impaired oxygenation and
nutrition in tissue.
(pg. 293)
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.
32
Clinical Features of NonInsulinDependent Diabetes Mellitus (cont.)
33
Oral Complications of NonInsulinDependent Diabetes Mellitus
Patients may have an increased prevalence of

oral candidiasis.
(pgs. 293-294)
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.
34
Oral Complications of NonInsulinDependent Diabetes Mellitus (cont.)
35
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.
36
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
37
Blood Disorders
Disorders of Red Blood Cells and

Hemoglobin
Disorders of White Blood Cells
Bleeding Disorders
38
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.
39
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
40
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
41
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
42
Iron Deficiency Anemia
An insufficient amount of iron is supplied to bone

marrow for red blood cell development.
(pg. 295)
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
43

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
44

of Iron Deficiency Anemia (cont.)
45
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
46
Pernicious Anemia
Probably an autoimmune disorder in most

situations
(pgs. 295-296)
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
47

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
48

of Pernicious Anemia (cont.)
49

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
50
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
51
Oral Manifestations of Folic Acid and

Vitamin B12 Deficiency Anemia
Oral manifestations are indistinguishable

from those of pernicious anemia.
52
Diagnosis and Treatment of Folic Acid

and Vitamin B12 Deficiency Anemia
Based upon laboratory tests serum

assays of folic acid and vitamin B12
53
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.
54

Manifestations of Thalassemia
Yellow skin pallor, fever, malaise, and

weakness
(pg. 296)
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.
55
Treatment of Thalassemia
Experimental
May include blood transfusions and

splenectomy
Poor prognosis
56
Sickle Cell Anemia
An inherited blood disorder
(pg. 297)
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.
57

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.
58

of Sickle Cell Anemia (cont.)
59
Diagnosis and Treatment of Sickle

Cell Anemia
The sickle-shaped cells may be seen on a

blood smear.
(pg. 297)
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.
60
Diagnosis and Treatment of Sickle

Cell Anemia (cont.)
61
Celiac Sprue
A chronic disorder
(pgs. 297-298)
Sensitivity to wheat gluten
Ingestion causes injury to intestinal

mucosa.
This injury may cause malabsorption of

nutrients and a resulting anemia.
62

Manifestations of Celiac Sprue
Symptoms include diarrhea, nervousness,

and paresthesia.
Painful, burning tongue, atrophy of papillae,

and ulceration of oral mucosa
63

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

disease is controlled.
64
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
65
Aplastic Anemia (cont.)
66
Oral Manifestations of Aplastic

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

petechiae, and purpuric spots
67

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.
68
Polycythemia
Polycythemia Vera
Secondary Polycythemia
Relative Polycythemia
69
Polycythemia (cont.)
Characterized by an increase in the

number of circulating red blood cells
(pg. 298)
May be absolute or relative
The three forms of polycythemia are
Polycythemia Vera
70
Polycythemia Vera
(Primary Polycythemia)
A neoplastic proliferation of bone marrow

stem cells causes an abnormally high
number of circulating red blood cells.
(pg. 298)
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.
71
(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
72
(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.
73
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.
74

Polycythemia
(pg. 299)
Laboratory testing and measurement of

hemoglobin and hematocrit
May include removal of causative factors,

chemotherapy, and phlebotomy
75
Agranulocytosis
Cyclic Neutropenia
Leukemia
76

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

found in circulation.
Granulocytes
Neutrophils (PMNs), eosinophils, and basophils
Lymphocytes
Monocytes
77
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
78
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
79

Manifestations of Agranulocytosis
(pg. 300)
Sudden onset of fever, chills, jaundice,

weakness, and sore throat
Oral infection
80

Agranulocytosis
(pg. 300)
Laboratory testing
Marked reduction in WBC count
Treatment
Transfusions, antibiotics
Removal of the cause for the secondary form
81
Cyclic Neutropenia
(pg. 300)
A cyclic decrease in the number of

circulating neutrophilic leukocytes
Discussed on pages 208-209
82
Leukemia
Malignant neoplasms of hematopoietic

stem cells
(pgs. 300-301) (Box 9-2)
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.
83
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.
84
Clinical Features of Acute

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

nodes, and bleeding
85
Oral Manifestations of Acute

Leukemias
Gingival enlargement
Oral infection
Bleeding gums, petechiae and ecchymosis
86
Diagnosis and Treatment of Acute

Leukemias
Laboratory findings include elevated white

blood cell count, anemia, and low platelet
count
Treatment
Bone marrow transplant
87
Chronic Leukemias
(pg. 301)
Slow onset
Primarily affect adults
88

Manifestations of Chronic Leukemias
Easy fatigability, weakness, weight loss,

anorexia
Pallor of lips and gingiva, gingival
enlargement, petechiae and ecchymosis,
gingival bleeding
89

Chronic Leukemias
High white blood cell count

Treatment
Bone marrow transplant
90
Bleeding Disorders
Hemostasis
Purpura
Hemophilia
91
Hemostasis (cont.)
92
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.
93
Hemostasis (cont.)
94
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
95
Bleeding Time
(pg. 302)
The adequacy of platelet function

Normal is between 1 and 6 minutes.
Prolonged is greater than 5 or 10 minutes.
96
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.
97
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
98
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.
99
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
100
Clinical and Oral Manifestations of

Spontaneous purpuric or hemorrhagic

lesions on the skin
Patients bruise easily, may have blood in urine,

and have frequent nosebleeds.
101

Laboratory tests show a significant

decrease in platelets.
Treatment
May include transfusions, corticosteroids, and

splenectomy
102
Nonthrombocytopenic Purpura
Bleeding disorders that can result from

either a defect in capillary walls or
disorders of platelet function
(pg. 304)
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.
103
Spontaneous gingival bleeding, petechiae,

ecchymoses, and hemorrhagic blisters
104

Systemic corticosteroids, splenectomy,

and discontinuation of the causative agent
105
Hemophilia
(pg. 304)
A disorder of blood coagulation
Results in severely prolonged clotting time

Due to a deficiency in plasma proteins involved
in coagulation
106
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
107
Oral Manifestations of Hemophilia
Spontaneous gingival bleeding, petechiae,

and ecchymosis
108

Hemophilia
The bleeding time and PT in hemophilia

are normal; the PTT is prolonged.
Diagnosis involves identifying the missing
factor; treatment involves replacing it.
109
Immunodeficiency
Can involve the different parts of the

immune system either alone or together
(pgs. 304-305)
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
110
Primary Immunodeficiencies
Of genetic origin
(pg. 305)
May involve B cells, T cells, or both
Very rare
Bruton disease (X linked congenital

agammaglobulinemia)
DiGeorge syndrome (thymic hypoplasia)
Severe combined immunodeficiency
111
Secondary Immunodeficiencies
(Cont.)
112
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 Hodgkins disease
May occur with immunosuppressive drugs,
drugs used along with radiation, chemotherapy
113
Oral Manifestations of Therapy for

Oral Cancer
(pgs. 305-307)
Radiation Therapy
Chemotherapy
114
Oral Manifestations of Therapy for

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

radiation therapy, or chemotherapy, or a
combination.
115
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.
116
Radiation Therapy (cont.)
(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.
117
Radiation Therapy (cont.)
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
118
Chemotherapy
Drugs used for cancer chemotherapy

affect basal cells of the epithelium.
(pgs. 306-307)
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.
119
(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.
120

(cont.)
121

(cont.)
122

(cont.)
Tetracycline can cause tooth discoloration.

Phenytoin and nifedipine can cause
gingival enlargement.
Cyclosporine may cause gingival
enlargement.
123
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?
124

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Chapter 9

Oral Manifestations of Systemic

Oral Manifestations of Systemic

Many systemic diseases are reflected in the oral

Mucosal changes may include ulceration or mucosal

Oral Manifestations of Systemic

Local factors may be involved in the

The mucosa may be more easily injured due to

These may include

Endocrine disorders, disorders of red and white

The endocrine system consists of a group

The secretion is controlled by feedback

Diseases may result from conditions

Excess hormone production by the

Caused most often by a benign tumor (pituitary

Clinical Features and Oral

Affects both men and women, most commonly

Patients experience poor vision, light sensitivity,

Enlargement of maxilla and mandible may cause

May have thickened lips and macroglossia

Clinical Features and Oral Manifestations

Diagnosis and Treatment of

Diagnosis involves measurement of

Excess production of thyroid hormone

More common in women than men

Appears to be due to an autoimmune disorder in which

Other causes include hyperplasia of the gland,

Rosy complexion, erythema of the palms,

The patient may have exophthalmos.

May lead to premature exfoliation of

Osteoporosis may affect alveolar bone.

May include surgery, medications to

A decreased output of thyroid hormone

Causes include developmental disturbances,

Due to excessive secretion of parathyroid

The four parathyroid glands are located near

Parathyroid hormone plays a role in

May be the result of hyperplasia of

Found in middle-aged adults

Parathyroid hormone increases the uptake of

Mild cases may be asymptomatic, or may

Lethargy and coma may occur with severe

Well-defined unilocular or multilocular

Microscopically, they appear to be CGCG

Diagnosis and Treatment

Measurement of parathyroid hormone

May include serum calcium and phosphorous

Treatment is directed at correcting the

Causes may include tumors, renal disease,

A chronic disorder of carbohydrate

These result from a lack of insulin, defective

Diabetes Mellitus (cont.)

Diabetes Mellitus (cont.)

Glucose normally signals beta cells of the

The hormone is then secreted into the

Diabetes Mellitus (cont.)

Without insulin, tissue is broken down to

A severe hyperglycemia can lead to diabetic

Phagocytic activity of macrophages is

Insulin-dependent diabetes mellitus

Noninsulin-dependent diabetes mellitus

Thought to be an autoimmune disease

Can occur at any age, the peak is at 20

These patients will require insulin their