Chapter 9
Oral Manifestations of Systemic
Diseases
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
1

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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
2
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
3
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
4
Endocrine Disorders






Hyperpituitarism
Hyperthyroidism
Hypothyroidism
Hyperparathyroidism
Diabetes Mellitus
Addison Disease
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
5
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
6
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
7
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
8
Clinical Features and Oral Manifestations
of Hyperpituitarism (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
9
Diagnosis and Treatment of
Hyperpituitarism


Diagnosis involves measurement of
growth hormone.
Treatment often includes pituitary gland
surgery.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
13
Treatment of Hyperthyroidism

May include surgery, medications to
suppress thyroid activity, or administration
of radioactive iodine
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
15
Hypothyroidism (cont.)

Oral manifestations

In infants
• Thickened lips, enlarged tongue, and delayed
eruption of teeth

In adults
• Enlarged tongue
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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).
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
17
Hyperparathyroidism (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
20
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
23
Diabetes Mellitus (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
24
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
25
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
26
Types of Diabetes

Insulin-dependent diabetes mellitus


Type 1
Non–insulin-dependent diabetes mellitus

Type 2
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
28
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).
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
29
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
30
Non–Insulin-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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
31
Clinical Features of Non–InsulinDependent 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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
32
Clinical Features of Non–InsulinDependent Diabetes Mellitus (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
33
Oral Complications of Non–InsulinDependent 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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
34
Oral Complications of Non–InsulinDependent Diabetes Mellitus (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
37
Blood Disorders



Disorders of Red Blood Cells and
Hemoglobin
Disorders of White Blood Cells
Bleeding Disorders
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
43
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
44
Clinical Features and Oral Manifestations
of Iron Deficiency Anemia (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
47
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
48
Clinical Features and Oral Manifestations
of Pernicious Anemia (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
49
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
51
Oral Manifestations of Folic Acid and
Vitamin B12 Deficiency Anemia

Oral manifestations are indistinguishable
from those of pernicious anemia.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
52
Diagnosis and Treatment of Folic Acid
and Vitamin B12 Deficiency Anemia

Based upon laboratory tests – serum
assays of folic acid and vitamin B12
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
54
Clinical Features and Oral
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
55
Treatment of Thalassemia

Experimental


May include blood transfusions and
splenectomy
Poor prognosis
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
57
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
58
Clinical Features and Oral Manifestations
of Sickle Cell Anemia (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
60
Diagnosis and Treatment of Sickle
Cell Anemia (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
62
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
63
Diagnosis and Treatment of
Celiac Sprue

The patient must avoid wheat gluten.

Oral manifestations resolve when the systemic
disease is controlled.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
65
Aplastic Anemia (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
66
Oral Manifestations of Aplastic
Anemia


(pgs. 298-299)
Infection, spontaneous bleeding,
petechiae, and purpuric spots
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
67
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
68
Polycythemia



Polycythemia Vera
Secondary Polycythemia
Relative Polycythemia
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Secondary Polycythemia
Relative Polycythemia
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
71
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
72
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
73
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
74
Diagnosis and Treatment of
Polycythemia


(pg. 299)
Laboratory testing and measurement of
hemoglobin and hematocrit

May include removal of causative factors,
chemotherapy, and phlebotomy
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
75
Disorders of White Blood Cells



Agranulocytosis
Cyclic Neutropenia
Leukemia
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
76
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
79
Clinical Features and Oral
Manifestations of Agranulocytosis


(pg. 300)
Sudden onset of fever, chills, jaundice,
weakness, and sore throat

Oral infection
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
80
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
81
Cyclic Neutropenia


(pg. 300)
A cyclic decrease in the number of
circulating neutrophilic leukocytes

Discussed on pages 208-209
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
84
Clinical Features of Acute
Leukemias


(pg. 301)
Weakness, fever, enlargement of lymph
nodes, and bleeding
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
85
Oral Manifestations of Acute
Leukemias



Gingival enlargement
Oral infection
Bleeding gums, petechiae and ecchymosis
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
86
Diagnosis and Treatment of Acute
Leukemias


Laboratory findings include elevated white
blood cell count, anemia, and low platelet
count
Treatment

Bone marrow transplant
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
87
Chronic Leukemias


(pg. 301)
Slow onset

Primarily affect adults
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
88
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
89
Diagnosis and Treatment of
Chronic Leukemias


High white blood cell count
Treatment

Bone marrow transplant
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
90
Bleeding Disorders



Hemostasis
Purpura
Hemophilia
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
91
Hemostasis (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
93
Hemostasis (cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
100
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
101
Diagnosis and Treatment of
Thrombocytopenic Purpura


Laboratory tests show a significant
decrease in platelets.
Treatment

May include transfusions, corticosteroids, and
splenectomy
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
103
Oral Manifestations of
Nonthrombocytopenic Purpura

Spontaneous gingival bleeding, petechiae,
ecchymoses, and hemorrhagic blisters
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
104
Diagnosis and Treatment of
Nonthrombocytopenic Purpura

Systemic corticosteroids, splenectomy,
and discontinuation of the causative agent
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
107
Oral Manifestations of Hemophilia

Spontaneous gingival bleeding, petechiae,
and ecchymosis
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
108
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
111
Secondary Immunodeficiencies
(Cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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 Hodgkin’s disease
May occur with immunosuppressive drugs,
drugs used along with radiation, chemotherapy
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
113
Oral Manifestations of Therapy for
Oral Cancer



(pgs. 305-307)
Radiation Therapy
Chemotherapy
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
119
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
120
Effects of Drugs on the Oral Cavity
(cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
121
Effects of Drugs on the Oral Cavity
(cont.)
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
122
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.
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
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?
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc.
124