Oral Pathology Review List

(Based on NDEB OSCE Entities)

Disturbances in shape of teeth

Gemination: aka twinning
-attempt of tooth bud to form
two teeth
-may cause shift in the midline
-characterized radiographically
with widened root, enlarged shared
root canal

Concrescence
-joining of two teeth by way of
cementum only
-two tooth buds form two teeth,
but due to close proximity, there is
joining
-often the result of
overproduction of cementum
(hypercementosis)
-occurs late in development of
the teeth

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Cusplike elevation located in the central groove
of mandibular first bicuspid.
Talon cusp – specific form of dens evaginatus
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Fusion – two tooth buds combine to
form one large tooth (1 less than
normal amount of teeth)
Dens evaginatus
-accessory cusp on posterior
teeth (mostly premolar affected)
-usally, bilaterally symmetrical
-also, has pulp chamber. if
remove b/c may affect pulp
-can interfere with occlusion,
but have to be careful not to
just grind cusp away because
there may be pulp tissue inside
- A developmental anomaly
characterized by a cusplike
supernumerary focal enamel
protrusion on the occlusal or
lingual surface of the crown.
Talon cusp
-extra cusp on the lingual
surface of the maxillary anterior (esp.
lateral) teeth
-very frequently there is pulp
tissue existing in the extra cusp
-may cause occlusion problems
(interference)
 Den invaginatus (dens in dente = tooth
within a tooth)
-deep surface invagination of
the crown of the tooth
-most commonly affected tooth
is maxillary permanent lateral tooth
-radiographically, you can see
space/pit near cingulum area (looks
like key hole)
-air filled
-problem is bacteria invasion
into the dens invaginatus
leading to decay and pulpal
infection b/c not self-cleansing
and also very close to pulp
-treatment and management:
identify early, place restorative
material at opening

Hypercementosis: increased amount

of cementum (may lead to
concrescence)
-unlike enamel, cementum is
living tissue and thus undergoing
changes
-this may occur due to
inflammation that stimulate
cementoblasts to deposit more
-opposing tooth in dentition is
missing, and this causes over-
eruption and hypercementosis
-neoplasm may stimulate or
assist formation of more cementum
-significance: upon extraction,
rather than root tapering to the
apex, root is more bulbous at
the apex of the tooth and thus
more difficult to extract, root
canal treatment-the apical area
configuration is secure b/c
extra cementum
-more difficult to detect apex
of the tooth

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 Dilaceration: a sharp bend in tooth
structure, mainly root
-once a tooth is completely
formed, it will not bend
-however, if there was
something that caused a bend
in Hertzwig’s Epithelial
Sheaths (soft tissue), it will
cause a bend during formation
-extraction will be difficult and
could lead to fracture of the
root and root canal will be
difficult b/c curve

Supernumerary roots
-due to extra Hertzwig’s
Epithelial Root Sheaths
-consequences: difficulty of
extraction, roots may be very
fragile, endodontic treatment
will require one to know how
many root canals must be filled
-sometimes will see radiolucency at
apex of tooth—careful, it may
represent that tooth is still forming and
not fully calcified
Maxillary premolar with three roots
rather than the usual two.

Disturbances in structure of teeth

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 Dentinogenesis imperfecta (aka
Hereditary Opalescent Dentin)
-hereditary condition
-osteogenesis imperfecta looks
very similar to the above
condition, but bone is also
affected
-translucent looking teeth,
-weeakness of enameodentin
junction
-prone to fractures
-opalescent appearance to tooth
structure, enamel is normal but
dentin is not
Dentinogenesis imperfecta (DI). A, Radiograph of the teeth of a -junction between enamel and
young patient that reveals the globe-shaped crowns caused by
cervical constriction and obliteration of the coronal pulp. B, dentin is abnormal and thus
Panoramic radiograph revealing the coronal shape and complete enamel often chips off
obliteration of the pulpal chambers of nearly all teeth.
**radiographically, crown tends
to be more bulbous and there is
no pulp (Classic presentation of
this condition)
-vitality test may indicate no
vitality of tooth
-“Shell teeth”—looks very similar
radiographically, but extremely
rare

genetic condition: amelogenesis

imperfecta and this can present as enamel
hypoplasia (enamel normal, but there
is less of it) and hypocalcification
(normal amount of enamel, but poorly
mineralized)
-enamel may be soft,
discoloration
-excessive loss of tooth structure,
decreasing vertical dimension
-this may be difficult when
placing crowns because you need
enough tooth structure to hold
restorative material

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 Dentin dysplasia
a) Type I: more common
-crown appears normal, but
radiographically there is abnormalities
-appearance radiographically will
show very short roots, teeth
become mobile, and frequently
Dentin dysplasia (DD), type I. Patient there is radiolucency at the apex
exhibits normally shaped and colored teeth. representing an unknown
inflammatory response, pulps
may be completely lost by
obliteration or there may be
remnants of the pulp
Type II: quite rare
-affects deciduous teeth
-clinical abnormality of crown but
root is normal, so no mobility
-permanent teeth are normal
clinically, but the roots of
Dentin dysplasia (DD), type I. permanent teeth will exhibit
Panoramic radiograph depicting the calcification in the pulp chambers
obliteration of the pulp except for the
occasional chevron radiolucency,
shortened and W-shaped roots, and
periapical radiolucency.

Dentin dysplasia (DD), type II. Periapical

radiographs indicating teeth with relatively
normal roots and pulp chambers that contain
large pulp stones.

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 Regional odontodysplasia (aka ghost
teeth)
-enamel, dentin and cementum all
affected
-may be local vascular problem
causing teeth to be affected during
formation
-radiographically, teeth will
appear not very dense at all…almost
invisible

Internal resorption

External resorption

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 Attrition – loss of tooth structure due to
tooth to tooth contact.

Enamel hypoplasia/Turners tooth

-if there is decreased amount of
enamel matrix but normal
calcification, this would cause
decreased thickness of enamel but
still normal enamel
laterally symmetrically bilaterally occurs
Congenital absence of succedaneous
tooth/teeth

Disturbances of eruption of teeth

Impacted teeth
-not every impacted tooth extracted
because too much damage may be caused
-consequences: temporary or
permanent paresthesia of half of lip
if the impacted tooth has close
association with inferior alveolar
nerve

Impacted teeth. Completely (A) and partially impacted (B)

mandibular third molars. A large area of dental caries is present
on the distal aspect of the adjacent molar tooth. C, Vertically
impacted (embedded) premolar teeth.

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 ankylosis of teeth
-fusion of cementum to bone
-will halt eruption of tooth
-if tooth is fully erupted and
ankylosis occurs, extraction will be
difficult and often will cause the
crown to break
-often occurs with second
deciduous molar; result of
hypodontia (retained “E”)
Deciduous molar well below the occlusal
-as a consequence, overtime
plane of the adjacent teeth.
there is fusion of root to bone
-non-formation of second
premolar

Radiograph of an ankylosed deciduous

molar. Note the lack of periodontal
ligament space.

Developmental Defects of the Oral and Maxillofacial Region

Commissural lip pits: quite common
-depression found on the lips in the
commisure area

Fordyce’s granules
-occur most frequently on buccal mucosa
-elevations are yellowish in color
-represent ectopic (not in normal position)
sebaceous glands
-sebaceous glands are associated
with hair follicles because they
produce sebum which is an oily
substance
-histologically, you can see sebaceous
glands—located very superficially

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 Leukoedema: quite common (star)
-often visible in dark skinned individuals
who have a whitish corregated surface on
the buccal mucosa compared to lateral
tissue
-epithelial cells have an increased amount
of fluid in the cytoplasm and thus there is
increased relative thickness compared to
adjacent cells
-when you stretch the cheek, the whiteness
disappears

Fissured tongue: quite common and

asymptomatic
-more pronounced in elderly patients
-will exhibit furrowing and cracking of the
tongue near midline
-prominent fissuring of the tongue: may
harbour bacteria
-asymptomatic and does not need to be
treated other than brushing of dorsal
surface

Benign migratory glossitis (aka

geographic tongue, erythema migrams)
-usually asymptomatic, but some patients
may have a burning sensation
-in those cases, can be managed
with glucocorticosteroid (anti-
inflammatory)
-usually caused by hypersensitivity
to a stimulus
-filiform papilla is lost creating patches
(reddish appearance); fungiform papilla is
present which has increased keratin giving
them a whiter appearance
-patches will be surrounded by a
reddish/yellowish/white border—over a
period of days, filiform papilla may be re-
established but other regions will lose their
filiform papilla (therefore, movement of
redness created name erythema migrams)
-may rarely occur off the dorsal surface of

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 the tongue on ventral surface: reddish
appearance caused by decreased thickness
of the epithelium
-*geographic tongue and fissured tongue
frequently occurs together

(Black) Hairy tongue

-elongated filiform papilla
-caused by keratin deposit on the dorsal
surface of the tongue, and thus will cause
discoloration of white pigmented filiform
papilla
-not to be confused with hairy leukoplakia
(to be dealt with later)
-may treat with tongue scrapers to
exfoliate keratin

Buccal exostoses
-usually affects posterior regions
-increased amount of NORMAL bone
formation
-asymptomatic but if the extension is so
far to trap food underneath, may warrant
treatment
-if the patient requires dentures, then the
great undercut would not accept a denture
very well and thus may need pre-
prosthetic surgery
- radiographic ↑density
-biopsy: normal appearing bone

Varicosity/varicosities.
Oral Varices and thrombosed varix
-abnormally dilated veins
-common location on the ventral surface
of the tongue
-caused by increased intravascular
pressure
-blood flow will be slower, it causes a
greater tendency for clotting (thrombosed
varix)

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 -may find on the lower lip
-the fear is always an embolis,
which may travel to important
vasculature to cause damage (ie.
stroke)
-if oral varices, we would expect a positive
diascopy test; but if it is a thrombis, then
we would expect a negative diascopy test

Palatal or mandibular tori (torus palatinus,

torus mandibularis)
Torus palatines
- An exophytic nodular growth of dense
cortical bone located on the midline of the
hard palate.
-occurs on the midline of the palate
-usually asymptomatic, but again, may
require treatment for denture patients

Torus mandibularis: same concept

-may see radiographically due to increased
radiopacities (a lot of white oval circles on
the roots of the teeth)

Stafne bone defect (static bone cavity)

Entity: Lingual mandibular salivary gland
depression (Stafne bone cavity)

Clinical Signs/Features: Asymptomatic

radiolucency inferior to inferior alveolar nerve
canal in posterior region of mandible
(submandibular gland region). Thought that gland
disrupts development of mandible in this region
creating a depression.

Radiographic features: Radiolucency inferior to

inferior alveolar nerve canal in posterior mandible.

Treatment: Incisional biopsy to induce healing

Pulpal and Periapical Disease

Pulpitis (acute irreversible pulpitis, chronic irreversible pulpitis
i. Acute irreversible pulpitis
 Symptom
- severe throbbing pain without stimulation
- severe pain to thermal change: usually more pain from heat
- pain tends to be worse at night because as they lie down, blood fl

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 will increase to head region
 EPT
- Reading will be very high nearing or reaching 80/80

 Histologic findings
- main cells involved: PMNs (neutrophils), macrophages (histiocy

 Treatments: endodontic treatment (remove necrotic pulp), extraction

 Radiographic findings
- widening of PDL space at the apex of the tooth
- loss of lamina dura (if you look at normal teeth, you may not be
able to
see lamina dura all around the root of the tooth due to limitation of radiograph
ii. Chronic irreversible pulpitis
 Symptoms
- may have a dull ache
- heat/cold – no pain
 EPT
- 80/80
 Cause
- usually indicative of someone who suffers traumatic blow to the
face
 Histological findings
-main cells involved: macrophages, lymphocytes, plasma cells

 Treatments: endodontic treatment (remove necrotic pulp), extraction

Pulpal calcifications

Periapical abscess
 Sign and symptoms
- redness, heat, swelling, pain
- liquifaction of tissue forming localized collection of pus causing
pain
- no sensation of heat or cold
- the patient can still feel a lot of pain -nerves within the bone at th
apex of the tooth will cause the pain thus, another procedure is
percussion test

 parulis
 treatment
- I & D incision and drainage
- endodontics to relieve the pressure in the pulp chamber if there
not excessive swelling
- extraction
 EPT
- Not registering on the EPT (80/80)

 Radiographic findings
- Periapical radiolucency, usually with ill-defined borders

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 Parulis/fistula (star)

Hyperplastic pulpitis (pulp polyp)

iii. Chronic hyperplastic pulpitis (pulp polyp)
Specific type of chronic irreversible pulpitis
 Sign & Symptoms
- patient does not have significant symptoms
- usually a young patient
- bombed out crown due to caries--with pulpal exposure;
exposure to bacteria
- red mass growi
out of the pulp
- -usual treatmen
is extraction b/c cannot be cleaned out properly
FIGURE 3-22
Hyperplastic pulpitis.

Post surgical defect/scar (periapical fibrous scar) (star)

-if a patient has a periapical periodontitis and there exists an abscess that is draining
through the mucosa; there is breakage through the cortex
-if the patient has NSRT treatment and it doesn’t work, then will have to do SRT

-the hole created by SRT will usually heal up properly, however sometimes there is def
in bone (ie. abscess has broken through cortex and draining through) and after resolutio
of the noxious stimulus, there is healing by laying down of dense fibrous connective tis
leading to a periapical scar—will also present as radiolucency
-therefore, it becomes difficult to detect whether there is active inflammation or it is an
asymptomatic scar from looking at a radiograph

Figure 3-21 ♦ Periapical fibrous scar.

Periapical radiolucency of maxilla at the previous site of extraction in
which both cortical plates were lost. The site was filled with dense
collagenous tissue.

Acute periradicular abscess/acute periradicular periodontitis

Chronic periradicular periodontitis

Chronic periradicular abscess/suppurative periradicular

periodontitis

Periodontal Diseases

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Parulis (gingival abscess) in maxillary
mucosa and representing pus extension
from a periapical abscess.
Fig 4-8. Necrotizing ulcerative gingivitis
(NUG). Gingiva is friable and hemorrhagic
with necrosis of the interdental papillae.
Fig. 4-31 Periodontal abscess. Localized
erythematous gingival enlargement with central
purulent drainage.
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Gingival abscess (star)
Gingivitis associated with plaque only
Necrotizing ulcerative gingivitis - In a classic
case of NUG, the interdental papillae are
highly inflamed, edematous, and hemorrhagic.
Typically, the affected papillae are blunted and
demonstrate areas of “punched-out,” craterlike
necrosis that are covered with a gray
pseudomembrane (Fig. 4-8). A fetid odor,
exquisite pain, spontaneous hemorrhage, and
accumulations of necrotic debris usually are
noted. Although a bad odor is not always
noted, its absence in a patient without
predisposing factors should raise concern for
other pathoses such as gonorrhea (see page
193). Occasional ancillary clinical features
include lymphadenopathy, fever, and malaise
Generalized aggressive periodontitis
Periodontal abscess - A periodontal abscess
appears as a zone of gingival enlargement
along the lateral aspect of a tooth. The involved
gingiva may be erythematous and edematous,
with a slick, red surface, or it may be
hemorrhagic, with a dark-red coloration
Fig. 4-32 Periodontal abscess. Same patient as
depicted in Fig. 4-31. Note extensive loss of bone
support associated with the maxillary cuspid.

Fig. 4-33 Periodontal abscess. Dark-red and

hemorrhagic enlargement of the interdental papilla
between the maxillary right lateral incisor and
cuspid.

Necrotizing ulcerative periodontitis - NUP

presents similarly to NUG (see page 157), but
it also demonstrates loss of clinical attachment
and alveolar bone. This destructive form of
periodontitis may arise within a zone of
preexisting periodontitis, or it may represent a
sequela of a single or multiple episodes of
NUG. Many believe that NUG and NUP
represent different stages of the same infection.
Patients affected with this pattern frequently
are younger than most patients affected with
chronic periodontitis and often demonstrate
immunosuppression or malnutrition.

Generalized chronic periodontitis > 30% of

sites with pockets 4mm or greater.

Localized aggressive periodontitis - Localized

aggressive periodontitis typically begins
around the ages of 11 to 13 years and has a
strong familial tendency. The following
specific features have been delineated by the
American Academy of Periodontology:

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 • Circumpubertal onset
• Robust serum antibody response to
infecting agents
• Attachment loss localized to the first
molars and incisors, with involvement of no
more than two teeth other than the first molars
and incisors
In classic cases an arc-shaped zone of bone
loss extends from the distal aspect of the
second bicuspid to the mesial aspect of the
second molar. Similar involvement is
apparent around the anterior teeth. Tooth
migration and mobility are common. If
untreated, then the process often continues
until the teeth are exfoliated. In about one
third of patients affected with localized
aggressive periodontitis, progression to
more generalized disease occurs.

Localized chronic periodontitis < 30% of sites

with pockets of 4mm or greater

Drug influenced gingival

enlargement/hyperplasia

Mild phenytoin-related gingival hyperplasia.

Gingival enlargement present predominantly in the interdental
papillae.

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 Pericoronitis
Painful erythematous enlargement of the soft tissues overlying
the crown of the partially erupted right mandibular third molar.

Mucogingival deformity

Bacterial Infections
Syphilis (mucous patches of secondary
syphilis) (star)

Primary syphilis (chancre)

Mucous patch of secondary syphilis. Circumscribed

white plaque on the lower labial mucosa.

Tertiary syphilis; palatal fistula resulting from a

gumma.

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 Maxillary sinusitis
Rhinogenic
- History of URTI
- Bilateral sinus pain
- No halo sign
- Teeth vital
- Multiple teeth are percussion sensitive
- Antibiotics or surgery

Odontogenic

Fig 26-11 Halo sign suggests odontogenic •No history of URTI

infection (necrotic tooth) and less
commonly a root fracture •Unilateral sinus pain
•Halo sign
•Non-vital tooth
•Single tooth is percussion sensitive (dead tooth
most percussion sensitive)
Endodontics or extraction
Fluid level in sinus – not convex, changes with
head posture

Fungal Infections
Candidiasis
Acute pseudomembranous Candidiasis
-white lesion that can be wiped off (picture
shown, looks like “cottage cheese”)
-white lesion being wiped off represents pure
colonies
-underneath often red mucosa: burning
sensation
-rapidly proliferating
-common in infants: because their immune
Candidiasis, pseudomembranous type. response is based on mother’s passive
immunity and will have to wait until their
immune system fully develops

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 Chronic hyperplastic Candidiasis
-white lesion that cannot be wiped off;
looks like leukoplakia (picture shown)
-white lesion due to increased
proliferation of epithelium
-if we treat the fungal infection, the
thickness will decrease back to normal

Hyperplastic candidiasis. This lesion of the anterior

buccal mucosa clinically resembles a leukoplakia
because it is a white plaque that cannot be removed
by rubbing. With antifungal therapy, such a lesion
should resolve completely.

Acute atrophic Candidiasis

-burning sensation associated erythematous
lesion
-red lesion because there is inflammation
triggered by fungus
-thinning of mucosa under the lesion
-picture shown of palate with red lesion
(erythematous candidiasis = atrophic
candidiasis)

Erythematous candidiasis. A, Severe presentation of

central papillary atrophy. In this patient the lesion
was asymptomatic. B, Marked regeneration of the
dorsal tongue papillae occurred 2 weeks after
antifungal therapy with fluconazole.

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 Chronic atrophic Candidiasis
-patient may have minimal symptoms
-found frequently under an ill-fitting, poorly
maintained appliance
-red lesion

Angular cheilitis - crusting on side of mouth

Median rhomboid glossitis

-depapillated lesion
-midline of dorsal tongue
-just anterior to foramen cecum
-cases of fungus causes depapillation
-should also look at posterior palate

Viral Infections

Herpes simplex virus: HSV-1 is spread

predominantly through infected saliva or
active perioral lesions. HSV-1 is adapted best
and performs more efficiently in the oral,
facial, and ocular areas. The pharynx,
intraoral sites, lips, eyes, and skin above the
waist are involved most frequently.
HSV-2 is adapted best to the genital zones, is
transmitted predominantly through sexual
contact, and typically involves the genitalia
and skin below the waist. Exceptions to these
rules do occur, and HSV-1 can be seen in a
pattern similar to that of HSV-2 and vice
versa.

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Fig. 7-8 Intraoral recurrent herpetic
infection. Multiple coalescing ulcerations
on the hard palate.
Fig. 7-6 Herpes labialis. Multiple sites of
recurrent herpetic infection secondary to
spread of viral fluid over cracked lips.
Fig. 7-1 Acute herpetic gingivostomatitis.
Widespread yellowish mucosal
ulcerations. (Courtesy of Dr. David
Johnsen.)
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Recurrent herpes simplex (herpes labialis,
cold sore, fever blister)
The most common site of recurrence for
HSV-1 is the vermilion border and
adjacent skin of the lips. This is known as
herpes labialis (“cold sore” or “fever
blister”). Recurrent herpes simplex
usually only occurs on bound down
mucosa
Primary herpetic gingivostomatitis. Acute
herpetic gingivostomatitis (primary
herpes) is the most common pattern of
symptomatic primary HSV infection, and
more than 90% are the result of HSV-1. Most
cases of acute herpetic gingivostomatitis arise
between the ages of 6 months and 5 years,
with the peak prevalence occurring between 2
and 3 years of age. Initially the affected
mucosa develops numerous pinhead vesicles,
which rapidly collapse to form numerous
small, red lesions. These initial lesions
enlarge slightly and develop central areas of
ulceration, which are covered by yellow
fibrin (Fig. 7-1). Adjacent ulcerations may
coalesce to form larger, shallow, irregular
ulcerations (Fig. 7-2). Both the movable and
attached oral mucosa can be affected, and the
number of lesions is highly variable. In all
cases the gingiva is enlarged, painful, and
extremely erythematous. Mild cases usually
resolve within 5 to 7 days; severe cases may
extend to 2 weeks.
 Herpes zoster
-Varicella-Zoster virus
-first exposure is chicken
pox, recurrent condition is known as shingles
-when a person has shingles, it’s a segment of
tissue that is involved by vesicles: usually on
trunk of back that does not cross midline
-present intraorally by travelling along
division of 2nd or 3rd division of
trigeminal…does NOT cross midline (key
feature!)
-picture shown of guy with white patches all
over one side of face
Oral lesions occur with trigeminal nerve
involvement and may be present on the
movable or bound mucosa.

Fig. 7-18 Herpes zoster. Numerous

crusting facial vesicles that extend to the
midline.

Fig. 7-19 Herpes zoster. Numerous white

opaque vesicles on the right buccal
mucosa of the same patient depicted in
Fig. 7-18. (star)

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Fig. 7-23 Herpangina. Numerous
aphthouslike ulcerations of the soft palate.
(star)
Physical and Chemical Injuries
Fig. 8-1 Linea alba. White line of
hyperkeratosis on the right buccal mucosa
at the level of the occlusal plane.
Fig. 8-2 Morsicatio buccarum. Thickened,
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Herpangina: -caused by Coxsackie virus
-presents with acute onset sore throat,
pharyngitis, fever and malaise
-in the posterior aspect of oral cavity
(pharynx, soft palate), little vesicles will form
and break down
-very contagious
-picture shown of red looking ulcers in
posterior palate
Most cases, however, are mild or subclinical.
A small number of oral lesions, usually two
to six, develop in the posterior areas of the
mouth, usually the soft palate or tonsillar
pillars (Fig. 7-23). The affected areas begin as
red macules, which form fragile vesicles that
rapidly ulcerate. The ulcerations average 2 to
4 μm in diameter. The systemic symptoms
resolve within a few days; as would be
expected, the ulcerations usually take 7 to 10
days to heal.
Linea alba: Linea alba (“white line”) is a
common alteration of the buccal mucosa
that most likely is associated with pressure,
frictional irritation, or sucking trauma from
the facial surfaces of the teeth.
Morsicatio buccarum (chronic check bites,
cheek/lip biting) (star)
Most frequently, the lesions in patients
with morsicatio are found bilaterally on the
anterior buccal mucosa. They also may be
unilateral, combined with lesions of the
lips or the tongue, or isolated to the lips or
tongue. Thickened, shredded, white areas
may be combined with intervening zones
of erythema, erosion, or focal traumatic
ulceration (Figs. 8-2 and 8-3). The areas of
white mucosa demonstrate an irregular
shredded areas of white hyperkeratosis of ragged surface, and the patient may
the left buccal mucosa. describe being able to remove shreds of
white material from the involved area.

Mucosal burn
Clinical Signs/Features: Caused by physical
(e.g. heat, electrical) or chemical (e.g. aspiring
burn, sodium hypochlorite, acid etch) means.

Treatment: Remove source of cause and allow

injury to heal.

Figure 8-13 ♦ Electrical burn.

Yellow charred area of necrosis along the left oral commissure. (Courtesy of Dr. Patricia
Hagen.)

Figure 8-14 ♦ Thermal food burn.

Area of yellow epithelial necrosis of the posterior soft palate on the left side. Damage was due
to attempted ingestion of hot pizza.

Figure 8-15 ♦ Aspirin burn.

Extensive area of white epithelial necrosis of the left buccal mucosa caused by aspirin
placement in an attempt to alleviate dental pain.

Figure 8-16 ♦ Hydrogen peroxide burn.

Extensive epithelial necrosis of the anterior maxillary gingiva secondary to interproximal
placement of hydrogen peroxide with cotton swabs.

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Figure 8-19 ♦ Cotton roll burn.
Zone of white epithelial necrosis and erythema of the maxillary alveolar mucosa.
Amalgam tattoo (foreign body)
Caused by foreign material in tissue (e.g.
amalgam embedded in tissue may cause
amalgam tattoo). Usually occurs in area where
material was used (e.g. restorative material).
Determine what it is via “guilty by
association”. A common example is an
amalgam tattoo – in most cases no
inflammatory reaction (same with glass).
Materials can become embedded in tissue when
Figure 8-38 ♦ Amalgam tattoo. being drilled out. Common location is hard
Area of mucosal discoloration of the floor of the mouth on the patient's left side.
palatal mucosa or gingiva.

Radiographic features: If large enough, foreign

body (e.g. amalgam, graphite) may show up
radiographically.

Treatment: Monitor lesion unless it is getting

larger – then biopsy. (make sure that it is not
something else b/c can look like nevus, oral
melanotic macule, melanoma).

Figure 8-39 ♦ Amalgam tattoo.

Area of mucosal discoloration of the mandibular alveolar ridge immediately below the bridge
pontic.

Figure 8-40 ♦ Amalgam tattoo.

Radiograph of the same patient depicted in Figure 8-39. Note the radiopaque metallic fragment
present at the site of mucosal discoloration.

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Figure 8-41 ♦ Amalgam tattoo.
Radiographic appearance of amalgam tattoo of lingual gingival mucosa adjacent to the
mandibular third molar. Note the pinpoint radiopaque metallic fragments overlying the crestal
and mesial portions of the root (arrows).

Physiologic/racial pigmentation
Most common on attached gingiva in
darker complexioned patients

Fig. 10-79 Tobacco pouch keratosis, mild. A

soft, fissured, gray-white lesion of the lower
labial mucosa located in the area of chronic
snuff placement. The gingival melanosis is
racial pigmentation and not associated with
the keratosis.
Antral pseudocyst/maxillary sinus retention
cyst
Clinical Signs/Features: Accumulation of fluid
between the mucosa and floor of the maxillary
sinus.

Radiographic features: Dome shaped lesion in

maxillary sinus area – appears as relative
radiopacity because cyst filled with fluid which
is more radiopaque than air. Not known why it
Figure 8-52 ♦ Antral pseudocyst. occurs – may be due to an inflammatory
reaction (i.e. nonvital tooth)

Treatment: None. Recognize it for what it is.

(only treat tooth if associated with a nonvital
tooth)

27
 Denture induced trauma
Denture related injuries caused by ill fitting or
poorly maintained dentures:

i) Entity: Traumatic ulcer

-very common

Clinical Signs/Features: Caused by ill-fitting,

overextended denture. Sufficiently high grade
Figure 6-8 ♦ Denture stomatitis.
irritation to cause ulceration.
Denture stomatitis in association with an interim partial denture. Note that the mucosal
alteration is confined to the denture-bearing mucosa.
Treatment: Adjust denture to correct
impingement. If irritation removed, ulcer
should heal within 10-14 days. (if doesn’t –
reassess b/c probably something else!)

ii) Entity: Denture stomatitis

Clinical Signs/Features: Occurs under denture

bearing area. Low grade inflammatory
condition caused by ill-fitting, poorly
Figure 6-9 ♦ Denture stomatitis. maintained denture. With present as erythrema
Denture stomatitis, not associated with Candida albicans, confined to the denture-bearing
mucosa of a maxillary partial denture framework. due to inflammation. Patient may report
burning sensation. May be associated with
Candida infection.

Treatment: Reline or replace denture. Patient

education on how to keep denture clean, take
denture out at night.

iii) Entity: Inflammatory fibrous hyperplasia

Clinical Signs/Features: Proliferation of

fibrous connective tissue due to inflammatory
cause. Can occur in association with an ill-
fitting denture – i.e. overextended denture
flange.

Treatment: Remove irritation (fix denture or

replace it) to remove the inflammatory
Figure 12-12 ♦ Epulis fissuratum. condition. Excise and biopsy hyperplastic
A, Several folds of hyperplastic tissue in the maxillary vestibule. B, An ill-fitting denture fits
into the fissure between two of the folds. tissue.

Epulis fissuratum – (epulis = lump, fissuratum

= groove) name given to this entity when cause
is specifically associated with a denture.

iv) Entity: Inflammatory papillary hyperplasia

Clinical Signs/Features: Occurs on palate

underneath ill-fitting denture. Proliferation of
Figure 12-13 ♦ Epulis fissuratum. epithelium due to inflammatory cause. Heavily
Redundant folds of tissue arising in the floor of the mouth in association with a mandibular roughened surface due to epithelial
denture.
proliferation. Can appear as red papillary
lesion that is diffuse. May be associated with
fungal infection (patient may experience

28
 burning sensation in this case).

Treatment: Remove denture for 10-14 days to

resolve infection (fix or replace denture).
Papillated surface will still remain and may
need to be surgically removed.

v) Entity: Denture Allergy (rare)

Clinical Signs/Features: Redness in denture

Figure 12-16 ♦ Inflammatory papillary hyperplasia. (star) bearing area. Patient may experience burning
Erythematous, pebbly appearance of the palatal vault.
sensation within minutes of contact with
denture. May be caused by incomplete curing
of the denture material. Partial denture patients
may react to the metal component (metal
allergy).

Treatment: Remove denture and symptoms will

resolve within hours.

Figure 12-17 ♦ Inflammatory papillary hyperplasia. (star)

An advanced case exhibiting more pronounced papular lesions of the hard palate.

Tooth brush induced trauma

Entity: Abrasion

Clinical Signs/Features: Loss of tooth structure

via physical means due to non-tooth to tooth
contact. Examples include tooth brush
abrasion, loss of enamel due to opening beer
bottles with teeth, carpenter with grooves in
teeth for nails.

Figure 2-11 ♦ Abrasion.

Horizontal cervical notches on the anterior mandibular dentition.

Occlusal trauma
Entity: Attrition

Clinical Signs/Features: Loss of tooth structure

with age due to physical tooth to tooth contact.
-bruxism may speed up the process
-process becomes faster once dentin reached
-severe anterior attrition occurs when there are
no posterior contacts in occlusion
Figure 2-10 ♦ Attrition.
Extensive loss of coronal tooth height without pulp exposure in patient with anterior edge-to- Radiographic features: loss of cusp tips
edge occlusion.

Occlusal trauma (primary) – normal

periodontal support, but tooth mobility
due to large oclusal forces.
Occlusal trauma (secondary) – normal
occlusal forces, but tooth mobility due

29
 to decreased periodontal support.
Traumatic purpura (hematoma, petechiae,
ecchymosis)
Entity: Hematoma, ecchymosis, petechiae

Clinical Signs/Features: Trauma resulting in

breakage of blood vessels. Appears as
collection of blood, diffuse bleed, pinpoint
bleed respectively.

Treatment: Will resolve on own in 10-14 days.

Figure 13-11 ♦ Thrombocytopenia.
This dark palatal lesion represents a hematoma caused by a lack of normal coagulation,
Hematoma – localized collection of
characteristic of thrombocytopenia.
blood
Ecchymosis – diffuse collection of
blood
Petechiae – pinpoint bleed

Figure 8-34 ♦ Palatal petechiae from fellatio.

Submucosal hemorrhage of the soft palate resulting from the effects of negative pressure.

Subcutaneous emphysema
Entity: Cervicofacial emphysema

Clinical Signs/Features: Patient presents with

swollen face, crepitus (crackling sensation on
palpation because air is moving along the facial
planes)
-caused by breach where air is getting in; air
may be contaminated with bacteria therefore
patient is given antibiotics
-reason why we do not blow air into
periodontal pockets or root canals
-most cases occur within 1 hour postoperatively

Treatment: Prescribe antibiotics for bacteria

(body will take care of air).
Figure 8-56 ♦ Cervicofacial emphysema.
Periorbital and facial enlargement caused by use of an air-driven handpiece during third molar
removal.

Denture stomatitis – see denture related

injuries above

30
 Radiation mucositis - Painful acute
mucositis and dermatitis are the most
frequently encountered side effects of
radiation, but several chronic alterations
continue to plague patients long after their
courses of therapy are completed. (star)

Fig. 8-22 Radiation mucositis. A, Squamous cell

carcinoma before radiation therapy. Granular
erythroplakia of the floor of the mouth on the
patient's right side. B, Same lesion after initiation of
radiation therapy. Note the large, irregular area of
epithelial necrosis and ulceration of the anterior floor
of the mouth on the patient's right side. C, Normal
oral mucosa after radiation therapy. Note resolution
of the tumor and the radiation mucositis.
Nicotine stomatitis
Entity: Nicotine stomatitis

Clinical Signs/Features: White elevations with

red centers on hard and soft palate representing
dilated and inflamed minor salivary glands. It
is the heat from smoking rather than the
chemicals that causes the inflammation
(condition due to chronic exposure to heat).
Figure 10-84 ♦ Nicotine stomatitis.
This extensive leathery, white change of the hard palate in a pipe smoker is sprinkled
throughout with numerous red papules, which represent inflamed salivary duct openings. The Treatment: Advise patient to quit smoking and
gingival mucosa also is keratotic. condition should regress.

31
Figure 10-85 ♦ Nicotine stomatitis. (star)
Close-up of the inflamed ductal openings of involved salivary glands of the hard palate. Note
the white keratotic ring at the lip of many of the inflamed ducts.

Allergies and Immunologic/immune-mediated Diseases

Aphthous ulcers (major, minor, herpetiform)

Minor: Patients with minor aphthous

ulcerations experience the fewest
recurrences, and the individual lesions
exhibit the shortest duration of the three
variants. The ulcers arise almost
exclusively on nonkeratinized mucosa
and may be preceded by an erythematous
Fig. 9-6 Minor aphthous ulceration. Single macule in association with prodromal
ulceration of the anterior buccal mucosa. symptoms of burning, itching, or
stinging. The ulceration demonstrates a
yellow-white, removable fibrinopurulent
membrane that is encircled by an
erythematous halo (Fig. 9-4). Classically,
the ulcerations measure between 3 and 10
mm in diameter and heal without
scarring in 7 to 14 days.

Fig. 9-7 Major aphthous ulceration. Large, Major: Major aphthous ulcerations are
deep, and irregular ulceration of the larger than minor aphthae and
posterior buccal mucosa. Note extensive demonstrate the longest duration per
scarring of the anterior buccal mucosa episode. The number of lesions usually is
from previous ulcerations. (star) intermediate between that seen in the
minor and herpetiform variants. The
ulcerations are deeper than the minor
variant, measure from 1 to 3 cm in
diameter, take from 2 to 6 weeks to heal,
and may cause scarring (Fig. 9-7).

Herpetiform: Herpetiform aphthous

32
 ulcerations demonstrate the greatest
number of lesions and the most frequent
recurrences. The individual lesions are
small, averaging 1 to 3 mm in diameter,
with as many as 100 ulcers present in a
single recurrence. Because of their small
size and large number, the lesions bear a
superficial resemblance to a primary
HSV infection, leading to the confusing
designation, herpetiform. It is common
Fig. 9-8 Major aphthous ulceration. Large, for individual lesions to coalesce into
irregular ulceration of the soft palate. larger irregular ulcerations (Fig. 9-9).
The ulcerations heal within 7 to 10 days,
but the recurrences tend to be closely
spaced. Many patients are affected
almost constantly for periods as long as 3
years. Although the nonkeratinized,
movable mucosa is affected most
frequently, any oral mucosal surface may
be involved. There is a female
predominance, and typically the onset is
Fig. 9-9 Herpetiform aphthous ulcerations. in adulthood.
Numerous pinhead ulcerations of the
ventral surface of the tongue, several of
which have coalesced into larger, more
irregular areas of ulceration.
Allergic reactions
An allergic reaction of the oral mucosa to the
systemic administration of a medication is
called stomatitis medicamentosa. Besides
erythema multiforme (see page 776),
several different patterns of oral mucosal
disease can be seen:
• Anaphylactic stomatitis
• Intraoral fixed drug eruptions
• Lichenoid drug reactions
Figure 9-29 ♦ Allergic mucosal reaction to systemic drug administration.
Large irregular erosion of the right ventral surface of the tongue. The lesion arose • Lupus erythematosus–like eruptions
secondary to use of oxaprozin, a nonsteroidal anti-inflammatory drug.
• Pemphigus-like drug reactions
• Nonspecific vesiculoerosive or
aphthouslike lesions

Entity: Allergic reactions

i) Stomatitis medicamentosa
-inflammation of mucous membrane of oral
cavity due to systemic administration of a
medication
Figure 9-27 ♦ Allergic mucosal reaction to systemic drug administration.
Mucosal lesions associated with use of oxybutynin chloride (anticholinergic therapy for ii) Stomatitis venenata

33
urinary incontinence). Note lichen planus-like striae. In addition, multiple superficial
mucoceles occurred on the soft palate, floor of the mouth, and bilaterally on the buccal
-contact of material/agent directly to oral cavity
mucosa. causing allergic reaction
-similar to poison ivy contacting the skin

-plasma cell gingivitis: identified with burning

sensation and pronounced erythema of gingiva –
occurs frequently in teenage females
-believed to be caused by a reaction to
constituent(s) of products such as chewing gum,
mouthwash, prophy paste etc
-lips, eyes very susceptible

Figure 9-30 ♦ Allergic contact stomatitis to aluminum chloride.

Mucosal erythema and vesicles of the lower labial mucosa caused by use of aluminum
chloride on gingival retraction cord.

Figure 9-31 ♦ Allergic contact stomatitis to toothpaste.

Erythematous mucosa with superficial epithelial desquamation.

Pemphigus vulgaris
Pemphigous Vulgaris (vulgaris meaning
“common”)
-autoimmune disorder, rare
-clinical presentation is a bulla on
mucosa, skin
-target site of pemphigous is intercellular
attachment of epithelium, basement
membrane is still intact
Fig. 16-49 Pemphigus vulgaris. Multiple -blister forms but basal cells are still
erosions of the left buccal mucosa. attached to underlying lamina propria but
above basal cells, epithelial cells are
separating from each other
-very dramatic Nikolsky
sign…extremely difficult to do biopsy
-again, two biopsies will be
required as above
-picture shown of person with skin all
over body just peeling offmust see

34

Fig. 16-50 Pemphigus vulgaris. Large,
irregularly shaped ulcerations involving
the floor of the mouth and ventral tongue.
(star)
Fig. 16-63 Mucous membrane pemphigoid. -pemphigoid is a condition that has
One or more intraoral vesicles, as seen on
the soft palate, may be detected in patients occur on mucous membrane or skin only
with cicatricial pemphigoid. Usually,
ulcerations of the oral mucosa are also
present.
Fig. 16-65 Mucous membrane pemphigoid.
Often the gingival tissues are the only
affected site, resulting in a clinical pattern
known as desquamative gingivitis. Such a
pattern may also be seen with lichen
planus and pemphigus vulgaris. (star)
35
dermatologist immediately
-treatment is glucocorticosteroids: HIGH
DOSE
Cicatrical pemphigoid (benign mucous
membrane pemphigoid)
Mucous membrane pemphigoid
-autoimmune disorder
-immune system is producing antibodies
that are destroying specific antigens
-target site is basement membrane
between epithelium and lamina propria;
on skin, target is on basement membrane
between epidermis and dermis
multiple subtypes, some scar, some only
and thus presentations are many
-clinical presentation, all above subtypes
look the same but the target antigens are
different for different subtypes
-appears as a large blister, or bulla, and
this forms because basement membrane
is destroyed and thus outer layer of
blister is epithelium, inner layer is lamina
dura and blisters breakdown to form
ulcer—basement membrane no longer
present to hold two layers together
-picture shown of white lesion on buccal
mucosa (looks like a large white blister)

Fig. 16-74 Erythema multiforme. The
concentric erythematous pattern of the
cutaneous lesions on the fingers resembles
a target or bull's-eye. (star)
Fig. 16-75 Erythema multiforme. Diffuse
ulcerations and erosions involving the
dorsal surface of this patient's tongue.
Star)
Fig. 16-76 Erythema multiforme.
Ulceration of the labial mucosa, with
hemorrhagic crusting of the vermilion
zone of the lips.
36
Erythema multiforme
Erythema multiforme
-multiple presentations as indicated
by name
-intraorally, can be lesions that can
be erythema, ulcerations, blisters
-classic skin lesion that occurs in
conjunction: “bullseye, target, iris” are
common name given to concentric rings of
different coloured pigmentation
-approx. 50% cases, can determine cause of
lesion and it is due to immunologic reaction
to a herpes simplex infection
-may be related to medication intake,
following a vaccination, following radiation
-approx. 50% of cases, can’t determine what
triggers the condition
-prognosis variable (mild to life threatening)
-picture shown of little girl’s back with
multifocal brown skin lesions
-close up view of skin lesion: bullseye target
shape…blister in middle surrounded by
white ring
-intraoral lesion showing collapsed blister on
ventral surface of tongue
i) Stevens-Johnson syndrome
-severe form of disease, but
will run its course
-tends to occur in males in
their 20s, explosive progression
-significant oral, eye,
genital, and skin lesions
ii) Toxic epidermal necrolysis
-life threatening condition
-sheets of skin peel right off
-picture shown of individual
who underwent autopsy

Fig. 16-92 Lichen planus. The interlacing
white lines are typical of reticular lichen
planus involving the posterior buccal
mucosa, the most common site of oral
involvement.
Fig. 16-94 Lichen planus. Reticular lesions
of the lower lip vermilion.
Fig. 16-97 Lichen planus. Ulceration of the
buccal mucosa shows peripheral radiating
keratotic striae, characteristic of oral
erosive lichen planus.
37
Lichen planus
-muco-cutaneous disorder and thus will skin
and/or oral lesions
-skin lesions: described by the 4 P’s-
-purple, papules, polygonal, pruritic (itchy)
-tend to occur on the
extremities, bilaterally symmetrical
-tend to occur on insides of
wrists, elbows, behind knee
-picture shown of wrist
with little pimples
-oral lesions: various presentations
i) reticular (most common)
-asymptomatic,
recognize it but no treatment
-most common
location is buccal mucosa
-presents as tiny white papules that string out
to form a spiderweb, lace-like appearance
known as Striations of Wickham
-picture shown of stringy white lesion on
buccal mucosa
-may evolve into another form of lichen
planus that need to treat
ii) plaque like
-not a common presentation
of lichen planus
-dorsal of tongue is common
location, gingiva
-tiny white papules, instead of forming
spiderweb, will coalesce to form a plaque-
like patch
-picture shown of white powdery looking
patch on dorsal tongue
-asymptomatic, does not need to be treated
iii) atrophic
-symptomatic:
burning sensation
-reticular like appearance with red
background because the epithelium is thinner
in that region (representative of atrophic
lesion), spicy foods will cause burning
-may resolve into a reticular form, or my
evolve to erosive form
iv) erosive
-significant pain
associated, ulcers present
-picture shown of
white striations beside an ulcer, erythema
-this presentation is
like a combination of all the above

Fig. 16-114 Systemic lupus erythematosus
(SLE). The erythematous patches seen in
the malar regions are a characteristic sign.
Fig. 16-115 Systemic lupus erythematosus
(SLE). Irregularly shaped ulcerations of
the buccal mucosa.
38
conditions
-if left untreated, chronic ulceration and
resolve will lead to fibrous deposition on
cheek
-Etiogenesis: hypersensitivity reaction; too
much of an immune response, band like of
inflammation made up of lymphocytes
attacking basal cells above epithelium
(vacuolapathy: early destruction of basal
cells)
-Treatment and management with
immunosuppressant medications such as
glucocorticosteroids—can be administered as
a topical (good for skin lesions, but orally
more difficult b/c of saliva), injection into
the lesion, pill form (Prednisone)
Lupus erythematosus (star)
-autoimmune disorder
-antibodies are produced against
certain target sites: nuclear material of
cells
-systemic condition is serious
disease, life threatening
-classic lesion associated with this
condition is “butterfly rash” which is an
erythema that goes over bridge of nose
going over to malar surfaces of the face
-two other forms are common
-chronic cutaneous lesions are non-
specific: may present as erythema,
ulceration
-picture shown of characteristic lesion:
erythema with peripheral white striations
-biopsy of lesion will give certain
histologic features to give clues
Fig. 16-117 Chronic cutaneous lupus
erythematosus (CCLE). Radiating
keratotic striae surround erythematous
zones of the buccal mucosa. These features
are similar to those of erosive lichen
planus.

Epithelial Lesions
Entity: Papilloma

Clinical Signs/Features: Asymptomatic. Elevated

lesion, firm to palpation. Tends to be pale and
whitish in color. Roughened papillated surface.
May be pedunculated or sessile.

Treatment: Excisional biopsy.

Figure 10-1 ♦ Squamous papilloma.

An exophytic lesion of the soft palate with multiple short, white surface projections.

Figure 10-2 ♦ Squamous papilloma.

A pedunculated lingual mass with numerous long, pointed, and white surface
projections. Note the smaller projections around the base of the lesion.

Entity: Verruca vulgaris

Clinical Signs/Features: Virally induced lesion

(caused by human papilloma virus HPV).Has a
verruciform (wart-like) appearance. Pale, elevated
wart like appearance. Lesion may be transmitted to
other areas because virus caused.

Treatment: On skin- use chemicals. In oral cavity -

Figure 10-6 ♦ Verruca vulgaris.
excisional biopsy. Removal of lesion does not
Several warts on the finger, exhibiting a rough, papillary surface.

39
 guarantee elimination of virus therefore lesion may
recur.

Figure 10-7 ♦ Verruca vulgaris.

Exophytic, white, papillary lesion of the lateral soft palate.

Oral melanotic nevus/macule

Entity: Acquired melanocytic nevus (nevus)

Clinical Signs/Features: Benign neoplasm of

Figure 10-44 ♦ Melanocytic (intradermal) nevus.
A pigmented, well-demarcated, dome-shaped papule is seen at the edge of the
vermilion border of the upper lip.
melanocytes. May appear as flat or elevated lesion
brown or black in color. Flat lesion will appear
similar to oral melanotic macule or melanoma.
Slow in growth. Common on skin, much less
common in oral cavity.
Types:
i) Junctional – theques of cells at junction of
basement membrane an lamina propria.
ii) Compound – theques of cells in both basement
membrane and lamina propria.
iii) Intradermal – theques of cells in lamina propria.

Treatment: Excisional biopsy to make sure it is not

a melanoma.

Figure 10-46 ♦ Intramucosal melanocytic nevus.

Pigmented lesion of the anterior hard palate. (Courtesy of Dr. Lewis Claman.)

Figure 10-47 ♦ Intramucosal melanocytic nevus.

This intramucosal nevus (arrow) of the mandibular gingiva is nonpigmented. (Courtesy
of Dr. John Lenox.)

40
 Leukoplakia – clinical term only – not a term
used in diagnosis
-white patch that:
a) cannot be wiped off
b) does not resolve significantly within 10 – 14 days
after removal of suspected stimulus
c) for which a more specific diagnosis cannot be
made

Leukoplakias represent:
Figure 10-59 ♦ Early or thin leukoplakia.
This early lesion of the ventral tongue is smooth, white, and well demarcated from the 1)hyperkeratosis and/or acanthosis (80% of
surrounding normal mucosa. leukoplakia):
-hyperkeratosis - increased production of keratin –
appears white due to increased thickness of
epithelium
-acanthosis – increased number of spinous cell
layers – thicker epithelium

2)hyperkeratosis an/or acanthosis with epithelial

dysplasia (18% of leukoplakia):
-represents pre-malignant condition
Figure 10-60 ♦ Homogeneous or thick leukoplakia.
A diffuse, corrugated white patch on the right ventral surface of the tongue and floor of
mild – 25% epithelium affected, moderate -50%,
mouth. severe -75%, carcinoma in situ -100%

3) Squamous cell carcinoma (2% or leukoplakias)

Treatment: Excisional biopsy

Figure 10-61 ♦ Homogeneous or thick leukoplakia.

Extensive buccal mucosa lesion with an uneven whiteness and fissures. Moderate
epithelial dysplasia was noted on histopathologic evaluation, and squamous cell
carcinoma later developed in this area.

Hairy leukoplakia
Although EBV is thought to be associated
with several forms of lymphoma in HIV-
infected patients, the most common EBV-
related lesion in patients with AIDS is oral
hairy leukoplakia (OHL). This lesion
clinically presents as a white mucosal
plaque that does not rub off

Fig. 7-34 HIV-associated oral hairy

leukoplakia (OHL). Vertical streaks of
keratin along the lateral border of the
tongue.

41
 Erythroplakia
Erythroplakia – clinical term only – not a term
used in diagnosis
Same as above except a red patch.
-red because decreased thickness of epithelium
-red patch that doesn’t look like inflammation or
dilation of blood vessels etc.
-not common
-90% show epithelial dysplasia or squamous cell
Figure 10-75 ♦ Erythroplakia.
carcinoma (more likely to be SCC than leukoplakia)
An erythematous macular lesion is seen on the right floor of the mouth with no
associated leukoplakia. Biopsy showed early invasive squamous cell carcinoma.
Treatment: Excisional biopsy
Tobacco or snuff patch
Entity: Smokeless Tobacco induced lesions

Clinical Signs/Features: Appears as white patch in

area tobacco is retained – often occurs as white
patch in buccal vestibule/lower lip. Use of
smokeless tobacco can cause pre-cancerous or
cancerous lesions in the area used, but usually is a
reversible lesion. Incidence of cancer much less
than smoking tobacco.

Treatment: Lesion should heal within 10-14 days of

Figure 10-77 ♦ Tobacco pouch keratosis, mild.
A soft, fissured, gray-white lesion of the lower labial mucosa located in the area of cessation of tobacco use. If lesion persists, perform
racial
chronic snuff placement. The gingival melanosis is biopsy.
pigmentation and not associated with the keratosis.

Figure 10-78 ♦ Tobacco pouch keratosis, severe. Star)

A somewhat leathery, white, fissured plaque of the posterior mandibular vestibule,
which is located in the area of chronic chewing tobacco placement.

Figure 10-82 ♦ Tobacco pouch keratosis.

A, Moderately severe lesion of the lower anterior vestibule and lip in a 15-year-old
male, which demonstrates a grayish-white surface change and fissuring. The patient
had been placing snuff in the area for several years. B, Two weeks after cessation of the
tobacco habit the mucosa has returned to an almost normal appearance.

42
 Entity: Squamous cell carcinoma

Clinical Signs/Features: Most Common form of

cancer in the oral cavity. High risk sites: lateral
border/ventral surface of tongue, floor of the
mouth.
Common appearances:
1)Leukoplakia
2)Erythroplakia
3)Speckled erythroplakia
Figure 10-99 ♦ Squamous cell carcinoma.
An exophytic lesion of the posterior lateral tongue demonstrates surface nodularity and 4)An out growing lesion (exophytic mass)
minimal surface keratin production. It is painless and indurated. 5)Unhealing ulcer with raised, rolled borders with
induration (more of an ulcer than an elevation
because grows invasively) * Most common
appearance
Extraorally – common location is lower lip

Treatment: Excisional biopsy (to identify)

Figure 10-100 ♦ Squamous cell carcinoma.

An exophytic buccal lesion shows a roughened and irregular surface with areas of
erythema admixed with small areas of white keratosis. Surface ulceration is evident.

Figure 10-104 ♦ Squamous cell carcinoma.

Small, crusted ulcer of the lower lip vermilion.

Figure 10-107 ♦ Squamous cell carcinoma.

Ulcerated lesion with surrounding leukoplakia on the posterior lateral and ventral
tongue.

43
 Frictional traumatic keratosis
Entity: Frictional keratosis

Clinical Signs/Features: Low grade chronic trauma

from friction. Results in increased keratin
production as a protective mechanism. Common
location is the edentulous ridge due to chewing with
an ill-fitting denture.

Treatment: Fix or replace denture. Should resolve

once irritaton removed

Figure 10-57 ♦ Frictional keratosis.

There is a rough, hyperkeratotic change to the posterior mandibular alveolar ridge
(“ridge keratosis”), because this area is now edentulous and becomes traumatized from
mastication. Such frictional keratoses should resolve when the source of irritation is
eliminated and should not be mistaken for true leukoplakia.

Entity: Verrucous carcinoma

Clinical Signs/Features: Wart like appearance but

much larger than verruca vulgaris. Most commonly
on maxillary mucosa area going into the buccal
vesibule. Can also be found on palate. Grows
laterally instead of invasively. Slow in metastasis
therefore good prognosis. Tend to be large at
diagnosis.

Treatment: Surgery.
Figure 10-120 ♦ Verrucous carcinoma.
Extensive papillary, white lesion of the maxillary vestibule.

Figure 10-121 ♦ Verrucous carcinoma.

Large, exophytic, papillary mass of the maxillary alveolar ridge.

Entity: Melanoma

Clinical Signs/Features: Extremely rare in oral

cavity, but poor prognosis because quick to
metastasize. Malignant neoplasm of melanocytes.
Common on hard palate and gingiva.
ABCDE of melanomas:
A = Asymmetry
B = Irregular borders
C = Color variegation (color variation)
D = Diameter > 6 mm
Figure 10-137 ♦ Oral melanoma

44
This discrete area of pigmentation, measuring approximately 5 mm in diameter, was
discovered on the posterior hard palate of a middle-aged woman during a routine oral
E = Evolving larger size
examination. Biopsy revealed melanoma in situ.

Treatment: Surgical excision.

Figure 10-138 ♦ Oral melanoma.

Diffuse, splotchy area of pigmentation of the lateral hard palate. (Courtesy of Dr. Len
Morrow.)

Figure 10-139 ♦ Oral melanoma.

Ulcerated pigmented mass of the posterior maxillary alveolar ridge.

Inflammatory papillary hyperplasia

See denture injuries
White sponge nevus
-autosomal dominant condition, not
common
-white patches (leukoplakias) identified at
birth on mucosal surfaces (most common
location)
-picture shown of young patient white
patch on tongue lips
-can diagnose with cytologic smear
Fig. 16-4 White sponge nevus. -can be excised but recurrence may occur
Diffuse, thickened white plaques of the
buccal mucosa.

Salivary Gland Lesions

45
 Mucocele
Entity: Mucus extravasation phenomenon
(mucocele)

Clinical Signs/Features: Due to severing of minor

salivary gland duct, mucin pools in subepithelial
region producing a swelling. Swelling eventually
ruptures releasing mucin and process occurs again.
Most common location is lower labial mucosa due
Figure 11-1 ♦ Mucocele.
Blue-pigmented nodule on the lower lip.
to the presence of many glands. Clinically will
appear as a vesicle or bulla; often has a bluish color.

Treatment: Excisional biopsy of minor salivary

gland.

Ranula: large mucus retention phenomenon due

severing of sublingual or submandibular duct.
Treatment – incise and allow healing or removal of
part of salivary gland.
Figure 11-2 ♦ Mucocele.
Nodule on the posterior buccal mucosa.

Figure 11-3 ♦ Mucocele.

Exophytic lesion on the anterior ventral tongue.

Figure 11-4 ♦ Superficial mucocele.

Vesicle-like lesion on the soft palate.

Figure 11-7 ♦ Ranula.

Blue-pigmented swelling in the left floor of the mouth.

Ranula – see above

46
 Sialoliths
Entity: Sialolithiasis (salivary stone)

Clinical Signs/Features: Calcium and phosphate

deposits in minor or major salivary glands which
form stones. Most common location is
submandibular gland duct due to its length, the
parotid duct (Stenson’s duct) is another less
common location. Patient feels fullness and pain
Figure 11-12 ♦ Sialolithiasis. (star) upon salivation. Hardness is felt upon palpation of
Hard mass at the orifice of Wharton's duct.
the duct

Radiographic features: Radiopacity in salivary

gland duct region.

Treatment: Surgical removal of stone.

Figure 11-13 ♦ Sialolithiasis.

Occlusal radiograph demonstrating radiopaque stone in Wharton's duct.

Figure 11-14 ♦ Sialolithiasis. (star)

Periapical film of the same sialolith as depicted in Figure 11-13. A radiopacity (arrow)
is superimposed on the mandible. Care must be taken not to confuse such lesions with
intrabony pathosis.

Figure 11-15 ♦ Sialolithiasis.

Minor salivary gland sialolith presenting as a hard nodule in the upper lip.

47
Figure 11-16 ♦ Sialolithiasis.
Soft tissue radiograph of the same lesion depicted in Figure 11-15. A laminated
calcified mass is revealed.

Sialadenitis
Entity: Sialadenitis

Clinical Signs/Features: Inflammation of salivary

gland tissue. Spectrum of inflammation from acute
to chronic:
1) Acute – PMN’s main cells involved, pain
associated with condition.
Figure 11-18 ♦ Sialadenitis.
2) Chronic – long term condition with lymphocytes
Tender swelling of the submandibular gland. associated.

Bacterial sialadenitis – most common form – caused

by bacterial infiltration of salivary gland tissue –
Treatment = antibiotics, stimulation of salivary
flow.

Viral sialadenitis – most commonly caused by

mumps.

Figure 11-19 ♦ Sialadenitis.

A purulent exudate can be seen arising from Stensen's duct when the parotid gland is
massaged.

Figure 11-20 ♦ Chronic sialadenitis.

Parotid sialogram demonstrating ductal dilatation proximal to an area of obstruction.
(Courtesy of Dr. George Blozis.)

Pleomorphic adenoma (salivary gland

adenoma)
Entity: Pleomorphic adenoma – most common
neoplasm of salivary gland origin

Clinical Signs/Features: Within major salivary

glands, most commonly found in parotid (#1 benign
neoplasm found in parotid). Presents as swelling
firm to palpation, slow in growth. Within minor
salivary glands, most commonly found in posterior
palate.

Treatment: Excisional biopsy.

Figure 11-33 ♦ Pleomorphic adenoma.
Slowly growing tumor of the parotid gland.

48
Figure 11-36 ♦ Pleomorphic adenoma.
Firm mass of the hard palate lateral to the midline.

Figure 11-37 ♦ Pleomorphic adenoma.

Tumor of the pterygomandibular area.

Mucoepidermoid carcinoma
Entity: Mucoepidermoid carcinoma

Clinical Signs/Features: Most common malignancy

of parotid gland. Also a common malignancy of
minor salivary glands.

Treatment: Excisional biopsy.

Figure 11-54 ♦ Mucoepidermoid carcinoma.

Blue-pigmented mass of the posterior lateral hard palate. (Courtesy of Dr. James F.
Drummond.)

Figure 11-55 ♦ Mucoepidermoid carcinoma.

Mass of the tongue.

Adenoid cystic carcinoma

Entity: Adenoid cystic carcinoma

Clinical Signs/Features: Characteristic histological

“Swiss cheese appearance”. Most common
malignancy of submandibular gland. Also a
common malignancy of minor salivary glands.

Figure 11-68 ♦ Adenoid cystic carcinoma. Treatment: Excisional biopsy.

Painful mass of the hard palate and maxillary alveolar ridge. (Courtesy of Dr. George
Blozis.)

Connective Tissue Lesions

49
 Traumatic fibroma (fibroepithelial polyp)
Entity: Fibroma (aka irritating or traumatic fibroma)

Clinical Signs/Features: Benign neoplasm of fibrous

Figure 12-1 ♦ Fibroma.
Pink nodule of the posterior buccal mucosa near the level of the occlusal plane.
CT. Most common neoplasm of the oral cavity.
Dome shaped elevated lesion, non-fluid filled.
Common location is buccal mucosa and side of
tongue at level of occlusion (cheek bite). Can also
occur on labial mucosa, tip of tongue. Will have
same color as surrounding tissue or slightly pale
unless irritated.

Treatment: Excisional biopsy.

Figure 12-2 ♦ Fibroma.

Black patient with a smooth-surfaced pigmented nodule on the buccal mucosa near the
commissure.

Figure 12-3 ♦ Fibroma.

Lesion on the lateral border of the tongue.

Figure 12-4 ♦ Fibroma.

Smooth-surfaced, pink nodular mass of the palatal gingiva between the cuspid and first
bicuspid.

Epulis fissuratum (inflammatory fibrous

hyperplasia) – see denture related injuries

50
 Pyogenic granuloma
The pyogenic granuloma is a smooth or
lobulated mass that is usually
pedunculated, although some lesions are
sessile (Figs. 12-30 to 12-32). The surface
is characteristically ulcerated and ranges
from pink to red to purple, depending on
the age of the lesion. Young pyogenic
granulomas are highly vascular in
appearance; older lesions tend to become
more collagenized and pink. They vary
from small growths only a few millimeters
in size to larger lesions that may measure
several centimeters in diameter. Typically,
the mass is painless, although it often
bleeds easily because of its extreme
vascularity.
Fig. 12-33 Pyogenic granuloma. A, Large Pyogenic granulomas of the gingiva
gingival mass in a pregnant woman just frequently develop in pregnant women, so
before childbirth. B, The mass has much so that the terms pregnancy tumor or
decreased in size and undergone fibrous granuloma gravidarum often are used.
maturation 3 months after childbirth.
(Courtesy of Dr. George Blozis.)

Fig. 12-30 Pyogenic granuloma.

Erythematous, hemorrhagic mass
arising from the maxillary anterior
gingiva.

51

Fig. 12-37 Peripheral giant cell
granuloma. Nodular blue-purple mass of
the mandibular gingiva.
Fig. 12-38 Peripheral giant cell
granuloma. Ulcerated mass of the
mandibular gingiva.
Fig. 12-41 Peripheral ossifying fibroma.
Red, ulcerated mass of the maxillary
gingiva. Such ulcerated lesions are easily
mistaken for a pyogenic granuloma.
52
Peripheral giant cell granuloma
The peripheral giant cell granuloma occurs
exclusively on the gingiva or edentulous
alveolar ridge, presenting as a red or red-
blue nodular mass (Figs. 12-37 and 12-38).
Most lesions are smaller than 2 cm in
diameter, although larger ones are seen
occasionally. The lesion can be sessile or
pedunculated and may or may not be
ulcerated. The clinical appearance is
similar to the more common pyogenic
granuloma of the gingiva (see page 517),
although the peripheral giant cell
granuloma often is more blue-purple
compared with the bright red of a typical
pyogenic granuloma.
The treatment of the peripheral giant cell
granuloma consists of local surgical
excision down to the underlying bone. The
adjacent teeth should be carefully scaled to
remove any source of irritation and to
minimize the risk of recurrence.
Approximately 10% of lesions are reported
to recur, and reexcision must be performed.
Peripheral cementifying and/or ossifying
fibroma
The peripheral ossifying fibroma occurs
exclusively on the gingiva. It appears as a
nodular mass, either pedunculated or
sessile, that usually emanates from the
interdental papilla (Figs. 12-41 and 12-42).
The color ranges from red to pink, and the
surface is frequently, but not always,
ulcerated. The growth probably begins as
an ulcerated lesion; older ones are more
likely to demonstrate healing of the ulcer
and an intact surface. Red, ulcerated
lesions often are mistaken for pyogenic
granulomas; the pink, nonulcerated ones
are clinically similar to irritation fibromas.
Most lesions are less than 2 cm in size,
although larger ones occasionally occur.
The lesion often has been present for many

Fig. 12-42 Peripheral ossifying fibroma.
Pink, nonulcerated mass arising from
the maxillary gingiva. The remaining
roots of the first molar are present.
Figure 12-46 ♦ Lipoma.
Nodular mass of the posterior buccal mucosa.
Fig. 12-49 Traumatic neuroma. Painful
nodule of the mental nerve as it exits the
mental foramen (arrow).
Fig. 12-50 Traumatic neuroma. Note the
53
weeks or months before the diagnosis is
made.
The peripheral ossifying fibroma is
predominantly a lesion of teenagers and
young adults, with peak prevalence
between the ages of 10 and 19. Almost two
thirds of all cases occur in females. There
is a slight predilection for the maxillary
arch, and more than 50% of all cases occur
in the incisor-cuspid region. Usually, the
teeth are unaffected; rarely, there can be
migration and loosening of adjacent teeth.
Lipoma
Entity: Lipoma
Clinical Signs/Features: Common on skin, less
common in oral cavity. Benign neoplasm of fat.
Dome shaped elevated lesion, non-fluid filled. May
look like fibroma, but softer upon palpation and
may appear yellowish.
Treatment: Excisional biopsy.
Traumatic neuroma – reactive lesion
Traumatic neuromas of the oral mucosa are
typically smooth-surfaced, nonulcerated
nodules. They can develop at any location
but are most common in the mental
foramen area, tongue, and lower lip (Figs.
12-49 and 12-50). A history of trauma
often can be elicited; some lesions arise
subsequent to tooth extraction or other
surgical procedures.
The treatment of choice for the patient with
a traumatic neuroma is surgical excision,
including a small portion of the involved
nerve bundle. Most lesions do not recur; in
some cases, however, the pain persists or
returns at a later date.
irregular nodular proliferation along the
mental nerve that is being exposed at the
time of surgery.
Granular cell tumor
Entity: Granular cell tumor

Clinical Signs/Features: Rare condition in the oral

cavity, but most common location in the whole
body is the dorsal surface of the tongue. Elevated
lesion firm to palpation. Has a whitish appearance
and a roughened surface.

Figure 12-79 ♦ Granular cell tumor. Treatment: Excisional biopsy.

Submucosal nodule on the dorsum of the tongue.

Figure 12-80 ♦ Granular cell tumor.

Nodular mass of the buccal mucosa near the commissure.

Hemangioma
Entity: Hemangioma

Clinical Signs/Features: Benign neoplasm derived

from blood vessels. Presents as reddish or bluish
lesion either localized or diffuse.

Two Types:
1) Those present at birth and may spontaneously
regress. Some are quite large and difficult to
Figure 12-87 ♦ Hemangioma. manage
Infant with two red, nodular masses on the posterior scalp and neck (“strawberry”
hemangioma). Treatment = surgery, laser therapy, injection of
chemicals (no radiation b/c can trigger malignancy).

2) Those not present at birth and do not regress at

puberty (true hemangiomas)
-presents as elevated lesion that is red or blue, soft
to palpation
-positive diascopy test

Treatment: Excisional biopsy.

Central hemangioma: Hemangioma within bone

-patient at risk to bleeding out if tooth extracted in
region of hemangioma
-should palpate region and take radiograph before
treating
-angiogram can detect it

Radiographic features: unilocular or multilocular

radiolucency in area of central hemangioma (may

54
 have soap bubble appearance)
Kaposi’s sarcoma
Kaposi’s sarcoma (type of angiosarcoma):
-most common malignancy associated with
HIV/AIDS
-occurs in immunocompromised patients

Figure 7-48 ♦ HIV-associated Kaposi's sarcoma (KS).

Large zones of KS exhibiting as a flat, brownish, and M-shaped discoloration of the
hard palate.

Figure 7-49 ♦ HIV-associated Kaposi's sarcoma (KS).

Raised, dark-red enlargement of the mandibular anterior facial gingiva on the left side.

Fig. 7-41 HIV-associated Kaposi's sarcoma (KS). Diffuse, red-blue nodular

enlargement of the left hard palate.

Bone Lesions

Focal osteoporotic marrow defect

Fig. 14-8 Focal osteoporotic marrow
defect. Circumscribed radiolucency with
central trabeculations in the extraction site an incidental finding on a radiographic
of a mandibular molar. (Courtesy of Dr.
The focal osteoporotic marrow defect
is an area of hematopoietic marrow that
is sufficient in size to produce an area of
radiolucency that may be confused with
an intraosseous neoplasm. The area does
not represent a pathologic process, but its
radiographic features may be confused
with a variety of pathoses. The
pathogenesis of this condition is
unknown.
The focal osteoporotic marrow defect is
typically asymptomatic and detected as
examination. The area appears as a

55
R. Sidney Jones.) radiolucent lesion, varying in size from
several millimeters to several centimeters
in diameter. In many instances, when
discovered in panoramic radiographs, the
area appears radiolucent and somewhat
circumscribed; however, on review of
more highly detailed periapical
radiographs, the defect typically exhibits
ill-defined borders and fine central
trabeculations (Fig. 14-8). More than
75% of all cases are discovered in adult
women. About 70% occur in the
posterior mandible, most often in
edentulous areas. No expansion of the
jaw is noted clinically.

Enostosis/dense bone island/osteosclerosis

Same as below?
Idiopathic osteosclerosis (enostosis/dense
bone island/osteosclerosis)
Entity: Idiopathic osteosclerosis – very common

Clinical Signs/Features: tooth is vital,

asymptomatic (no symptoms or signs)
-often occurs in the mandibular molar/premolar
region – not known why
Figure 14-10 ♦ Idiopathic osteosclerosis.
A, An asymptomatic area of bone sclerosis is seen between and apical to the roots of the -often identified during teenage years
first and second mandibular molars. B, No appreciable change can be seen on this
radiograph taken 10 years later.
Radiographic signs, features: increased density of
bone, radiopaque lesion
-increase radiopacity near apex of tooth
-tooth is vital
-periapical radiopacity
-very rarely leads to resorption of root

Population affected: autosomal dominant

hereditary condition

56
 Simple/traumatic bone cyst
Entity: Traumatic bone cyst (aka idiopathic bone
cyst - not actually a cyst)

Clinical Signs/Features: Asymptomatic bone

cavity. May be due to trauma. More common in
teenage males.

Radiographic features: Characteristic

radiolucency - radiolucency with scalloped
superior borders. Follows outline of roots. More
common in posterior mandible. Cavity often
filled with air.

Treatment: May spontaneously regress. Surgeon

can induce healing scraping cavity to promote
bleeding.
Figure 14-25 ♦ Simple bone cyst.
Periapical radiograph showing a radiolucent area in the apical region of the anterior
mandible. The incisor teeth responded normally to vitality testing, and no restorations are
present.

Figure 14-26 ♦ Simple bone cyst.

Panoramic film showing a large simple bone cyst of the mandible in a 12-year-old girl. The
scalloping superior aspect of the cyst between the roots of the teeth is highly suggestive of,
but not diagnostic for, a simple bone cyst. (Courtesy of Dr. Lon Doles.)

Figure 14-27 ♦ Simple bone cyst.

Panoramic film showing a large multilocular simple bone cyst of the mandible in a 16-
year-old white male.

Fibrous dysplasia
Entity: Fibrous dysplasia – Two Types
Clinical Signs/Features of both: can affect any
region of bone, but jaws are a common location
- bone will grow to certain degree then stabilize
- enlargement of bone, displacement of teeth

1) Monostotic (85% of cases) involves one bone,

but maxilla with adjacent bones are included in
this category

Figure 14-31 ♦ Fibrous dysplasia. Clinical Signs/Features: slow, painless

Expansile mass of the left maxilla in a 45-year-old woman. This lesion was known to have
been present for at least 20 years. enlargement of bone
-tends to occur in younger individuals

57
 -more common in maxilla than mandible

Radiographic signs, features: characteristic

ground glass radiographic appearance,
indistinct borders
-displacement of teeth
-loss of lamina dura
-solitary radiopacity, or mixed
Figure 14-32 ♦ Fibrous dysplasia. radiolucency/radiopacity (intermediate stage)
Panoramic radiograph of the patient shown in Figure 14-31. A diffuse “ground-glass”
radiopacity is evident. not necessarily contacting teeth

Treatment: contour bone back to normal

morphology (normal done after bone growth has
stabilized to prevent stimulating increased bone
growth)

2) Polyostotic (15% of cases) – same features as

monostotic except multiple bones affected
- architecture of bones may be compromised and
Figure 14-33 ♦ Fibrous dysplasia. there is increased risk of fracture
Periapical radiograph showing a diffuse “ground-glass” radiographic appearance.
-Can be associated with McCune-Albright
syndrome: multiple pigmentations of the skin;
has endocrine disorders; precocious puberty—
young individual has secondary sex features very
early in age

Figure 14-34 ♦ Fibrous dysplasia.

Occlusal radiograph showing localized expansion of the mandible and the “ground-glass”
radiographic appearance. The margins of the lesion are not well defined and blend into the
adjacent bone.

Figure 14-36 ♦ Polyostotic fibrous dysplasia.

Jaffe-Lichtenstein syndrome: A, young man exhibiting enlargement of the right maxilla
and mandible; B, intraoral photograph showing unilateral maxillary expansion; C,
panoramic radiograph showing ill-defined lesions of the right side of both jaws.

58
 Periapical cemento-osseous dysplasia
Entity: Cemento-osseous dysplasias (non-
neoplastic reactive lesions, no expansion, no
pain)
-most common of all entities of odontogenic
origin

Three subcategories:

i) periapical

Clinical signs/features: No pain, no bony

expansion, vital teeth, asymptomatic.

Radiographic signs/feature: At early stage

Figure 14-41 ♦ Periapical cemento-osseous dysplasia.Periapical radiograph showing
multiple radiolucent lesions at the apices of the anterior mandibular teeth.
presents as radiolucency, but calcifications form
with time and lesion occurs as radiopacity with a
thin rim of radiolucency surrounding it. Tends to
occur in mandibular anterior region – apices of
anterior teeth. (periapical mixed
radiolucency/radiopacity intermediate-late stage)

Treatment: No treatment required, just document.

ii) focal

Clinical signs/features Asymptomatic.

Radiographic signs/feature: At early stage

presents as radiolucency, late stage – more
radiopaque. Occurs in mandibular posterior
region as solitary lesion. Do not confuse with
hypercementosis b/c in this lesion, PDL space
visible between lesion and root. (periapical mixed
radiolucency/radiopacity intermediate-late stage)

Treatment: No treatment required.

iii) florid
Figure 14-42 ♦ Periapical cemento-osseous dysplasia.
Later stage lesions exhibiting significant mineralization.
Clinical signs/features Tends to occur in middle
aged females. Asymptomatic, no expansion.
Bone has decreased vascularity – try not to
introduce another infection.

Radiographic signs/feature: At early stage

presents as radiolucency, late stage – more
radiopaque. Occurs in multiple quadrants.
(periapical mixed radiolucency/radiopacity
intermediate-late stage)

Treatment: Try to retain teeth – ie don’t attempt

biopsy b/c will introduce infection, and extraction
of teeth will cause bone to resorb.

59
Figure 14-43 ♦ Periapical cemento-osseous dysplasia.
Later stage lesions exhibiting significant mineralization.

.
Figure 14-40 ♦ Focal cemento-osseous dysplasia.
A, A radiolucent area involves the edentulous first molar area and the apical area of the
second molar. B, Radiograph of the same patient taken 9 years later showing a mixed
radiolucent and radiopaque pattern.

Figure 14-44 ♦ Florid cemento-osseous dysplasia.

Multiple mixed radiolucent and radiopaque lesions involving the anterior and posterior
regions of the mandible.

Figure 14-46 ♦ Florid cemento-osseous dysplasia.

Densely sclerotic lesions involve the four posterior quadrants. The mass in the upper right
quadrant is exposed to the mouth and is sequestrating.
Alveolar osteitis
Dry socket (alveolar osteitis)
-recognized complication
following extraction predominantly in

60
 difficult extractions
-3-5% occurrence rate
-shows up 2-3 days after
extraction—extreme pain
-fetid odour
-counsel patient not to smoke because
this will disturb blood clot, gently irrigate
with saline, cover socket with medicated
dressing

Osteomyelitis
acute vs. chronic
chronic focal sclerosing
osteomyelitis (condensing osteitis)
rarefying and condensing osteitis
chronic osteomyelitits with
proliferative peroistitis

Entity: Osteomyelitis – Multiple types

-inflammation of bone and bone marrow
Figure 3-47 ♦ Acute osteomyelitis.
Ill-defined area of radiolucency of the right body of the mandible.
A) Acute Osteomyleitis
Clinical Signs/Features: patient will report pain
due to inflammation at apex of a non-vital tooth

Radiographic signs, features: radiolucency at the

apex of a tooth with ill-defined borders (indicates
rapidly destructive process)
- Radiographically – radiolucencies with
Figure 3-49 ♦ Chronic osteomyelitis. ragged, ill defined borders
A, Ill-defined area of radiolucency of the right body of the mandible adjacent to a recent
extraction site. B, After the initial intervention, the patient failed to return for follow-up
because of lack of significant pain. An enlarged, ill-defined radiolucency of the right body Population affected: person’s whose immune
of the mandible was discovered 2 years after the initial surgery.
systems are down, virulence of infection is high

Treatment: remove source of inflammation,

curettage, drain, may use antibiotics (if systemic
involvement)
Note: when there is decreased vascularity
associated with dead bone, or increased density of
bone antibiotics will not diffuse well to the site of
action

B) Chronic osteomyelitis
-similar concept but low grade form
Figure 3-52 ♦ Diffuse sclerosing osteomyelitis.
-treatment is same: remove source of problem,
Diffuse area of increased radiodensity of the right body of the mandible in the tooth-
bearing area. No other quadrants were involved.
curette out dead bone, necrotic tissue and
antibiotics

C) Chronic focal sclerosing osteomyelitis

(condensing osteitis)
-we’ve learned this before
-localized inflammatory condition that is such
low grade that causes osteoblasts to form bone as

61
 opposed to bone destruction
-radiographs shown of radiopaque lesion at the
apex of a non-vital tooth

D) Chronic diffuse sclerosing osteomyelitis

-same concept but now involving a much larger
region of bone
-low grade enough that it is also producing bone
-“cotton wool” appearance (5 small radiographs
shown together in one slide)
-mixed radiolucency/radiopacity not
necessarily contacting teeth (intermediate-late
stage)

E) Chronic osteomyelitis with proliferating

periostitis
-we’ve learned this before -young individual,
Fig. 3-54 Proliferative periostitis. A, Firm swelling of the lateral and inferior border good tissue resistance
of the right mandible that arose after traumatic injury. B, Computed tomography
(CT) image demonstrating new periosteal bone growth with onionskin laminations. C,
-most frequently in the jaws, radiolucency at the
Panoramic radiograph exhibiting new periosteal bone formation along the right apex
inferior border of the mandible. (Courtesy of Drs. Sherif Mekhail and Benjamin Lin.)
-instead of causing pain, the person may start
developing minimally painful expansion of the
jaw: stimulating periosteum to lay down bone
-“onion-skinning” appearance
-treatment is extraction, RCT; swelling should go
down in 6 months
-mixed radiolucency/radiopacity not
necessarily contacting teeth

Odontogenic Cysts
Apical radicular cyst
Entity: Apical radicular cyst

Clinical Signs/Features: Occurs at apex of non-vital

tooth. Less painful than abscess upon percussion.

Radiographic signs, features: Apical radiolucency

(well defined) secondary to pulpal pathosis.
(solitary radiolucency)

Treatment: Extraction (biopsy tissue if extracted) or

root canal therapy.
FIG. 20-1
Radicular cysts. In A, note that the epicenter is apical to the lateral incisor and the
presence of a peripheral cortex (arrows). In B, note the lack of a well-defined peripheral
cortex as this cyst was secondarily infected and that the root canal of the lateral incisor
is abnormally wide as it is visible at the root apex.

62
FIG. 21-12
A cropped panoramic radiograph of an ameloblastoma (arrow) that has a unicystic
appearance in the body of the right mandible. The lesion, which has a well-defined,
corticated border, has caused apical root resorption of the mesial root of tooth no. 31.
This lesion easily could be misdiagnosed as a radicular cyst.
Residual cyst
Entity: Residual cyst.

Clinical Signs/Features: Occurs at approximate

position of apex of tooth following extraction
(history of extraction) of tooth and does not resolve
(should usually resolve within 6 months).
(essentially an apical or lateral radicular cyst in
which the tooth no longer remains)

Radiographic signs, features: Radiolucency at

approximate position of apex of tooth following
extraction. Well-delineated border. (solitary
radiolucency?)

Treatment: Remove cyst surgically (biopsy).

Figure 3-30 ♦ Residual periapical cyst.

Persistent radiolucency of the mandibular body at site of previous tooth extraction.

Figure 3-31 ♦ Residual periapical cyst.

A, Well-defined radiolucency of the posterior maxilla. B, Clinical photograph
exhibiting soft-tissue cyst extruding from the maxillary alveolar ridge after surgical
exposure of the site.

63
Figure 3-32 ♦ Residual periapical cyst.
Radiolucency with central radiopacity of the right mandibular body.
Dentigerious cyst
Entity: Dentigerous cyst - aka follicular cyst.

Clinical Signs/Features: Tooth may be displaced if

cyst large. Occurs most commonly on those teeth
that erupt late – impacted third molars are prone.
May cause pain or swelling if it becomes
secondarily infected. May present clinically as a
bluish bulge known as an eruption cyst.
-looks the same as odontogenic keratocyst

Radiographic signs, features: Large radiolucency

Figure 15-2 ♦ Dentigerous cyst.
Central type showing the crown projecting into the cystic cavity.
above crown of erupting tooth – represents fluid
between reduced enamel epethelium and erupting
tooth. Must be differentiated from dental follical
which surrounds crown of developing tooth, but is
smaller. (solitary radiolucency) Encloses the crown
of an unerupted tooth and is attached at the CEJ.

Treatment: Extraction (must biopsy to determine

what it is).

Figure 15-3 ♦ Dentigerous cyst.

Lateral variety showing a large cyst along the mesial root of the unerupted molar. This
cyst exhibited mucous cell prosoplasia.

Figure 15-4 ♦ Dentigerous cyst.

Circumferential variety showing cyst extension along the mesial and distal roots of the
unerupted tooth.

64
Figure 15-5 ♦ Dentigerous cyst or enlarged follicle.
Radiolucent lesion involving the crown of an unerupted mandibular premolar.
Distinction between a dentigerous cyst and an enlarged follicle for a lesion of this size
by radiographic and even histopathologic means is difficult, if not impossible.

Eruption cyst
The eruption cyst is the soft tissue analogue of
the dentigerous cyst. The cyst develops as a
result of separation of the dental follicle from
around the crown of an erupting tooth that is
within the soft tissues overlying the alveolar
bone.
The eruption cyst appears as a soft, often
translucent swelling in the gingival mucosa
overlying the crown of an erupting
deciduous or permanent tooth. Most
Fig. 15-9 Eruption cyst. This soft
examples are seen in children younger than
gingival swelling contains considerable age 10. Although the cyst may occur with
blood and can also be designated as an
any erupting tooth, the lesion is most
eruption hematoma. commonly associated with the deciduous
mandibular central incisors, the first
permanent molars, and the deciduous
maxillary incisors
Odontogenic keratocyst
Entity: Odontogenic keratocyst.
-ultimate diagnosis made microscopically
-has features of dentigerous cyst, lateral periodontal
cyst, primordial cyst

Clinical Signs/Features: Common location is

posterior mandible. Appears similar to lateral
periodontal cyst or primordial cyst (or dentigerous
cyst when associated with an unerupted tooth). Can
be locally aggressive/destructive. Tendency to
recur.
Figure 15-13 ♦ Odontogenic keratocyst.
Large, multilocular cyst involving most of the ascending ramus.
Radiographic signs, features: Unilocular or
multilocular radiolucency often in posterior
mandible region. (Solitary radiolucency,
multilocular radiolucency) May be associated with
unerupted tooth in some cases (makes it look like
dentigerous cyst). Does not cause obvious bone
expansion (whereas a dentigerous cyst of similar

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 size will).

Treatment: Remove cyst (biopsy). Cyst may

reoccur; therefore patient must be informed and
monitored.

Odontogenic Keratocyst may be associated with

Figure 15-14 ♦ Odontogenic keratocyst.
This cyst involves the crown of an unerupted premolar. Radiographically, this lesion
cannot be differentiated from a dentigerous cyst.
basal cell nevus syndrome (Gorlin Syndrome).
-autosomal hereditary condition
- increased distance between pupils of eyes
(hypertelorism)
- prominent forehead, elongated face, bifid rib
- pits of the skin: prominent on palms, soles of feet;
many of these develop into basal cell carcinomas
-multiple OKC of the jaw – marker for presence
of this syndrome

Figure 15-16 ♦ Odontogenic keratocyst.

This cyst cannot be radiographically differentiated from a lateral periodontal cyst.

QuickTime™ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.

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 QuickTime™ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.

QuickTime™ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.

G
Gingival cyst (of the newborn and of the adult)
Entity: Gingival cyst

i) Gingival cyst of the newborn

- occur on soft tissue
- multiple cysts of gingiva
- often located on crest of gingiva
- present at birth
- fairly common condition; rupture spontaneously
and go away quickly
- NO treatment necessary
Figure 15-28 ♦ Gingival cyst of the newborn.
Multiple whitish papules on the alveolar ridge of a newborn infant. ii) Gingival cyst of the adult

- soft tissue counterpart of lateral periodontal cyst –

both occur commonly around the canine/premolar
region
-looks like periodontal cyst under microscope

Clinical Signs/Features: Occur on soft tissue on

gingival or junction of gingival/alveolar mucosa
(cyst so fluid filled - vesicle? Bulla?)

Treatment: Excise (biopsy).

Figure 15-29 ♦ Gingival cyst of the adult.
Tense, fluid-filled swelling on the facial gingiva.

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 Lateral periodontal cyst
Entity: Lateral periodontal cyst.

Clinical Signs/Features: Tooth is vital! Most often

occurs in the mandibular canine; first/second
premolar region. Differentiate from lateral radicular
cyst because teeth are vital.

Radiographic signs, features: Radiolucency lateral

to root. Radiolucency often in mandibular canine;
first/second premolar region. (solitary radiolucency)

Treatment: Surgical curettage of cyst, enuculation

(removal of something that tends to be removed in
one piece). Do not extract teeth – they are vital!!!

Subcategory
Figure 15-33 ♦ Lateral periodontal cyst.
Radiolucent lesion between the roots of a vital mandibular canine and first premolar.
-Botryoid (grapelike) odontogenic cyst
– may present radiographically as a multilocular
radiolucency. (differentiates it from lateral
periodontal cyst).
-teeth are vital

Figure 15-34 ♦ Lateral periodontal cyst.

A larger lesion causing root divergence.

Non-Odontogenic Cysts
Nasopalatine duct cyst
Entity: Nasopalatine duct cyst (aka incisive canal
cyst)

Clinical Signs/Features: Due to cystic

transformation of epithelium during fetal
development. Cyst may cause expansion of anterior
hard palate, or become infected. Cyst wall is NOT
inflamed b/c condition is not inflammatory in orgin.
-teeth are vital(do not extract teeth!)

Radiographic signs, features: Solitary radiolucency.

- Key feature – normal incisive foramen is about 6
Figure 1-56 ♦ Nasopalatine duct cyst.
Fluctuant swelling of the anterior hard palate.
mm, becomes larger with this entity

Treatment: Curettage out cyst (biopsy).

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Figure 1-57 ♦ Nasopalatine duct cyst.
Well-circumscribed radiolucency between and apical to the roots of the maxillary
central incisors.

Figure 1-58 ♦ Nasopalatine duct cyst.

Large destructive cyst of the palate.

Odontogenic Tumors

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 Ameloblastoma
Entity: Ameloblastoma
-3 three subtypes
-most common location on posterior mandible

i) Solid/multicystic (most common of three)

Clinical signs/features: Slow in growth, painless,

but may be locally aggressive. Tends to occur in
30-40 age group.
-teeth may be displaced, expansion of mandible

Radiographic signs/feature: Multilocular

radiolucency (multilocular radiolucency of
mandible think ameloblastoma). Teeth, inferior
alveolar nerve canal may be displaced.

Figure 15-52 ♦ Ameloblastoma. Treatment: If lesion small – curette lesion out

Large expansile mass of the anterior mandible.
(biopsy). If large, en bloc resection of the bone
involved may be required. Recurrence is possible.

ii) Unicystic (less common)

Clinical signs/features: Tends to occur in younger

individuals – teenage years.

Radiographic signs/feature: Solitary radiolucency

Figure 15-53 ♦ Ameloblastoma.
Prominent expansion of the lingual alveolus caused by a large ameloblastoma of the
mandibular symphysis. The radiograph of the patient is shown in Figure 15-57.
around crown of unerupted tooth.
- appears similar to dentigerous cyst (differentiate –
dentigerous cyst usually ends at CEJ where
unicystic ameloblastoma ends past CEJ further
apically but must differentiate histologically
because treatment much different).

Treatment: Remove tooth and scoop out neoplastic

tissue (biopsy). Prognosis better than multicystic.

iii) peripheral (ie occurs in soft tissue)

Clinical signs/features: Occurs as lump on gingival.

Treatment: Excise (biopsy). Prognosis very good.

Figure 15-54 ♦ Ameloblastoma.

Massive tumor of the anterior mandible.

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Figure 15-55 ♦ Ameloblastoma.
Large multilocular lesion involving the mandibular angle and ascending ramus. The
large loculations show the “soap bubble” appearance. An unerupted third molar has
been displaced high into the ramus.

Figure 15-56 ♦ Ameloblastoma.

Periapical films showing the “honeycombed” appearance.

Figure 15-57 ♦ Ameloblastoma.

Destructive radiolucent lesion associated with root resorption of the anterior teeth.

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Figure 15-58 ♦ Ameloblastoma.
This small unilocular radiolucency lesion could easily be mistaken for a lateral
periodontal cyst.

Figure 15-68 ♦ Unicystic ameloblastoma.

A large radiolucency in a 7-year-old boy with displacement of the developing second
molar to the inferior border of the mandible. This was believed to be a large
dentigerous cyst.

Adenomatoid odontogenic tumor

Entity: Adenomatoid odontogenic tumor

Clinical signs/features: Most frequently occurs in

young teenage years, more common in females than
males. Most commonly associated with
unerupted maxillary canine teeth (but can be
found with other teeth). Looks like glandular tissue
upon removal.

Radiographic signs/feature: Solitary radiolucency,

Figure 15-80 ♦ Adenomatoid odontogenic tumor (follicular type). pericoronal mixed radiolucent/radiopaque (may
Radiolucent lesion involving an unerupted mandibular first premolar. Fine snowflake
calcifications are present in the radiolucent area. In contrast to the usual dentigerous
appear as either). Can produce calcified tissue
cyst, the radiolucency extends almost to the apex of the tooth. (radiolucent/radiopaque presentation).
Radiolucency ends past CEJ (differentiates from
dentigerous cyst which usually ends AT CEJ. Most
commonly associated with unerupted maxillary
canine teeth

Treatment: Remove lesion (biopsy), does not have

recurrence rate. May include sacrificing tooth as
well.

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Figure 15-81 ♦ Adenomatoid odontogenic tumor (extrafollicular type).
A small radiolucency is present between the roots of the lateral incisor and canine.

Figure 15-82 ♦ Adenomatoid odontogenic tumor.

A wellcircumscribed solid mass can be seen enveloping the crown of this tooth.

Cementoblastoma
Entity: Cementoblastoma. (third most common
lesion) – rare, distinctive lesion.

Clinical signs/features: Tends to occur in late

teenage, early twenties age range.
Figure 14-66 ♦ Cementoblastoma.
A, A densely mineralized mass is seen at the apex of the distal root of the first molar.
The root is partially resorbed. B, The surgical specimen shows that the mass is attached
Radiographic signs/feature: Circular radiopaque
to the root. lesion connected to root of tooth and radiolucent
rim surrounding lesion (periapical
radiolucency/radiopacity). Neoplasm, therefore will
be expansion of bone over time due to
cementoblasts producing excess cementum.
Frequently involves mandibular first molar,
premolars, or second molars.

Treatment: Removal of tooth and neoplasm.

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 Odontoma
Entity: Odontoma
-second most common lesion of odontogenic
neoplasms behind cemento-osseous dysplasia
-most well differentiated neoplasm of all the lesions
-will contain dentin, enamel, pulp within lesion

Two forms:

i) Compound

Clinical signs/features: Present as cluster of tiny

Figure 15-101 ♦ Compound odontoma. teeth (well organized) – may prevent normal teeth
A small cluster of toothlike structures is preventing the eruption of the maxillary
canine. from erupting.

Radiographic signs/feature: Pericoronal mixed

radiolucent/radiopaque appearance (intermediate-
late stage) or mixed radiolucent/radiopaque lesion
not necessarily contacting teeth (intermediate-late
stage). Tend to occur in anterior region.
Radiopacity surrounded by radiolucent rim.

Treatment: Decide treatment by determining the

cost/benefit of removing it (depends on
severity/situation).

ii) Complex

Clinical signs/features: Haphazard arrangement of

components of tooth structure (poorly organized
Figure 15-102 ♦ Compound odontoma. enamel, dentin and pulp tissue). Can become large.
Multiple toothlets preventing the eruption of the mandibular cuspid.

Radiographic signs/feature: Pericoronal mixed

radiolucent/radiopaque appearance (intermediate-
late stage) or mixed radiolucent/radiopaque lesion
not necessarily contacting teeth (intermediate-late
stage). Tend to occur in posterior region.
Radiopacity surrounded by radiolucent rim.

Treatment: Decide treatment by determining the

Figure 15-103 ♦ Complex odontoma.
cost/benefit of removing it (depends on
A large radiopaque mass is overlying the crown of the mandibular right second molar, severity/situation).
which has been displaced to the inferior border of the mandible.

Other Dental Lesions

Caries/extensive caries
Transposition
Ectopic eruption
Arrested root development
Restored tooth
Retained deciduous tooth
Discolored tooth

Other Soft tissue lesions

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Soft tissue hyperplasia (general term)
Soft tissue laceration (general term)
Muscle hypertrophy
Edema

Anatomical Structures
Stensen’s duct orifice (parotid gland)
Wharton’s duct orifice
Lingual tonsil/foliate papillae
Mental foramen
Mandibular foramen
Mandibular canal
Submandibular salivary gland fossa
Maxillary sinus
Pterygomaxillary fissure
Developing root apex
Canine fossa
Nutrient canal.
Nasopalatine foramen
Nose
Nasal septum
Hamular process
Coronoid process
Zygomatic arch
Mylohyoid ridge (internal oblique ridge)
External oblique ridge
Torus
Retained root
Hyoid bone
Antral septum
Soft palate
Cervical spine
Inferior concha
Ghost image
Post extraction socket
Calcifying tooth crown
Calcification of root canals
Calcification of pulp chamber
Calcified lymph nodes
Calcified stylohyoid ligament
Pulp stones
Root fracture
Fractured tooth
Rotated or tipped tooth
Atrophic mandible/maxilla
Endodontic/periodontic lesion

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