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Chapter 2

Inflammation and Repair

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Outline
Injury
Natural (Innate) Defenses Against Injury
Inflammation
Regeneration and Repair
Injuries to Teeth
Injuries to Soft Tissues
Reactive Connective Tissue Hyperplasia
Inflammatory Periapical Lesions

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Inflammation and Repair
(pg. 34)
The bodys response to injury
Inflammation
Allows the body to eliminated injurious agents,
contain injuries, and heal defects

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Injury
(pg. 34)
An alteration in the environment that
causes tissue damage
Examples include
Physical
Chemical
Microorganisms
Nutritional deficiencies

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Natural (Innate) Defenses
Against Injury
(pg. 34)
Intact skin or mucosa is a physical barrier.
Enzymes in saliva have an antibacterial
activity.
Flushing action of tears, saliva, urine, and
diarrhea removes foreign substances.

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Inflammation
(pgs. 34-44)
Microscopic Events and Clinical Signs of
Inflammation
White Blood Cells and Their Involvement
in the Inflammatory Response
Biochemical Mediators of Inflammation
Systemic Manifestations of Inflammation
Chronic Inflammation
Hyperplasia, Hypertrophy, and Atrophy

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Inflammation (cont.)
(pgs. 34-35)
A nonspecific response to injury
Occurs in the same manner regardless of the
nature of the injury
May be local and limited to the area of injury, or
may be extensive if the injury is extensive
May be acute or chronic

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Microscopic Events and Clinical
Signs of Inflammation (Cont.)

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Microscopic Events and Clinical
Signs of Inflammation (Cont.)
(pgs. 35-37) (Table 2-1)

Local clinical changes are classic signs of


inflammation.
Redness, heat, swelling, pain, loss of normal
tissue function
Systemic signs may include
Increase in body temperature
Increase in the number of white blood cells
Enlargement of lymph nodes

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Microscopic Events and Clinical
Signs of Inflammation (cont.)

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Microscopic Events and Clinical
Signs of Inflammation (cont.)
Microscopic events involve
microcirculation.
Arterioles, capillaries, venules in the area of
injury
White blood cells
Chemical mediators
Usually, an exchange of oxygen and
nutrition is seen in these vessels.
Most of the fluid reenters circulation through
venules.
Lymphatic system carries away fluid that does
not reenter the blood vessels.
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Sequence of Microscopic Events
(pg. 36)
Injury to tissue
Constriction of microcirculation
Dilation of microcirculation
Increase in permeability
Exudate leaves microcirculation.
Increased blood viscosity
Decreased blood flow
Margination and pavementing of white blood
cells (WBCs)
WBCs enter tissue.
WBCs ingest foreign material.
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Sequence of Microscopic Events
(cont.)
(pg. 36)
Hyperemia
Increased blood flow in capillary beds of injured tissue
Will produce redness and heat
Exudate
Increased blood plasma and proteins in injured tissue
Helps dilute injurious agents, but results in excess fluid in
tissues edema
Serous exudate
Mainly plasma fluids and proteins, few WBCs
Purulent exudate (suppuration)
Contains plasma fluids and proteins, tissue debris, and
many WBCs

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Sequence of Microscopic Events
(cont.)
(pgs. 36-38)
Swelling develops as exudate escapes into tissue.
May flow out as a thin, clear exudate (serous) or a thick
white-to-yellow pus (purulent)
Drainage may occur through a fistula.
Incision and drainage (I & D) may be required.
A drainage tube may be placed.
Medication may be administered to treat infection and
reduce inflammation.
Pressure from exudate and chemical mediators may cause
pain.
Blood viscosity may increase due to loss of plasma fluids.
Margination
White blood cells migrate to the periphery of the
vessel.
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Sequence of Microscopic Events
(cont.)

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Sequence of Microscopic Events
(cont.)

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Sequence of Microscopic Events
(cont.)
(pgs. 37, 39)
Emigration
The process by which WBCs escape from
blood vessels through gaps in endothelial cells
Chemotaxis
Directed movement of WBCs toward the site of
injury
Phagocytosis
The process by which WBCs ingest and then
digest foreign substances.
May include pathogenic organisms and tissue
debris
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Sequence of Microscopic Events
(cont.)

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White Blood Cells and Their Involvement
in the Inflammatory Response
(pgs. 37, 39)
There are six different kinds of WBCs.
Neutrophils
First to arrive at the site of injury
Primary cell in acute inflammation
Monocytes (Macrophage)
Second cell in inflammatory response
Lymphocytes and Plasma Cells
Seen in chronic inflammation and the immune response
Eosinophils and Mast Cells
Seen in both inflammation and the immune response

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White Blood Cells and Their Involvement
in the Inflammatory Response (cont.)
(pgs. 39-40)
Changes occur in the proportion of WBCs
as the inflammatory response continues.
The neutrophil is the most common
inflammatory cell in acute monocyte (in blood)
becomes a macrophage as it enters tissue
inflammation.
The circulating.
Neutrophils decrease in number.
Macrophages, lymphocytes, and plasma cells
become predominant with chronic
inflammation.
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White Blood Cells and Their Involvement
in the Inflammatory Response (cont.)

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White Blood Cells and Their Involvement
in the Inflammatory Response (cont.)

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Neutrophils (PMNs)
(pgs. 39-40)
60% to 70% of WBC population
Granular leukocytes along with basophils and
eosinophils
Derived from stem cells in bone marrow
Contain lysosomal enzymes
Function is phagocytosis and then
enzymatic destruction of foreign
substances.
Neutrophils then perish.
The enzymes can leak, causing further tissue
damage.
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Neutrophils (PMNs) (cont.)

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Macrophages
(pgs. 40-41)
3% to 8% of WBC population
Derived from stem cells in bone marrow
Has a single, round nucleus and a nongranular
cytoplasm
Responds to chemotactic factors, is mobile,
can phagocytize also plays a role in the
immune system

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Macrophages (cont.)

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Biochemical Mediators of
Inflammation
(pgs. 40-41)
Cause many of the events in the
inflammatory response
Basic mediators can recruit other mediators
and immune mechanisms.
May be derived from
Blood
Endothelial cells
White blood cells and platelets
Pathogenic organisms as they injure the tissue

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Biochemical Mediators of
Inflammation (cont.)
(pgs. 40-41)
Three interrelated systems
Interaction takes place during activation,
among their products, and within their various
actions
Kinin system
Clotting mechanism
Complement system

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Kinin System
(pg. 40)
Active in early phases of inflammation
Activated by substances in plasma and
injured tissue
Causes increased
Dilation of blood vessels at the site of injury
Permeability of local blood vessels
Induces pain

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Clotting Mechanism
(pg. 41)
Clots blood and mediates inflammation
Some of the clotting mechanisms products that
are activated during tissue injury cause local
vascular dilation and permeability by activating
kinin.

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Complement System
(pg. 41)
Involves the production of a sequential cascade of plasma
proteins
They are present in blood in an inactive form.
A trigger (usually an antibody/antigen complex) initiates the
sequence of steps.
These plasma proteins function in inflammation and immunity.
Some components cause WBCs known as mast cells to
release histamine.
Histamine causes an increase in vascular permeability and
vasodilation.
Other components cause cell death, form chemotactic
factors for WBCs, and enhance phagocytosis.

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Other Biochemical Mediators of
Inflammation
(pg. 41)
Released by the body
Prostaglandins
Cause increased vascular dilation and permeability,
tissue pain and redness, and changes in connective
tissue
Lysosomal enzymes
Act as chemotactic factors
May cause damage to connective tissues and to the
clot

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Other Biochemical Mediators of
Inflammation (cont.)
(pg. 41)
Released by pathogenic microorganisms
Endotoxin
Produced by cell walls of gram-negative bacteria
Serves as chemotactic factor, can activate
complement, function as an antigen, and damage
bone and tissue
Lysosomal enzymes
Have a similar chemical composition and action as
those released by WBCs

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Antiinflammatory Drugs
(pg. 41)
Block or suppress the inflammatory
response
Prevent or reduce clinical signs of inflammation
and adverse reactions to the injury
Examples
Nonsteroidal antiinflammatory agents
Aspirin, ibuprofen, celecoxib
Steroidal antiinflammatory drug
Prednisone

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Systemic Manifestations of
Inflammation
(pgs. 41-42)
May include
Fever
Leukocytosis
Elevated C-reactive protein
Lymphadenopathy

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Fever
(pg. 42)
Controlled by the hypothalamus
Associated with systemic inflammatory
response
Pyrogens
Fever producing substances produced by
WBCs and pathogens
Pyrogens act on the hypothalamus.
The hypothalamus increases body
temperature by way of prostaglandins.

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Leukocytosis
(pg. 42)
A systemic inflammatory response can
increase the number of WBCs from the
normal 4000 to 10,000/mm of blood to
10,000 to 30,000/mm.
The primary cell involved is the neutrophil.
The rate of formation is increased and
immature forms are released from bone
marrow into the blood.
The body is attempting to produce more cells
for phagocytosis.
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Elevated C-Reactive Protein
(pg. 42)
C-reactive protein is produced in the liver and
plays the important role of interacting with the
complement system.
Elevated levels are present during episodes of acute
inflammation or infection.
May continue with chronic inflammation
Levels can be used to help assess rheumatoid
arthritis and systemic lupus erythematosus.
A chronic increased level is associated with an
increased risk for cardiovascular disease.

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Lymphadenopathy
(pgs. 42-43)
Enlarged and palpable superficial lymph
nodes
Follows route of lymphatic drainage
The enlarged nodes occur due to changes
in lymphocytes, which are the primary cells
of the immune response.
Hyperplasia
An increase in the number of cells
Hypertrophy
Enlargement of individual cells

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Lymphadenopathy (cont.)

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Chronic Inflammation
(pgs. 42-43)
Due to persistent injuries
Cells involved include macrophages,
lymphocytes, and plasma cells as well as
neutrophils and monocytes present in acute
inflammation.
May include proliferation of fibroblasts and
formation of granulomas

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Chronic Inflammation (cont.)
(pgs. 42-43)
Granuloma
Microscopic groupings of macrophages
surrounded by lymphocytes and plasma cells
Usually contain multinucleated giant cells
Large macrophages with multiple nuclei
Associated with foreign body reactions and
some infections such as tuberculosis

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Hyperplasia, Hypertrophy, and
Atrophy
(pgs. 43-44)
Hyperplasia
An increase in the number of cells often in response to
chronic irritation or abrasion
May return to normal if the insult subsides, or may
persist following removal of the irritant
Hypertrophy
An increase in the size of cells
May be seen in cardiac muscle as a response to
hypertension
Atrophy
A decrease in size or function of a cell, tissue, organ, or
entire body

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Hyperplasia, Hypertrophy, and
Atrophy (cont.)

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Regeneration and Repair
(pgs. 44-46)
Microscopic Events That Occur During
Repair
Types of Repair
Bone Tissue Repair

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Regeneration and Repair (cont.)
(pg. 44)
Regeneration
If the inflamed area returns to normal structure
and function
Repair
Occurs when the damage is too great for the
tissue to return to normal
Functioning cells and tissue often are replaced
with nonfunctioning scar tissue.

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Microscopic Events That Occur
During Repair
(pgs. 44-45)
Takes about 2 weeks
Occurs almost simultaneously in both
epithelium and connective tissue

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Microscopic Events That Occur
During Repair (cont.)

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Day of Injury
(pg. 45)
Blood flows into injured tissue to produce a
clot.
The clot contains fibrin, clumped red blood
cells (RBCs), and platelets.

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One Day After Injury
(pg. 45)
Neutrophils migrate from the
microcirculation into injured tissue in an
acute inflammatory response.
They phagocytize foreign material and necrotic
tissue.

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Two Days After Injury
(pg. 45)
Monocytes migrate from microcirculation and become macrophages
in tissue.
They also phagocytize.
Fibroblasts increase in number and produce new collagen fibers.
Granulation tissue is formed in the connective tissue portion of
injury.
This growth may be excessive.
New surface epithelium is formed in the epithelial tissue portion
of injury.
They use the fibrin meshwork to migrate.
This meshwork also protects newly formed tissue from
additional injury.
Lymphocytes and plasma cells migrate to the area as chronic
inflammation and the immune response begins.
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Seven Days After Injury
(pg. 45)
Fibrin is digested by tissue enzymes.
It sloughs off and the initial repair is complete.
The new tissue is relatively red.
New epithelium is thin.
New connective tissue is highly vascularized.

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Two Weeks After Injury
(pg. 45)
Initial granulation tissue and its fibers are
remodeled.
The new tissue is scar tissue.
It is whiter and paler due to increased collagen
and decreased vascularity.

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Types of Repair
(pgs. 45-46)
Healing by primary intention
Healing of an injury where there is little loss of
tissue
The margins are close together and very little
granulation tissue forms.
Healing by secondary intention
The edges of the injury cannot be joined during
healing.
A large clot forms, resulting in increased
granulation tissue.
May result in excess scar tissue a keloid
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Types of Repair (cont.)

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Healing by Tertiary Intention
(pg. 46)
Delaying surgical tissue repair until
infection is resolved
An injured area may become infected
especially with puncture wounds.
In some situations, an infected injury is left
open until infection is controlled.

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Factors That Impair Healing
(pg. 46)
Local factors that impair healing
Bacterial infection
Tissue destruction and necrosis
Hematoma
Excessive movement of injured tissue
Poor blood supply
Systemic factors
Malnutrition
Immunosuppression
Genetic connective tissue disorders
Metabolic disorders
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Bone Tissue Repair
(pg. 46)
Osteoblasts create new bone tissue.
May be delayed by
Increased movement of bone
Edema
Infection in the tissue
Excessive or inadequate movement of bone tissue

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Injuries to Teeth
Attrition
Abrasion
Abfraction
Erosion
Methamphetamine abuse

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Attrition
(pgs. 47-48)
Tooth-to-tooth wear
May be observed both in
primary and permanent
dentition

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Bruxism
(pgs. 47-48)
Grinding and clenching teeth for nonfunctional
purposes
Signs and symptoms include
Wear facets, abnormal rate of attrition, hypertrophy of
masticatory muscles, increased muscle tone, muscle
tenderness, muscle fatigue, cheek biting, pain in the TM joint
area, tooth mobility, and pulpal sensitivity to cold
May be due to local factors such as occlusal
interferences in combination with stress and tension
Management includes fabrication of an acrylic splint and
elimination of occlusal interferences through occlusal
adjustments.

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Bruxism (cont.)

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Abrasion
(pg. 48)
Wearing away of tooth structure from a
repetitive mechanical habit
Most frequently seen as a notching on root
surfaces with gingival recession
May occur from back-and-forth toothbrushing
technique
May be seen in patients who are
seamstresses, musicians, or pipe smokers

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Abrasion (cont.)

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Abfraction
(pg. 48)
Typically appears as wedge-shaped
lesions at the cervical areas of teeth
May be related to fatigue, flexure, fracture, and
deformation of tooth structure
May occur in combination with abrasion

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Erosion
(pgs. 48-49)
Loss of tooth structure
due to chemicals
Tooth structure may be lost
around a restoration,
making the restoration
stand out.
Occlusal surfaces may be
cupped out.
May be on facial surfaces
from food and lingual
surfaces from vomiting due
to bulimia

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Bulimia
(pg. 49)
Self-induced purging (vomiting)
after eating
The bulimic maintains normal body
weight.
May see electrolyte imbalance
and/or malnutrition
Management may include
fluoride rinse and toothpaste.
Rinsing with water after purging

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Methamphetamine Abuse
(pgs. 49-50)
Rapid destruction of
teeth
Due to acid content of
methamphetamine,
decreased salivary flow,
craving for high sugar
beverages with lack of
oral hygiene

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Injuries to Oral Soft Tissues
Aspirin Burn Traumatic Ulcer Melanosis
Phenol Burns Frictional Keratosis Solar Cheilitis
Electric Burns Linea Alba Mucocele
Other Burns Nicotinic Stomatitis Necrotizing
Lesions Tobacco Pouch Sialometaplasia
Associated with Keratosis Sialolith
Cocaine Use Traumatic Neuroma Acute and
Lesions from Amalgam Tattoo Chronic
Self-Induced Sialadenitis
Injuries
Hematoma

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Aspirin Burn
(pgs. 49-50)
Topical application is a
common misuse of this
product.
The tissue becomes
necrotic and white.
The surface may slough off
leaving a painful ulcer.
The ulcer usually heals in 7
to 21 days.

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Phenol Burn
(pgs. 50-51)
Used in dentistry as a cavity sterilizing
agent and a cauterizing agent
Will cause whitening and sloughing of the area
as a result of tissue destruction

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Electric Burn
(pg. 50)
May be seen in infants or young children
who have chewed an electrical cord
May be quite extensive, damaging oral tissue
and even tooth buds
May cause constriction of the commissure

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Other Burns
(pgs. 50-51)
Hot food burns
From soup or cheese on pizza
Products containing hydrogen peroxide or
eugenol

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Lesions Associated with Cocaine
Use
(pgs. 50-51) (Fig. 2-28C)
Lesions located at the midline of the hard palate may
vary from ulcers to keratotic lesions to exophytic
reactive lesions as a result of smoking crack cocaine.
Necrotic ulcers of the tongue and epiglottis have been
reported as a result of free-basing cocaine.

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Lesions from Self-Induced Injuries
(pgs. 51, 53-54)
A factitious injury
Due to a habit such as chronic lip, cheek or
tongue biting, or trauma to the teeth from a
fingernail
Lesions may range from ulceration to epithelial
hyperplasia and hyperkeratosis.

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Lesions from Self-Induced Injuries
(cont.)

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Hematoma
(pgs. 51-52)
A bruise inside the
mouth
Blood in an
extravascular space
Appears as a red to
purple to bluish-gray
mass
Most frequently seen
on labial or buccal
mucosa

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Traumatic Ulcer
(pgs. 51-53)
May be due to such events as biting the cheek,
lip, or tongue, irritation from a complete or partial
denture, mucosal injury from sharp edges of food,
or removal of a dry cotton roll after a dental
procedure (some patients are sensitive to the
starch in a cotton roll)
Persistent trauma may cause a hard (indurated), raised
traumatic granuloma.
Treatment
Usually heals within 7 to 14 days unless the trauma
persists
May require a biopsy

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Traumatic Ulcer (cont.)

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Frictional Keratosis
(pgs. 52, 54)
Due to chronic rubbing or friction against an oral
mucosal surface
A form of hyperkeratosis
Resembles a callus on skin
Results in a opaque white appearance
Treatment
Identify the traumatic cause of the lesion whether it be an
opposing third molar, chronic cheek or tongue chewing, or
some other entity.
Eliminate the cause.
Must be differentiated from idiopathic leukoplakia
because leukoplakia may be premalignant

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Frictional Keratosis (cont.)

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Linea Alba
(pgs. 52, 54)
A white, raised line most commonly on the buccal
mucosa at the occlusal plane
May be the result of a teeth clenching habit
Sometimes the pattern of the teeth can be seen in the
lesion.
Due to epithelial hyperplasia and hyperkeratosis
Treatment
None
May be used to evaluate severity of bruxing
and/or tongue thrusting habit

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Linea Alba (cont.)

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Nicotinic Stomatitis
(pgs. 52, 55)
A benign lesion typically associated with
pipe and/or cigar smoking; may also occur
with cigarette smoking
Presence indicates increased risk for
development of malignancy.
Initially, erythema is seen, but over time
keratinization takes place, resulting in
increased opacity.
Raised red areas may be seen at the openings of
ducts of minor salivary glands on the palatal surface.
This is due to obstruction by keratin at the mucosal
openings of the ducts.

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Nicotinic Stomatitis (cont.)

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Tobacco Pouch Keratosis
(pgs. 52, 55)
A white lesion located where chewing tobacco is
placed, most often in the mucobuccal fold
Early lesions may have a granular or wrinkled
appearance.
Long standing lesions may be more opaquely white and
have a corrugated surface.
Treatment
May require biopsy
Long-term exposure to chewing tobacco has been
associated with increased risk of squamous cell carcinoma.

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Tobacco Pouch Keratosis (cont.)

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Traumatic Neuroma
(pg. 53)
A lesion caused by injury to a peripheral nerve
When the nerve sheath of Schwann is disrupted,
occasionally the proximal end of damaged nerve
proliferates into a mass of nerve and Schwann cells
mixed with dense fibrous scar tissue.
Painful, ranging from pain on palpation to severe,
intractable pain
Diagnosis
Biopsy and microscopic examination
Treatment
Surgical excision

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Amalgam Tattoo
(pgs. 53, 55)
A flat, bluish-gray lesion of oral mucosa due to the
introduction of amalgam into tissue
May occur during placement or removal of an amalgam
restoration or during an extraction
May be seen in any location in the oral cavity, most
commonly on gingiva or alveolar ridge
Amalgam particles may be seen on radiograph, aiding in
diagnosis.
Diagnosis
Patient history and radiographs may help.
Must be differentiated from malignant melanoma
Treatment
None providing melanoma has been ruled out
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Amalgam Tattoo (cont.)

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Melanosis
(pgs. 54-55)
(see also pgs. 9, 24 and Figs. 1-18, 1-51)
Normal physiologic pigmentation of oral
mucosa
May be genetic
May occur as a result of inflammation due to
retained hemosiderin (a blood pigment)
retained in tissue

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Melanosis (cont.)

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Melanosis (cont.)
Oral Melanotic Macule
A flat, well-circumscribed lesion of unknown
cause
Less than 1 cm in diameter
Smokers Melanosis
Melanin pigmentation associated with smoking
More common in women than in men
Most common in anterior labial gingiva
Melanosis may also be associated with
genetic, bone, and systemic diseases.

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Solar Cheilitis (Actinic Cheilitis)
(pg. 56)
A degeneration of the tissue of the lips due to exposure to the sun
Occurs particularly in fair-skinned individuals
The lower lip is usually more involved than the upper lip.
The epithelium is thinner than normal; the vermilion appears
pale pink and mottled.
The interface between lips and skin is indistinct.
Treatment
No specific treatment
Biopsy may be indicated for persistent scaling or ulceration.
A relationship is found between these epithelial and
connective tissue changes and the development of basal
cell carcinoma of the skin or squamous cell carcinoma of
the lips and skin.

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Solar Cheilitis (Actinic Cheilitis)
(cont.)

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Mucocele
(pgs. 56-57)
A lesion that forms when a minor salivary gland duct is damaged
Not a true cyst
The mucous salivary gland secretion is walled off by granulation
tissue to form a cystlike structure lined by compressed granulation
tissue.
Most commonly found in the lower lip
It may increase or decrease in size over time.
May appear bluish if near the surface
Treatment
If persistent, they are surgically removed.
May observe a mucus cyst or mucus retention cyst
Usually in people over age 50
Treated by removal of affected salivary glands
These lesions must be differentiated from mucoepidermoid
carcinoma.
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Mucocele (cont.)

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Ranula
(pg. 56)
A unilateral mucocele-like lesion that forms
on the floor of the mouth
Associated with the ducts of submandibular
and sublingual glands

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Necrotizing Sialometaplasia
(pgs. 57-58)
A benign condition of salivary glands
Moderately painful swelling and ulceration
Thought to result from blockage of the blood
supply to the affected area
Necrosis of the salivary glands is seen histologically.
Salivary gland epithelium is replaced by squamous
epithelium (metaplasia).
The ulcer usually heals by secondary intention.

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Necrotizing Sialometaplasia (cont.)

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Sialolith
(pgs. 57-59)
A salivary gland stone
May be found in both minor and major salivary
glands
Formed by precipitation of calcium salts
around a central core
May often be seen on radiograph
Treatment
Sometimes the calcification can be milked
from the duct.
It may require surgical removal, this may
damage the duct.
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Sialolith (cont.)

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Acute and Chronic Sialadenitis
(pg. 58)
Painful swelling of the involved salivary
gland due to obstruction of the salivary
gland duct
May occur as result of infection
Diagnosis
May involve injection of a radiopaque dye into
the gland followed by a radiograph
(sialography)
Treatment
May require antibiotics

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Reactive Connective Tissue
Hyperplasia
(pgs. 58-63)
Pyogenic Granuloma
Giant Cell Granuloma
Irritation Fibroma
Denture-Induced Fibrous Hyperplasia
Papillary Hyperplasia of the Palate
Gingival Enlargement
Chronic Hyperplastic Pulpitis

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Reactive Connective Tissue
Hyperplasia (cont.)
(pg. 58)
Proliferating, exuberant granulation tissue
and dense fibrous connective tissue
resulting from overzealous repair
May be a response to a single event or chronic
low-grade injury

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Pyogenic Granuloma
(pgs. 58-59)
A proliferation of connective tissue
containing numerous blood vessels and
inflammatory cells occurring as a response
to injury
The name is a misnomer; the lesion is neither
pyogenic (pus forming) nor a true granuloma.

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Pyogenic Granuloma (cont.)

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Pyogenic Granuloma (cont.)
The lesion is usually ulcerated, soft to palpation,
and bleeds easily.
It is deep red to purple.
Generally elevated, may be sessile or pedunculated
Most commonly observed on the gingiva, it may be seen
on other intraoral areas
May vary in size from a few millimeters to several
centimeters
Usually develop rapidly and then remain static
Most common in teenagers and young adults, but may
occur at any age
If seen in a pregnant female, it is called a pregnancy
tumor.
Treatment
Surgically excised if it does not regress spontaneously

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Pregnancy Tumor
(pg. 58)
A pyogenic granuloma seen in a pregnant
woman
The lesions are identical to those seen in men
and nonpregnant women.
May be caused by hormonal changes and
increased response to plaque
They often regress after delivery.

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Pregnancy Tumor (cont.)

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Peripheral Giant Cell Granuloma
(pgs. 58, 60)
A lesion that contains many
multinucleated giant cells, well-
vascularized connective tissue, RBCs,
and chronic inflammatory cells
Occurs only in the jaws
Seems to originate from periodontal
ligament or periosteum in response to
injury
Peripheral
Lesions occurring outside of bone
Central
Lesions within bone of the mandible or
maxilla
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Peripheral Giant Cell Granuloma
(cont.)
Occurs on gingiva or alveolar process,
usually anterior to the molars
Vary in size from 0.5 to 1.5 cm
Usually dark red from vascularization
Most frequent in people from 40 to 60 years of
age
More common in women than in men
Treatment
Surgical excision

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Central Giant Cell Granuloma
(pgs. 58)
Occurs within the bone of the maxilla or mandible
Most frequent in children and young adults
More common in females than in males
Pain is not a common feature.
Usually discovered on routine radiographs
Radiolucent
Borders may be sclerotic or ill-defined.
Lesion may be unilocular or multilocular.
May cause divergence of roots of adjacent teeth
Treatment
Surgical removal
May recur

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Irritation Fibroma
(pgs. 60-61)
The most common mass on the
gingiva
A broad-based, persistent
exophytic lesion composed of
dense, scarlike connective tissue
with few blood vessels
The result of trauma such as cheek
chewing or cheek biting
Usually a small lesion, less than 1
cm in diameter
Most often occurs on buccal mucosa
May occur on tongue, lips, and palate

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Irritation Fibroma (cont.)
Usually lighter than surrounding mucosa
The surface is covered by stratified squamous
epithelium.
May be opaque if thick or ulcerated due to local
secondary trauma
Treatment
Surgically removed
Must be differentiated from many soft tissue
tumors

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Denture-Induced Fibrous Hyperplasia
(Epulis fissuratum) (Inflammatory
hyperplasia)
(pgs. 60-61)
Observed in the vestibule as elongated
folds of tissue into which of an ill-fitting
denture fits
Composed of dense, fibrous connective tissue
with a surface of stratified squamous
epithelium
The surface may be ulcerated.
Treatment
Surgical removal of excess tissue and
construction of a new denture

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Denture-Induced Fibrous Hyperplasia (Epulis
fissuratum) (Inflammatory hyperplasia) (cont.)

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Papillary Hyperplasia of the Palate
(Palatal papillomatosis)
(pgs. 60-62)
Almost always associated with a removable full or
partial denture or orthodontic appliance that is
worn continuously
The palatal vault is covered by multiple papillary
projections.
Each projection consists of fibrous connective tissue,
usually chronically inflamed and surfaced by stratified
squamous epithelium.
The cause is unknown.
Treatment
Surgical removal of the projections prior to construction
of a new denture

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Papillary Hyperplasia of the Palate
(Palatal papillomatosis) (cont.)

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Gingival Enlargement
(pgs. 61-62)
An increase in the bulk of free and
attached gingiva, especially the interdental
papillae
Gingival margins are rounded.
Color may vary from normal pink to pale or
erythematous depending upon the degree of
inflammation and vascularity.
May be generalized or localized

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Gingival Enlargement (cont.)

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Gingival Enlargement (cont.)
May vary from focal enlargement of interdental papillae
to severe generalized gingival enlargement that may
cover the crowns of teeth
Usually an unusual tissue response to chronic
inflammation associated with local irritants such
as plaque or calculus
May be from an increased response to local
tissue factors due to
Hormonal changes during pregnancy or puberty
Certain drugs such as phenytoin, calcium channel
blockers, and cyclosporine
May be hereditary

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Gingival Enlargement (cont.)
Treatment
Gingivoplasty
Reshaping the gingiva
Gingivectomy
Removing gingival tissue
Tissue may need to undergo a biopsy to
rule out gingival enlargement seen in
individuals with leukemia.

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Chronic Hyperplastic Pulpitis
(Pulp polyp)
(pg. 62)
An excessive proliferation of chronically
inflamed dental pulp tissue
In children and young adults, it occurs in teeth
with large, open carious lesions often in
primary and permanent molars.

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Chronic Hyperplastic Pulpitis
(Pulp polyp) (cont.)

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Chronic Hyperplastic Pulpitis
A red or pink nodule that fills the entire
cavity of the tooth, with tissue protruding
from the pulp chamber
Usually asymptomatic
May be related to the large root opening and
blood supply of the involved tooth
Primarily granulation tissue surfaced by a
stratified squamous epithelium
Treatment
Extraction or endodontic treatment of the
involved tooth

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Inflammatory Periapical Lesions
Periapical Abscess
Dental or Periapical Granuloma
Radicular Cyst (Periapical Cyst)
Resorption of Teeth
Focal Sclerosing Osteomyelitis
Alveolar Osteitis (Dry Socket)

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Inflammatory Periapical Lesions
(cont.)
(pg. 63)
Caries or trauma may result in
Inflammation
Infection
Chronic hyperplastic pulpitis
Necrosis of the pulp
The inflammatory process begins in pulp
and then extends to the periapical area.
Accessory canals may lead to areas of
inflammation on the lateral portion of the root.

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Periapical Abscess
(pgs. 38, 63)
Purulent exudate surrounded by
connective tissue containing neutrophils
and lymphocytes
Inflammation produces severe pain.
May develop directly from inflammation in
the pulp
More commonly develops in an area of
previously existing chronic inflammation

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Periapical Abscess (cont.)

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Periapical Abscess (cont.)
The pus may cause a fistula to form.
The tooth may be extruded.
If the acute abscess forms directly from
pulpal inflammation
There may be no radiographic changes except
for a slight thickening of the apical periodontal
ligament space.
If the abscess forms in a preexisting area
of periapical chronic inflammation
A distinct radiographic lucency may be seen at
the apex.
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Periapical Abscess
Treatment
May require incision and drainage of the
abscess
Endodontics or extraction

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Dental or Periapical Granuloma
(pgs. 63-64)
A localized mass of chronically inflamed
granula that forms at the opening of the
pulp canal, generally at the apex of a
nonvital tooth root
Granulation tissue with lymphocytes, plasma
cells and macrophages neutrophils may be
present
Usually asymptomatic
May be sensitive to pressure or percussion

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Dental or Periapical Granuloma
(cont.)

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Dental or Periapical Granuloma
(cont.)
The tooth may be slightly extruded from
the socket.
Radiographic
May vary from slight thickening of the
periodontal ligament space to a diffuse
radiolucency, to a distinct, well-circumscribed
radiolucency surrounding the root apex
Treatment
Endodontia or extraction

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Radicular Cyst (Periapical Cyst)
(pgs. 64-65)
A true epithelium-lined cyst
Associated with the root of a nonvital tooth
The most commonly occurring cyst in the
oral region
A result of proliferation of the rests of Malassez
Usually asymptomatic and discovered on
radiograph

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Radicular Cyst (Periapical Cyst)
(cont.)

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Radicular Cyst
Radiographic
The appearance is the same as for a periapical
granuloma.
Treatment
Endodontia, apicoectomy, or extraction and
curettage of periapical tissue

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Resorption of Teeth
(pgs. 65-66)
May occur when inflammation is present
Occurs in deciduous teeth during exfoliation
Can occur with excessive occlusal or
orthodontic forces or with benign or
malignant tumors
Rapid orthodontic movement in an adult may
cause external root resorption
A reimplanted tooth will resorb.
May be classified as external or internal

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External Root Resorption
(pg. 65)
Initially appears as a slight
raggedness or blunting of the
root apex
Not reversible
Progression can be avoided if
the cause is identified and
removed
Impacted teeth may resorb.

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Internal Tooth or Root Resorption
(pg. 65)
Idiopathic, thought to be associated with an
inflammatory response in the pulp
If seen within the crown, the tooth will appear pink due
to inflamed vascular connective tissue Pink tooth of
Mummery.
If seen within the root, it will be seen radiographically.
Treatment
If the root is not perforated, calcium hydroxide is placed
and endodontics performed in an attempt to save the
tooth.
If the tooth is perforated, it must be removed.

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Focal Sclerosing Osteomyelitis
(Condensing Osteitis)
(pgs. 65-66)
A change in the bone
near the apices of teeth
Thought to be a reaction to
low-grade infection
Generally asymptomatic;
if painful, may be
associated with pulpal
inflammatory disease

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Focal Sclerosing Osteomyelitis
Radiographic
Appears as a radiopaque area, most commonly
associated with the mandibular first molar
Borders may be diffuse or well-defined
Treatment
Usually not necessary
Biopsy may be required to rule out other
radiopaque lesions such as osteoma, complex
odontoma, or ossifying fibroma.

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Alveolar Osteitis (Dry Socket)
(pg. 66)
A postoperative complication following tooth
removal.
Most often in the area of the mandibular third molar
The blood clot is lost before healing can take
place, leaving raw, exposed nerve endings.
The patient may complain of pain, bad odor, and bad
taste.
Treatment
Daily application of Dry Socket Paste containing
eucalyptol until symptoms are relieved

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Discussion Questions
What cells appear first during an inflammatory
response?
What is the difference between healing by primary,
secondary, and tertiary intention?
What is the difference between regeneration and repair?
What is the difference between attrition, abrasion, and
erosion?
What injuries to oral soft tissues may be observed within
the oral cavity?
What is the definition of reactive tissue hyperplasia and
what forms may be observed within the oral cavity?
What inflammatory periapical lesions may be observed
within the oral cavity?

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