Contents

Section I.
Diagnostic and Descriptive Terminology
Macule. Patch. ErOSIon. Ulcer. Wheal. SCar. FISSUre.

SinuS

Papule. Plaque. Nodule. Tumor. Vesicle. Pustule,

Bullil. Cyst

Section II.
Oral Conditions Affecting Infants
and Children

Section III.

Conditions Pecull.ar to the Up

Actinic Cheilitis (Solar Elastosis). Monilial CheilitiS.
Angular Cheilitis {PerJecheJ. ExfoliatIVe CheilitIS

34

P.r.aul Swellings

Congenital EpullS of the NevvtX:II'n. MelClnotlC

BOdl

32

Neuroectodermal Tumor of Infancy. Dental Lamina

Cysts. Natal Teeth. GingIVal Eruption Cyst lEruption
Hemat()ll"l<lj. Congenital lymphangioma. Thrush
,candidiaSIs. MonIliaSIS). Parulis {Gum

Nodules of the Up
Mucocele {Mucous Retention Phenomenon,
Mxous RetentJon Cyst). Accesscxy salivary
Gland Tumor. Nasolabial CYSI {Nasoalveolar Cyst).
ImplantatIOn Cyst (EpltheliallncJusl()(l Cystl.
Me<ienchyrrlal Tumors

,1

Abnormalities by Anatomic Location

Palatal Tori (Torus Palatinus), Incisive Canal Cyst

INasopala!ine Duct Cyst), Periapical ,Abscess.
Benign LymphOid Hyperplasia /Follicular
lymphoid HyperplaSia)

36

Necroozlng SIaJometapiasla, Benign Accessory

Salivary Gland Neoplasm, Malignant Accessory Salivai)'
Gland Neoplasm, Primary lymphoma of the Palate

38

AJterations In Tooth Morphology

Microdontla and Macrodontia. FUSion and Gemination.

Swellings of the Floor of the Mouth

Dens Invagmatus IDens In

lleong's Tuberclel

Demloid CYSl Ranula /MucOCele of the

Sublingual Gland). salivai)' Calcu~. Mucous
Retention Phenomenon

Demel and Dens Evaglnarus

t2

40

Alt.'iltlons In Numbers of Teeth

Hypodontia. HyperdOntia. Cleidocranial Dysplasia.
Gardner's Syndrome

14

Alt.rations In Tooth Structure

Enamel Hypoplasia. Amefogenesis Imperfeeta.
DentJnogene5'S Imperfeaa. Dentin DysplaSIa

16

Acquired Defects of Teeth

Caries. Pulp Polyp. Attrition. Abrasion. Erosion

18

LocaUzed Glngtval Lesions

Pyogefllc Granuloma. Peripheral GIiirlt Cell
GranulOma. PerIpheral FlbrorTIa WIth
CalCification (Peripheral Cemenl~fying
Fibro~/. Gingival Carcino~.
Parulis (Gumboil). Pericoronitis /OperculitiS).
Periodontal Abscess. Epulis Fissuratum
{Irri(aoon Hyperplasia)

20

22

Conditions Peculiar to the Tongue

Normal Tongue Anatomy. Fissured Tongue
{Plicated Tongue, SCrotal Tongue!, Ankyloglossia,
lKlgual Yancosity rPhlebectasiaJ

42

SCalloped Tongue ICremated Tongue!.

Macroglossia, H.my Tongue ILJngua Villosa.
Coated Tongue). Hairy leukoplakia

44

GeographIC Tongue lBenign MigratOl}'

GlossitJs, Erythema Migrans. Wandeong Rashl,
Anerma. Xerrntorma

46

fv1edian Rhomboid GlossJliS (Central PapillaI}'

IWophy of the Tonguel. Granular Cell Tumor
(Granular Cell MyobIastomaj, Ungual Thyroid,
Cym of B1andin-Num IUnguaI Mucous Retention Cyst)

48

Gener.nzlRd Gingival Enlargements

Section f\I.

Hereditary FibromatOSIS GingNae. Dr'ug-{nduced

Gingival Hyperplasia. Mouthbreathing,
Gingival Ede~ of Hypothyroidism

Intraoral Findings by Color Changes

24

Gingivitis
GingMtis, Acute NecrooZJr"IQ UJcerauve GingIVitis.
ActinomycotIC GingMtlS. Honnonal GingivitIS
(Pregnancy GingivitIS), Diabetic Gingivitis

26

Spont.aneGus Gingival BI. .dlng

Leukemic GingivitiS. AgranUlocytosis (Neutropenia/
and Cyclic Neutropenia, ThtQmbotytopenic and
TlYombocytopathic Purpura

28

sw.mngs of the Up
AnglC)edema /tVlgioneurotic Edema), Cheilitis
Glandularis. Cheilitis Granulomatosa, Trauma. Cellulitis

30

51

White Lesions
Fordyce's Granules. Linea,AJba Buccalis,
LeuKoedema. Morsic:atio Buccarum IMucosal Cha.vingJ

52

White Sponge Nevus IFamll.ia1 \Mlite Folded

DysplaSI3!. TraumatIC WhIte lesions V<ute
Trauma. Chemical Burns and Peripheral
Scar). Leukoplakia

54

TalNtco Assod.ted White Lesions

Cigarette KeralOSls, Nicotine StomatilJS {Pipe
Smokm Palate). Snuff Dipper'S Patch (Tobacco
Che'vver's ~~ion. Snuff Keratosis), Vefrucous
Carcinoma (of Ackerman/IOral Florid PapiliomatosiSl

56

XIII

Red Lesions
Purpura Wetechiae, EcChymoses. Hematoma).
Varicosity (Varix). Thrombus. Hemangioma

58

HeredJtary Hemorrhagic: Telangieaa5ia

fRendu-OsIer-VleberJ. Sturge-Weber Syndrome
(Encepl1alOtrigemlnal AnglOffiCltosis)

60

Red tlnd RedlWhite Lesions

Erythroplakia. EryrhroIeukoplakia and Speckled
Erythroplakia. Squamous Cell carcinoma

62

lichen Planus. ElecUogalvanic White lesfO(l

64

lupus Erythematosus. lKhenoid and lupus-like

Drug Eruption

66

Acute Pseudomembranous Candidiasis (Thrush),

Chronic Keratotic Candidiasis IHyperplasricl.
Acute Atrophic candidiasis jAntlbiotic Sore Mouth).
Angular Cheilils, Chronic Atrophic candidiasis
/Demure StomatinS)

68

Varicella (Chickenpox), Herpes Zoster (Shingles).

Hand-foot-and-Mouth Disease

86

Allergic Reactions

88

Erythema MultJforme. Stevens-Johnson Syndrome

90

Pemphigus \AJlgans, Benign Mucous Membrane

(Cicatricial). Pemphigoid and Bullous PemptligOld

92

UlceratIve Lesions
Traumatic Ulcer. Recurrent fl,phthous Stomatitis.
IMinor Aphthae, Aphthous Ulcer). Pseudoaphthous Ulcer

94

Major Aphlhous lPenadenltis Mucosa NecfOtlCa

Recurrens /PMNRj. Sunon's Disease, SCanfylng
Stomatitis. Recurrent SCarring Aphthous UlCer).
Herpetiform Ulceration. Behcet's Syndrome
IOCulo-Oral-Genital Syndrome)

96

Granulomatous Ulcer. Squamous Cell carcinoma.

ChernoherapeutJC Ulcer

98

Pigmented Lesions
Melanoplakia, Tattoo, Ephelis [Freckle). Smoker's
Melanosis (TobacCo-Associated Pigmentation)

70

Oral Melanotic Macule. Nevus. Mallgnam Melanoma

72

Section VI.
Sexually Related and Infectious
Conditions

101

Sexually Related tlnd Infectious Conditions

Peutz-Jeghers Syndrome /Hereditary Intestinal
PoIyposisj. Add1SOfl'S DIsease !Adrenal Cortical
JnsufficlO1C}1. Heavy Metal PIgmentatIOn

Section \f.
Intraoral Findings by Surface Change

Traumatic Conditions. sexually Transmiaed Pharyngitis,

InfectIoUS Mononucleosis. Syphilis

74
77

Irritation Fibroma and Peripheral OdontogenJC Fibroma,

Upoma, Upofibroma.
Traumatic Neuroma /Amputation Neuroma).
Neurofibroma

104

Oral Viral Infections. Oral N'ialignancles

106

Appendices

Appendix I Rx Abbreviations

109

78

Appendix II Therapeutic Protocols

113

80

Appendix III Guide to Diagnosis and

Management of Common Oral

Papulonodules
Paprlloma ISquamous Paprlloma), Verruca \ll.Jlgans,
CondylOma Acuminarum jVenereal Wart!,

lymphangioma

HIV Infection ilnd AIDS

Oral Baaerlcll Infections. Oral Fungal Infections

NOdules
Rettoeuspid Paprlla, lymphoepithelial C~ Torus,
Exostosis and Osteomar

82

XIV

84

~s1ons

125

Appendix IV self-Assessment Quiz

141

Appendix V Glossary

147

VesiculobuJlous Lesions
Primary Herpetic Gingivostomatitis, Recurrent
Herpes Simplex.. Herpangina

102

I Index

161

DIAGNOSTIC AND DESCRIPTIVE TERMINOLOGY

Macule IFig. 1-1) A macule is a circumscribed area of
epidermis or mucosa dislinguished by color from its
surroundings. The macule may appear as a slain or spot
that is blue. brown. or black in color. This lesion is neither
elevated nor depressed and may be of any size. MOSI
frequently the tenn "macule" is reserved for lesions I em
or smaller. The oral melanotic macule is an example of this
condilion.

Wheal (Fig. 1-5) A wheal is an edematous papule or

plaque that results from acute extravasation of serum into
the upper dennis. Generally. wheals are pale red. pruritic.
and of shorl duration: they often occur in allergic
individuals. Wheals may be seen following insect bites. an
allergic reaction to food. or mechanical irritation such as
in patients who have dennatographia.

Patch IFig. 121 A patch is a circumscribed area that is

larger than the macule and differentiated from the
surrounding epidennis by color, or lexture, or both. Like
the macule, the patch is neither elevated nor depressed.
Lichen planus. mucous parch of secondary syphilis, and
snuff dipper's patch represent patch.like lesions that may
be seen immorally.

Scar (Fig. '-6) A scar is a permanent mark or cicatrix

remaining after a wound heals. These lesions are visible
signs that indicate a disruption in the integrity of the
epidennis and dermis. Scars are infrequently found in the
oral cavity, but may be of any shape or size. The color of
an intraoral scar is usually lighter than the adjacent
mucosa. Periapical surgery or intraoral trauma may
induce scar fonnation.

Erosion (Fig. 1-31 Erosion is a clinical term that

describes a soft tissue lesion in which the epithelium above
!he basal cell layer is denuded. Erosions are moist. slightly
depressed. and often result from a broken vesicle or
Inuma. Healing rarely results in scaning. Pemphigus is a
chsease that proctuces mucocutaneous erosions.

Ulcer (Fig. 1-41 An ulcer is an uncovered wound of

cutaneous or mucosal tissue that exhibits gradual tissue
disintegration and necrosis. Ulcers extend beyond the basal
layer of the epithelium and into the dennis: thus scarring
may follow healing. Ulcers may result from aphthous
stomatitis. or infection by viruses such as herpes simplex.
variola (smallpox), and varicella zoster (chickenpox and
shingles). Ulcers are usually painful and often require
topical drug therapy for effective management

Fissure (Fig. 1-71 A fissure is a normal or abnormal

linear cleft in the epidermis that typically affects the lips
and perioral tissues. When pathogenic organisms infect a
fissure pain. ulceration. and innammation often result.
Angular cheilitis and exfoliative cheilitis are examples of
this condition.

Sinus fFig. 181 A sinus is an abnonnal tract or fistula

that leads from a suppurative cavity, cyst, or abscess to
the surface of the epidermis. An abscessed tooth ohen
produces a sinus tract together with a clinically evident
parulis. which is the terminal end of the sinus.
Actinomycosis is a condition characterized by multiple
sinus tracts that appear yellow in color.

DIAGNOSTIC AND DESCRIPTIVE TERMINOLOGY

...---------....,

Macule

t""tg. 1-1. Macule. A (l((umscnbed area of epIdeft11lS

II'.e1!'d 11"I cokr from its surroundIngS

Erosion

Fig. 13. Erosion. AdenudatJOn of epithelium abOve

-ne basal celllayff.

Wheal/~~

Fig. 1-5. Wheal. A plnkred. edematous. serufT'l.filJed

papule or plaque

Fissure

Fig. 17. Fissure. A linear crack In the eptdemlts

Patch

Fig. 1-2. Patch. A (Jrcumscnbed plgmenled or textured

area larger Chan the macule.

Ulcer

Fig. 1-4. Ulcer. A los! of epttheIum that extends /:leIoIN'

the basal cell layer

Scar /

Fig. 1-6. Scar. A permanent mark inchcatrve of prevIOUs

INOUnd healing

Sinus

Fig. 1-8. Sinus. A tract leading from a suppuratNe

Cavity. cyst or abscess..

DIAGNOSTIC AND DESCRIPTIVE TERMINOLOGY

Papule fFig. 2-1 J A p;tpule is a superficial. elev3tl'd.
solid lesion thai i~ smaller than I em in diameter. Papules
may be of any color and may be attached by a stalk or firm

base. Examples of papules include the following

conditions: condyloma acumm:uum. parulis. and squamous

papilloma.

Plaque {Fig. 2-21 A plaque is a flar. solid. raised area

that is greater than I em in diameter. Though essentially
superficial. plaques may extend deeper into the dermis Ihan
papules. The edges may be sloped. and sometimes surface
keratin proliferates. a condition known as lichenification.
Lichen planus. leukoplakia or melanoma may initially

appear as a plaque.

Nodule (Fig. 2-3) A nodule is a solid mass of tissue

that has the dimension of depth. like papules. these lesions
are less than I em in diameter. but nodules extend dttper
inlO the dermis. Palpalion provides deleclion of the nodule.
The overlying epidermis is usually nonfixed and can be
easily moved over the lesion. Benign mesenchymallUmors
such as Ihe fibroma. lipoma. lipofibroma. and neuroma
often appear as oral nodules.

Tumor /Fig. 2-41 "Tumor" is a term used to represent

a !ootid mass of tissue larger than I em in diameter. The
term is also used to represent a neoplasm - a new.
independent growth of tissue with uncontrolled and
progressive mulliplicution of cells that have no
physiologic use. Tumors may be of any color and may be
located in any intraoral soft tissue. Tumors often appear
as raised rounded lesions Ihal have the dimension of
depth. Persistent lumors may be umbilicated or ulceraled
In the center. The term tumor is often used to describe a
benign tissue mass such as a neurofibroma. granular cell
tumor. and pregnancy lumor.

Vesicle 'Fig. 251 A \-esicle i~ a circumscribed. fluid

filled elevalion in the epidermis thai is less than I em in
diameter. The fluid of a vesicle generally consists of lymph
or serum. but may conlain blood. 1be epithelial lining of wa
vesicle is thin and will e\emually breakdown. thus giving
rise 10 an ulcer and eschar. Vesicles are common in viral
infeclions such as herpes simplex. herpes zoster.
chickenpox. and smallpox.

Pustu'e IFig. 2--6) A pustule is a circumscribed elevation

filled with purulent exudate resulting from an infection.
Pustules are less than I cm in diameter and may be preceded
by a vesicle or papule. They appear creamy white or
yellowish in color and are often associated with an epidennal
pore. Intraorally the pustule is represented by a pointing
abscess. Herpes zoster is another condilion that produces
pustules thai eventually ulcerate and cause intense pain.

Bulla 'Fig. 271 When a vesicle achieves a diameter

greater than I em. il is termed a bulla. This condition
develops from the accumulation of fluid in the epidermal
dermis junction or a split in the epidermis. Bullae are
commonly seen in pemphigus. pemphigoid. bums. and
epidermolysis bullosa.

Cyst IFig. 2-81 A cyst is an epitheliaJly lined. often fluidfilled mass in the dermis or subcutaneous tissue. CystS
range in diameter from a few millimeters to several
centimeters. Aspiration of a cyst mayor may not yield
luminal fluid. depending on the nature of the cyst. CYStS
that contain clear fluid clinically appear pink. to blue.
whereas keratin-filled cyslS often appear yellow or creamy
white. There are many types of oral cysls. A small list
includes the demloid cyst. eruption cyst. implantation cyst.
incisive canal cyst. Iymphoepithelial cySt. mucous retention
cySt. nasoalveolar cyst. and radicular cysi.

.....--------...,

DIAGNOSTIC AND DESCRIPTIVE TERMINOLOGY

Plaque

Papule

F.. .9 . 2-1. Papule. An elevated. solid lesion less than I

"T' Io'l diameter.

Fig. 2-2. Plaque. A flat raised area greater than I em

In diameter

oduIe

Fig. 2-3. Nodule. A raised, solid mass with the

dimenSIon of depth and IS less than 1 em In diameter.

Vesicle

Fig. 2-4. Thmot A solid. raIsed mass larger than J em

in diameH'( with the dlmenslQ(l of depth

-----

Fig. 2-5. Vesicle. A CIrcumscribed. f1uid-fined skin

Jess lhan I em In dlClmeter

eieval:fOI1

Pustule/

Fig.

2~.

Pustule. A vesICle filled With purulent

exudate.

Cyst

Fig. 2-7. Bulla. A flUid-filled skrn elevalJon greater than

em Ir'I diameter

Fig. 2-8. Cyst. M epithelial lined. t1uid-frlled m.m In

the dermIS

or sutx:utaneous tissue
5

ORAL CONDmONS AFFECTING INFANTS AND CHILDREN

Congenital Epulis ot the Newborn (Fig. 3-1 J
The congenital epulis of the newborn is a soft tissue
polypoid growth arising from the gingiva of the edentulous
alveolar ridge of newborn infants, It usually occurs in the
anterior maxilla, and is len times more likely to occur in
females than in males. The neoplasm is mOSI likely of
pericyte origin and histologically resembles a granular cell
tumor. Clinically the lesion is pink. soft, and compressible.
It usually an3ches to the alveolar ridge by a pedunculated
stalk and may reach several centimeters in diameter.
Treatment is complete excision, and recurrence is unlikely.

Gingival Eruption Cyst (Eruption Hematoma)

(Fig. 3-51 The eruption cyst is a soft tissue variant of the
dentigerous Cysl Ihal fonns around a.'l erupting lOOlh crown.
It is usually associated with primary teeth and manifests as
a small. dome-shaped, bluish flucluant swelling. The cyst is
lined by odontogenic epithelium and filled wilh blood or
serum. No treatment is usually necessary, as the erupting
loolh will eventually break the cystic membrane.
Symptomatic relief can be obtained by incising the lesion
and allowing the fluid to drain.

Melanotic Neuroectodermal Tumor of Infancy

IFig. 3-21 The melanotic ncuroeclodermal tumor of
infancy is a benign. rapidly growing neuroblastic neoplasm
commonly located in the anterior maxilla of infants less
than 6 months old. The tumor shows no sexual predileclion
and begins as a small pink or red-purple nodule that
resembles an eruption cyst. Localized and irregular
destruction of underlying alveolar bone is the usual
radiographic picture a... well as a primary tooth bud floating
in a son tissue mass. Treatment is conservative excision.
Histologic examination often reveals pigmentation.
Recurrence and melaSlasis are rarely documenled
complications.

Congenital Lymphangioma (Fig. 3-61 The

congenital lymphangioma is a benign neoplasm of dilated
Iymphalic channels Ihat occasionally occurs within the
mouth of infants. The tongue, labial mucosa, and alveolar
ridge are common locations. No sexual predileclion is
evident. The lesion Iypically produces a swelling that is
asymptomatic. compressible. and negative to diascopy.
When superficial. the swelling is composed of single or
multiple discrete papulonodules that may be pink to dark
blue in color. Deep-seated tumors produce diffuse
swellings with no alteration of the color of the overlying
tissue. Large lymphangiomas of the neck are referred to as
cystic hygromas. Surgical excision is the lreatment of
choice for intraorllilymphangioma~.

Dental Lamina Cysts (Fig. 3-3) Remnants of the

dental lamina that fail to develop into a tooth bud may
degenerate 10 fonn dental lamina cysls. These cysls are
classified, according to the clinical location in which they
are found. as eilher Epslein's pearls or Bohn's nodules.
Epstein's pearls are palatal keratin-filled cysts that develop
from islands of epithelial cells that persist at Ihe site of
fusion of opposing embryonic palatal shelves. The pearls
are usually small, firm, and whitish, and are found in
groups of about three. They are usually localed on the
midline of the pahlle or at the junction of the hard and soft
paJales. Bohn's nodules. or gingival cysts. appear similar to
Epstein's pearls. but are restricted to the alveolar ridge of
infanls. Dental lamina cysts vary in size from 1 mm to I em,
and both types are self-limiting. Resolution of Bohn's
nodules occurs upon tooth eruption, whereas palatal cysts
may be incised if they fail to resolve spontaneously.
Nata. Teeth fFig. 3-41 Natal teeth are supernumerary
odontogenic structures that appear occasionally in infants;
mOSI often as a familiaJ trait. These predeciduous teelh are
commonly located in the anterior mandible and frequently
consist only of cornified and calcific material. Root formation is dislinclly absent. and mobility is a common feature.
Natal teeth are believed to arise from an accessory tooth
bud. and simple eXlraction is the recommended treatment.
Natal teeth should be distinguished from a prematurely
erupting deciduous looth by taking the appropriate
radiograph prior to dental treatment.
8

Thrush (Candidiasis, Moniliasis) jFig. 3-71

Thrush. or acute pseudomembranous candidiasis. is a
fungal infection of mucosal membranes that is caused by
Candida albicalls and is primarily seen in infants. Thrush
is a surface infection that produces milky-white curds on
the oral mucosa. These curds are easily wiped off. leaving
a red. raw. painful surface. The buccal mucosa. palate. and
tongue are common locations of infection. Newborns often
acquire the infeclion from the mother's birth canal during
partuition and show clinical signs of disease within the first
few weeks of life. Fever and gaslrointestinal irritation may
accompany the disorder. Treatment consists of antifungal
agents applied topically.
Parulis fGum Bolli fFlg. 3-8) The parulis is an
inflammatory response to a chronic bacterial infeclion of
a non-vital tooth draining through a sinus tract. The
condition is most common in children following the
spread of pulpal infection to the furcal area of a posterior
tooth. It clinically appears as a small. raised. fluctuanl
yellow-to-red boil that is located near the mucogingivat
junction adjacent to the affected tooth. Pressure to the
area and the resulting discharge of pus is
pathognomonic. Spontaneous pain is not a feature.
although palpation of the lesion, looth. or surrounding
structures may elicit pain. Elimination of the
odontogenic infection leads to resolution.

ORAL CONDITIONS AFFECTING INFANTS AND CHILDREN

Fig. 3-1. Conge"it... epulis of the newborn.

-ourresy Dr Sheryl Hunter)

Fig. ]-). Dental lamina cysts on the maxillary alveolar

~ and epstein pear'IEPJ on median palatal raphe

Fig. 3-2. FIOOllng tooth In the mel..notic neuroectodermal tumor of Inl..ncy. ICourresy Or Chris NortJt?j

Fig. 3-4. Mandibular n ..tal teeth. (COUrtesy Dr Ron

.Jo(genson,

Fig. )-5. Dome-shaped ginglviI' eruption cyst.

,.. :1Urtesy Dr F Garcia-Godoyl

Fig. 36. Congenital alveolar lymphangioma.

f g. 37. Thrush caused by Cilndlda alblcam

Fig. 3-8. Parulis; nOrt-Vltal prUll<'lry first rnoI<lr

/Courtesy Dr Allugoj

Dr qon Jorgensonl

(Courtesy Dr Ron Jorgensonl

SECTION

III
Abnormalities
by Anatomic
Location

II

ALTERATIONS IN TOOTH MORPHOLOGY

Microdontia (Figs. 4-1and 4-21 and Macrodontia
Microdonlia refers to permanent teeth thaI are considerably
smaller than normal. II usually occurs bilaterally and is
oftcn a familial tr"il. Microdontia may occur as an isolalcd
finding. as a relative condition. or in a generali1-cd paltem.
The most common form occurs as an isolated finding
involving a single pemlanem tooth. usually the maxillary
lateral incisor. The term "peg lateral" is often used to
describe this variant. because the tooth is cone~ or pegshaped. Third molars are the second-most frequently
affected teeth.
When microdontia occurs in a generalized pallern il
may be relative to the size of the jaws. True generalized
microdontia is rare and occurs when the size of the jaws is
nonnal and the actual tooth size is small. Generalized
microdontia has been associated with pituitary dwarfism
and cancer therapy during the formative stage of tooth
development. True microdonts should be distinguished
from small overretained primary teelh and examined for
the presence of a frequently coexisting anomaly. the dens
in dente (see Fig. 4-7).
Macrodontia is Ihe opposite of microdontia and refers to
an abnormal increase in tOOlh size. This condition may
affect one. several or infrequently all teeth. It is usually a relative phenomenon. Macrodontia is often seen in incisors. in
mandibular third molars. and in a developmental condition
known as hemihypertrophy. in which the affected side is
larger than the unaffected side. A single macrodont should
be distinguished from fusion or gemination. a common fmd+
ing of incisors and cuspids. True generalized macrodontia is
rare and may be a result of pituitary gigantism.

Fusion IFigs. 4-3 and 4-41 and Gemination

IFigs. 4-5 and 4-6J Fusion and gemination are opposite
conditions that involve alterations in tooth morphology
resulting from a developmental disturbance during tooth
formation. In fusion the union of twO 1000h buds at the
level of the dentin forms a single tooth. This condition is
often hereditary. and it affects the primary teeth more commonly than the permanent teeth. Incisor teeth are the most
frequently involved. Clinically one sees an enlarged crown.
often with an extra cusp. a notch at the incisal edge. and a
vertical groove of variable length in the enamel.
Radiographically a single large root or two roots with separate pulp canals may be observed. In rare instances. a normal tooth bud fuses wilh a developing supernumerary
tooth. thus greatly resembling gemination.
Geminmion is the condition in which one tooth allempts
to split in two. It appears as an incompletely divided or
bifid tooth. The teeth most often affected are the primary

12

mandibular incisors and permanent maxillary incisors.

Heredity appears to be an important etiologic factor.
The two developmental anomalies. fusion and gemination. appear similar clinically and radiographically.
and may be difficult to distinguish. Geminated teeth
appear wide in the mesio-distal dimension. and more
commonly lack the vertical groove that delineates the
two crowns. To confirm the diagnosis the teeth should be
counted. If a clinically large tooth is seen and there is no
increase or decrease in tooth number. the condition is
gemination. If an enlarged tooth is seen and a neighboring tooth is missing. fusion has occurred. Treatment is
usually cosmelic. in which case the pulp chambers
should be located radiographically prior to crown preparation or endodontic treatment.

Dens Invaginatus 'Dens in Dente) (Fig. 4-7)

and Dens Evaginatus fuong~ Tubercle, {Fig.
48} About I % of the population has dens invaginatus. a
developmental anomaly in which enamel and dentin of the
crown invaginate in an apical direction into the pulp chamber along the palatal or lingual aspect of the tooth. There
are various degrees of invagination and the tenn "dens in
dente." which literally means a tooth within a tooth. should
be reserved for only the most severe fonn of this disorder.
Dens invaginatus is usually bilateml. and the cingulum of
maxillary lateral incisors is the most frequent point of
invagination. followed by the maxillary central incisors.
mesiodens. cuspids. and mandibular laleral incisors.
Clinically. the condition may appear as either a deep crevice
or an accentuated lingual pil. Food can easily impact in the
invagination. resulting in caries. which can rapidly lead to
pulpal necrosis and periapical innammation. Generally. prophylactic restorations are placed if the risk is high for carious involvement. Radiographically. one sees longitudinal
and bulb-shaped layers of enamel. dentin. and pulp centmlly located within the crown of the tooth. The disturbance
may extend apically to involve the entire root.
Dens evaginatus is less common than dens invaginatus.
II is represented by a small. dome-shaped accessory cusp
emanating from either the central groove of the occlusal
surface or the lingual incline of the buccal cusp of a pennanent posterior tooth. This condition occurs almost exclusively in mandibular premolars. and as such has been
termed Leong's tubercle. Persons of Mongolian descent
exhibit Leong's tubercle more frequently than others. The
tubercle consists of enamel. dentin, and a prominent pulp
chamber. Care should be taken to prevent pulp injury during tooth preparation. Pathologic exposure of the pulp may
occur with atmtion.

ALTERATIONS IN TOOTH MORPHOLOGY

Fig. 4-1. Mlcrodontla; peg-lateral inCISor.

Fig. 4-2. Periapical radiograph of a microdont (peg

lateri'll incisor).

Fig. 4-3. Bilateral fusion of primary mandibular

IncIsors. (Courtesy Dr Rick Myers)

Fig. 4-4. Periapical radiograph of fusion; primary

Fig. 4-5. Gemination of mancllbular Iateral.f"'l(ISOI".

Fig. 4-6. PeriapICal radiograph of gemination.

Fig. 4-7 _PenaplcaJ radiograph of dens invaginatus

maxi/leuy incisors

Fig. 4-8. Dens evaglnatus of mandibular second

",,,,,,,,,,

13

ALTERATIONS IN NUMBERS OF TEETH

Hypodontia (Figs. 5-1 and 5-21 Hypodomia is the
congenital absence of one or a rev. teeth because of agene
sis. Similar in meaning is the lenn oligodontia. which is
u~d (0 refer to "lImemus congenitally missing leeth. The
term anodontia is reserved for the rare condition involving
the failure of allteelh to develop. When missing teeth are
discovered. careful patient questioning is required to determine the reason for hypodontia. If teeth are missing for
reasons such as prior removal or lack of eruption. the use
of the term hypodolliia is inappropriate.
Hypodontia may involve either sex. any race. and the
primary or pennancnI teeth: however. it 110 most common in
the permanent dentition. About 5% of the population is
affected. and a familial tendency is quite common. The
most frequent congenitally missing teelh are the third
molars. follo~ed by the mandibular second premolars. the
maxillary second premolars. and the maxillary lateral
incisors. Visible space or over~retained primary teeth are
oftcn the clinicul signs of a missing tooth. Counting the
teeth together with radiographs confirms the condition.
Many syndromes are associated with congenitally missing teeth. They include Book's syndrome. chondroectodermal dysplasia. ectodermal dysplasia. incontinentia pigmenti, otodcntal dysplusia. and Rieger's syndrome. Both
head and neck therapeutic radialion to infants or children
and rubella (measles) during pregnancy have been implicated in the failure of tooth development.
Excess space is a sequela of missing teeth that may
result in drifling. tipping. 'and supraeruption of adjacent or
opposing teeth. Alterations in occlusion may require
orthodontic and proslhodontic therapy 10 restore function
and aesthetics.
Hyperdontla IFigs. 5-] and 5-4) Hyperdontia is a
term describing an extra or supernumerary deciduous or
permanent tooth. It occurs approximately eight times more
frequently in the maxilla than in the mandible, and most
often in the pennanent dentition. The most common supernumerary tooth is the mesiodens, which is located, either
erupted or impacted. between the maxillary cenlral
incisors. It may be of nonnal size and shape. but is usually
a small tooth with a conically shaped crown and short root.
The second most common supernumerary tooth is the
maxillary fourth molar. which can be fully developed or
microdontic in size. If the fourth molar is bocca.l or lingual to
the erupted third molar. the term "paramolar" is used: if it is
positioned behind the third molar, the term "distomolar" is
used. Mandibular premolars are occasionally supernumerary.
Supernumerary teeth are usually afunctional and may
cause inflammation, food impaction. interference with
tooth eruption. as well as positional. aesthetic. and masticatory problems. In addition, impacted supernumerary teeth
may give rise to dentigerous cysls. Because hyperdonti:t
occurs in association with cleidocranial dysplasia and

14

Gardner's syndrome. investigations should be performed to

rule out these disordcrs.

Cleidocranial Dysplasia (Figs. 5-5 and 5-6)

Cleidocranial dysplasia is an autosomal dominant hcreditary disturbance of unknown etiology. This syndrome
affects women and men equally. and b usually discovered
during childhood or early adolescence.
Cleidocranial dysplasia is a dcvelopmental disorder characterized by defective ossification of the clavicles and Cfillli
urn together with oral and sometimes long bone disturbances. Prominent features include delayed closure of the
frontal, pariet:!l. and occipital fontanelles of the skull. short
stature. broad shoulders, prominent frontal eminences with
bossing. small p:mmasal sinuses. an underdeveloped maxilla
with a high narrow palate. and relative prognathism of the
mandible. The clavicles may be absent or underdeveloped.
permilling hypermobility of the shoulders whereby patient...
can bring their shoulders togcther in front of the chest.
The oral changes are dramatic. particularly on the
panoramic radiograph. which can lead to early diagnosis of
the condition. There is prolonged retention of the primary
dentition. numerous unerupted supernumerary teeth, especially in the premolar and molar areas. and delayed eruption of the pemlanenl leeth. The pernlallem teeth are often
short-rooted and lack cellular cementum. which may be the
cause of the defective eruption pattern. Treaunent is compie-x. requiring surgical and orthodontic considerations.
Gardner~ Syndrome (Figs. 5-7 and 5-8) Gardner's
syndrome is an autosomal dominant condition with promi
nent orofacial features characterized by hyperdontia.
impacted supernumerary teeth. and jaw osteomas. In addition to these features. patients have multiple epidermal
cysts, multiple dermoid tumors. and multiple intestinal
polyps. The osteomas occur most frequently in the craniofacial skeleton, especially in the mandible and paranasal
sinuses: however, osteomas of the long bones are possible.
Maxillofacial radiographs often demonstrate numcrous
round osteomas and multiple diffuse enostoses that impart
a collon-wool appearance to the jaws. When superficial in
the skin. these slow-growing tumors are clinically
detectable as rock-hard nodules. The skin cysts (epidermoid. dermoid. or sebaceous) are smooth-surfaced lumps
that are commonly located on the ventral and dorsal thorax. Lipomas. fibromas. leiomyomas. and/or desmoid
tumors may accompany this disorder.
The most serious consideration of Gardner's syndrome
are the multiple polyps that affect the colorectal mucosa.
These intestinal polyps have an extremely high potential
for malignant transformation. resulting in adenocarcinoma
of the colon in nearly 100% of patients by the age of 40.
Early recognition of the orofacial manifestations necessitates prompt referral to a gastroenterologist together with
genetic counselling.

ALTERATIONS IN NUMBERS OF TEETH

F~.

5-1. Hypodontla; congeflllally rT!ISSI09 rnanc:l1Oular

~"'"

Fig. 5-3. Hype,dontla. 1'.J:tyerupr:ed ~

Fig. 5-5. Absent

clav,{~

In a patient with cleldoc:'itnial

d)'spliUi...

Fig. 57. Facial osteomas of Gardner's syndrome.

/COUrtesy Dr GeZd Terezhalmvl

Fig. 5-2. Pendplcdl raa,ogl<lpn reve<lhng it (Ongen'l

fTVSsang rn.w1Jy lal:ef<llII'l(ISQ'". CXdmpIt.' 01 hypodontla.

Fig. 5-4. Hyperdontla eKl.'d~ldtef.'.ll1l'lC1SOf

Fig. 5-6. Mult,ple supernumerary and rmp<'Clf'd tet'lh?f

c:leidoc,anlitl dyspliUI".

Fig. 5-8. PanoramK rilCllOgr",O/1 of d patient

syndrome.

With

Gardner's

15

ALTERATIONS IN TOOTH STRUCTURE

Enamel Hypoplasia IFigs. 6-1 and 6-21 Enamel that
is decreased in quantity is [cnned hypoplastic. This condition
results from a disturbance in enamel deposition during amelogenesis. A variety of interfering influences, including genetic
raclors (amelogenesis imperfocla). local [aclOrs (trauma). or

systemic factors (fluOJlY.)is. exanthemalic microbial infections.

and nutrilional deficiencies). may be involved. Depending on
lhe severilY of hypoplasia enamel discolorations. surface pil-

ling. or distinct horizontal grooves may appear. The pattern of

enamel hypoplasia depends on the nature of the influencing
factor. the phase of arneloblastic production at lhe lime of lhe

insult. and the duration of the insult. If the enlire phase of

amelogenesis is affected, the enamel of the entire dentition
will be thin and may appear "snow-capped:' yellowishbrown. rough. pined. or m()(tled. If the influence is systemic
and lasts only a short lime. only enamel then being formed is
affecled. producing a linear band of hypocalcificatiOll OIlleeth
developing during Ihis period. If the injury is local. such as
with trauma from an intruded primary tooth. damage to the
labial enamel surface of the permanent successor is likely.
Enamel hypoplasia of a single permanent looth thai results
from periapical or peri furcal inflammation of a deciduous
tOOlh is referred 10 as a "Turner's tooth."
Am~logenesis

Imperfecta (Figs. 6-3 and 6-41

Amelogenesis imperfecla is a heredilary disorder that is
characterized by a genemlized defect in enamel formation
of the primary andlor permanent dentilion. The condition
has been divided into four main types (hypoplaslic. hypo.
malure. hypocalcified. and hypomaturalionhypoplasia
with taunxionlism) and II subtypes according to clinical.
histologic. radiographic. and genelic features.
TIle most common fonn. the hypoplastic type. is deficiem
in normal enameL causing the crowns of Ihe leeth 10 appear
blanched. "snow-capped." yellow-brown. pined. or grooved.
Radiographically a full complement of teeth is usually seen;
however. the crowns of the teelh demonstrate either very thin
or absent enamel. The teeth resemble crown preparations
wilh characlerislic excessive imerdental spacing.
The hypomature type has quantitatively normal amounts
of enamel, bUI Ihe enamel is soft and poorly mineralized;
Iherefore a denial explorer under pressure will pit the enamel
surface. In this Iype. Ihe crowns COniaCI inlerproximally but
appear chalky. rough. grooved. and discolored. Fracturing of
the enamel is common.
The hypocalcified type. like the hypomature type, has
soft enamel bUI loses il at a much faster rale. resulting in
exposed dentin soon after eruption. PatienlS wilh hypocal
cified amelogenesis imperfecta usually have honey-colored
teelh with roughened surface texlure. mulliple unerupted
teelh. and an anterior open bite.
The hypomaturalion-hypoplasia with taurodontism Iype
exhibits yellowish teeth with opaque monling. cervical pit16

ting. attrition. and taurodontism. Trealmem for all forms of

amelogenesis imperfecla is usually full veneer coverage for
esthetic reasons.

Dentinogenesis Imperfecta {Figs. 6-5 and 6-6)

Dentinogenesis imperfecla is a hereditary disorder that
affecls the developmem of dentin. Three types have been
classified according 10 systemic involvement. clinical fealUres. and hislologic findings. They are Shields Type L
Shields Type" (heredilary opalescem demin). and Shields
Type III (Brandywine type).
Dentinogenesis impeJfecta Shields Type I is a manifestation of osteogenesis impeJfecta. a systemic condition involving bone fragility. blue sclerae. joint laxity, and hearing
impairment. It is caused by a defect in collagen fonnation.
Shields Type 1I demonstrates the same dentinal features as
Type I. bul no osteogenic oornponem is presenl. Persons with
Shields Type '" have leelh that are opalescent in color like
Types I and U. but the leeth have a shell-like appearance.
Dentinogenesis imperfecta affects the primary and per
manent teeth, the latter less severely. Clinically. the teeth
look normal when they first erupt, bUI shortly thereafter
become discolored gray-brown or opalescent: Ihe incisal
and occlusal surfaces chip and flake away. resulting in fissuring and significant anrition. Radiographically one sees
bulbous crowns. exaggeraled cervical constrictions. shon
tapered roots. and progressive obliteration of the rool
canal. Affected teeth are more susceptible to root fractures.
Dentin Dysplasia fFigs. b-7 and 6-8) Dentin dysplasia is a hereditary disorder of dentin characterized by alterations in pulp configuration - the presence of pulp stones.
and idiopathic radiolucencies of the root apices. The tenn
"roolless leelh" has been used to describe Ihis condilion.
The abnonnality has been classified into two types: Type I.
radicular dentin dysplasia. and Type II. coronal demin dysplasia. Both types are autosomal dominant and may affect
the primary and permanent dentition.
The distinclion belween Types I and II is based on mdiographic and histopalhological findings. In Type Ilhe primary and permanem leeth look clinically normaL bUI radiographs reveal defeclive rool developmenl with almoSI complete absence of root formalion. as well as large pulp stones
and complete pulpal obliteration of the primary teeth before
tooth eruption. Loose teeth and multiple periapical radiolucencies of unknown etiology are characteristic.
In Type II the pulp canals of !he primary leelh are often
completely obliterated as Ihey are wilh deminogenesis
imperfect3. The permanent leeth, in conlfast. clinically
appear normal excepl for narrower. Ihistle-shaped pulp
canals that are frequemly occupied by denticles. The roots
may be shan. blunted. and tapered. and may have horizonlal radiolucent lines.

ALTERATIONS IN TOOTH STRUCTURE

G!; 6-1. Do~na grooves of ~namel hypoplasia.

'3'

63. Teeth of ame/ogene"!,, imperfecU.

type lhat resembles crown preparaoons..

~Jtic

==

11 6-S. B ",e sclerilC of osteogenesis Imperfecta

Type I. ICourresy Dr Jerald Katz)

Fig. 6-2. Turner\; teeth; maxlll<lry first premolars

Fig. 6-4.

Hon~y-(oJored

teeth 01 amelogenesis

ImlMrfecta. hypocaltified type:.

Fig. 6-6. DIscOlored tee"ll of dentinogenesis imperfecta

~.

Shields Type I. (Courtesy Dr Charies ,'''oms)

~ag

Fig. 68. TMtle-rube pu:p chclmbe'rs and pulp calerflC<llrons In

the same patient WIth dentin dysplas-ia as If'! Fig 67

6-7. Op<oieSCenl hue of teeth WIth dentin dysplasl..

II.

17

ACQUIRED DEFECTS QF TEETH

Caries (Figs. 7-1 and 7-21 Denial caries is one of the
most common bacterial infections of man. characterized by
demineralization and destruction of the organic matrix of
leeth. Development of caries results from an intcmclion of
b<Jcterial plaque. diet components. altered host responses.
and lime. Electrochemical changes produced by acid
generation and ion flow appear to be causative. The
primary pathogen. S'repIO('o'CIIS 111111011.\', together with
AClil/om)'ces I'iSCO$IIS. Lac/oboeillll! species. and
S,replOcoccUS .wnglli.~ arc closely involved in lOoth
adherence and the production of lactic acid necessary for
the dissolUlion of enamel.

There are two types of caries. which arc classified

according to location: fissural and smooth surface. Fissural
caries is the most common fonn. It occurs most often in
deep fis.'>ures in the chewing surfaces of the posterior teeth.
Smooth surface caries usually occurs at places that are
protecled from plaque removal such as just below the
interproximal contact. at the gingival _margin. and on the
root surface.
Caries begins as an enamel decalcification that appears
as a Chlilky white spot or fissure. A dental explorer tip is
used to delect the soft lesion. Maturation of the lesion
permits progression through the enamel. then laterally
along the dentin-enamel junclion. and evemually IOward
the pulp. Sensitivity to hot. cold. and sweets are usual
symptoms; however. color changes. loss of hard tissue. or
infeclion of the pulp may occur before Ihe patiem becomes
llware of the disease. When caries occurs at an extremely
rapid pace. as in some children and young adulls. Ihe tenn
"rampant caries" is used. "Radiation. or amputation
caries." is another form of caries that occurs in
radiotherapy patients who lack the protective aClion of
saliva. "Nursing boltle caries" is the result of prolonged
comact of teeth with sugar-comaining liquids in infants.
"Root caries" are moSt frequently a result of xerostomia.

Pulp Polyp (Fig. 7-31 The pulp polyp is an

inflammatory and hyperplastic response of a wide open
pulp chamber to a chronic bacterial infection.
Extensively carious deciduous molars lind 6-year molars
of young children are most frequently affected.
Clinically the soft. red. non painful. pedunculated mass is
seen projecting up from the pulp chamber beyond the
broken-down occlusal surface of the tooth. Although the
tooth is initially vital. the condition will eventually erode
and result in nonvitality. Treatment is extraclion or
endodontic therapy.
Attrition (Fig. 7-4J Attrition. considered a physiologic
process. is the loss of occlusal or incisal tooth structure due
to chronic tooth-Io-tooth frictional contact. Although the
condition occurs most frequenl1y in the elderly population.
the primary teelh of young children may be affected.
Attrition is usually a generalized condition accelerated by

18

bruxism or abnormal use of selective teeth. Flattening of

the interproximal region is a common sequela. whereas
pulp exposure is a rare complication. since the deposition
of secondary dentin and pulpal recession occur
concurrently with the process. Close examination will
reveal a smooth llnd highly polished tooth surface. Ihe
outline of the dentin-enamel junction. and the receded pulp
chamber. Restoration of worn teeth may be challenging
becllUse of acquired changes in venical dimension.
Abrasion {Figs. 75 and 7-61 Abrasion is the
pathologic loss of tooth struclure due 10 abnormal
mechanical wear. A variety 9f agents can cause abrasion.
but the most common fonn is "toothbrush abrasion." which
produces a V-shaped notch in the cervical portion of the
facial aspect of the toolh. The abraded area is usually shiny
and yellow because of exposed dentin. and often the
deepest portion of the groove is sensitive to the tine of the
explorer. In addition to dentinal sensitivity. complications
of abrasion are eve11lual pulp exposure or tooth fraclure.
Abrasive notching of the teeth can be created by clasps
of partial dentures. pins or nails habitually held with the
teeth. or a pipe stem persistently clamped between the teeth.
Abrasion of the .incisal and occlusal surfaces often results
from exposure to abrasive substances in the diet and
occlusal wear from porcelain restorations placed in
occlusion. The abrasive process is slow and chronic.
requiring many years before giving rise to symptoms.
Restoration of normal tooth contour may be unsuccessful if
the patient is not made aware of the causative faclors.
Erosion {Figs. 77 and 781 Erosion refers to the loss
of tooth structure due to chemical action. Any chemical
Ihat is placed in prolonged contact with the tooth and
produces a drop in pH can produce erosion. The labial and
buccal surfaces of Ihe teeth arc most commonly affected.
The pattern of tooth erosion often indicates the
causative agent or a particular habit. For example. lemon
sucking produces characteristic changes of the faciaJ
surfaces of Ihe maxillary incisors. Horizontal ridges are
initially apparent. followed by smooth, cupped-oul.
yellowish depressions. A similar erosive pattern may be
seen in dedicated swimmers who chronically expose their
anterior teeth to chlorinated swimming pools.

Erosion of the lingual surfaces of the maxillary teeth.

together with amalgams that show generalized raised
margins. may indicate chronic regurgitation due to bulimia.
anorexia. pregnancy. or hiatal hernia. Sensitivity of the
exposed area is an early symptom. Excessive consumption
of sweetened carbohydrate beverages may accelerate the
condition. Fluoride treatments for early erosions and
restorations that cover exposed dentin for more extensive
lesions are the treatment of choice. Habit elimination or
behavior modification is required for success.

 caUIRED DEFECTS OF TEETH

:::.,. 1-1. "lerprWlJrr;a1 <Inc! occlus.'!1 Ci'lries.

Fig. ]-2. Radlogrilpl1lC evtdence of (aries of ~me p<ltlenl

Fig, 7-1

::"9 ]-3.1leOCl sn. exuberant pUlp polyp Pro.te<tJfl9 up rrom

"""'''''

Fig. ]-4. Signs of attrition YI100ttl yeI\owlSh oenon

e;o;posecl on mastlC<11ory surfaces

=''9 ]-5. Toothbrush abrasion aJong (efVlCa! margns of

Fig. ]-6. Abrasion d the rn<ncliOUlar IflOSOfS from Chronc:

fnc:t>on ag<WlSl porce&a-'l

F"'9 77. Lemon-sucking erosion.

Fig. 78. ungual erosion of bulimia.

19

LOCAUZED GINGIVAL LESIONS

Pyogenic Granuloma (Figs. B-1 and 8-21 The leon
pyogenic granuloma is a misnomer. since it is neither pusfilled nor a granuloma: instead. it represcms a form of
inflammatory hyperplasia rich in neocapillaries and immalure fibrous connective tissue. The exuberam growth is an
exaggemlcd response to irritation and appears bright red.
fleshy. and soft. The surface is glossy and the border is erythematous and ulcerated. The base may be polypoid or
pedunculated. Allhough usually asymptomatic. minor
manipulation will induce copious bleeding because of the
thinn~d epithelium and highly vascular tissue. Maturation
of Ihc lesion resulls in increased fibrosis. decreased vascu
larity. and decreased intensity of color.
Pyogenic granulomas are prone 10 develop in palienu
who have poor oral hygiene or a chronic or.ll irritant such as
overhanging restorations and calculus. Females a~ more
susceplible to !he condilioo because of honnonal influences.
Pyogenic granulomas may correspond with honnonal imbalances thal occur during puberty. pregnancy. or menopause.
and in such cases a~ called "hormonal or pregnancy
tumors." About 1% of pregnant women develop this lesion.
Pyogenic granulomas most frequently arise from the interdental papilla and enlarge from the labial and lingual aspects
to several centimeters if left untreated. Other sites of devel
opment include the tongue. lips. buccal mucosa. and edentu
lous ridge. Treatment is surgical excision which. in the gravid
female. should be delayed until afler panuition. Recurrence is
possible. especially if excision and local debridement are
incomplete or if plaque control is inadequate.

Peripheral Giant Cell Granuloma IFigs. 83 and

8-41 The peripheral giant cell granuloma is a reactive
epulis-like growth on the gingiva that is generally associated with a history of trauma or irritation. It is thought to
originate from the mucoperiosteum or periodontal ligament; therefore. the peripheral giant cell granuloma
demonstrates a restricted area of development - the dentu
lous or edentulous ridge. The mandibular gingiva anterior
to the molars is particularly affected. especially in females
between the ages of JO and 40. Histologically multinucle
ated giant cells and fibroblasts are numerous throughout
the sp;x:imen.
The peripheral giant cell granuloma is characterized by
a well-defined. finn swelling that seldom ulcerates. The
base is sessile. the surface is smooth or slightly granular.
and the color is pink to dark red-purple. The nodule is usually a few millimeters to Icm in diameter. although rapid
enlargement may produce a large growth that encroaches
on adjacent teeth. The lesion is generally asymptomatic.
but because of its aggressive nature the underlying alveolar
bone is often involved. prooudng a pathognomonic superficial "peripheralcuff radiolucency. Treatment is surgical
excision including the base of the lesion and curettage of
lhe underlying bone. Incomplete ~moval results in a

20

marked tendency for recurrence. Histologically, this lesion

cannot be distinguished from the central giant cell granuloma and the brown tumor of hyperparathyroidism.

Peripheral Fibroma with Calcification {Peri

pheral Cemento-Ossitying FJbroma' (Figs. 8-5
and 8--6) The etiology of the peripheral fibroma with cal
cification is uncertain. but innammatory hyperplasia of
superficial periodontal ligament origin has been suggested.
It arises exclusively from the gingiva. usually the interden
tal papillae. When calcifications are present they may con
sist of bone. cementum, or dystrophic calcification. which
are often difficult to distinguish microscopic.llly.
The peripheral fibroma with calcification is a reactive
growth that is especially prone to occur in the anterior
region of the maxilla of young and middle-aged females.
The salient clinical features of this solitary swelling are
finnness. pink color. and sessile allachmenl. An imponant
diagnostic clue is the condition's marked tendency to cause
displacement of adjacent teeth. The chief complaint often
involves an asymptomatic. slowgrowing round or nodular
swelling. Immature lesions are soft and bleed easily.
whereas older lesions become firm and fibrotic.
Radiographs m3Y reveal central radiopaque foci and mild
resorption of the crest of the ridge at its base. Treatment is
excision. Care should be taken to avoid damage to lhe
adjacent teeth. The recurrence rate is low.

Gingival Carcinoma IFigs. 8-7 and 8-81 The gingiva accounts for approximately 5 to 10% of all cases of
squamous cell carcinoma within the mouth. Generally. at
the time of diagnosis the disease is advanced because of its.
asymptomatic nature and posterior location, and because of
delay of examination.
Gingival carcinoma has a varied appearance. It usually
appears as a reddish mass with focal white areas prolifer3ting from the gingiva. but may mimic benign inflammatory
gingival conditions. erythroplakia. leukoplakia. or a simple
ulceration. Carcinoma should be suspected when close
examination reveals a pebbly surface. the presence of
many small blood vessels in the overlying epithelium_ and
surface ulceration. Etiologic factors include tobacco ,use.
alcoholism. and poor oral hygiene. Elderly males are espe
cially susceptible. and the condition seems to have a slight
predilection for the edentulous alveolar ridge of the poste
rior mandible. Completely dentulous persons rarely have
this disease.
Gingival carcinoma may extend onto the floor of the
mouth or mucobuccal fold. or it may invade the underlying
bone. Radiographs may reveal a "cupping out" of the alve
olar crest. Metastasis to regional lymph nodes occurs fre
quently. These nodes are finn. rubbery. matted. nonmov
able. and non-painful. Treatment consists of surgery and
radiotherapy.

_lXAlIZED GINGIVAL LESIONS

Fig. S-2. Pregnillncy turnor; thR'e day!;

post-pattultJOn.

&-3 JTIOCXtKUrfacea perfpheril' giant-cell grany.

'rom marginal 91l191'l/a jCourresy Dr Ed Heslop)

Fig. 8-4. A rapKlly enlarging perfpheril' giantoCitll

granuloma. 'Courtesy Drs.James Cottone & SIeve Bnckefl

&.5. Peripheral fibroma with c..lc:iflUltJon ansng

O"{~ paprlae ICourtesy Or .James COttonet

Fig. 8-6. F.'m. pw1k peripheral fibroma with

c.alclfic"tion. [COUrtesy Dr Pele Semon)

8-7. Glnglv<l. colIrclnomil concurrent Wlttl poor oral

advanced age. r Courtesy Dr Jack Shermanl

U1rdnoma of the gi"gll;'4I. (Courtesy Dr Tom ,A,ufClemone)

leY' """'d

Fig. 3-8. ReddISh, granular surface of sq"ilmous nil

2.

LOCALIZED GINGIVAL LESIONS

Parulis fGumboil) lFigs. 9-1 and 9-21 The parulis.
or "gumboil"" - a

s)'nonymou~

tenn rCS/,"l"\cd for children-

is a locnlized area of inflammalOry hyperplasia that occurs

at the endpoint of a draining dental sinus tract. It appears
a.'> a soI'l. solitary reddish papule. located apical and facial

to a chronically abscessed 1001h. usually on or near Ihe

labial mucogingival junction. Occasionally the parulis is
slightly yellow in the center and emits a purulent yclJo~ish
exudate upon palpation. Acute swelling and pain may
accompany the condition if the sinus lract is obstructed.
To locate Ihc non-vital looth from which the parulis
arises. a sterile gutta-peTeha poinl may be inserted into the
fistuhL Periapical radiographs are then taken to demonstrate the proximity of the gUlla-percha point 10 the apex
of the offending tooth. Afler diagnosing the non-vital
tooth. the treatment of choice is root canal therapy.
Regression of the parulis usually ensue:. shonly mercafter.
If the problematic tooth is left untreated. the parulis may
persist for years. A persistent lesion may mature into a
pink-colored fibroma.

Pericoronitis 'OperculltlsJ {Figs. 9-] and 9-41

Pericoronitis is inllammation of the soft tissue surrounding
the crown of a partially erupted or impacled tooth.
Pericoronitis may develop at any age. but mosl frequently
occurs in children and young adults whose teeth are erupting. Generally. it is associated with an erupting mandibular
Ihird molar that is in good alignment but is limited in its
eruption by insufficient spacc. Radiographs of the region
reveal a flame shaped radiolucency surrounding the tooth.
with the cortical outline on the dislal a<;pect of the lucency
either absent or di:.tinctly thickened because of the deposition of reactive bone.
Pericoronitis de\elops from bacterial contamination
beneath the operculum. resulting in gingival swelling. redness. and halitosis. The presence of pain is variable and
may be extreme. but the discomfort usu:llly resembles that
of gingivitis. a periodontal abscess, or tonsillitis. Regional
lymphadenopathy. malaise. and low-grade fever are common. If edema or cellulitis extends 10 involve the masseter
muscle. trismus often accompanies the condition.
Pericoronitis is frequently complicated by pain induced by
tmuma from the opposing toolh during closure.
Pericoronitis is best managed by entering the follicular
space. llushing the purulent material from the gingival sulcus with saline solution. and eliminating "ny occlusal trauIn". Definitive treatment is usually extraction of the
involved tooth. Antibiotic coverage is ~ommended when
conslitutional symptoms are present and the spread of
infection is likely. Recurrences and chronicilY are likely if
the condition is managed only with antibiolics.

22

Periodontal Abscess {Figs. 9-5 and 961 A periodontal abscess is a fluctuant !'>welling of the gingiva
resulting from pathogenic bacteria that are occluded in the
gingival crevice. The condition is evidcnced clinically by a
smooth fluctuant nodule. increased mobility of the periodontal1y involved tooth. purulence. and tissue necrosis.
Chamcleristically the attached gingiva is mised. redpurple.
and without stippling or a free marginal groove. Patients
often complain of well-localized. dull. and c;minuous pain.
especially if the purulent exudate has no avenue for escape.
Intensification of pain occurs when vertical or horizomal
pressure is applied. or whcn the overlying soft lissuc is palpated. Diagnostic evaluation utilizing a periodontal probe
may initially produce discomfort. but is often therapeutic
for a short time because it may drain the ab!'>cess. An
unpleasant tasle oflen accompanies the condition.
The pulp of a tooth associated with a periodontal
abscess usually tests vital. unless the inflammatory process
has extended into the pulp via the apex or accessory canals.
Fever. mal"ise. and lymphadenopathy may coexist, and
radiographic evidence of localized bone loss may be seen.
Treatment should be directed toward necrotic material
removal. adequate dminage. localized pcriodonraltherapy.
and improved plaque control measures. Failure to fully
treat the problem can result in recurrence or spread of
infection along fascial planes.
Epulis Fissuratum ,Irritation Hyperplasia, {Figs.
9-7 and 981 TIle epulis lissuratum is a reaclive inflanuna~
tory fibrous hyperplasia caused by :I chronic irritant. usually the
flange area of 1m old. poorly fining complete or partial denture.
Initially the overextended denture margin produces an ulcer that
heals incompletely because of repeated tmuma. Hyperplastic
healing results and a pinkred. fleshy exuberance of mature
granulation tissue is produced. 1lle hyperplastic lesion. located
where the denture flange rests. is found most commonly in
females. It is nonpainfuL grows slowly on either side of the
denture. and causes the p<ltient lime concern.
The epulis fissuraturn in the early stages consists of a sin.)
gle fold of smOOlh soft tissue. As the swelling grows, a central cleft or multiple clefts become apparent. the boundaries
of which may drape over the denture flange. "The mucolabial
fold of the anterior region of the maxilla is the most common
location. followed by the mandibular alveolar ridge and me
mandibular lingual sulcus. Adjustment of the denture or construction of a new denture may reduce the trauma and
inflammation. but will not cause the underlying fibrous tissue
to regress. Likewise, surgical excision without alteration of
the dentures promotes recurrence. Successful treaunel1l usually requires surgical removal of the redundant tissue. micro-.!>Copit examination of me excised tissue. and correction or
reconstruction of the denture.

_OCALIZED GINGIVAL LESIONS

Fig. 9-2. PInk parulis at moc:ogll19....dI }JllCtlOfl adjaCent to it

fl()(l-VIt<!1 first molar

~-.3

97.

Pericoronitis surrounarng a partially erupled

Fig. 9-4. Flafne..wpe<l radiolucency of pericoronitis .ma

o~tems

underlYIng

Wnl swelling caused by a periodontal

Fig. 9-6. Dlamlng of puruleflt m<ltenal from the periodontal

abscess evident In Fig 9-5

~stl( fc>lm

at M epulis fissu,,,tum (<,used

a (lert!u-e Range

Fig. 9-8. Epulis ffssuratum where the p,:!rtial denture

flange ''''''

23

GENERALIZED GINGIVAL ENLARGEMENTS

Hereditary Fibromatosis Gingivae (Figs. '0-1
and 10-21 Hereditary fibromatosis gingivae is a rare progressive fibrous enlargement of the gingiva that is inherited as an autosomal dominant nail. The condition has an
early childhood onset and becomes more prominent with
age. The enlargement is usually generalized and noninflammatory. affecting the buccal and lingual surfaces of
bOlh jaws equally. The free. interproximal. and marginal
gingiva are enlarged, ullifonnl)' pink in color, finn. non
hemorrhagic. and often nodular.
There are two varieties of hereditary fibromatosis gingi.
vae: generalized and localized The generalized type is nodular and diffuse. exhibiting multiple coalesced areas of globular
gingival overgrowths that encroach on and eventually cover
the crowns of the leeth, The localized variely is occasionally
seen in which solitary overgrowths are limited to the palatal
vaull of the maxillary tuberosity or the lingual gingiva of the
mandibular arch. These gingival overgro"1hs appear smooth.
finn. and symmetrically round. The localized involvement
may be unilateral or bilater.t1. and the term "focal gingival
fibromatosis" has been suggested for this variant.
Hereditary fibromatosis gingivae may interfere with
tooth eruption. mastication. and oral hygiene. In severe
cases. noneruption of the primary or pennanent teeth may
be the chief complaint of the patient. Regression is not a
fealUre of this disease. even with effective oral hygiene
measures. Gingivectomy, with either a blade or a carbon
dioxide laser. is the treatment of choice. Continued growth
may require multiple operations. The condition may be
accompanied by acromegalic facial features. hypertrichosis. or mental deficits.
Drug-Induced Gingival Hyperplasia (Figs. 10-3
and '0-4} In approximately 25 to 50% of patients taking
the therapeutic prescription drugs phenytoin (Dilantin).
nifedipine (Procardia). and cyclosporin-A. bulbous
enlargement of the gingiva is a common side effect. The
condition is usually seen in young patients after pUberty,
and can occur in either sex. Though the enlargement
results from a hyperplastic response. an inflammatory
component induced by dental bacterial plaque often coexists and tends to exacerbate the condition. The gingival
enlargement is usually generalized and often appears most
exaggerated on the labial aspects of the anterior teeth.
The overgrowth begins at the interdental papillae and
enlarges to fonn soft red lumpy nodules that bleed easily.
Progressive growth results in fibrotic changes: the interdental tissue becomes enlarged. pink. finn. and resiliem to
palpation. With time the condition can completely engulf
the crowns of the teeth. which aggravates home care. limits
mastication. and compromises aesthetics. Treatment may
involve changing drug therapy and/or minimizing the overgrowth with meticulous plaque control measures. The gingival swelling usually does not completely regress even

24

with reduced drug doses: thus. once present. the excess tissue often requires surgical removal.
Mouthbreathing {Figs. 10-5 and T0-61 Chronic
mouthbreathing is characterized by nasal obstruction. a
high narrow palatal vault. snoring. xerostomia. a sore
throat upon wakening. and a chamcleristiC' form of gingivitis. Classically the gingival changes are limited to the ante
rior labial gingiva of the maxilla and, sometimes. the
mandibular gingiva. These changes may be an incidental
finding. or may be noticed in conjunction with caries limited to the incisors. Therefore. multiple anterior restorations
often sen'e as a diagnostic clue.
Early changes involve diffuse redness of the labial.
marginal and interdental gingiva. Shortly thereafter. the
interproximal papillae become red. bulbous. and hemor
rhagic. Progression of the condition results in inflamma~
tory changes of the entire attached gingiva and bleeding
upon probing. Improved oral hygiene will reduce the features. but will not resolve the condition.
The diagnosis of mouthbreathing is made by objective
and subjective information. Confirmation is achieved when
healing occurs after a protective dressing is placed on the
affected gingiva al night. together with the return of gingivitis upon discontinuance of the dressings. Treatment
should address the re-establishment of a patent nasal airway: thus. the aid of an otorhinolaryngologist is often
required to effectively manage this condition.
Gingival Edema of Hypothyroidism IFigs. 10-7
and 10-81 Hypothyroidism is a relatively common disorder in which clinical manifestations are dependent on the
age of onset. duration. and severity of the thyroid insufficiency. When the patient is deficient in hormone at an early
age. cretinism results. This disease is characterized by
soon stature. menial retardation, disproponionate head-tobody size. delayed tooth eruption. mandibular micrognathism. and swollen lips and tongue. Regardless of the
age of onset, hypothyroid patients exhibit coarse. dry. yellowish skin. intolerance to cold. and lethargy. Swelling is
the classic feature and is most prominent in the face. particularly around the eyes.
Intraorally macroglossia and macrocheilia are common
and may cause an altered speech pattern. The gingiva
appears unifonnly enlarged, pale pink in color. and compressible. Swelling occurs in all directions on both the
facial and lingual sides of the dental arches. When secondary inflammation is present. the tissues become red and
boggy and have a tendency to bleed easily. Treatment for
the gingival condition depends on the degree of thyroid
deficiency. Patients marginally deficient require only strict
oral hygiene measures. whereas frank cases require supplemental thyroid therapy to achieve resolution of the systemic and oral condition.

::il:

ERALIZED GINGIVAL ENLARGEMENTS

!)oJ, :::ieneralllM glngrval enlargement of heredlt..ry

"";"__
~m gIngivae. I(ourtesy Dr Kenneth AbramoVltchj

~3.

Oilantin-induced gingival hyperpliula.

:r -"'!I"""IeS (otlOf1ej

~s Early ginglvi'l' inflammation as\.Ooated

. ' ; '"'~.uthing.

With

Fig. T0-2. Fibromatosis gingivae, localized type,

limited to the tuDermrly ICourtesy Dr Ron Jorgenson)

Fig. T0-4. Fibrotic ginglv..' hyperplasl.. inolcalNe of

prolonged dllantln therapy

Fig. 10-6. Progressive glngllo'o1' changes

and caries seen

In a chronic mouthbreather. lCoortesy Dr Charles Morris)

Fig. '0-8. GeneraliZed gingival edemi1 of l1ypothyroldlsm;

same patient as In Fig 10-7

25

GINGIVITIS
Gingivitis (Figs. II) and 11-2) Inflammation of the
gingiva. or gingivitis. is the result of bacterial infection.
Initially, gram-positive streptococcal organisms predominate. Over a 3-week period. however. gram-positive rods
species. specifically Actinomyces. gram-negative organisms such as Fusobacterium, Veil/of/ella. and spirochetal
organisms including Treponema colonize the gingival sulcus. Persistence of supragingival microbial plaque results
in characteristic gingival changes and the eventual establishment of subgingival microbial populations that may
lead 10 periodontitis. Gingivitis can occur at any age, bUI
most frequently arises during adolescence. It has no sexual
or racial predilection.
Gingivitis can be classified according to distribution.
duration, etiology, pathogenesis. and severity. The distribution may be general, local, marginal, or papillary; the duration acute or chronic. An abbreviated list of the different
types of gingivitis based on etiology includes: actinomycotic, diabetic, hormonal, leukemic, plasma celL psoriasifonn. scorbutic, and human immunodeficiency virus (H1V).
Gingivitis is most often chronic and nonpainfuL but
acute, painful episodes may superimpose over the chronic
state. The severity is often judged by the alterations in
color, contour. and consistency, and by the presence of
bleeding. Chronic gingivitis features red swollen marginal
gingiva with bulbous interdental papillae that have a redpurple tinge. Stippling is lost as the marginal tissues
enlarge. The condition may be difficult for the patient 10
control because hemorrhage and pain are induced by the
slightest provocation; therefore patients will reduce brushing frequency and effectiveness. Treatment for acute and
chronic forms of gingivitis consists of removal of dental
plaque followed by daily oral hygiene measures.
Acute Necrotizing Ulcerative Gingivitis (Fig.
11-31 A type of acute gingivitis that is linked to specific
bacterial species and stress is termed "acute necrotil-ing
ulcerative gingivitis"' (ANUG). also known as Vinl:ent's
infection. or "trench mouth."' This multifactorial disease
has a bacterial population high in fusiform bacillae and
spirochetes that can be demonstrated in smears using darkfield microscopy.
ANUG is charactcril-ed by fever. lymphadenopathy.
malaise. fiery red gingiva. extreme oral pain. hypersaliva
tion. and an unmistakable fetor oris. The interdental papillae are punched out. ulcerated and covered with a grayish
pseudomembrane. ANUG is common in persons between
the ages of 15 and 25. particularly students and military
recruits enduring times of increased stress and reduced
host resistance. and in patients with HIV infection. In rare
instances the condition can extend onto other oral mucosal
surfaces. or recur if mismanaged. Treatment of ANUG
requires irrigation. gentle debridement. antibiotics (if constitutional symptoms are present). and stress reduction.

26

Partial loss of the interdental papillae can be expected

despite nonnal healing.
Actinomycotic Gingivitis {Fig. 11-41 Actinomycotic
gingivitis is a rare intraoral finding that may appear as a
fonn of marginal gingivitis. Redness, intense burning pain.
and lack of a response to nonnal therapeutic regimens are
common features. A tissue biopsy reveals the Mn-acid fast.
filamentous fungal organism. Gingivectomy or long-tenn
antibiotic therapy provides effective treatment.
Hormonal Gingivitis (Pregnancy Glngivitisl
(Figs. 11-5 and 11-6) Honnonal gingivitis is an inflammatory hyperplastic reaction to microbial plaque that generally affects females during puberty. pregnancy, or
menopause. Although alteration in estrogen/progesterone
levels as a result of hormonal shifts and the use of birth
control pills have been implicated. the exact causative
mechanism remains unknown.
The condition begins at the marginal and interdental
gingiva and becomes most prominent interproximally. The
marginal gingiva appears fiery red. swollen, and tender,
while the papillae become compressible. swollen. and
lumpy. Close inspection reveals hyperemic engorgement of
the inflamed tissue. Severity is related to microbial accumulation; thus poor oral hygiene can exacerbate the condition, which is often the case with the gravid female, since
tooth brushing may precipitate nausea. Honnonal gingivitis
is usually transitory and responds to meticulous horne care
and frequent oral prophylaxis.
Diabetic Gingivitis (Figs. 11-7 and 11-8) Diabetes
mellitus is a common disease affecting approximately I to
3% of the population in the United States. It is a progressive metabolic disorder characterized by hyperglycemia.
glucosuria. polyuria. polydipsia. pruritis. and weight loss.
Poor control of blood glul:ose levels is related to lack of
production or utilization of insulin. Complications of diabetes include a variety of vascular-related problems such
as atherosclerosis, retinopathy. peripheral forms of neuropathy. and renal failure. In addition. altered neutrophil
chemotaxis increases the diabetic's risk of infection. A dry
mouth. burning tongue. persistent gingivitis. or candida I
infection may be the first intraoral signs of the disease.
The severity of diabetic gingivitis depends on the stage
of the disease and the patient's oral hygiene. In the unC()lltrolled diabetic peculiar proliferations of exuberant tissue
arise from the marginal and attached gingiva. The welldemarcated swellings are soft. red. irregular. and hemorrhagic. The surface of the hyperplastic tissue is usually
bulbous and. in some cases. papulonodular. This type of
gingivitis is difficult to manage when blood glucose level ..
remain elevated. Successful treatment requires meticuloU',
home care and control of the blood glucose concentration
with diet. hypoglycemic agents. or insulin.

'~"(j IVI TI S

1-1

UJe-lnduced marginal gingivitis.

Fig. 1 1-2. Chronic gingivitis exten<Jlng onto me attached

gingiva (Courtesy Dr Tom McD<lVidl

...

'-3
({'ff't1 papin",..: acute necrotizing
. . . ._ _
e gingivitis iANUGI ICoorte~y Dr Bril BClker)

1-5. Hormonal gingivitis In a pubertal female

1-7 _Gingivitis In a 19-year-{)lcl woman With

diabetes mellitus.

Fig. T1-4. Red, ,nfBmed IT'i1ndlbular gingiva (!U~ed by

AclJOOmyce.s Inff;.'(liofl of gingiva

Fig. 11-6. Severe glr'lgNill ch<1nges associated With

pregnallC)': hormona' ginigivitis.

Fig. I 1-8. Inflamed, papulonodu!ar hyperplasia of the

gingiva In a diabetic patient.ICouttesy Dr Iv1<Irgol Van Dis)

27

SPONTANEOUS GINGIVAL BLEEDING

Leukemic Gingivitis fFigs. 12-' and 12-21
Leukemia. a malignant condition characterized by while
blood cell overproduction. is classified according to cell morphology (monocytic. myelogenous. or lymphoblastic) and

the clinical course of the disease (acute or chronic). Oral

manifestations are more frequently encountered in acute
leukemia of the monocytic and myelogenous subtypes. Oral
features occur early in the course of the disease because of
neoplastic proliferation of one blood cell type. which reduces
the normal production of the other hematopoietic cells.

Consislenl signs of acute leukemia afe cervical lymphadenopathy, malaise, anemic pallor. leukopenia-induced
ulcerations. and gingival changes. Leukemic gingival tissues are usually red. tender. and spongy. and tend to peel
away from the teeth. With progression of the disease the
swollen gingiva becomes purple and shiny. Stippling of the
tissue is lost and spontaneous bleeding from the gingival
sulcus eventually occurs. The edematous tissue is most
prominent interdentally and results from leukemic infiltration of white blood cells. In certain patients the neoplastic
cells may invade pulpal and osseous tissue, inducing vague
symptoms of pain without corresponding radiographic evi
dence of pathosis. Purpuric features such as petechial
lesions and ecchymoses on pale mucosal membranes.
togelher with gingival hemorrhage. occur frequently.
Systemic control of leukemia often involves intensive
radiOlherapy, chemotherapy. blood transfusions, and bone
marrow transplantation. Difficulty may be encountered in
maintaining optimal oral health because of the chemotherapeutic-induced oral ulcerations. Meticulous oral hygiene
combined with antimicrobial rinses is recommended 10
reduce the innammatory and ulcerative sequelae of
chemotherapy.

Agranulocytosis (Neutropenia) and Cyclic

Neutropenia IFlgs. 12-3 and 12-41 Neutropenia
refers to a disease characterized by a decrease in the num
ber of circulating polymorphonuclear neutrophils (PMNs).
In most instances. the condition is recognized by its clinical symptoms. which consist of chronic infections and an
almost complete absence of neutrophils in laboratory blood
tests. Anti-metabolic. antibiotic. and cytotoxic drugs are
the etiologic agents involved in over half of all cases. In
rare instances the condition may be congenital. An uncontrollable infection in the neutropenic patient can resuil in
bacterial pneumonia, sepsis, or death.
A distinct fonn of agranulocytosis is cyclic neutropenia.
which is characterized by a periodic dimunition of circulating PMNs that occurs about every 3 weeks and lasts for
about 5 days. The condition is idiopathic and usually
begins in childhood. II is sometimes accompanied by
arthritis. pharyngitis. fever. headache, and Iymphadenopa-

28

thy. A history of repeated infections of the ear and upper

respiralory tract is common.
Intraorally patients demonstrate inflammalory gingival
changes and mucosal ulceralions. The ulcerations are usually large. oval. and persistent. They vary in size and location; sometimes found on ttfe aU8ched gingiva and other
times on the tongue and buccal mucosa. The gingivitis is
periodic and ulcerative. At stages corresponding to elevated
levels of PMNs. minimal inflammation is evident. In contrast, when the level of PMNs drops precipitously. general
ized inflammatory hyperplasia and erythema occurs. If left
untreated Ihe condition is exacerbated by the presence of
local factors such as plaque and calculus. resulting in alveolar bone loss. tooth mobility. and early exfoliation of leeth.
The periodic appearance and spontaneous regression of
signs and symptoms should cause the clinician to suspect
cyclic neutropenia. Daily repetition of the white blood cC'1I
count is required to diagnose this condition. Curative treatment is unavailable: therefore management is palliative,
with antibiotic and antimicrobial therapy together with
repeated oral prophylaxis.

Thrombocytopenic and Thrombocytopathlc

Purpura IFlgs. 12-5 through 12-81 Platelets play an
integral role in maintaining hemostasis by providing the primary hemostatic plug and by activating the intrinsic system
of coagulation. A decrease in the number of circulating
platelets (thrombocytopenia) may be idiopathic. or it may be
due 10 decreased platelet production in the bone marrow.
increased peripheral destruction. or increased splenic
sequestration. Decreased function of circulating plate leiS
(thrombocytopathia) is often related to hereditary syndromes
or acquired states such as druginduced bone marrow suppression, liver disease. or dysproteinemic states like uremia.
Vascular-related clinical manifestations of platelet disorders include petechiae. ecchymoses, epistaxis, hematuria.
hypennenorrhea. and gastrointestinal bleeding resulting in
melena. Spontaneous gingival bleeding is a frequent. early.
and dramatic occurrence. The blood oozes from the gingival sulcus profusely. eilher spontaneously or following
minor trauma such as toothbrushing. Later the fluid turns
into purplish-black globs of cloned blood that adhere to the
oral slTUctures. Occasionally, clotted blood may be swallowed. which results in nausea. Mild traumas. panicularly
at the occlusal line of the buccal mucosa and tongue. are
siles of extensive hemorrhage. Multifocal red petechial
spots on the so! palate is another frequent clinical sign of
bleeding disorders. The platelet count, clot retraction time.
tourniquet test, and template bleeding time should be
ordered to diagnose a platelet disorder. Platelet transfusions may be necessary if local measures prove ineffective
in controlling oral bleeding.

;oQNTANEOUS GINGIVAL BLEEDING

on shiny. l)leedWI9

~e"OUJ 'eukemi~.

glngJV~ of

a patient WIth

(Courtesy Dr Mornque

l-J Cyclic neutropenia assoclJlec! gingival

'C eo:heoal erosion

2-5 - ~ ","1m cirrhosis d ttle liver and a dotting- - . oef'kfc:ncy. lCOUrtesy Dr Rogef Raol

2-7 Thtombocytopenlil; 91119.....<11 bleedmg ana tl'Il!

'J{ Courtesy Dr l.ao'y Skoczylas)

Fig. 12-2. Acute lymphOcytic

men:;nj

leukem~; gtngwal eriarge--

sp::lnIaI'leOUs b/e.ltr9 (COUrtesy Dr o'.1onque MKhau<:lJ

Fig. 12-4. RiKllogl(1ph revealing loss Of penod()l'l[<ll support

and floating teettt; same patient WIth cydlc neutropenlil as
III

F'9 12-3

Fig. 12.(). Spont.lneolots gingiva' bleeding of same

paoent WI{h tirrhosls III FIQ 12-5 !Courtesy Dr Roger Raol

Fig. '2-8. RadIOgraphic: evidence of ctvonc Irrlt<l/1l:'.; thai:

caused tf1e bIeeCllf19 ~ ,n patlenl: WIth thrombocytopenhl

lnF'912-7

29

SWELLINGS OF THE LIP

Angioedema fAngioneurotic Edema, (Figs. 13-1
and T321 Angioedema is a hypersensitivity reaction characterized by the accumulation of fluid within the facial lissues. resulling in soft. swollen areas under the skin. It occurs
in hereditary and acquired fonns. and may be generalized or
localized. When the nonpainful swelling affects the lips it is
usually unifonn and diffuse. but may be asymmetrical,
involving pans of the lip in varying degrees. Angioedema
develops within minutes or gradually over a few hours. and
is of Iransient duration. The vermilion border appears

stretched, evened, pliable. and less distinct than usual,

whereas the surface epithelium remains normal in color, or
is slightly red. Swellings of the tongue. floor of the mouth.
eyelids. face. and extremities may accompany the condition,
and complaints of burning or itching are common.
Although Ihe cause of angioedema is poorly understood, foods, wine, drugs, and stressful situations may be
causative factors for the acquired type. In this fonn of the
disease. antigenic stimuli appear to trigger an
immunoglobulin-linked. histamine-mediated increase in
capillary penneability. The hereditary type. on the other
hand. appears 10 be linked 10 an enzyme deficiency.
Angioneurotic edema is usually recurrent and self-limiting. Generally it poses little threat to the patient.
Wilhdrawal of the allergen together with the administration
of antihistamines is the trealment of choice. In cases
involving swelling of the pharyngeal tissues. airway compromise is of prime concern.

Cheilitis GJandularls IFig. 13-31 Cheilitis glandularis is of unknown etiology and is most frequently
encountered in adult males. II is a chronic inflammatory
disorder of the accessory labial salivary glands. panicularIy those of the lower lip, that is characterized by diffuse
enlargement and eversion of the lip. Although poorly
understood. this condition may be associated with smoking. JXXlr oral hygiene. or chronic exposure to the sun and
wind; it may also be auributable to bacterial infection or
congenital disposition.
Cheilitis glandularis clinically produces a symmeuically
enlarged, evened. and finn lower lip. As time passes. the
inflammed labial accessory salivary glands become dilated
and appear as multiple small red spots. From these ductal
openings a viscous. yellowish. mucopurulent exudate is
secreted that can cover the entire lip. making it sticky.
Progression of the condition causes the lip to appear
atrophic, dr)'. fissured, and scaly. Distinction of the vennilion border is eventually losl. and secondary infection of a
deep labial fissure often results in fistulation and scarring.
Emollienls and sunscreens afford protection. but severe
cases require vennilionectomy. which produces an excellent esthetic result. Patients with cheilitis glandularis are at
an increased risk of malignant transformation.

30

Cheilitis Granulomatosa (Figs. 13-4 through' 3-(6)

Cheilitis granulomatosa is a noncascaling gntnulomatou.~
condilion resulting in nonpainful symmetric enlargement of
the lips. Its etiology is unknown. and it has no sexual
predilection. The swelling, which involves the entire lip. is
large and develops slowly at"il young age. BOIh lips may be
finn and swollen. but symmetric enlargement of the lower
lip is more common. The diffuse enlargement is asymptomatic and does not affect the color of the lip. but discrete
nodules can often be palpated. Granulomatous swellings of
the tongue. buccal mucosa. gingiva, palatal mucosa. and
face have also been associated with this condition. When
unilateral facial paralysis and a fissured pebbly tongue are
exhibited. the Melkersson-Rosenthal syndrome should be
suspeCted. Steroids and surgery have been used with limited
succcess. while in selected patients elimination of an odon
togenic infection has proved curdtive. Spontaneous regres
sian is possible.

Trauma (Fig. 13-71 Trauma to the lips often resullS in

edema thai is fluctuanl. irregular. and exquisitely painful.
The trauma may originate from an external source or it
may be self-induced. EXlemallrauma may damage the soft
tissue of the lip. resulting in laceration or hemorrhage.
Tooth fmcture may accompany the condition.
Traumatic enlargement of the lip is orten a problem of
children and menially handicapped patients who inadver
tently chew their lip while under local anesthesia. The best
management for this type of lip injury is to limilthe traumat
ic influence, apply ice compresses. and treat any lacemtions
or hemorrhage as soon as possible.

Cellulitis IFig. 13-81 Cellulitis, in the strictest sense.

means "inflammation of the cellular tissue:' This degeneralive process is caused by a bacterial infection in which
localization of purulent material has yet to occur. When of
dental origin. it typically produces grossly edematous
facial tissue lhat is warm and painful to touch and i
extremely hard to palpation.
A firm. diffusely swollen lip may be the first sign of
cellulitis of odontogenic origin. A nonvitaltOQth is usually
the root of the problem. and is where the bacterial invasion
begins. Failure of host defense mechanisms to control the
infection usually results in inOammatory edema. pus for
mation. and a clinically evident swelling of the vestibule.
cheek. and/or lip. Delay in initiating treatment can result in
cervical lymphadenopathy. malaise. trismus. encroachment
of the swelling on the lower eyelid. elevated temperature.
and increased pulse. Treatment involves extirpation of
necrotic pulpal tissue. drainage. cuhurt, antibiotic sensiti ...
ity testing, and antibiotic therapy. Injection of local anesIhetic into the inflammatory region should be avoided to
minimize spread of the infection.

"EWNGS OF THE LIP

en lO\Ne( Ifp of angioedema.

Otis)

Fig. 13-2. Reddish, edematous upper lip and philtrum

indicative of angioedema.

~<la

>3:-:

ged, everted 10000er lip with discrete red

dWilitis glandularis.

).-5

'T'If'trlC enlargement of the upper lip, SdfTlf'

Melkerson-Rosenthal syndrome as

.J.- - Traumatic swelling of the upper lip.

III

Fig. 13-4. MelkersonRosenthal syndrome.

cheilitis granulomatosa, and facial paralysis

Fig. 13-6. Fissured tongue; same pcltlent with

Melkerson-Rosenthal syndrome as in Fig 13-4

Fig. 13-8. Odontogenic infection resulting In cellulitis

and a swollen upper lip {Courtesy Dr Geza Terezhalmy!

31

NODULES OF THE LIP

Mucocele fMucous Retention Phenomenon,
Mucous Retention Cyst, (Figs. 14' and T4-2)

salivary gland neoplasia consists of surgical excision. If the

excision is incomplete, recurrences are possible,

The retention of mucous secretions in subepithelial tissue

is called a mucous retention phenomenon. which has been
subdivided into two types. The first type. the mucous
retention phenomenon-retention type. or mucous retention
cyst, is lined by ductal epithelium and results from the
pooling of mucous in an obslrucled and dilated c:<cretory
duct. The second type, the mucous retention phenomenonextravasation type, or mucous extravasation cyst, lacks an
epithelial lining. [t is usually surrounded by granulomatous
tissue and resuhs from traumatic severing of a duci followed by the subsequent pooling of mucous OUlSide of the
accessory salivary gland duct in the connective tissue.
The mucous retention phenomenon constitutes the most
common nodular swelling of the lower lip and. as such. is
specifically termed the mucocele. These swellings are
asymptomatic, soft. fluctuant. bluish-gray. and usually less
than I cm in diameter. Enlargement coincident with meals
may be an occasional finding. 1lle most common location is
the lower lip midway between the midline and commissure.
but other locations include the buccal mucosa, palate, floor
of the mouth, and venlral tongue. Children and young adults
are most frequently affected. Trauma is the etiologic agent,
which predisposes the lesions to recurrence. Patients usually
have esthetic concerns and desire surgical removal of the
lesion. The lesion is negative to diascopy. but yields a semiclear fluid upon aspiration_ Treatment is excisional biopsy
and histopathologic examination. Recurrence. though rare. is
possible if the mucocele is not properly excised or if (){her
ducts are severed during surgery.

Nasolabi<11 Cyst ,Nasoalveolar Cyst) 'Figs. 1 ~5

and 14-61 The nasolabial c),st. or nasoalveolar cyst. is a
fissural cyst of soft tissue located intraorally in the cuspidlateral incisor PQrtion of the upper lip. The etiology is
uncertain, and two theories have been suggested. The most
accepted theory is that epithelial remnants become
entrapped during the embryologic fusion of the lateral
nasal, globular, and maxillary processes. A more recent theory suggests that the tissue originates from the nasolacrimal
ducl. Proliferation and cystic degeneration of the entrapped
tissue usually do not become clinically evident until after
age 30, even though the tissue has been entrapped since
biM. The condition has a slight female predilection.
The nasolabial cyst is a palpable soft tissue mass under
the upper lip that may cause elevation of the ala of the
nose, as well as dilation of the nostril and alteration of the
nasolabial fold. The cyst may be tense or fluctuant.
depending on size, Aspiration will yield a yellowish or
straw-colored fluid. It is most often unilateraJ and is gener
ally not in contact with the adjacent bone; thus the maxillary teeth remain vital. Infrequently, if the nasolabial cyst
applies pressure to the adjacent bone. local resorption of
osseous structures can result. Treatment is simple excision.

Accessory Salivary Gland Tumor (Figs. 143

and 14-4) Nodular swellings of the upper lip are infrequent and are usually caused by benign neoplasia of the
minor salivary glands, i.e., the canalicular or monomorphic
adenoma, and the pleomorphic adenoma. Benign accessory
salivary gland tumors constitute approximately 10% of all
salivary gland tumors and are characterized by encapsulation, slow growth, and long duration (several months).
Persons over the age of 30 are usually affected. Clinically
the pleomorphic adenoma is a pink to purple dome-shaped
or multinodular lesion that commonly protrudes from the
inner aspect of the lip or vestibule. It is usually semi-solid,
freely movable, painless, and especially firm on palpation.
The border is well-circumscribed, and although it has unlimited potential for growth. the tumor generally remains less
than 2 em in diameter. Auctuance and surface ulceration are
nOl usual clinical features.
Malignant salivary gland tumors are rare in the upper lip
and may be distinguished from benign neoplasia by their
rapid and aggressive growth, short duration, and tendency
to ulcerate and cause neurologic symptoms. Treatment for

32

Implantation Cyst ,Epithelial Inclusion Cyst,

{Fig. 14-7} An implantation cyst is an unusual cyst arising from a foreign-body reaction to surface epithelium that
is implanted within epidermal structures after traumatic
laceration. The cyst can occur intraoraJly or extraoraJly, al
any age. and in any race or sex. Within the mouth the
lesion appears as a firm, dome-shaped. freely movable
nodule located at the site of impetus, which is often the lip.
Implantation cysts are usually small, solitary, and asymp
tomatic. Growth appears to remain constant, and the overlying mucosa appears smooth and pink. A previous history
of trauma should lead the clinician to suspect this lesion.
Surgical excision and histopathologic examination is Tt:commended.

Mesenchymal1\lmors (Fig. 1 ~8) A variety of mesenchymal tumors can cau~ nodular swellings of the lip.
One example is the neurofibroma, Neurofibromas may be
solitary or found in conjunction with von Recklinghausen's
disease. When solitary. the neurofibroma is usually an
asymptomatic, sessile. smooth-surfaced nodule of the buccal mucosa. gingiva, palate, or lips. Histologically the
tumor consists of connective tissue and nerve fibrils. The
discovery of a solitary neurofibroma requires close examination for multiple neurofibromatosis, since the latter condition is associated with a marked tendencj toward malignant transfonnation.

:JULES OF THE LIP

1m mucocele of the mandibular

....] Pleomorphic adenoma; a firm bluish

Fig. 14-2. Large dome-shaped mucocele that

appeared fOllOWing trauma.

Fig. 144. PurpliSh canalicular adenoma of the

f'TlaXlllary labial

.... 5 ""uolo1blal cyst; a fluctuant nodule on

mucosa

Fig. 14-6. Lateral skull radIOgraph of a nasolabial cyst

injeCted WIth contrast medium (COUrtesy Dr ChriS NortJe)

nc..;ced Implantation cyst.

Fig. 14-8. SmaR neurofibroma of the IO'Ner lip

ICOUftesy Dr John fv1cDowE."lIJ

..

CONDITIONS PECULIAR TO THE LIP

Actinic Cheilitis (Solar Elastosis) {Figs. 15-1
and 15-2) Actinic cheilitis is a clinical lesion of the
lower lip due to excessive solar radiation damage. Elderly
fair-skinned men with outdoor occupations are typically
affected. [n early stages, the lower lip is mildly keratotic
with a subtle blending of the vennilion border with the
adjacent skin. With increased exposure to the sun. focal
white zones that have distinct or diffuse borders become
apparent. Slowly the lip becomes finn, scaly. slightly
swollen, and evened. Ulceration with encrustation is typical
of the chronic condition. Development of ulcerations may
be due to loss of elasticity, or they may be an early sign of
carcinomatous transfonnation. Histologic features include
atrophic thinning of the epithelium, subepithelial basophilic
degeneration of collagen, and increased elastin fibers.
Biopsy is recommended to rule out other sun-related diseases that should be distinguished from actinic cheilitis,
including epithelial dysplasia, carcinoma in situ, basal cell
carcinoma, squamous cell carcinoma, malignant melanoma,
keralOacanthoma. cheilitis glandularis, and herpes labial is.
Actinic cheilitis is considered a precancerous condition
and should be treated accordingly, Clinicians should warn the
patient of the likelihlXXl of disease progression without the
use of sunscreen protectives. Dysplastic changes should be
treated surgically or by topical application of 5-tluorouracil.
Monilial Cheilitis (Figs, 15~3 and 15-4) Monilial
cheilitis is an inflammatory condition of the lips associated
with Candida albicans and a lip-licking habit. It is believed
that the candidal organisms obtain access to the surface layers of the labial epithelium following mucosal breakdown.
which is caused by repeated wetting and drying of the labial
tissues. Desquamation of the surface epithelium results, and a
fine whitish MOale consisting of dried salivary mucous may be
seen. In children the affected peri labial skin appears red,
atrophic, and fissured. Chapped. dry. itchy, burning lips and
the inability 10 eat hot spicy flXXls are frequent complaints.
Chronic situations are characterized by painful venical fissures that ulcerate and are slow to heal. A hypersensitivity
reaction to ingredients contained within lip balms or lip sticks
may mimic the condition. In monilial cheilitis the lip-licking
habit perpetuates the condition. Although nystatin ointment
is helpfuL ultimate resolution requires habit elimination,
AngUlar Cheilitis 'Perleche) {Figs. 15-5 and 15-6}
Angular cheilitis is a painful condition consisting of radiating erythemalOus fissures at the comers of the mouth. The

.4

condition is most commonly seen after the age of 50 and is

usually encountered in females and denture wearers. The
etiology is believed 10 be associated with a mixed infection
of Candida albicans and Sraphylococcus aureal/.I.
The linear abrasions of angular cheilitis result from
repeated pooling of saliva. Initially the mucocutaneous tissue at the comers of the mouth become soft. red. and ulcerated, With time the erythematous fissures become deep and
extend several centimeters from the commissure onto the
peri labial skin, or they ulcerate and involve the labial and
buccal mucosa. The ulcers frequently develop crusts that
split and reulcerate during normal oral function. Small yellow-brown granulomatous nodules may eventually appear.
Bleeding is infrequent.
Angular cheilitis is chronic, usually bilateraL and often
associated with denture stomatitis or glossitis. Predisposing conditions include anemia. poor oral hygiene, frequent use of broad-spectrum antibiotics, decreased vertical
dimension. flaccid perioral folds. and vitamin B-group
nutritional deficiency. Treatment should include preventive
measures (such as elimination of traumatic factors, meticulous oral hygiene, and reestablishment of the correct venical dimension) combined with topical antifungal and
antibiotic therapy. Vitamin supplementation may also
prove beneficial.

Exfoliative Cheilitis fFigs. 1 5~7 and 15-81 Exfoliative cheilitis is a persistent condition affecting the lips
that is characterized by fissuring, desquamation, and the
formation of hemorrhagic crusts. Candida albicans. oral
sepsis, stress, and habitual lip biting are etiologic agents,
This condition usually begins as a single fissure near the
midline of the lower lip and spreads to produce multipk
fissures. The fissures may ultimately develop a yel1owwhite scale or ulcerate and fonn hemorrhagic crusts over
the entire lip. The condition is often bothersome and
unsightly, with the lower lip being more adversely affected
than the upper lip. When the condition is symptomatic.
burning is the usual chief complaint. Exfoliative cheilitis
has a predisposition for teenage girls and young women.
and stress has been reponed to cause acute exacerbations.
Because the condition appears to be multifactorial, exfoliative cheilitis is difficult to manage and may persist for
many years, Treatment is best rendered through the elimination of predisposing factors together with topical application of antifungal ointments.

::DiNIDITIONS PECULIAR TO THE LIP

-;"'1 Actinic cheilitis; loss of the vermiJion

-e' p. due to chronic sun exposure.

associated WIth actinic cheilitis.

;"3 Monilial cheilitis with ch<'!racterisfic

'''Xl red Inflammatory borders jCourtesy

caused by Candida Infection; monilial cheilitis

~...,

'XJj perioral folds and angular cheilitis.

Fig. 15-2. KerCllotlC foci and thickened lower rip

Fig. 15-4. DesquamaliOn and fissunng of the lips

Fig. 15-6. Erythematous areas extending from the

cor~ of mouth IndiCatIVe of angular cheilitis.

Fig. 15-8. Hemorrhagic crusts of a severe case of

exfoliative cheilitis.

35

PAlATAL SWELLINGS
Palatal Tori fTorus PalatinusJ fFigs. 16-1 and
1621 A palatal IOrus is a form of bony exoslosis thai
affects approximately 20% of Ihe adult population. It is
frequently inherited: thus multiple family members are
affected. The incidence of palalal IOri is higher in femates
Ihan it is in males.
Tori vary greally in clinical size and shape. and they
lend 10 increase slowly in all dimensions after pubeny. The
IOCalion is always in Ihe midline of Ihe hard palale adjacent
10 either the bicuspid or molar leelh. The torus palatinus is
usually a single. smooth. dome-shaped. bony-hard swelling; however, bosselated versions are occasionally seen
with a midline groove and several locular outgrowths. The
covering mucosa is pale pink. thin, and delicate: the
boundary of the lesion is delineated from the palatal vault
by a raised oval contour.
The palatal torus is frequently asymptomatic unless
traumatized, and patients may insist that they were
unaware of the torus's presence until the traumatic episode
occurs. The resultant ulcer should always be observed until
resolution; if healing does not occur chronic irritants
should be identified and eliminated. Palatal tori should be
removed if they interfere with phonetics. mastication. or
the construction of prosthetic appliances.

Incisive Canal Cyst (Nasopalatine Duct Cyst)

(Figs. 16-3 and 16-4) 1lle incisive canal cyst is a developmental cyst that fonns from entrapped squamous or respiratory epithelial remnams. It may occur at any age and
anywhere along the course of the incisive canal. but generally the cyst is confined 10 the palatal bone between the
maxillary central incisors althe height of the incisive canal.
The incisive canal cysl is usually asymptomatic and is
discovered as an incidental finding during routine examination. Symptomatic cysts are usually bacterially infected.
Infrequently the cyst arises entirely in the soft tissue of the
incisive papilla. where it appears as a small. superficial,
fluctuant swelling. A well-developed incisive canal cyst
may swell the entire anterior third of the hard palate.
The radiographic features of the incisive canaJ cyst are
characteristic. The cyst appears as a well-delinealed, mid
line. symmetrically oval or hean-shaped radiolucency
located between the roots of vital maxillary central
incisors. The cystic border is contiguous with the incisive
canal and may vary greatly in size. Root divergence and
root resorption of the central incisors are occasional findings associated with large cystic lesions. A similar cyst thai
is located more posteriorly in the palate has been referred

36

to as the median palatal cyst. Current beliefs are that 1M

incisive canal cyst and the median palmal cyst represenl
the same anomaly found in slightly differenl location.
Treatment for both is surgical enuclealion.

Periapical Abscess {Figs. '6-5 and 16-61 A periapl

cal abscess is a flucluant sofl-lissue swelling consisling
purulent malerial that results from bacterial infection of the
pulp. It appears adjacent to a diseased tooth. which is often
tender 10 percussion, mobile. and slightly "high" in occlusion. Regional lymphadenopathy, fever. malaise. and trism~
are common accompanying features. Careful examination ol
the teeth and their supporling tissues along with diagnostic
testing reveals the offending nonvital tooth. Radiographicall)
an oval periapical radiolucency is usually seen.
Any abscessed maxillary toolh may produce a swelling
of the palate. Generally the swelling is red-purple. SOfL
tender. and laleral 10 the midline if a maxillary posterior
tooth is involved. In comraSI. an abscessed maxillary
incisor may cause a midline swelling in Ihe amerior third
of the palale. Aspiration or incision produces a creamy )ellow or yellow-green purulenl discharge. Immediate
drainage. endodomic Iherapy. or extraction is indicated 10
prevenl spread of !he infection. Antibiotics. analgesics. and
amipyretics may also be needed.

Benign Lymphoid Hyperplasia (Folllcula,

Lymphoid Hyperplasia) fFigs, 16-1 and 16-8)
Benign lymphoid hyperplasia is a rare. benign. reacti\e
process thai involves proliferation of the lymphoid tissr.ae
of the palale. Persons over the age of 50 are mosl common
ly affected. The etiology is unknown. Authorities dispule
whelher the proliferation is a reaction to regional or generalized stimuli.
Clinically the exuberant lesion arises at the poslerior
extent of the hard palate and grows slowly. either uniiaterally or bilalerally. The enlargemenl may reach 3 cm ID
diameter, yet palients rarely complain of pain. The surface of the mature lesion is pink to purple. nonulcerated.
and dome-shaped or lumpy. The mass is usually soft.
on occasion may be finn 10 palpation. Surgical excision
the lreatmem of choice. followed by radiation therap)
the lesion recurs. The condition may clinically resemb
pal alai lymphoma. benign Iymphoepilhelial lesion.
Sj(jgren's syndrome. whereas histological fealures oft
mimic nodular lymphoma. Fortunately. benign Iympho
hyperplasia fails 10 disseminale like lymphoma.

...........TAL SWELLINGS

.. ' Torus palatinuJ, slightly lobulated

Fig. 16-2. LObular torus palatinus with a denture SI(Wted

around the torus

>3.

Fig. 16-4. Heart-shapecl radiolucency characterIStIC of an

incisive tanaf cyst. (Courtesy Dr Olaf l.i.mgland)

-\..C..... nt
"f"'ll'

incisive canal cyst Invoiving the

PiJlate ICourtesy Dr Geza TerE'zhalmyl

..50 "Ie!"l..plc..,' abscess arISing from the non-vital

Fig. 16-6. Radiolucency typical of a periapical abscess.

"'=

1 Benign lymphoid hyperpl,i'I$ia ariSing at the

.=;nj soft palate, ICourtesy Dr Dale Mllesl

Fig. 16-8. Inappropriate management of benign lymphoid

hyperplasia. denture accomor::l<1tes nodule.seen In Fig, 16-7,
ICourtesy Dr Dale Milesl

37

PALATAL SWEWNGS
Necrotizing Sialometaplas'. IFigs. 17-' and 17-21
Necrotizing sialomelaplasia is a benign reaclive lesion.
chieOy of accessory palatal salivary glands. that has histologic features suggestive of malignancy. The inflammatory
lesion begins after trauma as a rapidly growing nodular
swelling on the lateral aspect of the hard palate. particularly of adult males. Tissue infarction as a result of vasoconstriction and ischemia has been implicated in the pathogenesis of this condition. Rarely Ihe sofl palate or buccal
mucosa is involved. and bilateral cases have been reported.
Initially. necrotizing sialomclaplasia is a small painless
nodule that eventually enlarges and ulcerates. causing pain.
The Si7..e of the SOfllissue swelling is variable. and growth up
(0 2 em is possible. A deep cenlTal ulcer with a grayish pseudomembrane is characteristic. The surface of the depressed
ulcer is irregular and pebbly. and the border is oflen rolled.
Healing occurs spontaneously over 4 to 8 weeks. Biopsy is
recommended to rule out similar-appearing lesions such as
salivary gland tumors and malignant lymphoma. Necrotizing
sialometaplasia demonstrates squamous metaplasia of ductal
epithelium. which may be misdiagnosed for mucoepidennoid
carcinoma or adenocarcinoma of the palate.
Ben'gn Accessory Salivary Gland Neoplasm
IFigs. 17-3 and' 7-4) The pleomorphic adenoma. or
benign mixed IUmor. is the mOSI common benign neoplasm
of accessory salivary glands. II occurs in major or minor
salivary glands. and the palate is the most common location
when accessory salivary glands are affected. Occurrences
are most frequent in females between the ages of 30 and 60.
They lend to occur Ialeralto the midline and distal to the
anterior third of the hard palate.
1lle classic clinical presentation of the pleomorphic adenoma is a finn painless. nonulceraled. irregularly domeshaped swelling. Palpation may reveal isolaled softer areas
and a smooth or lobulated surface. Slow persistent enlargement over a period of years is typical. and lesions may
achieve sizes greater than 1.5 cm in diameter. Histologically
this tumor has epithelial cells in a nestlike arrangement. with
pools of myxoid. chondroid. and mucoid material. A distinct
fibrous connective tissue capsule comaining tumor cells
surrounds and usually limits the extension of the tumor.
Thorough excisional biopsy is the recommended treatment.
since recurrences are frequent following simple enucleation
or incomplete excision. Tumorous involvement of the capsule may playa role in recurrence.
The monomorphic adenoma is a benign salivary gland
tumor that can occur in the palate. 11 consiSIS of a regular
glandular pattern. usually one cell type, and lacks a mesenchymal component like that of the pleomorphic adenoma. Treaunent is surgical excision.
Malignant Accessory Saltvary Gland Neoplasm
fFlgs. 1 ]-S and t 7-61 Adenoid cystic carcinoma (cylindroma) and mucoepidermoid carcinoma are the two most

J8

common immoral malignant accessory salivary gland ne0plasms. Persons between the ages of 20 and 50 are most fre
quently affected by the mucoepidennoid tumor. whereas the
adenoid cystic carcinoma usually occurs aller the age of 50. In
addition to Slllivary glands. adenoid cystic carcinoma occurs in
respiratory, gastrointestinal. and reproductive tissues. wherea!o
111ucoepidennoid tumor may occur in the skin. respir.lt~
tract. or centrally within bone. particularly the mandible.
Malignant accessory salivary gland neoplasms occur frequently in the posterior palate. Classically they are asympIOmatic. finn. domeshaped swellings that occur lateral to
the midline. The overlying tissue appears normal in tlK
early stages. but later lhe mucosa becomes erythematou
with multiple smalltelangieactactic surface vessels. Growth
is more rapid and more painful than with benign salivary
gland tumors. Induration and eventual sponlaneous ulceration are common. indicating rapid malignant growth. A
bluish appear.l.nce and/or a mucous exudate emanating from
the ulcerated surface of the swelling are distinctive for
mucoepidennoid carcinoma.
Treatment is usually radical excision. The prognosi
varies depending upon the degree of histologic differentiation. the extent of the lesion. and the presence of metasta
sis. Adenoid cystic carcinoma rarely metastasizes bul is an
infLItrating malignancy with a propensity for distam spread
by perineural invasion: therefore lifetime followup is necessary. In comrast. the mucoepidennoid tumor infrequently
metastasizes and is more easily cured by surgical means.

Primary Lymphoma of the Palate /Figs. 1]]

and 17-81 Malignant lymphomas are solid neoplastic
growths of lymphocytes or histiocytes that are classified
imo Hodgkin's or non-Hodgkin's lymphoma and subdivided between nodal and eXlranodal disease. Primary nooHodgkin's lymphoma may develop at any site at whle
lymphoid tissue is present, including the cervical lympll
nodes, mandible. and pal ale. When the primary lewoa
affecls the palate the condition is sometimes referred to
lymphoproliferatlve disease of the palate. Rarely lym
phoma may affectlhe gingiva.
Primary lymphomas ofthe palate occur most commonl.
in patients over the age of 60. but may be seen in young
patients. especially those with AIDS. Primary Iymphom
may be solitary or associated with widespread disease
though they usually precede disseminated disease
Clinically the lesion arises at the junclion of {he hard a
soft palates. The slow-growing palatal swelling is asym
10matie. soft. spongy. and nonulcerated. and rarely affe
the underlying palatal bone. The surface is often lump
and pink to blue-purple in color. Early recognition a
biopsy is extremely important. as the disease may be c
fined entirely to the palate in the early stages. Palatally
phomas are usually irradiated. whereas disseminated di
ease necessitates the use of chemotherapy.

"",,~:rAL

SWELLINGS

Fig. '7-2. CIne \-\!E'k later: necrotblng sialoml!tapli1sia

Clppeared as. a Iilrge depress!"d ulce< (Courtesy Dr J L .Jerlsenj

~f5!I

;ng ff"'l nod.ie. pleomorphic

Dr J<>mes COl!Of'lt'!

"'",COlIS l"~UOlf'lg 'rom ~

_ _ _ _.....m oid carcinoma. (CO..Jrtesy 0-- .kxk SherfTk'r;

lymphoma of the pal.Ue. f(ou"lesy

Fig. 17-4. ~omal'C monomorphic adenoma

year-olO fema:e fCoum"sy Dr S Bre"1l Dove;

II"'

a 25-

Fig. 17-6. RilPK1,y 9rowm9 /lOdUit' 'M111 \urfilCe UICefil,'Dn

adenoid cystic carcinomit.

Fig. '7-8. Primary lymphom01l of the palate appeanng

as il DHeller-al purplish swelling

39

SWEWNGS OF THE FLOOR OF THE MOUTH

Dermoid Cyst {Figs. 18-' and 18-2) The dermoid
cyst is a soft tissue swelling derived from the cystic degeneration of epithelium entrapped during embryonic development. The cyst may occur anywhere on the skin, bot has a
propensity for the noor of the mouth. Allhaugh a small
percentage appear very early in life, these cysts are more
frequently seen in young adults under the age of 35. There
is no sex predilection.
Tbe dennoid cysl classically appears as a painless mid
line, dome-shaped mass arising in the noor of the mouth.
The overlying mucosa is a natural pink, the tongue is
slightly elevated, and palpation yields a dough-like consistency. Palients may complain of difficulties in ealing and
speaking. Growth of the cyst is slow, but diameters in
excess of 5 em may be seen. Dermoid cysts may appear
below the floor of mouth if the original site of development is inferior to the mylohyoid muscle. In this inslance a
submental swelling is nOled. Histologically the lesion is
distinguished from an epideonoid cyst by the presence of
adnexal structures in the fibrous wall such as sebaceous
glands. sweat glands. and hair follicles. Dennoid cystS typical1y are lined with stratified squamous epithelium, but
respiratory epithelium may also be present. The lumen
contains semisolid keratin and sebum. which accounts for
the doughy consistency and makes aspiration difficult.
Surgical enucleation is the preferred treatment.
Ranula (Mucocele of the Sublingual Gland)
IFigs. 18-3 and 18-41 The ranula is a large mucin-eontaining cyst in the floor of the mouth. It is identical to the
mucous retention phenomenon except that the ranula is of
greater size. The ranula forms as a result of inhibition of
normal salivary flow through a dilated or severed major
excretory duct of the sublingual gland (Ranholin's duct) or
submandibular gland (Whanon's ducc). No sex predile<:tion
is apparent, and persons under the age of 40 are most commonlyaffected.
There are two types of ranulae - the more common
superficial ranula that appears as a soft compressible
swelling rising up from the floor of the mouth. and the dissecting or plunging ranula that penetrates below the mylohyoid muscle to produce a submental swelling. The superficial
ranula characteristically is tmnslucent or has a bluish cast. It
is unilateral, dome+shaped, and fluctuant. As the asymptomatic lesion enlarges. the mucosa becomes stretched,
thinned. and tense. Digital pressure will not cause the lesion
to pit. but rupture will cause the escape of mucous fluid. The
entire floor of the mouth may be fi1Jed by the swel1ing,
which elevates the tongue and hinders movement. This
impairs mastication, deglutition, and speech.

40

A ranula can be differentiated from other floor-of-themouth swellings such as a dermoid cyst and mucoepidermoid carcinoma of the submandibular gland by sialography. Treatment is excision or marsupialization (Pansch
operation). which consists of excising the regional mucosa
and suturing the remaining cystic lining to the floor of the
mouth. Incision and drainage is not the treatment of choice.
since it will lead to reaccumulation of fluid as healing
occurs. Recurrences are common in cases involving a
plunging ranula or superficial ranula that is ill-managed.
Removal of the affected major salivary gland is the indicated treatment for recurrent and plunging ranulae.
Salivary Calculi 'Figs. 185 and 1861 Sialoliths.
also known a salivary calculi or stones. are concretions of
calcium complexes within a salivary gland or duct that
may obstruct salivary flow and cause floor-of-the-mouth
swellings. Fonnation of stones occurs most frequently after
the age of 25. twice as often in males as in females. and
usually in the submandibular gland. The ascending course
of the excretory duct. along with high mucous content and
alkaline pH of the saliva, are significant factors in stone
foonation. Calculi are usually oval and smooth or irregularly surfaced.
Obstruction of salivary flow by a calculus results in a
f1oor-of-the-mouth swelling that is firm. tender. nnd
painful. Acute symptoms often recur at meal lime.
Swelling may extend along the course of the excretory duct
and last for hours or days. depending on the blockage. TIle
overlying mucosa usually remains pink. Secondary infe<:tion results in pus emanating from the ductal opening or in
redness of the swollen floor of the mouth. Treatment
involves appropriate occlusal radiographs. sialography (if
no infection is present). and surgical removal of the
sialolith. Localized cellulitis and fever require the use of
antibiotics prior to invasive procedures.
Mueous Retention Phenomenon {Figs. 18-7
and 18-8) The mucous retention phenomenon is a soft.
fluctuant lesion involving the retention of mucous fluid itt
subepithelial tissue. usually as a result of trauma. Thesr
clear or bluish swellings may occur on the lip. floor of
the mouth. ventral tongue, or buccal mucosa. They are
usually asymptomatic and less than I cm in diameter. The
base of the mucous retention phenomenon is commonl_
sessile. although pedunculated bases are possible
Children and young adults are most frequently affected.
Treatment is excisional biopsy along with histopathologic
examination. If the condition is managed properly. recurrences are rare.

WNGS OF THE FLOOR OF THE MOUTH

5-1 Dermoid cyst pl'OO\Jdll""'9 below the

""'""'

3 --<!ItlSIuCen[ fluctuant ranula; floor of the

3-5. Siillolith produCing a firm and tender

~the-mouth sweJllng.

8-7. Small POlYPOId mucocele on sublingual

Fig. 18-2. Dermoid cyst appeanng as a soft Issue

swelhng In me floor of the mouth

Fig. 18-4. large ranula eleVating the tongue

(Courlesy Dr Charles Morns)

fig. 18-6. Radlopilque (onere-nons of slaloliths which

obstructed salivary flow.

Fig. 18-8. Mucocele In the floor of the mouth (",used

by tri'luma dunng crown preparation

41

CONDmONS PECULIAR TO THE TONGUE

Normal Tongue Anatomy (Figs. 19-1 through
19-41 The tongue is a compact muscular organ covered by
a pfO(eclive layer of stratified squamous epithelium. II fullCtions primarily in deglutition. taste. and speech. The dorsum
of the longue has numerous mucosal projections forming
papillae. There are four types: filiform. fungifonn. circumvallate. and foliate papillae. Filifonn papillae are the smallest. bUI are also the most numerous. They are slender. hairlike, cornified stalks that may appear red. pink. or white.
depending on the degree of daily irritation experienced. In
contrast to filifonn papillae. the fungiform papillae are fewer
in number, brighter red in color, and broader in diameter;
they also contain taste buds. Fungiform papillae are noncornified. round or mushroom-shaped. and slightly elevated.
They are most numerous on the lateral border and anterior
tip of the tongue. Occasionally fungifonn papillae contain
brown pigmentation, especially in melanoderms.
The largest papillae are the circumvallate papillae,
which appear as 2- to 4-mm pink papules. They are surrounded by a narrow trench and also contain taste buds.
These papillae are 8 to 12 in number and are arranged in a
Vshaped row along the sulcus tenninalis at the posterior
aspect of the dorsum of the tongue. They anatomically
divide the tongue into two unequal sections. the anterior
two thirds and the posterior third.
If one looks carefully at the lateral border of the posterior region of the tongue the foliate papilla can be identified.
These papillae are leaflike projections oriented as venical
folds. Occasionally. corrugated hypenrophic lymphoid tissue (lingual tonsil) extending into this area from the posterior dorsal TOOl of the tongue may be mistakenly called foliate papillae. The plica fimbriata are linear projections on
the ventral surface of the tongue. Sometimes the plica fimbriata have a brown pigmentation.
Fissured Tongue fPlicated Tongue. Scrotal
Tongue) {Figs. 195 and '961 Fissured tongue is a
variation of nonnal tongue anatomy that consists of a single midline fissure. double fissures, or multiple fissures of
the dorsal surface of the anterior two thirds of the tongue.
Various fissural patterns, lengths, and depths have been
observed. The cause is unknown, but fissured tongue is
probably developmental and increases with age.
Fissured tongue affects about I to 5% of the population.

42

The frequency of occurrence is equal between both sexe _

Fissured tongue occurs commonly with Down's syndrome
and in combination with geographic tongue. It is a component of the Melkerson-Rosenthal syndrome (fissured
tongue. cheilitis granulomatosa. and unilateral facial nene
paralysis). The fissures may become secondaril~
inflammed and cause halitosis as a resull of food
impaction: therefore brushing the tongue to keep the fissures clean is recommended. The condition is benign.

Ankyloglossia 'Fig. 1971 The lingual frenum is normally auached to the ventral tongue and genial tubercles of
the mandible. If the frenum fails to attach properly to tlK
tongue and genial tubercles, but instead fuses to the floor of
the mouth or lingual gingiva and the ventral tip of th~
tongue, the condition is called ankyloglossia. or "tonguetie." This congenital condition is characterized by both an
abnormally short and mal positioned lingual frenum and a
tongue that cannot be extended or retracted. The fusion rna)
be partial or complete. Panial fusion is more common. If
the condition is severe. speech may be disturbed. SurgicaJ
correction and speech therapy are necessary if speech is
defective. or if a mandibular denture or removable panial
denture is planned. Ankyloglossia occurs with an estimated
frequency of one case per 1000 binhs.
Lingual Varicosity fPhlebectasia) 'Fig. 19-8)
Lingual varicosities. or venous dilations. are a common
finding in elderly adults. The etiology of these vascular
dililalions is either a blockage of the vein by an intemal
foreign body, such as a plaque. or the loss of elasticity of
the vascular wall as a result of aging. Intraoral varicosities most commonly appear superficially on the ventra!
surface of the anterior two thirds of the tongue and ma~
extend onto the lateral border. Males and females are
affecled equally.
Varicosities appear as red-blue to purple. fluctuant
nodular growths. Individual varices may be prominent and
tortuous. or small and punctale. Palpation elicits nu pain.
but can disperse the blood from the vessel, flattening the
surface appearance. When many lingual veins are prominent the condilion is called "phlebectasia linguae" or
"caviar longue." The lip and labial commissure are other
frequent sites of phlebectasia. No treatment is required of
this condition.

_u"OITlONS PECULIAR TO THE TONGUE

..,

ge pln~ circumvallate papillae

"'I<3ped

row

(Courtesy Dr Jilmes Cottonel

...3 Ungual tonsil apparent poslenor to the

~o

~-7

Ankyloglossia.

Fig. 194. Plica limbriata which IS pigmented in thiS

IndlVlClual

.at"

....5 Fissured tongue, a mild

Fig. 19-2. Foliate papilla on the lateral bOrder of the

tongue

case

fig. '9-6. Fissured tongue and subtle manifestations

of geographic tongue

Fig. 19-8. 1V1ultlpie purple lingual varicosities; ventral

tongue /Courtesy Dr linda OtJsj

4.

CONDmONS PECULIAR TO THE TONGUE

Scalloped Tongue 'Crenated Tongue' ,Figs. 201 and 2021 A scalloped longue is a common entity
characterized by indentations on the Imeral margins of the
longue. The condition is usually bilateral, but may be uni
laleral or isolated to a region where lhe longue is held in
close contact with the leeth. Abnormal pressure of the teeth
on the longue imprints the characteristic pattern. which
appears as depressed ovals thaI are circumscribed by a
raised white scalloped border. Causes of scalloped tongue
include situations thai cause abnonnal longue pressure
such as frictional movement of the tongue against teeth and
diastemata. longue thrusting, tongue sucking. clenching. or
an enlarged longue. A crenated longue may be seen in
association with temporomandibular join! disorders, systemic conditions such as acromegaly and amyloidosis. and
genetic disorders such as Down's syndrome. as well as in
normal patients. The condition is harmless and asymptomatic. Treatment is often aimed at habit elimination,

Macroglossia (Figs. 20-3 and 2().4J Macroglossia is

the term used to indicate an abnormally enlarged tongue.
To assess tongue size. the tongue should be completely
relaxed. The normal height of the dorsum of the tongue
should be even with the occlusal plane of the mandibular
teeth: lhe lateral borders of the tongue should be in contact
with. but nOI overlapping. Ihe lingual cusps of the
mandibular teeth. A tongue that extends beyond these
dimensions is said to be enlarged_
Macroglossia is either congenital or acquired. Congenital
macroglossia can be caused by idiopathic muscular hyperlrophy. muscular hemihypenrophy. benign lumors. hamartomas, or cysts. Idiopathic muscular hypenrophy is oflen
associated with a mental deficiency. or may be a component
of a syndrome such as Beckwith-Wiedemann's syndrome.
Acquired macroglossia may be the result of passive enlargement of the tongue when mandibular teeth are lost. In this
case the enlargement may be localized or diffuse, depending
on the size of the edentulous area. Systemic disease such as
acromegaly, cretinism, and amyloidosis. or malignant neoplasms. which can occlude lymphatic drainage and produce
a swollen tongue, can cause macroglossia. Indicators of an
enlarged longue are speech difficulties. displaced leeth. mal
occlusion. or a scalloped tongue. Often Ihe affected region
of the tongue demonstrates enlarged fungiform papillae. If
lhe enlarged longue is hindering function, eliminalion of the
primary cause and/or surgical correction is recommended.
Hairy Tongue (Ungua Vlllosa. Coated Tongue)
(Figs. 20-5 and 206) Hairy longue is an abnormal
elongation of the fLIiform papillae that gives the dorsum of
the tongue a hairlike appearance. The cause of Ihe hyper-

44

trophic response of the filiform papillae is poorl~

underslOod but seems to be related to either increased keralin deposition or delayed shedding of the cornified layer_
Patienls who fail to cleanse their longues are most commonly affected. Cancer Iherapy, infection with Candida
albicafls. inadiation. poor oral hygiene, change in oral pH.
smoking. and the use of antibiotics have also been associated with this condition.
Hairy tongue may be while. yellow. brown, or blacL.;
hence the names while coaled longue and yellow. brO\l;Q.
or black hairy longue. The color of the lesion is a result of
inlrinsic faclors (chromogenic organisms) combined with
eXlrinsic factors (food and tobacco stains). Hairy tongu~
occurs more frequently in males. primarily in persons O\ef
the age of 30. and the prevalence seems to increase witb
age. The lesion bcgios near the foramen cecum on the dorsal surface of the tongue and spreads laterally and anteriorly, The affected filiform papillae discolor, progressivel~
elongate, and may reach a lenglh of several millimelef'i
Usually the lOngue remains asymplomatic, but severe ca~
may become uncomfortable because of pruritis. Generall~.
hairy tongue is only of cosmetic concern. Vigorous brushing wilh abrasive pasles and topical antifungal agenls lead!
10 resolulion. In cases Ihal are rerraclory an underlyin~
endocrinopathy such as diabeles mellilus should be sought.

Hairy Leukoplakia 'Figs. 207 and 20-81 Han}

leukoplakia is a significant leukoplakic-Iike finding th.
indicates human immune deficiency virus (HIV: HTLV-III
infection and immunosuppression. This lesion is primant;.
localed on the lateral borders of the tongue. bul may exteoO
to cover the dorsal and ventral surfaces. A viral origin I
likely since Epstein-Barr virus has been idenlified wilh
the affected epithelial cells. Hairy leukoplakia is so named
because hair-like peeling of Ihe parakeratotic surface la)ef
is evident histologically. Candida albicans is frequend.
associated with this lesion.
Hairy leukoplakia produces white vertical raised fol
on the lateral border of the tongue. Initially the lesion tu.,
alternating faint white folds and adjacent nonnal pi
troughs thai produce a characteristic vertical while-banded
washboard appearance. The bands evenlually coalesc~
form discrele while plaques or extensive thick white COmlgated parches. Large lesions are usually asyrnptomallc
have poorly demarcated borders. and do not rub off_
bilateral occurrence is common. but unilateral lesions m
possibility. Hairy leukoplakic lesions have been docurnesaed on the palate and buccal mucosa. Antiviral agenls
reduce the size of the lesion. 001 do liltle to alter Ihe Cout1&.
of HIV infection.

r::.:::~-omONS

PECULIAR TO THE TONGUE

scalloped tongue caused by abnormal

.....-e against the teeth.

3: Hemihypertrophic tongue.

Fig. 20-2. Localized scalloping due to tongue

sucking.

Fig. 20-4. Macroglossia due to a hemangioma.

(Courtesy Dr Kenneth I\bramovitChl

ns White hairy tongue.

f. -.e"WIIe white corrugations of hairy leuko;:z~t with !\IDS.

ICourtesy Or Sol SHvermanj

Fig. 20-6. Brown hairy tongue in an individual that

smokes.

Fig. 20-a. Hairy leukopli'lkla in an Individual who just

received dental treatment. ICourtesy Dr Micheal Huberj

45

CONDITIONS PECULIAR TO THE TONGUE

Geographic Tongue 'Benign Migratory Glossitis, Erythema Migra"s. Wandering Rash}
IFigs. 21) through 21-6) Geographic tongue is a
benign intlammatory condition caused by desquamation of
superficial kcmtin and the filifonn papillae. The etiology is
unknown. but emotional stress, nutritional deficiencies. and
heredity have been suggested. The condition is usually
restricted to the dorsal and laleral borders of the anterior
two thirds of the tongue. affecting only the filiform papillae
and leaving the fungifonn papillae intact.
Geographic tongue is chamClcrized by single or multiple pink to red denuded patches of desquamated filiform
papillae that mayor may nOI be bordered by a raised white
serpiginous rim. An adjacent red band of inflammation al
the leading edge of the lesion may be concurrent. When
innammution is present. pain is often a feature. The lesion
continuously changes patterns and migrates from site to
sile; hence the synonymous name "benign migratory glossilis:' "erythema migrans," and "wandering rash."
Geographic tongue is common, affecting approximately
I to 2% of the population. Females and young to middleaged adults are most frequently affected. The condition
may appear suddenly and persist for months or years.
Spontaneous remissions and recurrences have been
observed. Geographic tongue is occasionally seen in association with a mucosal counlerpan. areata erythema
migrans (migratory mucositis, geographic stomatilis.
ectopic geographic tongue), and fissured tongue. Erythema
migrans. when asymptomatic, is harmless and requires no
treatment. More often than not, erythema migrans produces
red annular patches that bum. Topical aneslhelics or lopical
Sleroids may be given to the symptomatic patient.
Histologically Ihis lesion resembles psoriasis: however, it
is generally accepted that these conditions are distinct entilies, Ihough Ihey may sometimes co-exist.

Anemia fFig. 21-7) Anemia is a condition of impaired

oxygen delivery to bodily tissues that results from a deficiency in red blood cells, hemoglobin, or total blood volume.
Underlying causes of anemia include increased destruction of
red blood cells due to hemolysis, increased blood loss due to
hemorrhage. or a decreased production of red blood cells due
to a nutritional deficiency state or bone marrow suppression.
Anemia is not a final diagnosis. but a sign of an underlying
disease; thus the cause of anemia must always be sought.
Iron deficiency is the most common type of anemia, frequemly affecting middle-aged women and young teenagers.
Deficiencies in vitamin B Il and folic acid will also cause anemia and produce oral signs of the condition.
Anemia produces characteristic changes in the appearance of the oral mucous membranes. These manifestations.
although suggestive of anemia, are not helpful in distiguishing the lype of anemia causing lhe features seen. Analysis

46

of red blood cell morphology is recommended for a mo~

accurate diagnosis.
Imraoral manifeslations of anemia are most promiocm on
the tongue. The dorsum of the lOngue initially appears pale.
with fl3ttening of the filifom' papillae. Continued alrophy of
the papillae re..<;uhs in a surface devoid of papillae thaI appean
smooth. dry. and glazed. This condition is commonly referred
to as "bald tongue." In Ihe final stage. a beefy or fiery red
tongue is seen. possibly wim concurrent oral aphthae.
Anemic patients may complain of a sore. painful lOngue
(glossodynia) or burning longue (glossopyrosis). The lips
may be thinned and taut. while the width of the mouth ma~
develop a narrowed appearance. Other clinical signs associaled with anemia include angular cheilitis. 3phthous ulceration. dysphagia. mucosal erythema and erosions. pallor.
shonness of breath. fatigue. dizziness. and a bounding
pulse. Palienls with a vilamin B'l deficiency may complam
of weight loss, weakness. neurological diSlurbances such :b
numbness and lingling of Ihe extremilies. and difficully in
walking. Therapy should be directed loward correcling t~
underlying cause. Improvement after therapy is reneCled in
changes in the oral appearance.
Xerostomia IFlg_ 21--81 Saliva functions to keep the oral
cavily moisl and aids in mastication, deglutition. digestion.
speech. and immunologic neutralization. When impaired sa.1Jvary function causes a dry mourn Ihe condition, is called
xerostomia. Manifestations of decreased salivary flow can be
subtle with no patient complaints, or severe with a myriad of
complaints. Xerostomi3 may result from advancing age. anemia. avitaminosis. dehydration, diabetes. emotional stress.
mechanical blockage. surgery, collagen vascular disease. et"todermal dysplasia. mumps, Mikulicz's disease, multiple sclerosis. Sjogren's syndrome. acquired immunodeficiency syndrome. and head and neck irradiation. Many therapeulK
drugs. principally antidepressants, antihistamines. antihypertensive and cardi3C agents, decongestants, ganglionic bloc ing agents, and tmnquilizers will also produce xerostomia.
Mild cases of xerostomia are relatively free of symptoms, and the mucosa appears normal. In moderate case\
the tongue is dry. pale. red. and atrophic, with its dorsal surface wrinkled or smooth. In severe situations the tongue
may be devoid of papillae. fissured. and inflamed. The
mucosa appears dry. shiny. and sticky, while the lips awecracked and fissured. Stagnant. rope-like accumulations of
saliva on the tongue along with burning longue (glossop)rosis) and alterations in taste are usually presenL
Progression of xerostomia can result in halitosis. multiple
carious lesions evident at the gingival tooth margin. and difficulty with speech. maSlicalion. and retention
prosthodontic appliances_ Chronic xerostomia requires lODE
term multiphasic support. including such items as emollients, artificial saliva. pilocarpine. fluoride treatment. ora
hygiene instruclions. and nutritional counseling.

:::0

OIT/ONS PECULIAR TO THE TONGUE

.'

'1He<! ClenudallonS of filitorm papillae

geographic tongue.

O::Ofl"lo3tIC geographic tongue

n:'larnmatOl)' borders

1. -5 Erythema migrans of the L3bIal mucosa

___

:h bald. burning tongue, iron

"'Yanemia.

Fig. 21-2. ExtenSIVe CoClse of geographic tongue with

while orOndte borders jCourtesy Dr BJII &!O<Cfj

Fig. 21-4. SymptomaliC geographic tongue W1[h a

promncnt red-wtule ln~mma[oty bof(ler

Fig. 21-6. Annular pc1t1ern of syrnptornaoc erythema

mlgrans of the hard and soft palate

Fig. 21-8. Xerostomla-iIlduced dry. fi.ssured atrophK

tongue (COurtesy Dr Pete Bemon/

47

CONDITIONS PECUUAR TO THE TONGUE

Median Rhomboid Glossitis lCentral Papillary
Atrophy 01 the TongueJ {Figs. 221 through 22-

41 Median rhomboid glossitis was once thought to be a

developmental defect of incomplete desccm of the tuberculum impar. Recently this theory has fallen into disfavor: it is
now believed Ihat median rhomboid glossitis is a permanenl
end result of a Candida a/bicans infection in conjunction
with other factors (possibly smoking or a change in oral
pH). Median rhomboid glossitis frequently affects middleaged adult males and rarely affects children. Blacks and
whites are affected equally. Diabetics, immune-suppressed
patients. and patients who recemly completed a course of
broad spectrum antibiotics have a higher prevalence of this
condition.
Median rhomboid glossitis is a smooth. denuded. beefy
red patch devoid of filifonn papillae. With time lIle lesion
becomes granular. lobular. and induraled. The most common location is Ihe midline of Ihe dorsum of the lOngue.
jusl anlerior 10 the circulTl\'allale papillae. The size and
shape of Ihe lesion varies. bUI il frequently appears as a
well-demarcated I 10 2.5 cm oval or rhomboid with irregular bUI rounded borders. The condition is generally asymptomalic. Occasionally an erythematous palatal candida I
lesion is observed directly over the lesion of the tongue.
Median rhomboid glossitis is easily recognized by its
clinical appearance. characterislic location, and asymptomatic nature. Early recognition and treatmenl wilh anlimonilial agents may lead to resolution. End-slage median
rhomboid glossitis is usually asymptomalic but refractory 10
antifungal treatment. The rare possibility of anaplastk
transfonnation exists.
Granular Cell Tumor (Granular Cell Myoblastoma) fFigs. 22-5 and 22-6) The granular cell
lumor is a rare benign soft-tissue tumor composed of oval
cells lhat have an extremely granular cytoplasm. This tumor
may occur in a variety of cutaneous. mucosal. and visceral
sites, but its favorite oral site of occurrence is the dorsal-lateral surface of the tongue. Theories of histogenesis have
been controversial. Most investigalors believe Ihat the
tumor is actually a benign proliferalion of neurogenic cells.
The granular cell tumor can occur al any age and in any
race. but it has a slight predilection for females. Usually
the lesion consists of a symptomless. solitary. dome-shaped
submucosal nodule covered clinically by nonnal. yellow.
or white tissue. The surface may be ulcerated when it has
been traumatized. The granular celliumor is often sessile.
well-circumscribed. and finn to compression. Growlh is
very slow and painless. with some tumors achieving sever-

48

al cenlimeters in size. Larger lesions may demonstrate I

slightly depressed central area. Rarely these lesions art
found on lIle ventral surface of the tongue. Approximatel~
10% of affected patients experience multiple lesions.
The granular cell tumor is characterized by pseudoepitheliomatous hyperplasia and granular cells thai may histologically resemble epidennoid carcinoma and the con
genital epulis of the newborn. respectively. Conservati\e
local excision is the preferred treatment. and these lesions
do not tend 10 recur.

Lingual ThyrOid {Fig. 22-7J Lingual thyroid is an

uncommon nodule of thyroid lissue found jusl poslerior 10
the foramen cecum on Ihe posterior Ihird of Ihe tongue. 11
occurs when embryonic tissue from the thyroid gland fail
to migrate to the anterolateral surface of Ihe trachea.
Persistent thyroid tissue occurs much more frequently in
women Ihan in men (the ratio is 4: I) and may appear at
any age. If lIle remnant tissue becomes cystic the conditioo
becomes a Ihyroglossal duct cyst.
The lingual thyroid is a raised asymptomatic mass thaI usually measures about 2 em in diameter. Increased surface vascularity is a prominent feature. Hemorrhage. dysphagia. dysp~
nia, symptoms of hypothyroidism. and (rarely) pain can be
associated with the condition. The lesion may be differentiated
from similar lesions by confinning its distinctive location p0sterior to Ihe circumvallate papillae and by ulilizing radionuelide studies. Biopsy should be deferred until it is ascertLnc:d
that the remainder of the thyroid gland is present and function.
ing. In over 50% of patients with ectopic thyroid !he lingual
thyroid is the only active thyroid tissue present.
Cyst of Blandl~uhn (Ungual Mucous Retention Cyst) (Fig. 22-81 The glands of Blandin-Nuhn art
the accessory salivary glands on the venlral surface of Iht
tongue composed of mixed serous and mucous elements.
When trauma of the ventral tongue induces eXlravasatioo
of saliva into the surrounding tissues, a relatively smaU
painless swelling develops. which is termed the cysl
Blandin-Nuhn. This infrequent accessory salivary gland
cyst is located near the lip of Ihe ventral surface of t~
tongue. The borders are raised and well-demarcated, lhe
mucosal surface appears pink-red. and Ihe lesion is so
and fluctuant. When superficial. Ihe cyst has balloon-I"
features and a pedunculated base. Deeper lesions have seY
sile bases. Although usually lfaumatically induced. Ihe C)
of Blandin-Nuhn may be congenital. These cysts rarel.
exceed I cm in diameter. Trealment is excisional bioJ>$)
and recurrence is rare.

OITIONS PECULIAR TO THE TONGUE

~.

21-1. o-typertrophic median rhomboid

PUs.

Fig. 22-2. Smooth denuded patch with irregular borders;

median rhomboid glossitis. (Courtesy Dr lInda OtIS/

n-3. Cenual area of tongue dE'VOld of filiform

Fig. 224. Red palatal lesion of atrophic: candidiasis

dlrea:ly ~ medliV1 rhombclId g\o5sIs seen Ifl Fig 22-3

22-5 Granular cell tumor appearing as a pink

Fig. 22-6. Granular cell tumor; lateral VI~ of same

patient as In Fig 22-5. (Courtesy Dr Jerry Cioffi)

<'(,emIl( of median rhomboid gloni'is.

.JO.J1e (COUrtesy Dr Jerry Cioffi)

22-7

'Kular lingual thyroid; post('flor to the

.., - s ICOUrtesy Dr Tom AufdemotteJ

Fig. 22-8. Cyst of Blandin-Nuhn. (Courtesy Dr

James Cottone)

.9

SECTION

IV
Intraoral
Findings by
Color
Changes

51

WHITE LESIONS
Fordyce's Granules fFigs. 23-1 and 23-2) Fordyce's granules are ectopic sebaceous glands found within
the mouth thai are considered a variation of normal oral
mucosal anatomy. These granules consist of individual
sebaceous glands that arc 1 to 2 mm in diameter.
Characteristically they appellr on the buccal mucosa as
white. creamy white. or yellow slightly raised papules.
They usually occur in multiples. fonning clusters, plaques.
or patches. Clusters Ihal are enlarged may feel rough to
palpation. Occasionally they are an isolated finding. Less
common locations include the lip. labial mucosa. retromolar pad. allached gingiva. longue. and frenum.
Fordyce's granules arise from sebaceous glands embryologically entrapped during fusion of the maxillary and
mandibular processes. They become more apparent after
sexual maturity as the sebaceous system develops. Rarely an
intraoral hair may be seen in association with the condition.
Fordyce'S granules occur in approximately 80% of
adults. and no predilection in race or sex has been reponed.
Histologically. rounded neSlS of clear cells. 10 to 30 per
nes!. with darkly slaining. small. centrally located nuclei
are found encapsulaled in the lamina propria and submucosa. The clinical appearance is adequate for diagnosis of
Fordyce's granules: biopsy is not usually required.

Linea Alba Buccalis IFigs. 23-3 and 23-4) The

linea alba buccalis is a common intraoral finding that
appears as a raised while wavy line of variable length
located at the level of the occlusion on the buccal mucosa.
Generally this asymplOmalic cornified emily is I to 2 mm
in width and extends from the second molar 10 the canine
region of Ihe buccal mucosa. The lesion is usually found
bilaterally and cannot be rubbed off. The thickened epithelial changes consisl of hyperkeratotic lissue that is a
response to frictional aClivilY of the teelh. The condition is
often associated with crenated tongue and may be a sign of
bruxism. clenching. or negative oral pressure. The clinical
appearance is diagnostic and requires no treatment.

Leukoedema (Figs. 23-5 and 23-61 Leukoedema is

a common mucosal variant associated with dark-pigmemed
individuals. but may be seen infrequently in Iighler-pig-

52

mented persons. The incidence of leukoedema tends

increase with age. and 50% of black children and 92ttadult blacks are affected. Leukoedema usually appe
bilalerally on the buccal mucosa as an opalescenl. white.
gray thin surface film. The labial mucosa and soft palauare less common locations of occurrence.
Leukoedema is often faint and may be difficult to sec
Prominence of the lesion is related to the degree of under
lying melanin pigmenlalion. level of oral hygiene.
amounl of smoking. Close examination of leukoede
reveals fine white lines. wrinkles. or overlapping folds
lissue. The borders of the lesion are irregular and diffll5t::
Ihey fade into adjacent lissue making it difficult to determine where Ihe lesion begins and ends. Diagnosis
oblained by strelching the mucosa, causing the whitt
appearance 10 significantly diminish or disappear in some
cases. Wiping the lesion fails to remove it. The edolog)
leukoedema is unknown. No serious complications art
associated with this lesion, nor is treatment required.

Morsicatlo Buccarum ,Mucosal Chewing' {Figs..

23-7 and 23-8) Morsicalio buccarum. or cheek biting.
a common habit Ihat produces a progression of mucosa.
changes. Initially, slightly raised white plaques and fo1
appear in a diffuse pattern covering areas of Irauma.
Increased injury produces a hyperplastic response tha'
increases the size of the plaque. A linear or strialed patte...
is sometimes observed. with thick and thin areas seen sideby-side. Persislent injury leads to interadjacenl Iraumata.
erythema and ulceralion.
Mucosal chewing is usually seen on the buccal mucosa.
less frequently on the labial mucosa. The lesions rna) be
unilaleral or bilateral and can occur al any age. No sell:
race predileclion has been reponed. Diagnosis requires vi
al or verbal confirmation of the nervous habit. AlIhou_
morsicatio buccarum has no malignant polential. patienb
should be advised of the mucosal altemtions. Because of Ibc
similar clinical appearance. speckled leukoplakia and caDdidiasis should be ruled OUI. Microscopically Ihere is a nor
mal maturing epithelial surface wilh a corrugated parakentOlic surface and minor subepilhelial inflammation.

LESIONS

:J.

.~: ~e

--.iC0Scl

Z.J..3

creamy .......nlte fordyce granules

(Courtesy Dr lmda OtiS)

"':e wiNy linea alb.1l buccalis.

Fig. 23-2. Clusters of fordyce granules WIth a rare

Intraoral half (COUrtesy Dr Bill Baker)

Fig. 23-4. Keratotic linea alba buccalis WIth mild

leukoedema ICOUrtesy Dr Dale Mllesl

:.J.-S u!oIkoedema of the buccal mucosa in a

Fig. 23-6. P<'ltch-like distribullon of leukoedema;

:..J..

Fig- 23-8. Morsicatio buccarum of the labial

mucosa lCourtesy Dr Kenneth AbramoVitchl

:~ff'

o,!,ng prodUCing white plaques

:;' morsicatio buccarum.

bUccal mucosa

53

WHITE LESIONS
White Sponge Nevus ,Familial White Folded
Dysplasia) 'Figs. 24-1 and 24-2) White sponge nevus
is a relatively uncommon entity that usually appears al birth
or in early childhood bUI pe~ists throughout life. It is characterized by mucosal lesions that are asymptomatic, white.
folded. and spon!!y. Often the lesions exhibit a symmetric
wavy panem. The most common location is the buccal
mucosa. bilaterally. followed by the labial mucosa. alveolar
ridge, and noor of the mouth. This condilion may involve
the entire oral mucosa. or may be distributed unilaterally as
discrete while patches. The gingival margin and dorsal
longue are almost never affected. allhough the soft palate
and vcolml tongue are commonly involved. The size of the
lesions v:lrics from patient to patient and from time to time.
White sponge nevus exhibil.~ no race, sex or gender
predilection; however, because of this condition's autosomal dominant pattern of transmission. multiple family
members may manifest the disorder. Extraoral mucosal
sites may involve the nasal cavity, esophagus. larynx. vagina. and rectum. Concurrent skin lesions exclude the diagnosis. Causation has been attributed to a basic defeci in
epithelial maturation and exfoliation. No treatment is
required, and the lesions are hannless.
Traumatic White Lesions fAcute Trauma,
Chemical Burns and Peripheral Scar) fFigs. 24-3
through 24-61 Traumatic white lesions can be caused by
a variety of physical and chemical irritants such as friction
al trauma, heat, prolonged aspirin comact, and excessive
use of mouthwash or other caustic liquids. In particular.
frictional trauma is onen noted on the allached gingiva. It
is caused by excessive tooth brushing. movement of oral
prostheses. and chewing on the edentulous ridge. With
time the mucosa becomes thickened with a roughened
white surface. Pain is characteristically absent, and histologic examination reveals hyperonhokeratosis.
Severe trauma can produce a white lesion owing to the
loss of the superficial layers of mucosal epithelium.
Undemeath the white slough there is a raw. red, or bleeding
surface. Typically aCUie traumatic lesions appear as punctate white patches with diffuse and irregular borders.
Moveable mucosa is more susceptible to trauma than
allached mucosa. P-din of severdl days duration is common.
Trauma involving the subjacem dermal layers may
induce a fibrous healing response or scar. Scars are often
asymptomatic. linear. pale pink. and sharply delineated. A
thorough history may reveal previous injury, recurrent
ulcerative disease. seizure disorder. self-multilating behavior. or previous surgery.

54

Leukoplakia IFigs. 247 and 2481 Leukoplakia

a clinical tenn descriptive for a white plaque or patch
the oral mucosa that cannot be scraped off and cannot
classified as any other clinically diagnosable dise
Individuals of any age may be affected; however.
majority of cases occur in men between the ages of 45
65. Recent incidence figures indicate that the male
female ratio is decreasing, with women being an
almost as frequently as men.
Leukoplal.:ias are protective reactions against chronic UL
tants. Tobacco. alcohol, syphilis, vitamin deficiency, hol'Tlx.al imbalance, galvanism. chronic friction, and candidl
have been implicated in the cause of these lesi
Leukoplakia<; vary oonsidembly in size, location, and c1i
appearance. The preferential sites for leukoplakia are the
eral and ventral tongue, floor of mouth, alveolar mucosa.
soft paJateretromolar trigone. and mandibular attached
giva. The lesional surface may appear smooth and ho~
neous. thin and friable. fissured. corrugated. venucoid.
lar, or speckled. The color can take on subtle variations
faintly translucent white lesions to gray or brown-while.
A classification system offered by the World H
Organization (WHO) recommends tWO divisions for
leukoplakias: homogeneous and nonhomogeneous. K
homogeneous leukoplakias have been further subdh
into erythroleukoplakia. nroular. speckled. and verru~
The majority of leukoplakias (80%) are benign:'
remaining cases are dysplastic or cancerous. The cli
dilemma is in determining which leukoplakias are p
lignam or malignant. especially since 4 to 6% of all I
plakias progress to squamous cell carcinoma witma
years. High risk sites for malignancy include the flOO
the mouth, lateral and ventral tongue. uvulo-palatal
plex, and lips.
Leukoplakias with localized red areas also confer a
risk of carcinoma. For example, nonhomogeneous I
plakias. particularly oral speckled leukoplakias, rep
epithelial dysplasia in about half of the cases and ha\e
highest rate of malignant transformation among im
leukoplakias. Candida albicQ/ls. a fungal organism
associated with oral speckled leukoplakias. may lu\c
role in the dysplastic changes seen.
The initial step in the treatment of leukoplakia
eliminate any irritating and causative factors. then ob",~
for healing. The lesion mayor may not disappear. \Vhea
unexplained oral leukoplakia is persistent. biops}
mandatory. Multiple biopsy sites may be necessary for
fuse lesions. onhomogeneous areas of the lesion
always be selected for biopsy.

~rn=

LESIONS

1-4- T White sponge nevus affecting the buccal

Fig. 24-2. ThICk whIte plaques of white sponge

- pala:e, and retromolar pad

nevus in S<1me patten! sho\Nn In FIg 24-1 GlnglV(ll

margIn remalflS unaffooed

El;. ]-4.3. Frictional ker..tosis associ<lled with

Fig. 24-4. White pebbly frictional keratosis from

traumatic occlusion.

-h brushing

lLS Traumatic white lesion; white chemICal

;pnn placement ar it biopsy site

2'*-7 Leukoplakia; soft palate Biopsy revealed

eratoSI$

Fig. 24--6. Traumatic laceriltJOn at age 2 resulted In this

palatal sur.

Fig. 24-8. Leukoplakia of {he floor of the mouth and

ventral tongue. biopsy revealed mild eplthellill dysplasia

55

TOBACCO ASSOCIATED WHITE LESIONS

Cigarette Keratosis lFigs. 25-1

and 25-2)

Cigareue keratosis is a specific reaction evident in individuals who smoke noo-fillered or marijuana cigarenes to a very

short length. The lesions. which appro"imatc each other

upon lip closure. invoh'c both the upper and lower lip al the
location of cigareuc placemenl. These kcr.lIotic patches are
about 7 mm in diameter and in\lariably arc located lateral 10
the midline. Raised ",hile papules are evident throoghoullhe
pmch. producing a roughened texture and finnness to palpation. Occasionally cigarette ker.l1oses may extend onlo the
labial mucosa. but rarely is the vennilion border involved.
Elderly males are most commonly affected. Discontinuation
of the smoking habit usually brings about resolution. The
developmclll of ulcer and crust formation should raise the
suspicion of neoplastic transfonnation.

Nicotine Stomatitis 'Pipe Smoker's Palate)

{Figs. 25-] and 25-41 Nicotine stomatitis is a response
of palatal eClodennal structures to prolonged pipe and cigar
smoking. Usually found in middle-aged and elderly males.
posterior to the palatal rugae. this lesion shows progressive
changes with time. Initially the irritation causes the palate
to become diffusely erythematous, Eventually the palate
becomes grayish-white secondary to hyperkeratosis.
Multiple discrete keratotic papules with depressed red centers develop that correspond to dilated and inflamed minor
salivary gland excretory duct openings, 1be papules enlarge
as the irritation persists but fail to coalesce. producing a
characteristic cobblestone (parboiled) appearance of the
palale. Isolated but prominent red-centered papules are
common. Whether the lesion arises as a consequence of
heat or of tobacco is a mailer of debate. Reverse cigarette
smoking produces similar findings. Discontinuation of
smoking should result in regression.

Snuff Dippers Patch (Tobacco Chewer's

Lesion. Snuff Keratosis) IFigs. 25-5 and 25-61 A
wrinkled yellow-white area on the gingival mucosal flexure and mandibular buccal or labial mucosa is indicative of
intraoral use of unburned tobacco, Smokeless tobacco may

56

take various fonns (snuff. dip, plug. or quid), leaving

characteristic mark al the preferential site of tobacco pi
ment. Posterior sites are commonly utilized for dip. pi
or quid. whereas anterior sites are preferential for sn
Individuals who vary intraoral sites have multiple. I
prominent lesions. Male teenagers are most freque
affected. largely because of intensive marketing effOfu
tobacco companies.
Early snuff dipper's patches are pale pink in color. \1i
the surface appearing corrugated and wrinkled, A progm
sion to white, yellow-white. and yellow-brown may e
as hyperkeratosis and exogenous staining occur.
Chronic smokeless tobacco use is associated with
odontal alterations. caries, epidermal dysplastic chan
and verrucous carcinoma. To achieve resolution. cessa
of use is recommended. If normal appearance does
return 14 days after cessation. biopsy is necessary.

Verrucous Carcinoma (of Ackerman) lOr

Florid Papillomatosis' (Figs. 25-7 and 25-8J
wany, exophytic, cauliflower-like whitish mass is a v
malignant squamous cell tumor that is considered I
grade and nonmetastasizing. The buccal mucosa
mandibular gingiva are the most common locations. ~
over 60 years of age who use smokeless tobacco are
often affected, The disease is rare in persons under
years of age.
Verrucous carcinoma has a distinctive surface ap
ance. Characteristically there is a white keratotic surf
with pink-red pebbly papules throughout. Lateral g
leads to an increase in mass. and the tumor can ac
several centimeters or more in diameter. Large lesiOTb
be locally destructive by invading and eroding the uJXkrl
ing alveolar bone. Similar-appearing lesions include \
cous epithelial hyperplasia, pyostomatitis vegetans.
proliferating verrucous leukoplakia.
Recommended treatment is wide surgical exci
Radiation therapy is contraindicated. since there is a n
anaplastic transfonnalion to squamous cell carcinoma.

':C-J!:OACCO ASSOCIATED WHITE LESIONS

"r-ok:! male WIth Cigarette Smoking

ogarette keratosis.

"'cotine stomatitis prorT'Ilnent on <he soft

Fig. 25-2. Cigarette keratosis on lab""! mucosa of

patJenr In FIg 25-1

Fig. 25-4. Cobblestone appearance of nicotine

;: onto the buccal mucosa

stomatitis In a rt':"VefSe smolo:.er

placement of chewing lobaeeo,

snuff djpper~ patch.

Fig. 256. Wrinkled appearance of a snuff dippers

patch.

.,;.c: ng verrucous carcinoma of the

Fig. 25-8. ExtensJVf' pink nodular verrucous carcinoma;

alveolar ridge and palate, (COUrtesy Dr James Cottone)

-:~

many years of tobacco chevving

-~cer

Reddlngl

57

RED LESIONS
Purpura (Petechiae. Ecchymoses. Hematoma)
(Figs. 26-1 through 26-41 Purpum is a condition characterized by the pooling of extravasated blood. The stimulating factor can be i:urogcnic. (:letitia!. or accidenlallraurna to vascular tissues contained within Ihc dermis or submucosa. In circumstances where trauma b not involved,
deficits in the platelets either quantitative or qualitative.
dotting factors. or capillary fragility ~hould be suspected.
Initially purpura tlppcar bright red. but lend (0 discolor
with lime. becoming purplish-blue and laler brown-yellow.
Bec,lUse these lesions consist of extr::lVascular blood. they
do not blanch 011 pressure.
The three types of purpura - petechiae. ecchymoses.
and hemalOma are clas~ificd according to size and etiology.
Petechiae are pinpoint nonraised circular red spots. The
sofl palate is the most common intraorallocalion for multifocal petechiae. Palalal petechiae may represent an early
sign of infectious mononucleosis. scarlet fever. leukemia.
bleeding diatheses. or blood dyscrasia. They may also indicate rupture of palatal capillaries due 10 coughing. sneezing. vomiting, or fellatio. Suction petechiae under a maxillary denture are not true purpura. They evolve as a result of
candidal infection and the resulting inflammation of the
orifices of accessory salivary glands. not because of denture-created negative pressure as previously believed.
An area of extravasated blood usually greater than lem
in diameter is called an ecchymosis (common bruise).
Careful physical evalualion may reveal the cause 10 be
mechanical tr:mma. hemostatic disorders, Cushing's dis
case. neoplastic disease. primary idiopalhic or secondary
thrombocylopenic purpura. or use of anticoagulant drugs
such as bishydroxycoumarin. warfarin. or heparin.
Hematomas are large pools of eXlravasated blood re,.<>ulting from traumatic vascular severance. They occur most
commonly in the oml cavity as a result of a blow to the face,
tooth eruption. or rupture of the posterior superior alveolar
vein during local anesthetic administration. They are usually
dark redbrown or blue in color and tender to palpation.
Purpura fade with time and require no specific treatment.
Detemlining the underlying cause is the prime consideration.

Varicosity (Varix} IFig. 26-51 A varix is a red purple

flucluant swelling frequently seen in the elderly populalion. The swelling represents a venous dilation caused by
reduced elasticity of the vascular wall as a resuh of aging.
or by an internal blockage of the vein. The ventral surface
of the anterior 1'>'0 thirds of Ihe longue is a frequent location. The lip and labial commissure are other common
sites. Labial varices appear dark red 10 blue~purple. They
are most commonly single. round, dome-shaped. and fluctuant. Palpation of the lesion will disperse the blood frOnl

58

the vessel. flattening the surface appearance; therefo~

lesions are dia.'iCopypositive.
Varices are benign and asymplomatic. and requiR
trealmen!. If they are of cosmetic concern 10 the pat
varices can be surgically removed without signifi
bleeding. Occasionally they are slightly finn becau~
fibrotic changes. Thrombosis is a rare complication. \\
multiple veins on the ventral tongue are prominent the
dition is called phlebectasia linguae, or "caviar tongue_~
Thrombus (Fig. 26-6) The series of events that inel
trauma, activation of the clotting sequence. and fonnatl
of a blood clot typically results in the cessation of blee<l"'~
Several days later clot breakdown occurs and nonnal
flow resumes. In cenain cases. if the clot docs not di
blood flow stagnates and a thrombus is fonned.
Thrombi appear as raised red round nodules. typicaU.
the labial mucosa. They are finn 10 palpation and m3~
slightly tcnder. No sexual predilection is evident. but ""...~
bi are most commonly seen in patients over 30. Va
plugs can concentrically enlarge to occlude the entire I
of the vessel or mature and calcify to form a phlebol
Phleboliths 3re rare oral findings that occur in the c
lips, or tongue. Radiographically they appear as doug
like, circular. radiopaque foci with a radiolucent center.
Hemangioma {Figs. 26-7 and 26-81 Hemangi
are benign, enlarged. vascular hamartomas that ma~
seen in any soft-tissue intraoral location. They occur
in life and somewhat more commonly in females tlla
males. The dorsum of the tongue. gingiva. and bu..-:
mucosa are common localions. Histologically they IT).J.
capillary or cavernous.
Hemangiomas. when situated deep within the co
tive tissue. do not alter the color of the mucosal surf
Superficial hemangiomas. in contrast. are red, blue. or
pIe in color, flat or slightly elevated, smooth-surfaced.
somewhat finn. Hemangiomas are positive to diascop)
may vary in size from a few millimeters to several
timeters. The borders are usually diffuse, and lobular
faces are infrequent. Single hemangiomas are most
mon, whereas multiple tumors are seen in Maffucci's
drome. Facial and oral hemangiomas fonn a com~
Slurge~Weber syndrome.
Large soft tissue hemangiomas present manag,,,,"'4
problems. Surgical excision. sclerosing agents.
therapy. and radiation therapy have been used to eli ......
these lesions. A hemangioendothelioma is the mali
counterpan to the hemangioma, whereas Kaposi's sa<a-."j
is another malignant vascular tumor seen if}' about 3O'l
AIDS patients.
)

LESIONS

. '-..II pie red petechiae on the soft palate

Fig. 26-2. Ecchymosis following lip trauma In

it

heparinized pi;Jtient

::>3 l'urphsh-blue hematoma resulting from a

... face

Fig. 26-4. Red intriloral hematoma of patient In Fig.

26-3

2>5 Purple lip varix. ICourtesy Or Unda Otisl

Fig. 26-6. Blue organrLIng thrombus; labldl mucosa.

jCourtesy Dr Ed Heslop)

:"'>1 Dome-shaped hemangioma of the ventl",1

:ClJftesy Or Tom Razmusj

Fig. 26-8. Multinodular hemangioma of the buccal

mucosa.

59

RED LESIONS
Hereditary Hemorrhagic Telangiectasia fRenduOsler-Weber) (Figs. 27-1 through 27-4) Hereditary
hemorrhagic telangiectasia is a genetic disease that is inherited as an autosomal dominant trait. The disease is chardcterired by multiple telangiectasias, which are purplish red
macules or slightly red papules represeming pennanently
enlarged end-eapillaries of Ihe skin. mucosa. and other tissues. The lesions are usually I to 3 mm in size. lack central
pulsation. and blanch upon dia.<>eop)'. After pubcny the size
and number of lesions tend 10 increase with age. Males and
females are affected equally. Bleeding is a prominent feature of Ihis disease.
The lesions of hereditary hemorrhagic telangiectasia are
located immediately subjacent to the mucosa and are easily
traumatized. resulting in rupture, hemorrhage. and ulcer
fonnation. Skin lesions are less subject to rupture because
of the overlying cornified epithelium. The mosl common
locations on the skin are the palms. fingers, nail beds. face.
and neck. Mucosal lesions can be found on the lips.
tongue. nasal septum. and conjunclivae. The gingiva and
the hard palale are less commonly involved. Complications
include epistaxis. gastroinleslinal bleeding, melena. hematuria. cirrhosis. and pulmonary arleriovenous fislUlae.
PrecaUlions are recommended wilh Ihe use of inhalalion
analgesia. general anesthesia. oral surgical procedures, and
hepatotoxic and anti-hemostatic drugs. Rupture of a lelangieclasia may cause hemmorhage Ihat is best controlled by
pressure packs. History. clinical appearance. and hislologic
features are importanl in making the diagnosis.
Sturg~Weber Syndrome

,Encephalotrigeminal

Angiomatosis) fFigs. 27-5 through 27-8) SturgeWeber syndrome is a rare congenital disorder Ihat mani,

60

1 \\1\

fests venous angiomas of the leptomeninges of Ihe b

ipsilateral macular hemangiomas of Ihe face, neurom
lar deficits. and oculo-oral lesions. The macular he
gioma of Ihe facial skin. also tenned "pon-wine slain"nevus nammeus:' is the most slriking feature of !he s.
drome. The facial hemangioma is well-demarcated. fla
slightly raised. and red to purple in color. It blanches
pressure. It is present at binh. dislributed along a brandl
the lrigeminal nerve. and Iypically eXlends to the pala
midline without crossing 10 Ihe Olher side. The ophth
division of the trigeminal nerve is most frequently aE
No tenderness or innammation is associated \>. ith
hemangioma. and it does not enlarge with age.
The altered venous blood now caused by an angioma
the leptomeninges can resull in cerebral conical dege
lion. seizures, mental retardation. and hemiplegia. On I
al skull radiographs gyri form calcifications characlc
cally appear as double-contoured "tram-lines." Appro
imately 30% of patients have ocular abnonnaJities inc
ing angiomas. colobomas. or glaucoma.
Vascular hyperplasia involving the buccal mucosa
lips is the most frequenl oral finding. The palale. gin
and noor of the mouth may also be affCCled. Dislribu
of Ihe bright red oral palches is to areas supplied b~
branches of the trigeminal nerve. Like facial lesions.
palches stop abruptly al the midline. Involvement of
gingiva may produce edematous tissue and cause diffi
with hemostasis when surgical procedures involving
tissues are performed. Abnormal tooth eru
macrocheilia. macrodontia. and macroglossia are seq
of large vascular overgrowths. In areas of vascular hyper
plasia oral surgery should be perfonned in accordance
stricl hemostatic measures.

LESIONS

. oe lip tel<lngiectasias; hereditary

gic telangiectasia.

Fig. 27-2. Gingival telangiect.'lsias, .>arne patient as In Fig

27-1 With hereditary hemorrhagic telangiectasia.

J ... telangiectasias; hereditary hemorr

Ii!U:ngiectasla. ICourtesy Dr Iv1argot van Dis)

Fig. 2~-4. Blanching of telangiectasias on diascopy:

heredItary hemorrhagic telangiectasia. ICourtesy

_ _....~

r
~

~x ...vlne

stain; Sturge-Weber syndrome,

:? :..i.'rry Skoczylas)

:--1. _'" .ateral hemangioma of the palate;

eMr syndrome.

Dr Margot van Dis)

Fig. 27-6. Unilateral involvement of intraoral

hemangioma; same patient as in Fig. 27-5 with Sturge-

Weber syndrome. ICourtesy Dr Larry Skoczylas)

Fig. 278. Tram-line gyriform calcifications, lateral skull

radiograph"; same patient as in Fig, 27-7 with Sturge-

Weber syndrome.

61

RED AND REDIWHITE LESIONS

Erythroplakla (Figs. 28-1 through 28-4) Erythroplakia is defined as a persistent velvety red patch that cannot be characterized clinically as any other condition. This
term. like "leukoplakia," has no histologic connotation:
however. the majority of erythroplakias arc histologically
diagnosed as epithelial dysplasia or worse. and thus have a
much higher propensity for progression to carcinoma.
Erythroplakias may be located anywhere in the mouth. but
appear 10 be most prevalent in the mandibular mucobuccal
fold. oropharynx and floor of the mouth. The redness of
the lesion is a result of 3lrOphic mucosa overlying a highly
vascular submucosa. The border of the lesion is usually

well-demarcated. There is no sexual predilection and

patients over the age of 60 are most commonly affected.
Three clinical variants of erythroplakia have been recognized: (I) the homogenous foml, which is completely red in
appearance: (2) erythroleukoplakia, which has red patches
interspersed with occasionalleukoplakic areas; and (3) speckled
erythroplakia, which contains white specks or granules scattered throughout the lesion. Biopsy is mandatory for all types of
erythroplakia, because 91 % of erylhroplakias represent severe
dysplasia. C'".lJ'Cinoma in situ, or invasive squamous cell can:illl).mao Close inspection of the entire oral cavily is also required.
since 10 to 20% of these patients will have several erythroplakic areas. a phenomenon known as field cancerization.

Erythroleukoplakia and Speckled Erythroplakia

(Fig, 285) Erythroleukoplakia and speckled erylhroplakia, or "speckled leukoplakia," as some authors prefer,
are precancerous red and white lesions. Erythroleukoplakia
is a red patch with isolated leukoplakic areas. whereas
speckled erythroplakia is a red patch that contains white
speckles or granules throughout the entire lesion. A variant
red-white lesion thai has a nodular appearance is called
proliferative verrucous leukoplakia.
Erythroleukoplalda and speckled erythroplukia have a
male predilection, and most lesions are detected in patients
over age 50. They may occur at any intraoral site, but frequently affect the lateral border of the tongue, buccal
mucosa, and soft palale. These lesions are often associated
with heavy smoking, alcoholism, and poor oral hygiene.
Fungal infections are common in speckled erylhroplakias, Candida a/bicans. Ihe predominant organism, has
been isolated in the majority of cases: therefore the management of these lesions should include analysis for candida. The cause and effect relationship of candidiasis and
speckled leukoplakia is unknown. but erylhroplakia with
leukoplakic regions confers a greater risk for atypical cyla-logic changes. Because of the increased risk for carcinoma,
biopsy is mandatory of all red-white lesions.
Squamous Cell Carcinoma (Figs. 285 through
28-8' Squamous cell carcinoma is a malignant neoplasm
of mucosal origin. It is the mOSI common type of oral cancer. accounting for over 90% of all malignant neoplasms of

62

the oml cavity. Oml cancer may occur al any age. but
primarily a disease of Ihe elderly: greater than 95% of
cancers occur in persons over the age of 40. In Ihe pasL
prevalence was much higher in males, but the mak
female r.!tio has dramalically decreased in recent YC3f\
approximately 2: I. owing to the increased num~r
women who smoke.
The exaci cause of oml cancer is unknown. C}to
atypism and mutagenesis may be a resuh of multiple f
associated with aging and exposure to a variety of bi
chemical. and physical agents such as the following:
tion with Treponema pa/fidl/m. herpes simplex virus. h
papilloma virus, or Candida a/bicans: excessive use
tobacco and alcohol: nutritional deficiency states:
neglect: chronic trauma: radiation: and immune supp'~"".
The most common site for intraoral squamous cell
cinoma is the lateral border and ventral surface of
tongue. Other intraoral sites, in descending order
involvement, are the oropharynx, noor of the mouth.
va. buccal mucosa, lip. and palate. The occurrence of
mous cell carcinoma of the lip has decreased dramatl
in the pasl decade because of Ihe increased use of p
tive sunscreening agenls. The dorsal surface of Ihe t
is almost never affected.
The appearance of squamous cell carcinoma is hI_
variable. with over 90% of the cases having an e.",,""'"
kic component, and about 60% showing a leukop
component. A combination of colors and surface pal
such as a red and white lesion Ihat is exophytic. infil
or ulcer.lIed, indicates instability of the oral epilhelium
is highly suggestive of carcinoma. Early lesions are
asymptomatic and slow-growing. As the lesion de\c
the borders become diffuse and ragged. and induratioo
fixation ensue. U the mucosal surface becomes ulc
the mosl frequent oral complaint is that of a persl
"sore" or "irritation:' Not uncommonly, patients may
plain of numbness or a burning sensation. swelling. or
ficulty in speaking or swallowing. Extension of lesi
several centimeters in diameter can result if treatm
delayed. permitting large lesions to invade and de
vital osseous structures.
Spread of squamous cell carcinoma occurs b)
extension, or by way of the lymphatiC vessels. Slagl
the tumor according 10 size (T). regional lymph nodes
and distant melastases (M) affords assessmenl of the eof disease. Surgery and radial ion Iherapy have ben
principal forms of treatmenl for oral cancer.
The prognosis for oral cancer depends. in large
sure. on the site involved, the clinical stage at the u
diagnosis, the width of Ihe tumor al its greatest di
Ihe palient's access 10 adequate heah,>care, abilit} 10
and mounl an immunologic response. Early treat
paramount: therefore biopsy should be initialed if ~
suspicion of neoplasia.

AND REDIWHITE LESIONS

:3-1 Erythroplakia not discernible unlll the

>pressea as seen in Fig 28-2

Fig. 28-2. Erythroplakia with leul<oplak.lc border,

biopsy revealed epithelial dy<;plasia

erythroplakia along the ~ub):ngual

levedled carcinoma In s:tu. /Courtesy Dr

Fig. 28-4. Erythroplakia of the floor of the mouth:

biopsy revealed squamous ceil carCInoma

Erythroleukoplakia; biopsy rt"'VeaJed

l<lrClI'lO/1'1a

Fig. 28-6. Squamous cell carcinoma of the :orgue

<tdJdCenl. to itred ~ecn In FI9 28-5. exct!'1"ptc of field

.~

cancerization.

1:;-

e erythroleukoplakla that proved to

caronom.:l (Courtesy Dr Robert Cralgj

Fig. 28-8. Speckled erythroplakia; biopsy revealed

squamous cell carCinoma (Courtesy Dr Robert (ralgl

63

RED AND REDIWHITE LESIONS

Lichen Planus (Figs. 291 through 29-6) Lichen
planus is a common skin disease that frequently has
mucosal manifestations. The etiology and pathogenesis are
unknown. although evidence suggests thai lichen planus is
an immunologic disorder. possibl)' an autoimmune disease.
in which T.lymphocyles destroy the basal cell1ayer of the
affected epithelium. Both CD4 and COB T-cell subsets
have been identified in the submucosal lymphocyte population. Nervous and high-strung persons are predisposed to
Ii~hen planus. The majority of patients are females over the

age of 40. The disease exhibits a protracted course with

periods of remission and exacerbation.
The skin lesions of lichen planus initially consist of
small. flat-topped. red papules with a depressed central
area. The lesions may enlarge and become polygonal in
shape or coalesce into larger plaques. TIle papules progressively acquire a violaceous hue and surface lichenification,
which consists of fine white striae. The lesions usually itch
and may change color 10 yellow or brown before resolution.
Bilateral distribution on the flexor surfaces of the extremities is common. occasionally involving the fingernails.
Patients with characteristic purple. polygonal. pruritic
papules on the skin often have concurrent intraoral lesions.
Oral lesions of lichen planus may have one of four
appearances: atrophic, erosive. strialed (reticular). or
plaquelike. More thun one form may affect a single patient.
The most frequently affected sile is the buccal mucosa.
The tongue, lips. palale. gingiva. and floor of the mouth
may also be affected. Bilateral and relatively symmetrical
lesions are common. Patients with reticular oral lichen
planus characteristically have multiple delicate white lines
or papules arranged in a lacy. web~like network known as
"striae of Wickham." The glistening white areas are often
asymptomatic but of cosmetic concern. They may involve
large areas.
Atrophic lichen planus results from atrophy of the
epithelium and predominantly appears as a red. non-ulcerated mucosal patch. Wickham's striae are often present al
the border of the lesion. When the attached gingiva is
affected. the lerm "desquamative gingivitis" has been used.
Erosive lichen planus occurs if the surface epithelium is
completely lost and ulceralion results. The buccal mucosa
and tongue are commonly affected sites. Initially, a vesicle
or bulla may appear which eventually erodes producing
ulceralion. Mature lesions have irregular red borders. a yel
lowish necrolic central pseudomembrane, and an annular

64

white patch often at the periphery. The condition i

millently painful and may onset rapidly. All of theSt
lures are helpful in differentiating oral lichen planU5
other clinically similarappearing lesions such as I
plakia, erythroplakia. candidiasis. lupus er)'them
pemphigoid. and erythema multiforme.
The least common type of lichen planus is the
tommie plaque form. This lesion is a solid white plaqIR
patch that has a smooth to slightly irregular surface
asymmetric configuration. Lesions are commonly fOlD,.
buccal or glossal mucosa. Patients may be una.. arr
these lesions.
In many cases clinical appearance alone can confi
diagnosis of oral lichen planus. and a biopsy is not
sary. Asymptomatic intraoral lesions can be left
Biopsy of the atrophic or erosive form should be
formed at the border of Ihe lesion.
The oral lesions of lichen planus lend 10 be more
tent than those of the skin. A vacation, change in
or discharge of psychologically burdensome proble
bring about abrupt and dramalic resolution of (he
Chronic. symptomatic. erosive lichen planus lesi
best managed with lopical or syslemic steroids
immunosuppressants. A small number of patients "'1 .
lichen planus are diabetic and should be tested for
intolerance. Carcinomatous transformation has
reported (in less than 100 cases) 10 have an asso<"'-_
with erosive lichen planus and tobacco use. The true
and effeci relalionship. however. has yet 10 be esta
for squamous cell carcinoma and lichen planus.
Electrogalvanlc White Lesion fFigs. 297
29-8} Electrogalvanic while lesions closely resemble
hypenrophic form of lichen planus. This disorder IS
apparent after the age of 30 and frequenlly occurs
buccal mucosa. immediately adjacem to a melallic
tion. Mild cases are asymptomatic. whereas erosi\e
can cause a burning type of pain. Histologically this
mimics lichen planus. Electric microcurrents ind
dissimilar restoralions is one explanation for thu
nomenon. Inlerestingly, lichenoid drug reactions...
similar in appearance to electrogalvanic while lesioas:
be caused by the systemic application of the same
(mercury and gold) found in dental restorations. T
consists of replacing the reslOralion with a different
tive malerial. preferably gold. porcelain. glass iOOOlDl:E"
composite materials. 1be prognosis is excellent.

~:>

AND REDJWHITE LESIONS

.3CeClUS

skin plaque with lichenification on

. re of lichen planus.

ul denuded patches of erosive lichen

5 Red .. trophic lichen planus on buccal

_psy (Courtesy Dr Tom Razmusj

ElKtrogalvanic white lesion that has a

_ - '1( dent to the adjacent dass-V alloy

Fig. 29-2. Characteristic V/ickham striae of reticular

lichen planus. ICourtesy Dr Birgit Glass)

Fig. 29-4. Erosive lichen planus; same patient as in

Fig 29-3.

Fig. 29-6. Plaque form of lichen planus with

fevv striae.

Fig. 29-8. Electrogalvanic white lesion opposite

Side in the same pallent as seen in Fig. 29-7

65

RED AND REDIWHITE LESIONS

Lupus Erythematosus fFigs. 3D-' through 30-41
Lupus erythematosus (LE) exist'" in three ronns: chronic discoid lupus erythematosus (CDLE), which only involves the
skin: systemic lupus erythematosus (SLE), in which mulli
pie organ systems are involved: and subacute cutaneous
lupus erythematosus. a cutaneoUs varianl wiTh mild systemic
symptoms. The cause of all three types is unknown.
COLE. the benign form of the disease. is a purely
mucocutaneous disorder. II may appear al any age. but predominates in females over the age of 40. COLE is classically characterized by a red bUllerfly rash symmetrically
distributed across the bridge of the nose. Other prominenl
photosensitive areas of the face, including the cheeks.
malar areas. forehead. scalp. and ears. may be involved.
The lesions of LE are chronic wilh periods of exacerbation and remission. Mature lesions exhibit three zones: an
atrophic center lined by a hyperkemtotic middle zone which
is surrounded by an erythematous periphery. Frequently
there is hypopigmentation of the lesion resulting from
melanocytic damage at the epidermal-dermal junction.
Telangiectasias, blackheads. and a fine scale are common
dermal findings. The lesions are usually limiled to the
upper ponion of the body, particularly the head and neck.
Twenty to 40% of patients with LE have oral lesions.
These lesions may develop before or after skin lesions
develop. Lip lesions are red with a white 10 silvery. scaly
margin. A sun-exposed lower lip at the vermilion border is
a common site. whereas the upper lip is usually involved as
a result of direci extension of dermal lesions. Intraoral
lesions are frequently diffuse and erythematous. with
ulcerative and while components.
Occasionally COLE appears as isolated white plaques.
The buccal mucosa is the most frequent imraoral site. followed by Ihe tongue. palate and gingiva. Alternating parallel red and white lines in a radial arrangement are an imporlant diagnostic feature. along with the appearance of multiple lesions on several surfaces. These lesions may mimic
lichen planus; however, concurrent ear involvement helps
to exclude the diagnosis of lichen planus. Ulcerative lesions
are painful and require treatment. Avoidance of emolional
stress. cold. sunlighl. and hOI spicy foods is necessary. The
use of sunscreens. topical steroids. systemic steroids. and
antimalarial agents have proven effective. Patients using
antimalarial agents require close ophthalmologic foUowup.
SLE. an aUioimmune collagen disease. is characterized
by the production of antinuclear and anti-DNA antibodies
that participate in immunological1y mediated tiS5ue injury.

66

Patients often complain of fatigue. fever. and JOInt

Generalized nontender lymphadenopathy is often
Hepatomegaly, splenomegaly. peripheral neuropath.
hemalOlogic abnonnalities may also be seen. Strict
ance of sun exposure is necessary. since sunburn
gel' acute reactions. Involvement of the kidneys and
is a common occurrence that may prove fatal. S
oral lesions may accompany SLE. but there is little
of conversion from discoid to systemic lupus. PatieOB
SLE often suffer concurTemly from other autoimmtmr
lagen-vascular diseases such as Sjogren's syndromerheumatoid arthritis. Allergic mucositis. candidiasis.
plakia. erythroleukoplakia. and lichen planus must br
side red in the differential diagnosis of oral LE I~
Biopsy and histologic examination with immunon
cence confirms the diagnosis. Precautions are ad\
the denial treatmenl of patients with lupus erythe
who may be laking high doses of systemic St
because of their predisposition to delayed wound
the risk of infection. and the possibility of stressadrenal crisis characterized by cardiovascular co...'
These patients are also at risk for cardiomyopath~
requires antibiotic prophylaxis.
Uchenold and Lupus-llke Drug Eruption
)0-5 through 3o-BI Relicular or erosive lesiOfb
in appearance 10 lichen planus and lupus er)"the
may occur in association with a variety of systemic
tion~. Allhough the appearance may be quite varied..
linear plaques with red margins are common. The
may erupt upon immediate or afler prolonged use of ..
Persistent innammalOry changes may result in large er
matous areas. eventual mucosal ulceT'"dtion. and pam.
induced lupus erythematosus is often associated ",iIb
tis. fever. and renal disease. Hydralazine and p""........
are the most common instigators of lupus-like dna!
lions. Other drugs known to cause lupus-like e
include gold. griseofulvin. isonia~.id. mcthyldopa.
cillin. phcnytoin. procaillamide. Mreptomycin. and
dionc. Drugs known to induce lichenoid eruptioM
the following: chloroquine. dapsone. furosemide.
mercury. methyldopa. palladium. penicillamine.
iaLines. quinidine. thiaLides. certain antibiotics.
metals. Consultation with a physician and withdra",
offending medication will lead to regression of the
substitule drug is usually selected to manage thesystemic problem.

o REDIWHITE LESIONS

---

,,_."''''SU$.

rash; chronic discoid lupus

Fig. 30-2. Red scaly lip les'Orl of chronic discoid

lupus erythematosus (Courtesy Dr James Cottone)

'-19 radial red and white hoes,

oid lUpus erythematosus.

Fig. 30-4. Red aldwtvte cur\llhrl6:."W" plaq..Jc; chronic discoid lupus erythematosus. fCourtesY Dr James CextOf"'M?)

pus-like drug eruption fOllOWing the

_ am tnptytlne

opposIte buccal mucosa. same paClent

- 'e pliiques and wiae of a lichenoid

_..,DOn subsequent to furosemide therapy

Fig. 30-6. Ulcerated lupus.fike drug eruption

as In Fig

30-5

Fig. 30-8. Withdrawal of furosemide reSulted in

complete resolution of lichenoid drug eruption

seen In Fig

30-7.

67

RED AND REDIWHITE LESIONS

Acute Pseudomembranous Candidiasis (Thrush)
fFigs. 31-1 and 31-21 Acute pseudomembranous candidi-

asis, an opportunistic inft:ction, is caused by an overgrowth of

the superficial fungus Candida albicans. It appears as diffuse.
curdy. or velvety white mucosal plaques thai can be wiped off.

leaving a red. raw, or bleeding surface. The organism is a

common inhabil3m of the oral cavity. gastroinlcslinal1f3et.
and vagina. InfanlS whose mothers display vaginal thrush al
the time of binh and adults who have experienced an upset in
the normal oral microflora due 10 antibiotics. steroids, or systemic alterations such as diabetes. hypoparathyroidism.
immunodeficiency. or chemotherapy are frequently affected.

There is no racial or sexual predilection.

Acute pseudomembranous candidiasis is usually found
on the buccal mucosa. tongue. and soft palate. Clinically
the white plaques appear in clusters that have an erythematous border. A peculiar paltern is seen in asthmatic patienls
who use a steroid inhaler. The pattern appears as a circular
or oval reddish~white patch at the site of aerosol contact on
the palate. Diagnosis can be made by clinical examination.
fungal culture, or direct microscopic examination of tissue
scrapings. A potassium hydroxide (KOH). Grams. or periodic acid-Schiff (PAS)-stained cytologic smear will reveal
budding organisms with branching pseudohyphae. Topical
appJicalion of amifungal medication for 2 weeks usually
produces resolution.
Chronic Keratotic Candidiasis (Hyperplastic)
{Figs. 31-3 and 31-41 Chronic keratotic candidiasis is
caused by organisms of the candida sp. that penetrate the
mucosal surface and stimulate a hyperplastic response.
Chronic irritation. poor oral hygiene. and xerostomia are
predisposing factors: thus smokers and demure wearers are
commonly affected. Chiefly involved is the dorsum of the
tongue. palate. and labial commissures. The lesion invari
ably has a distinctive raised border and a white. pebbly sur
face with an occasional red area: thus the condition may
resemble leukoplakia or erythroleukoplakia. The scattered
erythematous comlX'nents are a result of mucosal cell layer
desuuction.
The white "latch of chronic keratotic candidiasis cannot
be peeled off. requiring the diagnosis to be made by biopsy. Microscopically the organisms may be identified by
routine hematoxylin and eosin stain or. more appropriately.
by the PAS stain. With adequate topical application of an
anti-fungal agent. resolution usually occurs. In some
instances surgical stripping may be required. All patienls
with chronic keratotic candidiasis should be followed
closely. since this fonn may be related to speckled erythroplakia. a lesion which is often premalignant or worse.
Acute Atrophic Candidiasis (Antibiotic Sore
Mouth) fFig. 3151 The use of broad spectrum antibiotics. panicularly tetracyclines. can result in the oral condi-

68

tion tennOO "acute atrophic candidiasis." This fungal

tion is the result of an imbalance in the oral eC(K.
between Laclobacillus acidophifus and Candida a
Antibiotics taken by the patient reduce the Lacrol..
population and pennit candidlll organisms to floun
infection produces desquamated areas of surface
that appear as diffuse. nonelevated red patches. 8
pain is the most frequent chief &mplaint. The dis
of the patches of acute atrophic candidiasis is so
indicative of the cause. Lesions affecting the
mucosa. lips. and oropharynx often suggest the
administration of antibiotics. whereas redness
tongue and palate are more common following the
antibiotic troches. When the tongue is affected a
devoid of filiform papillae is common. It is rare for
didiasis to affect the attached gingiva: if this is the
finding. then severe immune suppression is a disuna
sibility. The diagnosis of a candidal infection sh
confirmed by demonstration of budding organL
hypha I fOnTIS on a stained cytologic smear. Trea
wilh antifungal agents.

5,

Angular Cheilitis 'Fig. 31-6) Angular cheit

chronic painful condition involving the labial co
caused by Candida albicans. Clinically. angular
appears red and fissured. with the periphery of the
less erythematous than central areas. Crusting and
ish gmnulomatous nodules may be concurrent. Di
caused by opening the mouth may limit nonnal oral
tion. Predisposing factors and treatment have been
ously discussed.
Chronic Atrophic
Candidiasis (DenStomatitis) fFigs. 31] and 31-8) Chronic
candidiasis is the most common form of chronic "". ._
It is present in 15 to 65% of complete and partial
wearers. panicularly elderly females who wear their
tures at night; rarely dentate patients may also be
The mandible, however, is rarely involved. Misnomcro
this disease are the terms "denture sore mouth" and
lUre base allergy".
Chronic atrophic candidiasis is caused by candida)
isms located under the denture base. There are thrtt
of mucosa.! alterations. The earliest lesions are red
areas of hyperemia limited to the orifices of the
minor salivary glands. Progression produces a di~
merna of the hard palate that is sometimes accom
epithelial desquamation. Papillary hyperplasia is tbt
stage. It may be generalized or restricted to relief
Rarely a fourth stage is apparent; the enlarge~nt of _ _
papules to form red nodules on Ihe vault of the . . .~
Effective therapy requires antifungal treatment
mucosa and denture base. The role of trauma, sue.
rocking action of the denture. may perpetuate the 000","_

ae:

AND REDIWHITE LESIONS

.! .' Thrush In an immunosuppressed p.3tient.

:
)ol Sl'verman)

Fig. 31-2. Acute pseudomembranous candidiasis in a patient that uses a steroid inhaler, (Courtesy
Dr Geza Terezhalmyl

"
......
.-.',
',\

.~

.:.~~

-3 Chronic hyperplastic candidiasis at the

~'e which

extends onto the buccal mucosa

:", Acute atrophic candidiasis limited to

Fig. 31-4. White keratotic plaques of hyperplastic

candidiasis in a deblliated pallent

Fig. 31-6. Angular cheilitis. (Courtesy Dr JC1mes

:"-Dearing area, due to steroid Inhalant

Cottonel

Papillary hyperplasia; the third stage of

Fig. 31-8. Chronic atrophic candidiasis limited to

partial denture bearing area ICourtesy Dr Nancy rvlantlch)

-"J.! lCourtesy Dr Ken Abramovltchl

69

PIGMENTED LESIONS
Melanoplakia fFig. 32-1' Melanoplakia is a generalized and constant dark pigmentation of the oral mucosa.
commonly seen in dark-skinned persons (melanoderms).
The condition is physiologic, not pathologic, and results
from increased amounts of melanin, an endogenous pigment. that aTC deposited in the basal layer of the mucosa
and lamina propria. The most common site for observing
melanoplakia is the attached gingiva. It often appears as a
diffuse, ribbon-like, dark band with a well-demarcated and
curvilinear border that separates it from the alveolar
mucosa. Characteristically the region is symmetric and
asymptomatic. The degree of pigmentation varies from
light brown 10 dark brown. and infrequently may appear
blue-black. Other sites of occurrence are the buccal
mucosa. hard palate, lips and tongue. At these sites the
deposition of pigment often is multi focal and diffuse.
Melanoplakia should be differentiated from similar-appearing conditions that produce oral pigmentations, such as
Addison's disease. Albright'S syndrome, Peutz-Jeghers
syndrome, heavy metal pigmentation, and anti-malarial
drug ingestion.
Tattoo fFigs. 322 through 32-51 Tattoos are caused
by intentional or accidental implantation of exogenous pigments in the mucosa. The most common intraoral type is
the amalgam tattoo, which has been referred to by some as
"focal argyrosis:' The amalgam tatoo appears as a blueblack. non-elevated discoloration that is usually irregular
in shape and variable in size. It results from the entrapment
of amalgam in a soft tissue wound such as an extraction
socket or a gingival abrasion from a rotating bur.
Deterioration of the silver compounds of the amalgam
impart the characterislic blue-black color. Focal discolorations may occasionally appear green 10 dark gray
because of the deposition of high copper alloys.
Amalgam tattoos are usually seen in the gingiva in posterior arcas adjacent to a large amalgam restoration or gold
casting. These lesions are not limited 10 the gingiva and
may also be seen on the edentulous ridge. vestibular
mucosa, palate, buccal mucosa. and floor of the mouth. The
clinical diagnosis of an amalgam tattoo can be confirmed
by finding radiographic evidence of the foreign metal in the
paradental tissue. The radiographic appearance may vary
from no demonstrable particles to pinpoint or globular
radiopacities several millimeters in diameter. If radiographs
fail to demonstrate suspected metallic particles. a biopsy is
required 10 rule out more serious pigmented lesions.
Other types of tattoos seen in the oral ca\'ity are the
graphite pencil wound and India ink tattoos. The graphite

70

pencil wound appears following Irauma as a focal.

gray macule frequently located on the palate. The
the lesion can be easily ascertained by questionq
patient. Ordinary India ink tattoos are occasional
on the labial mucosa of the lower lip. In generaL la
hannless and of no clinical significance; however. ~
be indistinguishable from more potentially ominous

Ephelis ,Freckle) fFig. 32-61 An ephelis is a _

dark-brown macule that appears on the lip or skin ~
ing active deposition of melanin triggered by ex
sunlight. Unlike some pigmentations, this lesion ""
essentially unchanged in size with time. darl;
response 10 sunlight, and has a predilection for
skinned or red-headed persons. A single freckle is m......
ly distinguished from an oral melanotic macule b}
tory of a traumatic or inflammatory episode that
the development of the latter condition. Microsc
the ephelis shows an increase in melanin pigment ,.
an increase in the number of melanocytes. Multiple
les on the lip should be distinguished from the iden
ephelides seen in conjunction with palmar pigmt'
and intestinal polyposis of Peutz-Jeghers s~ .....~
Ephelides m3.Y be of cosmetic concern requiring
removal; othen,vise. observation is normally reco""'......
Smoker's Melanosis ITobacco-Assoclate-d
mentation) {Figs. 32-1 and 32-81 Smoking
imparts a characteristic color change to exposed
surfaces that is tenned smoker's melanosis. The
is not a nonnal physiologic process, but instead
principally from the deposition of melanin in lhe
layer of the mucosa. The relationship of s
melanosis and inflammatory changes that result f~
smoke inhalation. and the absorption of exogeous pi_
has not been detennined.
Smoker's melanosis affects older individuals
heavy smokers. It appears as a diffuse brown patch
centimeters in size. The mandibular anterior gin
buccal mucosa are the most frequently affected sj~
susceptible sites include the labial mucosa. palate,
floor of the mouth, and lips. The degree of pig........
ranges from light to dark brown and appears to be
related to the amount of tobacco consumed. Us
finds dark-brown foci asymmetrically distributed
out an ill-defined. light-brown patch. Brown-slaiDtd
and halitosis usually accompany the condition. 5
melanosis itself is not premalignant; however. the "'......
should closely inspect the adjacent tissues for 'otba
co-induced lesions.

NTED LESIONS

M~lanopl.. kia

dlSC/lbuted along the

_ ~~i.fJ. macular
_--e? OrosI

amalgam tattoo.

S Focal argyrosis from failed silver point

"

- Smoker's melanosis; lateral regions of the

Fig. 32-2. Ind!3-lnk tattoo. (COUrtesy Dr David Freed)

Fig. 32-4. R<lcflOgl'"aph of paLent n Fig 32-3 that reveals

~

oa'tlClcs bervvren the rlfSl molcV" elM second

blC\.lSpd. confirm.ng the atagnoslS Or amalgam tattoo.

Fig. 32-6. Multiple ephelides {frecklesl of the face and

lips

Fig. 32-8. Smoker$ melanosis of the weecl mucosa;

same pclclent as seen In Fig 32-7

71

PIGMENTED LESIONS
Oral Melanotic Macule {Figs. 33-1 and 33-2)
Within the mouth. an increased amount of melanin deposited
as a single. flat. well-circumscribed discoloration usually
less than I em in diameter is tcnned an oml melanotic macule. These endogenous pigmentations are common in lightskinned individuals between 25 and 45 years old and probably represent jX)Snraumatic or inflammatory pigmentation. a
condition analogous to po5linflammalory hypermelanosis on
the skin. The most common site is the lower lip close to the
midline. Other sites include the gingiva, buccal mucosa. and
palate. The color is uniform and may be blue. gray. brown.
or black. Biopsy is recommended. unless the lesioo has been
present for many years wilhoUi visible change and periodic
observation is provided.

Nevus (Figs. 33-3 through 33-61 The nevus is commonly seen on the skin and may. in rare instances. occur in
the mouth. Ahhough the histogenesis of the nevus is controversial. authorities suggest that it has a melanocyte or
Schwann cell derivation. There are a number of different
types of nevi. which are broadly classified as either con~
genital or acquired. Congenital nevi are present at binh and
are also known as birthmarks or "garment trunk" nevi.
They are usually larger than acquired nevi and have a higher incidence of malignanttl'3nsformation.
Acquired nevi. or moles. occur later in life and usually
appear as dari;:. slighlly raised papules or dome-shaped nodules. They may vary in pigment. and can be brown. gray.
blue. or black. Occasionally nevi are amelanotic and appear
pink. Intl'3orally the nevus is a rare finding. They are usually
small (only a few millimeters). pigmented, well-circumscribed, dome-shaped papules or nat macules that occur
more frequently on the palate and buccal mucosa of females.
Their size tends to remain constant after puberty. These
asymptomatic lesions do not blanch on pressure.
Benign nevi have been classified into four subtypes
according to the histologic appearance and location of the
nevus cells. which are arranged in nests. or 'theques.' In
order of decreasing frequency one finds the following nevi:
intramucosal nevus. blue nevus. compound nevus. and
junctional nevus.
The intra mucosal nevus, the most common nevus found
in the mouth and the Ixxly. has ovoid nevus cells located in
the connective tissue only. This entity is analogous to the
intradennal nevus. which appears as a dari;: raised papule on
the skin. often seen with a hair growing from iL It is rare,
however. to find a hair associated with the intramucosal
nevus of the mouth. Usually the intTamucosal nevus is
brown, raised. and between 0.4 and 0.8 cm in diameter.
The second most common intraoral nevus is the blue
ne\us. The name originates from the typical blue or blueblack color imparted by the spindle-shaped nevus cells
located deep in the connective tissue. These cells are

72

derivatives of neural crest cells that fail to migrate

region. A small. well-circumscribed blue macule b
ical appearance, although the color of the nevus one.
with age. The palate is the mOSI common
Malignant transformation of intraoral blue nevi
been reported.
The compound nevus. as the name implies.
posed of nevus cells located in the epithelium and_
na propria. Like the two previous nevi. the c
nevus rarely undergoes malignant transformal
junctional nevus is a subtype of acquired nevus
nevus cells at the junctional layer of the epilhelium.
lamina propria. These lesions are the rarest I)pe'
nevus and usually appear l1al. brown. and less m.
The palate and buccal mucosa are common locan
On rare occasions the melanolic frecl::le of H
(lentigo maligna) is found in Ihe mouth. More 00....the melanotic freckle is seen on Ihe face of pe
the age of 50. This lesion is flat. irregularly sha
diny gray-brown in color. It may spread superfi
horizontal direction and undergo malignant transf:
Nevi may be difficult to distinguiSh from IMU
nant counterparts; thus all intraoral pigmented
should be surgically removed and submi
hislOpalhologic examination. especially if they an:
to chronic irritation.

Malignant Melanoma IFigs. 337 and

Melanomas are malignant neoplasms of melan
may occur in the oral cavity. They occur appro
twice as frequently in males as in females and ~
sons over the age of 50. Approximalely 30% of ..."".
have been reported 10 arise from previously exi
mented lesions, particularly ones with a history of
Like the nevus. melanomas may be flat or rai
pigmenled or pigmented. When pigmented their
usually deep and varies from brown. gray. blot
black. The most frequent sites for occurrence art ~
illary alveolar ridge. palatal tissues. anterior gin
labial mucosa.
Inilially melanoma is a small. slightly raised p&its aggressiveness causes rapid growth in all d.
Eventually a prominent. non-moveable. dark leslon
The main distinguishing clinical features include
colors (Ihe combination of red together with blue
white is panicularly ominous), change in size. i""I'L_
illdefined margins, satellite lesions arising at the
of the lesion. signs of inflammation. such as a
zone of erythema. bleeding and ulceration. fi~
pation. and rock hard regional lymph nodes. . . . .<;Ii
malignant melanomas are extremely dangerous _. , , _
serious than their cutaneous counterpart. due to ea"
wide metastasis which resulls in a very poor progDD"

"_L

MENTED LESIONS

mOst common 5ne of the melanotic

er p

-"le

!3-3 Blue nevus Of the hard palate ICounesy Dr

- ch

O\Vfl flat compound nevus

"e (Courtesy Dr Dare Mllesl

3:3-5 3

on me

33-1 B.n P19memanon. p,npomr satellite 1es1OflS.

erythema charactenstlC of malignant
_ ......m ... ,Courtesy Dr GeZil Terezhalmyl

Fig. 33-2. Brown melanotic macule of the hard

palate

Fig. 33-4. Dark ptgmented blue nevus on the lateral

palatal vault fCOUrtesy Dr Tom McDavrd)

Fig. 33-6. Ratse<:! nooule adJerlt to firs! maxillary

molar. amelanotic intramucosal nevus. (COUrtesy

Or Curt Lundeen)

Fig. 338. vegetatIVe. amelanotlC malignant

melanoma; paklle and atveolar ridge (Courtesy Drs
AM Abrams (lnd JOhn Tall)

73

PIGMENTED LESIONS
Peutz-Jeghers Syndrome (Hereditary Intes-

tinal Polyposis, fFigs. 34-1 and 34-2) PeutzJeghers syndrome is an aUl050ma) dominant condition
associated with multiple melanotic mucocutaneous macnles and gastrointestinal jXllyposis. These multiple benign

intestinal polyps are hamartomatous tissue growths Ihal

usually occur in the ileum, bUI may also be found in the
stomach and colon. Symptoms such as intennillent colicky
pain and complaints of obstruction may be concurrent.

Of relative imponance to the dentisl are the muhiple.

asymptomatic. melanotic discolor.uions. These lesions are
usually small. flat, brown ovals that are prominently located
on the skin around the eyes. nose and mouth. as well as on
the lips. perineum. oral mucosa, gingiva, and palmar and
planlar surfaces of the hands and feel. The mOSI common
intraoral locations for these pigmentations are the lips and
buccal mucosa. In contrast to their cutaneous counterparts.
the inlrnOral spots tend to persist into adulthood, whereas the
dermal macules may fade with age. 0 treatment is necessary for the macules, which microscopically contain hyperpigmentation of the basal cell layer and lamina propria.
Although the macules are benign findings, they are of considerable clinical significance, since a small percentage of
affected patients are prone to develop gastrointestinal adenocarcinoma and are at an increased risk for tumors of the
reproductive system. The diagnosis of Peutz-Jeghers syndrome therefore necessitates prompt medical evaluation,

Addison's
Disease
,Adrenal
Cortical
Insufficiency' (Figs. 34-3 and 34-41Addison's disease most commonly results from aUioimmune-induced
destruction of Ihe adrenal gland. Other causes include
infectious diseases, adrenalectomy. gram-negalive sepsis.
pituitary insufficiency. and tumor invasion. Progression of
the disease results in anemia. anorexia. diarrhea. hypotension. lethargy. nausea. and weight loss,
A complication associated with this disorder is failure of
the feedback loop from the adrenal gland to the pituitary
gland. This causes an increase in adrenoconicotrophic hormone (ACTH). which induces melanocYle-stimulating hormone (MSH) and the deposition of melanin in the skin.
Classically the skin acquires :I bronze tan that persists following sun exposure. Darkening may be initially noted on
the knuckles. elbows. palmar creases. and intraoral mucosa.
IntraoraHy Ihe disease is characterized by hypermelanosis similar in :lppearance to melanoplakia. The puuern
is not unique and may consist of multiple focal blue-black
spots or generalized. diffuse streaks of dark-brown pigmentation. Usually the pigmented areas are macular, nonraised, brown, and varied in shape. The buccal mucosa and
gingiva are most commonly affected. bUI the pigmentation
may extend ontO Ihe tongue and lips as well. Biopsy is nol

74

diagnoslic and serum cortisol tests are recom

Replacement therapy with conicosteroids produ~
ual diminution of the hyperpigmentation: thus the
of oral pigmentation is a sensitive indicator of t"'~~
effectiveness. Transient changes in pigmentation in
ed patient may be an indication of inadequate the~

Heavy Metal Pigmentation (Figs. 34-5

""':0.;-

34-8J Excessive ingestion of heavy metals (bismu

mercury. silver) and cenain drugs (antimalarials.
chotics. binh control pills) can produce mucoc
pigmentalions, Bismuth is commonly found in
medications, which if used chronically will result m
deposition of the metal in the gingiva. The discol
confined to the marginal gingiva. panicularl) I
where inflammation is present. Typically the
line" appears blue to black in a linear distribution
gingival sulcus. A metallic taste and burning m
common complaints.
Lead poisoning, or plumbism. usually is a result
pational exposure to excessive doses of lead used
or plumbing. The most prominent intraoral chan__
early diagnostic sign is a gray-black "lead line" m.
from the deposition of lead sulfide in Ihe marginal
Spotty gray macules on the buccal mucosa. a coated
tremor of the extended tongue. and hypersaii\'
other intraoral findings. The condition is reversible
sure to lead is eliminated.
Mercury poisoning. or acrodynia. can be aeq
absorption, inhalation, or ingestion. Although u"",..,~
today. acrodynia was the end-result of treat
syphilis earlier in the century. Inadequate mercW)
measures such as handling mercury. brealhing
vapors. and spilling mercury place dental personnel
for acrodynia.
like bismuth and lead intoxication. mercul)
produces a dark mercury gingival line. In addition.
ease is often accompanied by a multitude of Sl
symptoms. including abdominal pain. anorexia. ~-=;:;.
psychological symptoms. venigo. oral ulcerations..
rhage, a metallic taste, sialorrhea, burning mouth._
adontal destruction.
Silver pigmentation, or argyria. is a rare occu~
most often results from prolonged exposure to si ~
laining ocular or nasal medications. Asymptomatic
tations accumulate in the sun-exposed areas of tK
along with the hair. fingernails, and oral mucosa.
gray pigmentation is characteristic. which once ~
irreversible. Nasal inhalation of solutions contaillUl!
salts have a propensity for deposition in the palata!
imparting a similar color to Ihal seen on the skin. T.......
is immediate withdrawal of the medication.
M

""CiMENTED LESIONS

flat. brown pl9menlaOOOS of me bps,

..._ ..... hers syndrome.

Fig. 34-2. Brown macules on he buccal mtJCQS.Cl. same

pattent WIth Peutz.Jeghers syndrome as If1 Fig 34--1

Fig. 34-4. Diffuse plgmenlClllon on the buccal mucosa

and lOngue, same patient With Addisons disease as
In Fig 34-3

:.pIe

J a....o wn pigmentatl9ns apparent on the lips,

_'"".~.s disease.

r----~...,

sh lead line dlwitx,.ned alOng

Fig. 34-6. lead line; same paTlCf1t as.seen In Fig 3 4-5

tenor marginal gll1glViI

7 Argyria In a pauenr that ChronlCaJly used

"y Ilao;al drops (Courtesy Dr Ch<'Irles Morns)

Fig. 34-8. Argyrosis of the palate In ano\tlef pdtlffit

'Nho used nose drops (Courtesy Dr Ch.'lrles Morris)

75

SECTION

v
Intraoral
Findings by
Surface
Change

77

NODULES
Retrocuspld Papilla fFigs. 351 and 35-21 This
anatomic structure is not seen in all individuals. It consists Of a finn. round. fibro-epilhelial papule. usually I 10
4 mro in diameter. located on the attached gingiva Iinguallo the mandibular cuspids jusl below or several millimeters below the marginal gmgl'.a. rhe surface mucosa
is usually pink. soft. and smooth. Rarely the lesions may
be pedunculated and the stalk can be lifted off lhe gingiva by a periodontal probe. This condition is a variation
of normal and is frequemly found bilaterally. Some
3U1horities stale thai the retrocuspid papilla is a developmental anomaly that represents a variant form of fibroma. Apparently the reuocuspid papilla is present in most
children, but regresses with maturity: lhus the incidence
and size decrease with increasing age. The retrocuspid
papilla has no sexual predilection. and no treatment is
necessary unless interference with a removable prosthesis is <lnticipated.
Lymphoepithelial Cyst 'Figs. 35-3 and 35-41 The
Iymphoepithelial cyst is an encapsulated. fluid-filled dennal
or submucosal mass that arises from epilhelium entrapped in
lymphoid tissue that has undergone cystic transfonnalion. It
is usually asymplomatic. but may enlarge and spontaneously
fistulate. Most appear in children and young adults. No sexual predilection has been demonstrated.
When the Iymphoepilhelial cyst is derived from degenerative tissue of the second branchial arch. il is referred to as a
branchial cleft cysl. and il appears on the IateraJ aspocl of the
neck JUSI amenor and deep to Ihe superior Ihird of the slernocleidomastoid muscle near the angle of the mandible.
Occa~ionally the cySi may occur in the proximity of the parotid
gland. The extraoral Iymphoepithelial cyst is a well-circumscribed. soft. fluctuant mass that is rubbery to Ihe touch.
Common sites for the intraoral lymphoepithelial cyst
are the floor of Ihe mouth, lingual frenum. ventral tongue,
and base of the tongue. These small swellings. rarely
exceeding I em in diameter. are ch<lracteristically well-circumscribed. soft. and doughy, with a yellow color. Palpation yields a slightly moveable nodule. When located in
the anterior floor. the lesion may resemble a mucous retention cyst Infrequently, multiple Iymphoepilhelial cysts can
be found.
Histologically. Iymphoepithelial cySts are usually lined
wilh Slratified squamous epithelium. but occasionally pseudostratified, columnar. or cuboidal epithelium is found. A
fibrous connective tissue wall surrounds the lesion. which

contains dark-staining lymphoid aggregates \Itnent germinal centers.The luminal fluid is yelloa
cous. Excisional biopsy should be performed
histologic confirmation. Recurrence of Ihe lym
Iial cyst is rare.
Torus. Exostosis. and Osteoma (Figs..
through 35-81 Tori. exostoses, and peripheral
are readily recognizable bony hard nodules that
lologically identical. The term used depends OIl
appearance, and systemic associations.
Bony protuberances of the jaws, localized to_
midline or mandibular lingual attached gingiva. :Ill'e
'tori". They are the most common intraorallesK.
exophytic by nature. Females are most frequentJ_
Tori have smooth rounded contours. nomml-appea
slightly pale mucosa. and a ~ssile b..1se. Often ton
to have a lobulated surface. Internally they are
conical bone with occasional areas of spongy borJ:'
Bony outgrowths in alternate locations ~
"exostoses". The facial aspect of the mumandibular alveolar ridge are common sites. I .
Ihe palatal alveolar ridge adjacent to maxillary
affected. Usually exoslOses are multiple hard no_-,
demonstrate crease-like folds belween distina
The surface mucosa is firm. taul, and while 10 par
Tori and exostoses tend to increase Slowl} in
increasing age. but remain asymptomatic unless ""_-=~
Following a traumalic incidem. patients may be
about neoplasia and insist that the bony mass is ",....",,-,.
that it was not presem prior 10 the injury. RertlO\
ally unnecessary unless prompted by cosmetic.
tic. psychological. or traumatic considerations.
Osteomas are considered to be neoplaslic
are distinct from the developmemat lesions. ton
toses. because osteomas have more growlh ~
to be larger. and may be confined to soft tissue
with osteomas should be examined radiogra
multiple impacted supernumerary teeth. which
cate the presence of Gardner's syndrome (see p.
autosomal dominant condition is characlerized
mas, dermal CYSIS, mulliple impacled and su"""".
teeth, and intestinal polyposis with a high p
malignant transformalion. The majority of ..."".,
Gardner's syndrome will demonstT'dte malignaa:
by age 40: Iherefore aLI patients with this conma..
close medical management.

78

OULES

rs-1 Retrocuspld papill'" appeanng i'lS a pink

-,

-~-

" Iymphoepithellal cyst on the

-'"9"e

.....s..e mandibular tori.

_>-.. .

Exostoses apparent at the mucoglngrval

'T'..2\, Ia and mandible

Fig. 35-2. Unusual elefllng of.-. retrocuspid papilla.

Fig. 35-4. Pinkish nodule rn the IIoor of the mouth

rejJfesentlng a lymphoeplthelial cyst.

Fig. 35-6. MultInodular mandibular tori.

Fig. 35-8. Paletta! exostoses. fCOUrtesy Dr Tom

McDCMd)

79

NODULES
Irritation Fibroma and Peripheral Odontogenic Fibroma IFigs. 36-1 and 36-2) The irritation
fibroma is one of the most common benign lesions of the
oral cavity. It results from reactive hyperplasia caused by a
chronic irritant; thus this lesion is nOI a true neoplasm as
the term "fibroma" seems 10 imply. True neoplastic fibromas are a Tarc intraoral finding.
Typically the irritation fibroma appears as a welldefined, pale-pink. slow-growing papule that with time
enlarges to form a nodule. This smooth and symmetrically
round lesion is finn and painless to palpation. Infrequently
a leukoplakic, roughened, or ulcerated surface is present.
The base is usually sessile. This growth can arise on any
soft tissue location in the mouth, including buccal mucosa,
labial mucosa, gingiva, or tongue. Histologically an interlacing mass of dense collagenous tissue is found subjacent
to thinned epithelium. Fibromas are best treated by removing the source of the irritation together with surgical excision. Fibromas recur infrequently if treated properly.
Multiple intraoral fibromas may be associated with the condition tuberous sclerosis (Bourneville-Pringle's disease),
which is characterized by seizures, mental deficiency, and
sebaceous adenomas that are in fact fibromas.
The peripheral odontogenic fibroma is clinically similar
to the irritation fibroma, but is characterized by its unique
location and tissue of origin. In most cases the peripheral
fibroma is found as a circumscribed swelling in the region
of the interdental papilla, generally located anterior to the
molar teeth. A cup-like erosion of the underlying alveolar
bone may be radiographically evident. It probably arises
from cellular components of the periodontal ligament.
Microscopically, clusters of odontogenic epithelium among
dense collagenous tissue is found.

Lipoma (Figs. 36-3 and 36-4) The lipoma is a common dermal tumor, but a rare intraoral finding. This benign
neoplasm is composed of mature fat cells surrounded by a
thin, fibrous connective tissue wall. Adults over the age of
30 years are commonly affected, and no sexual predilection exists. Imraorally the lipoma appears as a well-circumscribed, smooth~surfaced, dome-shaped or diffusely elevated nodule that is yellow to pale pink in color. Occasionally
lipomas may be polypoid, pedunculated. or lobulated.
Lipomas are slow-growing submucosal nodules that
occur on the buccal mucosa, tongue, floor of the mouth.
alveolar fold. and lip. The palate is a rare site of involvement. Palpation reveals a soft. movable. and compressible
submucosal mass that has a slightly doughy consistency.
Therapy consists of surgical removal, which includes the
base of the lesion. Lipomas rarely recur.
Lipofibroma (Fig. 36-5) The lipofibroma is a rare
benign intraoral neoplasm of mixed connective tissue origin. Microscopically it is a well-demarcated submucosal

80

mass that consists of mature lipid~containing

significant fibrous connective tissue componenL
the appearance is a blend of a fibroma and Ii
generally found on labial and buccal mucosa. Oa
the lesion is non~indurated, movable, painless_
firm depending on the lipoid-to-collagen con
lesions are slow growing, but if left untreated
grow to several centimeters in diameter.

Traumatic Neuroma fAmputatlon Ne

{Fig. 36-61 The traumatic neuroma results fl"()d
plastic response to nerve damage following se\
large nerve fiber. Intraorally the traumatic ne~
quently encountered in the mandibular mucobucat
the region adjacent to the mental foramen. Other
include the area facial to the mandibular incison..
lingual to the retromolar pad. and the ventral { _
of the lesion depends upon both the degree of
degree of hyperplastic response.
Traumatic neuromas are usually very small
suring less than 0.5 em in diameter. Visualization ~
cult if the lesion is located deep below normal ant.
Neuromas are painful when palpated. Pressure "PI....
neuroma elicits a response often described as all shock." Multiple neuromas discovered on lips.
palate may indicate the possibility of multiple endl"".
plasia Type lib. Treaunent of the trawnatic neuroma
excison or intralesional injection with corticosteroids..
may further damage the nerve and lead to recurrence.
Neurofibroma {Figs. 36-7 and 36-81
proliferation of all the elements of a perip~
including the sheath of Schwann, results in the
tumor neurofibroma. They most commonly apper
pink nodules. Clinically neurofibromas may be
diffuse, or over \000 in number. Solitary nod~
More commonly, multiple large neurofibromas ~
tered, which are associated with neurofibro
Recklinghausen's disease).
Neurofibromatosis is an autosomal dominaJll
characterized by skin pigmentations (cafe-au-lail
axillary freckling) and multiple neurofibromas llR""'"
skin. oral cavity, bone, and gastrointestinal trna.. ~
nomonic sign of this disorder is Crowe's sign. wbdt
of more than 5 cafe-au-Iail spots and axillary ~
Intraoral neurofibromas may be located OIl the cbI:a.
buccal mucosa. tongue, and lips. Most soft tissue ..,""......
are asymptomatic; however, those arising within dec;amay produce pain and paresthesia. Diffuse ne"",fib"",'"
striking for their firmness and irregular nooular surfxr
results in physical defonnity. In some cases ~:::~
undergo sarcomatous change, necessitating close fl
tar)' neurofibromas not associated with von Rec"~",,,,,,,,,!!
disease have no tendency for malignant transformatil:a

..cOULES

iHge nodule; irritation fibroma.

Fig. 36-2. PInk Interdental papule; peripheral

odontogenic fibroma.

Lipoma arising at the junction of the hard

Ie (Courtesy Dr Dale Miles)

Fig. 36-4. Diffuse lipoma of the lateral margin of the

tongue.

.Jo..S. "~yeIIOW1Sh mass; lipofibroma.

:J Srgll Glass!

....,

::<!'e..:.u-Icll{ spots and neurofibromas; von

It!f'l S Qisease

Fig. 36-6. PInk traumatic neuroma (near midline)

and a wtutlsh papilloma ICounesy Of Jeny ClOffiJ

Fig. 36-8. Neurofibroma of the lateral margin of the

tongue.
81

PAPULONODULES
Papilloma (Squamous Papilloma) fFigs. 37-1
and 37-2) Papillomas are the most common benign
epithelial neoplasm of the oral cavity. They appear as
smalL pink-white. exophytic masses that are usually less
than 1 em in diameter. The surface of the papule may be
smooth. pink. and pebbly. or have numerous small fingerlike projections. The base is pedunculated and well-circumscribed. Intraoral lesions are Iypically soft. whereas
those on exposed areas of the lips arc usually rough and
scaly. Solitary lesions are the general finding, bul multiple
lesions are occasionally seen. A viral etiology is probable
with a recent study implicating human papilloma virus
(HPV) Types 6 and 1 J in 35% of the squamous papillomas
examined. Because the papilloma is slow growing, any
rapidly advancing papillomatous lesion should be suspected to be a more aggressive lesion.
The mean age of occurrence of the papilloma is 35
years and more cases have been documented in males than
in females. The most common location is the uvulo
palatal complex, followed by the tongue and frenum, lips,
buccal mucosa, and gingiva. Other HPV-induced lesions
such as the condyloma acuminatum, focal epithelial
hyperplasia (Heck's disease). and verruca vulgaris share
similar clinical features, but are microscopically distinct.
Treatmem is complete excision, including the base.
Recurrence is rare. There have been no documented cases
of malignant transformation.
Verruca Vulgaris (Figs, 37-3 and 37-41 Verruca
vulgaris is a common skin growth that seldom occurs
intraorally. The etiologic agent is a papilloma virus,
Virally induced cellular changes result in the characteristic
clinical findings. Typically the lesional surface is rough
and raised with white finger-like projections. The white
ness of imraoral verrucae varies depending on the amount
of surface keratinization. Pink areas are not unusual at the
lesional base.
Verrucae are commonly located on the skin, vermilion
border. labial and buccal mucosa, tongue, and attached gin
giva. The base of the lesion is broad, but the size is usually
less than I em. Clinically a verruca may appear identical to
a papilloma, although the clefts are more shallow and the
mass more sessile, Viral inclusion bodies are frequently
seen histOlogically, Individuals with skin verrucae are
more likely to have oral lesions as a result of autoinocula
tion. Occasionally a lesion may regress spomaneously. If
not. treatment is complete excision or ablation with a car
bon dioxide laser,

82

Condyloma Acuminatum fVenere.ili

fFigs. 37-5 and 37-61 The condyloma acum_ _
transmissible papillomatous growth that may I
to the papilloma or fibroma, except for several
ing features. The oral condyloma occurs much
quently than the papilloma. It is seen more c
sexually active individuals and is much more
multiple. The warm, moist. intertriginous ~
anogenital sk.in and mucosa are frequent sites of _
Condyloma acuminata are usually multiple.
colored pink to dirty gray. The surface may be
more often pebbly and resembles a cauliflower. 1ksessile and the borders are raised and rounded.
spread may occur among the host and sexual ....."'.
When multiple lesions are present. proliferation ai
condylomas can form extensive clusters that ma~
a single mass. Any oral mucosal surface rna) be
but the labial mucosa is the most common site
logically condylomata exhibit parakeratosis. CTypIX
ination of comified cells, and koilocytosis. (her
condyloma acuminala have HPV Types 6 and 11
sent in the epithelium. Treatment of choice is ...
sion, since these lesions have a high rate of =.".,,=~
Occasional oncogenic transformation of longgrowths has been reported.
Lymphangioma (Figs. 377 and 37-8) L_
giomas are benign tumors of lymphatic channeJJi u.
op early in life with no sexual predilection. The)
on skin or mucous membrane. The oral cavity is ~
site. The most common intraoral sile is the dorsal
a1 surface of the anlerior portion of the tongue. f;
the lips and labial mucosa.
Small superficial lymphangiomas have irregtbIF
lary projections that resemble a papilloma. Tk.
and compressible, and vary in color from normal.
whitish. slightly translucent. or blue. DeepseatM
cause diffuse enlargement and stretching of me
mucosa. Macroglossia. macrocheilia. and cystic
are clinical deformities resulting from the diff~
Aspiration or diascopy is mandatory prior 10
excision of a lymphangioma to pre\'ent compLic
ciated with the similar-appearing hemangioma.
with a large, diffuse lesion often require hopltal .
monitor post-operative edema and possible air"..~
tion. Lymphangiomas do not undergo malignant
Some lymphangiomas. especially congenital types..
spontaneously during childhood.

;00.

"V'ULONODULES

unculClwd p.nk papilloma on the soft

-esy Dr (urt lundC'ffi)

Sh papilloma WIth surface proJe(fJons

"'-e ,Courtesy Dr Tom .\llcD.3vJd1

lOU""r condyloma acuminata on ventral

fig. 37-2. Firm whitish verruca vUlgaris.

Fig. 31-4. Mulllp'e verrucae vulgaris at commssure

o"he bps

Fig. 37-6. MUlliple gray.sh-p,/lt( condyloma

acuminata.

Fig. 37-8. Papulonodular surface of a Iymphagioma

of the lip In the SClme patlent.?ls In FIg 37-]

83

VESICULOBULLOUS LESIONS
Primary Herpetic Gingivostomatitis (Figs. 38-'
through 38-31 Herpes simple~ virus (HSV) Types I and
2 belong to the family Herpesviridae. which also includes

cytomegalovirus. varicella zoster virus. and Epstein-Barr

and the recently discovered human herpes virus VI. These
viruses are ubiquitous in nalUre and infect a wide variety of
animal speeies.
Approximately 80 to 90% of the adult human population
have been infected with HSV. Viral transmission occurs by
direct mucocutaneous contact of infected secretions, resulting in over half of a million cases of primary herpetic gingivostomatitis annually in the United States. HSY-l is the
causative organism in the majority of cases: however, Type

2 herpes virus. which has a propensity 10 infect the skin

below the waist. can cause herpetic gingivostomatitis by
oral-genital or oral-oral contactTIle manifestations of the primary infection may be trivial or fulminating. Trivial infections may produce subclinical signs of infection that often go unrecognized, or flulike symptoms. The initial infection of herpetic gingivostomatitis primarily affects children under the age of 10,
and secondarily young adults aged 15to 25 years.
The acute inflammatory response of the primary infection of
HSV usually follows a 3- to lO-day incubation period. The
infected individual will complain of fever, malaise, and irritability. Initially. focal areas of the marginal gingiva become fiery
red and edematous. The swollen interdental papillae bleed after
minUIe ttawna because of capillary fragility and increased permeability. Widespread inflammation of the marginal and
attached gingiva develops. and small clusters of vesicles rapidly
crupi throughout the mouth. The vesicles burst. fonning yellowish ulcers that are individually circumscribed by a red-halo.
Coalescence of adjacemlesions forms large ulcers of the buccal
mucosa. labial mucosa. gingiva, palate. tongue. and lips.
Shallow erosions of the perioral skin may be apparent.
Hemorrhagic crusts of the lips are characteristic. Headache.
lymphadenopalhy, and pharyngitis are usually present.
A significant problem in patients with primary herpetic
gingivostomatitis is the pain caused by the mouth ulcers.
Mastication and deglutition may be impared. resulting in
dehydration and subsequent elevation of temperature. Vrral
culluring. serum antibodies. and cytology are confirmatory.
Treatment is supportive and should include acyclovir in
severe cases.
Primary herpetic gingivostomatitis is a contagious disease
that usually regresses spontaneously within 12 10 20 days wilhout scarring. Complications associated with the primary infection include auto-inoculation of other epidennal sites. producing keratoconjunctivitis and herpetic whitlow: extensive epidermal infection in the atopic individual, which is tenned
Kaposi's varicelliform eruption; meningitis. encephalitis. and
disseminated infections in immunosuppressed patients.
Immunity to HSV is relative. and patients previously infected
with the virus may be reinfected with a different strain of HSV.

84

Recurrent Herpes Simplex fFigs. 38-4 :.,...,....~

38-7) Following the initial infection. HSV inti
nerve fibers. migrates to a regional neuronal _
becomes stably associated with the nucleus oftilr
cell in a latem and undetectable manner. Re
virus. replication of progeny panicles. and c renee occurs in approximately 40% of persons
the latent virus. Recrudescence is dependent on Or
immune mechanisms to eliminate reactivated H5'
rences are often precipitated by a triggering eH.
sunlight. heat. stress. trauma, or immunosup~
Recurrent herpes simplex (RHS) tends to P'<""'~
ters of vesicles that ulcerate. The vesicles repeated:
op at the same site following the distribution of
ed nerve. Recurrences on the vermilion bo~
(recurrent herpes labial is) are clinically more "'
"".
intraoral recurrences (recurrent herpetic st"" -"
lesions of recurrent herpes labialis are chara~
appearance of small clusters of vesicles that
lesce. and form slightly depressed. yello.... Ihat have distinct red halos. Spread to perioral
mono especially if greasy lip ointments are used
horizontal weeping of vesicular fluid. Contact
fluid with other epidennal structures can result in
ulation of the eye (keratoconjunctivitis). finger
whitlow). or genitalia (genila.! herpes). In relati\
persons, recurrent herpetic stomatitis is
periosteal-bound. keratinized mucosa cons
attached gingiva and hard palate. Recurrences
cal mucosa and tongue are infrequent. unless tbr: _ _;:.
immunosuppressed.
Most patients with RHS complain of pam
some individuals experience lillie discomfon.
neurogenic symptoms such as tingling. throl,.._:
burning often precede the eruption of lesions b) :Sunscreens are effective in the prevention of ':~~:~
Management also includes lysine, vitamin C. UId
drugs (acyclovir) in the immunosuppressed.

Herpangina (Fig. 38-8) Herpangina is a

infection involving the oral cavity. caused
Coxsack.ie viruses. This infection is seen maiDI
dren during the warmer months of summer......
contagious. Young adults are occasionally affecei
pangina produces light-gray papillary vesicles ..~ ,.....
to form multiple. discrete, shallow ulcers. 1lIC" :::.~~
an erythematous border and are limited to me .a
lars of the fauces, soft palate. uvula. and thtDiffuse pharyngeal erythema. dysphagia. and.
are common features, as are fever, malaise, head:&..
phadenitis, abdominal pain. and vomiting_
rarely occur. Treatment is palliative and spon,""",".
ing occurs within I to 2 weeks.

eo.

::5ICULOBULLOUS LESIONS

_";:~-~-'~_S:'W5!1ng lips, primary herpetic gingivo-

- 3. Prlm",y Infection of herpes simplex

typl!' I oreducing pcllnful gingIVitiS

Fig. 382. Multiple broken-down herpetic vesicles

with red halos, same patient as in Fig. 38-1,

Fig. 38-4. Viru.s-Idden vesICles of rec:urrent herpes

labla"s. (Courresy Dr James (ortonej

; Recurrent herpes simplex of the palate

Fig. 38-6. Patlefll In Fig 38-5 twO days later WIth

broken down herpetic vesicles.

] Herpetic whitlow. (COUrtesy Dr lmda

Fig. 38-8. Erythematous soft palate witn multiple

veSICles; herpangina. (Courtesy Dr Charles Morns)

85

VESICULOBULLOUS LESIONS
Varicella fChlckenpox) (Figs. 391 and 39-21
Varicella and herpes zoster are caused by the same herpetic
virus. varicella lOSler. Varicella is the highly contagious
primary infection. whereas herpes zoster is the recurrent
neurodermal infection. Typically. young children become
infected with the. virus during the latc winter and spring
months. Following exposure to the virus and a 2 to 3 week
incubation period. mild prodromal features appear.
Fever, malaise. and a distinctive red rash on the trunk are
the first recognizable signs of Ihis disease. The pruritic rash
quickly spreads to the neck. face and extremities, and is followed shonly by the eruption of papules that form vesicles
and puslUles. Individual vesicles burst, producing a "dew
drop on a rose petiLr' appearance. The first and largest skin
lesion is called the "herald spot:' It is often located on the
face and. if scratched. may heal with scarring.
Intraoral lesions of varicella are few and often go unnoticed. They appear as vesicular lesions that break down and
form ulcers with an erythematous halo. The soft palate is
the predominant site. followed by the buccal mucosa and
mucobuccal fold. Anorexia. chills, fever. nasopharyngitis.
and musculoskeletal aches may accompany the course of
the disease. Complications are infrequent. and vesicles
eventually cruSI over and resolve sponlaJleously within 7 10
10 days. Infection during pregnancy poses a significant risk
to the fctus.

Herpes Zoster fShingles, fFigs. 393 and 39-4)

Herpes zOSler is the recurrent infection of chickenpox.
Unknown factors result in reactivation of dormant varicella
virus from sensory ganglia and migration of virus along the
affected sensory nerves. Viral recrudescence usually
affeclS older adulls past age 50, but may be seen in young
adulls or children. Prior to eruption. prodromal signs of
itching, tingling, burning, pain. or paresthesia occur.
Lesions are characterized by acutely painful vesicular
eruptions of the skin and mucosa that are unilaterally dis
tributed along nerve pathways and stop abruptly at the
midline. Two areas are affected the most: the trunk
between venebras T3 and L2. and the face along the ophthalmic division of the trigeminal nerve.
Cutaneous lesions of shingles begin as erythematous
mncules that are followed by vesicular and pustular eruptions. Crust formation occurs within 7 to 10 days and persists for several weeks. Pain is intense. but usually dissipates when the cruSls fall off.
The imraoral lesions are vesicular and ulcerative with an

86

imense red. inflammatory border. A

hemotl~

nem is common. The lips. tongue. and bocc:aI::~:~::

have unilateral ulcerative lesions if the n
of the trigeminal nerve is affected. Invohe~
ond division of the trigeminal nerve typical]) po"'o=",.
lateral palatal ulcerations that extend up to tu
the palatal raphe. Considerable malaise. fe\er.
accompany herpes zoster. PatieniS often
inlense pain I to 2 days before the viral \"esi~
Herpes zoster usually heals withoul scar~.~~~
within about 3 weeks, but many patienls rna.
persistem pain after Ihe lesions have faded.
called "poslherpelic neuralgia:' may continue f .~~:
10 a year before regressing. It is resistant 10 . . . t
therapy. Patients who are immunosuppressed ae:
larly susceptible to shingles and have a hip - : : :
rate. In the past the rare occurrence of bilat ..
was termed "the death sign" because tho.:
inevitably died. Varicella ZOSler virus infeCtl"~OD::'_.~::
ally associated with the Ramsay Hunt S) n
zoster. unilateral facial paralysis. and ear e
Reye's syndrome (high fever. cerebral edema..
eration. high monalilY. and salicylate use).

HandFootandMouth

Disease (Figs.
through 39-8) Handfoot-and-mouth dise~
contagious disease caused by a number of COl"'....
B viruses. It usually affects children. but ma~
young adults. It typically occurs in spring andh_.,
the name implies, il produces small ulcerath"e:;:::~~
mouth logether with an erythematous and \ a
the dorsal and ventral surface of the hands, fi
soles of the feet. Muhiple pinpoint vesicles
crust are characterislic. There may be several to
100 pinpoint lesions wilh distinctive erylhe~
Oral lesions of handfootand-mouth diseue~' m.
tered mainly on the tongue. hard palate. and
labial mucosa. In time they coalesce to form la::areas. The oropharynx is usually unaffected- -..
number of intraoral lesions is usually less than
a common symptom. along with elevated 1
malaise. and lymphadenopathy. The diag
made by viral culture and serum antibody sllJl:hls..
er. the classic distribulion of lesions on lhe
hands, soles of feet, and oral mucosa is diagnoso,;:
instances. Healing occurs regardless of lR_-=~
approximately 10 days.

thal7:::

CULOBULLOUS LESIONS

Fig. 39-2. Intraoral vesICle of chickenpox

.... ]

-:eral erup!lon of herpes :zoster along

'r branch of lhe trigeminal nerve

_..., S ~
ill pinpoint lesion of hand-foot-andQueue n a young adult. {Courtesy Drs Birgit

_ , Handfoot-andmouth disease of the

(C).Jrtesy Drs BIrgIt & Tom Glass!

Fig. 39-4. pC! nfulln(raord' 1e<.lOns of pa{l(>nt in Fig 39-3

w,rh herpes zoster

Fig. 39-6. Erythematous border surrounding an ulcer;

hand-footandmouth disease. (Courtesy Drs Birgit
& Tom Glass)

Fig. 39-8. Paontut clusters of vesICles of hand-foot-

and-mouth disease, same priltlent.n 8gs. 39-5

through 39-8 (Courtesy Drs Blrgll & Tom GlasS)

87

VESICULOBULLOUS LESIONS
Allergic Reactions (Figs. 40-' through 40-81
Allergy is 3 condition of hypersensitivity 10 certain malerials
acquired by repeated exposure 10 an allergen.
Hypersensitivity reactions usually produce inappropriate tissue damage as a result of antigen-antibody reactions
(increase in antigenic stimuli or a heightened inunune stale).
M.anifesl31ions of allergy may be generalized or localized.
and may occur at any age. A genetic predisposition 10 allergy and persistenl sensitivity are common features.
Hypersensitivity reactions have been classified imo several types according to the following faclors: the speed
with which the symptoms occur (immediate or delayed);
clinical appearance; and cellular and (issue response (Type
I - IgE-medialed immediate hypersensitivity, Type II antibody-dependent cytolOxic hypersensitivity. Type 1II complex-mediated hypersensitivity. Type IV - cell-mediated. or delayed hypersensitivity. and Type V - stimulatory
hypersensitivity). Those of clinical significance to the dentist include immediate hypersensitivity Type I reactions
(anaphylaclic shock. urticaria. angioneurotic edema. allergic stomatitis) and delayed hypersensitivity Type IV reaclion (contact allergy).
Immediate allergic responses such as anaphylaxis are
histamine-mediated and occur within minutes of exposure
to antigens. When the condition is localized to superficial
blood vessels. IgE-mediated histamine release results in
vasodilation. increased capillary permeability, tissue
swelling. and pruritis. Typically. individual wheals. also
known as urticaria or 'hives". arise following the ingestion
of cenain foods such as shellfish. citrus fruits. chocolate,
or systemically administered drugs.
Angioedema is a hypersensitivity reaction characterized by the accumulation of serum within tissues, brought
about by histamine-mediated vasodilation. Hereditary and
acquired fonns exist. with the fonner more serious because
of possible visceral involvement.
Swelling is the most prominent feature of angioedema.
It appears rapidly and lasts for 24 to 36 hours. Sensations
of warmth. tenseness, and itchiness are concurrent. The
perioral and periorbital tissues are commonly affected.
Angioedema is often recurrent and unpredictable. If an
allergen can be identified, withdrawal of the agent and
administration of antihistamines is recommended.
Allergic stomatitis, also tenned "allergic mucositis:' is
an oral Type 1 hypersensitivity reaction to a systemically
administered drug or food. l1le oral manifestations of drugrelated eruptions are varied and may be clinically similar to
erythema multiforme, lichen planus. Of lupus erythematosus.
Intraorally a dry, glistening. red area is usually apparent.
Focal white areas may be adjacent. TIle fonnation of multiple
vesicles that desquamate and produce fibrin--covered ulcers
eventually results. An erythematous. inflammatory border
and a painful. burning sensation are common. The response

88

may be limited to the buccal mucosa, gingiva.. li~ 01

or may involve the entire oral cavily. Conc~ .....
lesions are possible. Treatment requires witlJdra,
allergen and administration of antihistamines.
Generalized anaphylaxis is an immediatt
hypersensitivity reaction that can be lifetlm~
laryngeal tissues are involved. It results fro"m:.;_;,::~~
antibody interaction that produces mast cell <:
and the release of vasoactive amines and medi
histamine. In fulminant cases, a generalized m=..., .
vascular penneability and smooth muscle con~
es urticaria. dyspnea. hypotension. laryngeal ~::.:
vascular collapse. Mild localized immediate h)l
ity reactions are treated with antihistamines.
epinephrine is required to effectively manage 5e'u:"
ali zed anaphylactic reactions. Treatment sh
include the elimination of the allergen.
Delayed hypersensitivity (Type IV) is a res
immune system to a locally or systemicall~
allergen thai usually develops slowly and reachei
mum size 24 to 48 hours after antigenic r
Topically applied allergens such as latex glo\1:5
cal disinfectants may produce a delayed hy~
response evident as itchy, erythematous skin tes.a
lact dermatitis) that eventually become inflamed
ated at the site of contact.
Another form of delayed hypersensitivit) ISo
stomatitis (stomatitis venenata). which may ocxw
intraoral mucosal site. It characteristically produc:es
rna at the site of contact with the topical
Reactions 10 lipstick or sunscreen preparations
the lips to appear red, swollen. fissured. or drl.
sation of burning may be present.
The gingiva can also show signs of delayed
tivity. Plasma cell gingivitis produces diffusel) ......''''~
and fiery red gingiva because of the flavoring
in some toothpastes and chewing gums. Often die ...,"'~
commissures are involved. resulting in cheilitis.
Antiseptics. antibiotic lozenges, topical "''''...~
eugenol preparalions. and mouthwashes may produ.;l..
lar burning lesions. These appear on the alveolar _""'_
dorsum of the tongue. or palate as erythemalous
are covered by a gray-white pseudomembrane.
restorations and partial denture frameworks 11m _
heavy metals such as coball, mercury. nickel. oralso induce delayed hypersensitivity reactio&..
mucosa adjacent 10 the restored area. Usuall~ cz:
red and ulcerated. and bums. Allergy to the ff:=~:~";
in dentures. once thought 10 be a common 0
now known to be rare.
Immediate localized hypersensitivity is m,,,,,,!,ol,,,,t
antihistamines, whereas delayed hypersensiti\
treated with corticosteroids.

",_""""Z

.'ESICULOBULLOUS LESIONS

-~I

~ 'leal
r

on the cheek Immediately following

of Chinese food: Type I

~sitivity.

{Courtesy Dr Michele Saunders)

Fig. 40-2. Lichenoid drug-eruption. Ulcerations

resolved following discontinuation of thlClllde therapy.

...;..3 S-ee-song-Induced palatal erythema, Type IV

sensitivity. (Courtesy Dr Carson Mader)

Fig. 40-4. Fingers of a dental ",ssistant with contact

dermatitis; 'TYpe IV hypersensitivity.

.....:-5 ,.. :er':l!<ve hypersensitivity IType II

Fig. 40-6. An erythematous reacrion to benzocaine:

Sit

,:,,-"nICI iln.

.....;_"! - ~ nflammed atl<lched gingiva of plasma

-JP!!'9.ivitis. ICourtesy Dr Steve Bricker)

contact stomatitis.

Fig. 40-8. Contact stomatitis to nickel In the

adjelCent GIst alloy

89

VESICULOBUUOUS LESIONS
Erythema Multiforme fFigs. 41-' through 41-4)
Erythema multiforme is a self-limiting disease of the skin
and mucous membranes. [\ commonly affects young
adults, particularly males, bUI may affect children and the
elderly as well. Low-grade fever, malaise. and headache
typically precede the emergence of lesions by 3 to 7 days.
Erythema multiforme has an unknown etiology; however, recent evidence suggest thai circulating immune complexes that provoke complement-mediated cytopathic
effects, combined with lymphocytic and neutrophilic stimulated vascular injury. may playa pathogenic role.
Precipitating factors include bacterial, fungal. and viral
infections such as herpes simplex and Mycoplasma pneumoniae. emotional stress, and allergy, especially to sulfaand barbiturate-containing drugs. In about 50% of the
cases no causative factor has been identified.
Although there is great variation in the clinical appearance of the disease. as the name "multiforme" suggests,
stomatitis and cutaneous lesions are the most prominent
features. The hallmarks of this disease are the red-white.
concentric, ring-like macules tenned "target," "bulls-eye."
or "iris" lesions that rapidly appear on the extensor surfaces of the anns and legs, knees, and palms of the hands.
The trunk of the body is classically exempt from lesions,
except in the most severe cases.
Initially the skin lesions are small, red, circular macules
that vary in size from 0.5 to 2.0 cm in diameter. Then the
macules enlarge and develop a pale white or central clear
area. Shortly thereafter the lesions fonn vesicles and bul~
lae. The vesicles may go unnoticed until they rupture and
become confluent. The ulcers fonned are large, raw. and
shallow, with an erythematous border. A necrotic slough
and a fibrinous pseudomembrane typically cover the
ulcers. Urticarial plaques that do not break down may also
be present.
Imraorally, red macular areas, multiple ulcerations, and
erosions with a gray-white fibrinous surface may be seen.
They are limited to the buccal mucosa, labial mucosa.
palate. or tongue. or involve all of those areas. Rarely is
the gingiva involved. Dark. red-brown, hemorrhagic crusts
are characteristically present on the lips, which aids in
making the diagnosis. Lesions are usually short-lived and
last about 2 weeks. Erythema multifonne rarely persists for
more than I month. Oral lesions without cutaneous lesions

90

have been reported. Recurrent and chronic fonns

Pain is the most common symptom. which rTU~
fere with normal oral activity. Oral hygiene
neglected, resulting in secondary bacterial ini
Treatment consists of topical palliative rinses and..
instances. low dose systemic steroids. CampI"
resulting from erythema multifonne are uncomnx.
the disease progresses to its major fonn, Stevenssyndrome.

Stevens-Johnson Syndrome {Figs. 415 th~..

41-81 The severe fonn or major variant of erythema
fonne is tenned "Stevens-Johnson syndrome," named
two investigators who firs! described the clinical ~:a::
of the disease in the early 19205. It frequently affecu
and young adults, predominantly males. The oral
Stevens-Johnson syndrome are similar to those of"'.....
multiforme, but there is more widespread invohcutaneous and stomatologic structures, together ... constitutional signs including fever, malaise. "'. . .
cough. chest pain. diarrhea. vomiting, and arthralgia..
The classic clinical triad of Stevens-Johnson ~
consists of eye lesions (conjunctivitis). genital lesKa
anitis. vulvovaginitis), and stomatitis. In addition
the characteristic target skin lesions on the face,
abdomen that later develop into painful "weepinglobullous lesions.
Like erythema multifonne, the gingiva is less
affected by desquamating bullae than the non-k.~
mucosa. Extensive ulcerative and hemorrhagic lesm.
lips and denuded areas of oral mucosa are imense:1);
and usually prevent affected patients from eating . .
lowing. Inadequate nutritional intake, dehydration.
itation are common sequelae that necessitate hospiiw......
Significant morbidity and mortality may oc
portive therapy is not provided. Treatment consists
venous fluid and nutritional therapy, short-tenn ..
steroids. and palliation consisting of oral anestheDc
agents that coat and protect the lesions. and
mouthwashes. Secondary infection is managed wi.s
oties. the ensuing fever with fluids and amipyrebO'
condition has a longer duration than erythema m
but usually resolves within 6 weeks. Fatalities ta..
documented in sulfa-induced Stevens-Johnson S)nd_.

00_.

::5ICULOBULLOUS LESIONS

-~rge(
~ Tom

>1.

lesion; erythema multiforme.

McDavldj

-1.13 ...w : pie erythematous ulcers on the d(l(sum

"i-.

.&

Fig. 41-2. Ulcerated lips. erythema multlforme.

(Courtesy Dr John McDowell)

Fig. 41-4. Ulcers of erythema multlforme on ventral

..-.g...e erythema multlforme. (Courtesy Dr

tongue. same patient In Figs 4' -2 through 4 r-4

::x".,\rell)

(Courtesy Or John McDowell)

1-5. Stevens-Johnson syndrome. (Courtesy

'cDavld)

, T-7 severe conJunctMtrs and weeping SIon

Stevens.Johnson syndrome.

Fig. 41-6. Extensive palatal ulcerations of StevensJohnson syndrome In.si'lme pallent as In Fig 41-5

/Courtesy Dr Tom McDavldl

Fig. 41-8. He'TlOlTaglC and crusted lips of chid seen In

Fig 41-7 Who has Steven.s-Johnson syndrome.

91

VESICULOBUUOUS LESIONS
Pemphigus Vulgar;s jFigs. 42-1 through 42-41
Pemphigus is a pOieniially falal. vesiculobullous disease
which has been categorized into four types: \'ulgaris and
\'egetans. which have inlr30ral manifestations. and foliaceous and er:,.thematosus, which are nOI believed to produce oral disease. The most imponant aspect of this condition is early recognition of the oral lesions. which usually
precede skin involvement by several months. In fact. or"l.I
lesions may be the only manifestation of the disease.
Diagnosis during the early stages greatly enhances the initiation of conicosleroid and immunosup'pressive therapy
and. therefore. the long-tenn prognosis.
Vulgaris. the mosl common type of inlraoral pemphigus.
usu311y develops between the ages of 30 and 50. It may be
seen in younger or older patients. but rarely does it develop
in patients beyond 60 years. It is seen with equal frequency
in males and females and is usually encountered in lightpigmented patients of Jewish or Mediterranean origin. Pemphigus vulgaris is probably an autoimmune disorder involving a reaction of IgG to an intercellular subtance. resulling
in epithelial cell-to-cell separation. ACUie and chronic fonns
exist. Ihe slow chronic fonn being the most common.
The most prominent clinical fealUTt of pemphigus is the
rapid development of mulliple bullae that tend to rupture
and leave erosions of the skin and oral mucous membranes. When there is syslemic involvement. severe debilitation may resull in death. Early mucocutaneous lesions
consist of "weeping" bullae or gelatinous plaques that are
clear and shimmering. TIle bullae are extremely fragile and
rapidly disintegrale. hemoJfhage, and crust. They tend to
recur in the same area and later spread 10 adjaceOl regions.
Light lateral pressure applied to a bulla will cause it to
enlarge by extension (Nikolsky's sign). A characteristic
and consistent finding is the appearance of a whitish superficial covering. which is the roof of a collapsed bulla Ihat
can easily be stripped away. Cases that show predominantly desquamative areas that affect the gingiva have been
clinically tenned "desquamative gingivitis."
Pemphigus may appear as an epithelial slough with
white tissue folds. an aphthous or traumatic ulcer or. in circumslances in\'olving multiple areas of the lips, buccal
mucosa. tongue. gingiva. palate. and oropharynx, the condition may resemble erythema multifonne. Individual lesions
orten have circular or serpiginous borders. whereas extensive erosions of the buccal mucosa are red and raw. and
have diffuse irregular borders. Frequent eruptions may be
superimposed over healing lesions so that periods of remission are absent. The longue is less commonly involved than
the lips, buccal mucosa. and gingiva. Thick hemorrhagic
cruSts and fetor oris are characteristic of extensive lesions.
Patients wilh pemphigus are often dislUrbed by the severe
pain associated with the condition.
The diagnosis of pemphigus is confinned by a positive

92

Nikolsky's sign. biopsy. and immunofluorescent

techniques. Prior to steroid therapy, dehydration
ticemia were fatal complications of pemphigus.

Benign
Mucous
Membrane
ICica
Pemphigoid and Bullous Pemphigoid (FIgSthrough 42-8) Pemphigoid is a chronic. self-I
mucocutaneous disease that is slightly more commor
oral cavity than pemphigus. but is associated with
morbidity and mortality. Two types that produce
oral lesions may be seen in the mouth: benign mucc:..
brane pemphigoid and bullous pemphigoid.
Bullous pemphigoid. which is the least com~
two. affects both the skin and the oral cavity. and
sexual or racial predisposition. Skin folds locate<!
axilla. inguinal. and abdominal regions are c
affected. The second type. benign mucous membnmr
phigoid (BMMP). also termed "cicatricial," is Ii
the mucous membranes. favoring the ocular and ora.
branes. This disease occurs twice as frequentl) in
than men usually after the age of 50. Occasionall)
persons are affected. There is no racial predilection.
Pemphigoid skin lesions usually precede oral
tend to be desquamative and localized, and heal
neously. The lips are rarely affected. Intraoral
usually small tense blebs that are yellow or hemor"
They fonn slowly and tend to favor the palate. gin_,
buccal mucosa. Because bullae of pemphigoid
a subepithelial separation. they are thicker-"alla:..
fragile. and longer-lasting than those of pemp
some instances patients may ha\'e bullae that pen
several days before rupture. and it is this intactoe'\
suggests the diagnosis of pemphigoid. Large.
ulcers can result from coalescence of several
lesions. The ulcers are surrounded by an er)
ring, exhibit a symmetrical pattern, and occasion
When the condition is limited 10 the gingi\'a.
occurs frequently, the clinical tenn "desquamative :
tis" has been used to describe the bright. red, bu
denuded gingiva. "Desquamative gingivitis" is a
live tenn and may represent several clinically si
ditions such as erosive lichen planus. pemphig
pemphigus for which a diagnosis is not yet obtained.
BMMP may affect the anal. vaginal. and
mucosa. but the most severe complication of B
ocular involvement producing conjunctivitis.
bullae. clouding of the cornea. and fibrous ",...,1IlI
Blindness is a serious sequela of protracted eye
Although pemphigoid is rarely fatal. close f<
suggested for progressive cases. since carcinom..
rectum and uterus have been associated with this
Modemte doses of corticosteroids alone. or in
with immunosuppressive agents such as azathiopna..
provided effective management.

ph..,..

'UICULOBULLOUS LESIONS

,
&2-1. T'oung child with extensive erosions of
_ .....,;,gus vulgaris.

tJ-). SuperfICIal clear bullae of ~mphigus

Courtesy Drs Tom McDavId and Martrn Tyterl

Fig. 42-2. up involvement of child In Fig 42-1 with

pemphigus vUlgaris.

Fig. 42-4. Ruptured and herr\o(rhagic bullae; ~mphJ

gus vUlgaris. (Courtesy Drs Tom McDavid and Martin
Tyler)

.oLI-S :JesquamativegIf'lQMtis"; benign mucous

_ _"',ne pemphigoid.

Fig. 42-6. DesquamatIVe 911lQival patCheS of benign

mucous membrane pemphigoid.

..._'~lu-7., O'sltys sign suggestive of benign

embrane pemphigoid; same patient In

Fig. 42-8. Corneal scarring; benign mucous

membrane pemphigoid.

,~

-rough 42-7

93

,
ULCERATIVE LESIONS
Traumatic Ulcer jFigs. 43-1 through 43-31 Recurrent oral ulceration is a common condition resulting from
several etiologies. trauma being the most common cause.
Ulcers may occur at any age and in either sex. Likely locations for traumatic ulcers arc the labial mucosa. buccal
mucosa. palate, and peripheral borders of the tongue.

Tmumatic ulcers may result from chemicals, heal. electricity. or mechanical force, and are often classified according to the
exact nature of the insult. Pressure from an ill-fitting denture
base or flange, or from a partial denture fmmework:. is a source
of a decubitous or pressure ulcer. Trophic, or ischemic ulcers.
occur particularly on the palate at the site of a previous injection. Dental injections have also been implicated in the traumatic ukemtions seen on the lower lip by children who chew their
lip after dental apJXlintments. In addition to faClitial injury,
young children and infants are prone to traumatic ulcers of the
soft palate from thumb sucking, called Bednar's aphthae.
Ulcers may be precipitated by contact with a fractured
tooth, a partial denture clasp. or inadvertent biting of the
mucosa. A bum from food or drinks that are too hot commonly occurs on the palate. Other traumatic ulcers are
caused by factitial injury from inappropriate use of fingernails on the oral mucosa. The diagnosis of these conditions
is simple and is often obtained from a careful history and
examination of the physical findings.
The appearance of a mechanically induced traumatic ulcer
varies according to the intensity and size of the agent. The
ulcer usually appears slightly depressed and oval in shape.
Initially an erythematous zone is found at the periphery,
which progressively lightens because of the keratinization
process. The center of the ulcer is usually yellow-gray.
Chemically dam<:tged mucosa. such as that with an aspirin
burn. is less well-defined and contains a loosely adherent.
coagulated surface slough. Following removal of the traumatic influence, the ulcer should heal within 2 weeks. if not
other causes should be suspected and a biopsy perfonned.
Recurrent Aphthous Stomatitis IMinor Aphthae,
Aphthous Ulcer) /Figs. 43-4 through 43-61
Recurrent aphthous stomatitis (RAS) is classified into three
categories according to size: minor aphthae, major aphthae,
and herpetifonn ulcers. Approximately 20% of the JXlpulation
is afflicted with minor aphthae, or "canker sores" as they are
commonly referred to by patient~. They may be seen in anyone, but females and young adults are slightly more susceptible. Familial patterns have been demonstrated and persons
who smoke are less frequently affected than non-smokers.
Factors that precipitate aphthae include atopy. trauma.
endocrinopathies, menstruation. nuuitional deficiences, stress,
and food allergies. Although the etiology is unknown, current
studies suggest an immunopathic process involving ceIl-mediated cytolytic activity in response to HLA or foreign antigens.
The L-fonn of streptococcus has been suggested to playa
causal role in the fonnation of aphthous ulceration.
94

Minor aphthous ulcers have a propensi~ t

mucosa that is situated over minor salivary gland
labial and buccal mucosa are frequently affec1l:lw..
ulcers arc rarely seen on heavily keratinized : : : :
the gingiva and hard palate. Occasionally. prod"
toms of paresthesia or hyperesthesia arc reponed
Minor aphthae appear as shallow, )eIlO'l\-,..
ulcers usually about 2 to 5 mm in diameter_ :\ -.,._
et)thematous border surrounds the fibrinous P'~-="'"
brane. No vesicle foonation is seen in this di~
tive diagnostic feature. Ulcers that occur
mucobuccal fold often appear more elongated..
Burning is a preliminary complaint that is
intense pain of a few days' duration. Tender
lar. anterior cervical. and parotid nodes are OI1et
particularly when the ulcer becomes secon~ :~;;~
Aphthae are invariably. recurrent. and the
occurrence varies. Most persons exhibit singk
or twice a year. beginning during childhood
cence. Occasionally the ulcers appear in crops.
less than five occur at one time. Patients Voulcers may have periods of several months I
ulcers are constant. Persistent ulceration!'
extremely painful and usually have a ragged
More extreme measures may be required 10
treat those patients. Minor aphthous ulcers
spontaneously without scar foonation within I..;.
Although no medication has been totall)
the treatment of aphthous stomatitis. patients
ded to antibiotic suspensions and coagulating.
and anti-inflammatory agents.

""""'=.

Pseudoaphthous Ulcer (Figs. 43-7

Pseudoaphthae is a term coined by Binney
recurrent, aphthous-like mucosal ulcers of
which are associated with nutritional deficiea.
Studies indicate that 20% of patients with ",=-~~1iI
thous stomatitis are deficient in folic acid, iron..
B!2' Pseudoaphthae are frequently cone
inflammatory bowel disease. Crohn's disease.
erance, and pernicious anemia.
Pseudoaphthae resemble aphthous ulcers. t..
acteristically more persistent. There is a slight
for females between the ages of 25 and 50. 1k
depressed, rounded, and painful. The bof'de=,.
raised and firm. but induration is seldom
Alterations of the tongue papillae may clue the
cian of an underlying nutritional deficienc) SDk
is slow, and patients may complain of never
ulceration. Chronic and persistent disease
evaluation for nutritional deficiencies. inchJdia!:
logic studies. If the laboratory results are al:inomlk
medical referral is required.

RATIVE LESIONS

.;. 3-1 :Jenture-flange-induced traumatic ulcer.

Fig. 432. Traumatic ulcer; same patient as In Fig

43-1.

.1.3-3 Tr.1umatlc ulcer due 10 the Ingestion of

Fig. 43-4. Oval aphthous ulcer on CllVeolar mucoXl

'oed ,Courtesy Dr Donna Wood)

3-S Aphthous ulcer WIth promn"lent red

Fig_ 4]-6. A ckJsler of .phthaul ulcers

mucosa. (Courtesy Dr Tom Schiff)

-3-7 -:. oe band of erythema SUrrounding a

'" ~ pa,lent wrCh Crohn'S disease.
OonnaWoodJ

Fig. 4]-8. Pseudoaphthous ulcer of Crohn'S

disease. (Courtesy Dr Donna Wood)

95

ULCERATIVE LESIONS
Major Aphthous (Peridadenitis Mucosa Nec-

rotica Recurrens IPMNRJ, Sutton's Disease.

Scarifying Stomatitis. Recurrent Scarring
Aphthous Ulcer) (Figs. 44-1 through 44-4) Major
aphthous is an exaggerated variant of minor aphthous that
produces larger and more destructive ulcers that last longer
and reCUT more frequcnlly. The etiology is unknown; some
suggest that an immune defect is involved. Others speculate
Ihal the large ulcer is a severe fonn of recurrent aphthous
slOmatitils. which results from the coalescence of several
smaller ulcers. Young female adults with anxious personality traits are most commonly affected.
Major aphthous ulcerations are often multiple. They
involve the soft palate, tonsillar fauces. labial mucosa. buccal mucosa. and tongue. occasionally extending onto the
attached gingiva. Characteristically the ulcers are asymmetric and unilateral. The most prominent feature is the
large si7-e together with a depressed. necrotic center. A red
raised innammatory border is common. Depending on size.
Lraumatic innuences, and secondary infection. ulcers may
last from several weeks to months. Because the ulcers
erode deep into the connective tissue. they heal with scar
formation and tissue distonion. Muscle destruction can
result in tissue fenestration. and if the periodontium is
involved, loss of tissue altachment may occur. Extreme
pain and lymphadenopathy are common symptoms.
Healing can be accelerated and scarring reduced with
the use of steroids. Ulcers similar to those of PMNR are
seen with some frequency in association with cyclic neutropenia. agranulocytosis. and gluten intolerance. Ulcers
located on the tongue may strongly resemble carcinoma.
The presence of scarring is of diagnostic importance to rule
out malignancy.

Herpetiform Ulceration (Figs. 44-5 and 44-61

Herpetifonn ulceration is a type of recurrent focal ulcerafion of the oral mucosa that clinically resembles the ulcers
seen in primary herpes; hence the name herpetifonn. This
condition. however. is probably a variant fonn of recurrent
aphthous ulceration. The prominent feature of the disease
is the numerous, pinhead-sized. gray-white erosions that
enlarge. coalesce. and become ill-defined. Initially the
ulcers are I to 2 mm in diameter and occur in clusters of 10
10 100. The mucosa adjacent to the ulcer is erythematous.
and pain is a predictable symptom.
Any pan of the oral mucosa may be affected by herpetifonn ulcerations, but panicularly affected is the anterior tip
of the tongue. margins of the tongue. and labial mucosa. The
smaller size of these ulcerations distinguishes them from aphthae, while their absence of vesicles and gingivitis together
with their recurrent nature distinguishes them from primary
herpes and other oral viral infections. Virus cannot be cul-

96

tured from these lesions. and the ulcers are not CO""",
The first episode of herpelifonn ulcerat
occurs in patients in their late twenties. lO)ean
peak incidence of aphthae. The duration of tbr
variable and unpredictable. and the etiolog) h:aI
detennined. Recurrent herpetifonn ulceratj
especially well to tetracycline suspensions. and
tion often regresses spontaneously after several ~
Beh~et'$ Syndrome 'Oculo-OraJ-Geni
dromeJ 'Figs. 44-7 and 44-8) Beh,et'.s

named for the Turkish physician who first de.scr'

ulcerJ.tive disorder. principally involves three SJle'I:"
oral cavity. and genitals. For this reason it has beaI
rized as a triple~symptom complex with ulcerati\~
tat ions. In its fully developed Slale. cutane
arthritis of the major joints. gastrointestinal
neurologic manifestations. and thrombophle
seen, though rarely are all components preseO! m
patient. The etiology remains unknown. but .a
hypersensitivity reaction. possibly involving HlA
immune complexes. and vasculitis. has been su
Be~et's syndrome is two to three times ~
in males than in females, with an onset bel',l,'een
20 and 30. Persons from Asia. the Mediterrat'Jll.":llr
and Great Britain are most commonly affected.
Eye manifestations of Be~t's syndrome u-0 _
phobia. conjunctivitis. and chronic recurrent
hypopyon that occasionally leads to blindness.
festations may be concurrent with or occur yean
and genital ulcers. Skin changes are characterized
taneous nodules and macular and papular e"". .vesiculate, ulcerate. and encrustate. Genital
involve the mucosa or skin. and tend to be smaUer
common than the oral lesions.
Oral ulcers. the most prevalent lesion of Be
drome. may be the initial sign of the disease. One_
crops of aphthous-like ulcers on the buccal
mucosa are characteristic; however. any oral mu..
may be involved. Similar to aphthous. the ulcm
shallow. and oval, with the size of the ulce~
Small lesions tend to occur more frequentl~ u..
lesions. A serofibrinous exudate covers the swfax
margins are red and well-demarcated. Complaiar.
are frequent. and recurrent periods of exace
remissions are characteristic. Patients with linuIc..
cutaneous involvement are managed sympton..."".-'"
topical and systemic steroids. Protracted diseasethe neuro-ocular structures requires the care of a
Azathioprine, cyclophosphamide. thalid
colchicine have been used successfully in sel
All of these agents have potentially serious sidt

LL-l j:I~lstent ulcers on marginal and attached

P<ltlent with m..jor ..phthous.

~3_

Painful major ..phthous of the gingiva.

~5 "~ul[lple

herpetiform ulcerations of the

OS<'! (Courtesy Dr Geza Terezh<llmyl

_ ~7 foung male with tonsillar ulceration of

.-..x:etJl syndrome. ICourtesy Dr Geza Terezh<llmyj

Fig. 44-2. Multiple tongue ulcers in patient with m.. jor

..phthous.

Fig. 44-4. Large irregular ulcer of the soft palale; same

patient with major aphthous as in Figs. 44-1 through
44-1

Fig. 44-6. Coolescing herpetiform ulcerations; same

patient <IS In Fig, 44-5 ICourtesy Dr Gez<l Terezhalmyj

Fig. 44-8. Multiple genit<ll ulcers in the same p<ltient <IS

seen In Fig 44-7; 8eh~etS syndrome. iCourtesy Dr
Gez;) Terezhalmyl
97

ULCERATIVE LESIONS
Granulomatous Ulcer IFigs. 45-1 and 45-21 Two
common granulomatous infections thai may produce oral
ulcers are tuberculosis (TB) and histoplasmosis. These are
rare lesions thaI are usually found in older adults after the
disease is far advanced. Underlying disorders such as
AIDS resull in a younger population group being affected.
Because pulmonary lesions oflen precede oral lesions. the
pulmonary complain! of persislent cough is an imponanl
historic finding.
Dissemination of organisms from the lungs 10 the mOUlh
via infected sputum can resull in oral infection. Oral TB
and histoplasmosis infection are characterized by ulceralion. These ulcers may occur on any mucosal surface: however. tuberculous lesions occur preferentially on the dorsum of the tongue and labial mucosa at the commissure.
The clinical picture varies and the ulcer may resemble a
traumatic ulcer or epidermoid carcinoma, particularly
when the lesion is located on the lateral border of the
tongue. Lesions on the alveolar ridge often resemble a
granulating extraction site. The center of the granuloma+
tous ulcer is yellow-gray or even bluish. necrotic, and
depressed several millimeters. The peripheral region of the
ulcer is undulating or lumpy and has been described as
"cobblestoned:' The margin of the lesion is irregular. welldemarcated. and undermined. odular and vegetative components are often seen in conjunction with the ulcers of
histoplasmosis. Cervical lymphadenopathy is a common
finding. Depending on the location and irritating factors.
some patients rarely complain of pain and the discovery
may be an incidental finding; other patients experience
severe, unremiuing discomfon. Tuberculous and histoplasmosis lesions are contagious. and active organisms can be
transmitted under appropriate conditions.
A biopsy or culturing is required to confirm the diagnosis. Histologic features and special stains demonstrate the
presence of the causative organisms. Treatment of the primary lung problem is with specific long-term antibiotics; for
TB, streptomycin is usually followed by isoniazid (INH); for
histoplasmosis. amphotericin B is administered. The primary lung problem should be treated prior to dental treatment.
Squamous Cell Carcinoma (Figs. 45-3 through
45-6) Squamous cell carcinoma often appears as an ulcer.
In the early stages the condition is usually small, nonpainful. and non-ulcerative: however. the persistent nature
of the disease results in neoplastic proliferation that soon
exhausts the blood supply. resulting in surface telangiectasia and eventual ulcer formation. Older ulcers tend to be
large and crateriform. covered by a central yellow-gray

98

necrotic slough. Red, raw foci are frequenL

ders are firm, raised. and sometimes fungatJ.a!.
Carcinomas mlly occur anywhere in I.bC"
most common siles are the posterior third
margin of the tongue and the floor of
Associated features may include pain. nu,n>i_ _
plakia. erylhroplakia. induration. fixallGa.
phadenopathy. Metaslatic Iymphadenopath) ~ c.....~
ized by nonpainful rubbery or hard nodes m. ale
the base and maned together. Excessive use .<I:'::~~
tobacco by the patient should heighlen ~ n
picion of oral carcinoma when a persistent .
heal within 14 days. Biopsy should be ped
clinician who provides the definithe treatmelll..

Chemotherapeutic Ulcer IFigs. 45-7

Patients receiving immunosuppressant
c- _

dru,,_,

of serious illnesses. including OfB:an ~~~~~~

aUlOimmune condilions. and neoplasia. nta)
ulceralions and stomatitis. Side effects of the
peutic drug may be directly or indirectly
oral mucosa. Antimetabolites such as me~
the replication of rapidly reproducing cell,. _ _""'"'"
oral epithelium, whereas alkaloids such b ~
phamide induce leukopenia and secondar) uJoc:
The chemotherapeutic ulcer. an early sign m ...., . , .
ity. appears during the second week of the~
persists for 2 weeks. These ulcers may occur
mucosal sile. The lips. buccal mucosa. tongue.. ~
mouth. and palate are affected most frequeml __
area is red and bums. The surface epithelium K
ulcer forms that is usually large. deep.
painful. The margins of the ulcer are irreglI-E.
characteristic red inflammatory border is om
because of the lack of an inflammatory re
host. If the pain becomes severe and the inta1:e
nutrition and fluids is impaired. a reduction ia
may be necessary.
Culturing is highly recommended for allleslca
of their propensity for infection with gram-nepIl"
isms and fungi. and because of the likelihool.
ulcers may represent recrudescence of latent
plex virus. Topical anesthetics are used to mi.... r
toms. whereas oral hygiene measures. includuJr
bial agents such as chlorhexidine. are criti
secondary infection. soft tissue necrosis. aDd
necrosis. Consultation and open communie.at:D
the physician and the dentist can help reduc.e ""......
and promote oral comfort.

-.."ii

=-

CERATIVE LESIONS

,"

.IS-I Granulomatous ulcer on anterior tongue

.' .,Q!)aetmum lubfrCUjOSIS (Courtesy Dr
_ " noz)

Fig. 45-2. Granulomatous ulcer on the dorsum of

the longue; histoplasmosis {Courtesy Dr Michael Huber)

Fig. 45-4. FfOQr-Qf-lhe-moulh ulceraoon; squamous

cell carcinoma. {Courtesy Dr Robert Craig)

Fig. 456. Squamous cell carcinoma In the same

pallenl as In FIQ 4S-S (COUrtesy Dr Tom McD<lVid)

-'5--7. Chemotherapeutic Induced ulceration

'"'II(

patient (Courtesy Dr Tom McDavid I

Fig. 45-8. Chemother..peutlc ulceration of the

buccal mucosa caused by methotrexate therapy_
(Courtesy Dr Jerry Cioffil

99

SECTION

v
Sexually
Related and
Infectious
Conditions

101

SEXUALLY RELATED AND INFECTIOUS CONDITIONS

Traumatic Conditions (Figs. 46-1 and 46-21
Injury to the lingual frenum lind fellatio syndrome are
common oral conditions associllled with sexual activity.
Ulceration of the lingual frenum may occur when the
longue is mechanically abraded against the incisal edges of
the mandibular incisors during orogenilal sexual activity. A
while fibrinous exudate and an erythematous border are
commonly seen. A hislory of cunnilingus confirms the
diagnosis and abstinence is recommended to pennil healing. Chronic irritation may lead to secondary bacterial
infection, development of leukoplakia, a tr::lUmatk fibroma.
or it may permit ingress of the human papilloma virus.
Fellatio. a sexually traumatic condition, produces erythema
and submucosal hemorrhage most commonly seen at the
junction of the hard and sort palate. Initially isolated bright
red petechiae appear. which eventually become a confluent
patch that bridges the palatal midline. The purpuric lesion
is painless and nonulcerative, does not blanch on diascopy.
and clinically resembles the petechial patch produced by
infectious mononucleosis; however. lymphadenopathy and
fever are characteristically absent. Petechiae darken and
fade away in about a week.
Sexually Transmitted Pharyngitis 'Figs. 463
and 46-4J Venereal organisms such as herpes simplex
virus Type 2. Neisseria gonorrhoeot'. and Chlamydia Ira
choma/is may cause pharyngitis by transmission from
direct contact with infected genital or oral secretions or
lesions. Herpetic stomatitis (Type II) is most prevalent after
sexual activity begins. usually occurring in persons
between 15 and 35 years of age. Limited reports indicate
that primary HSV-2 infection produces a prominent
pharyngotonsillitis and fever while inflammation of the
gingivae may be less severe than HSV-I primary infection.
Multiple small vesicles are usually apparent in the early
stages; the vesicles collapse to form ulcers that resolve in
JO to 21 days.
Gonococcal pharyngitis may produce a diffuse erythematous throat. small pustules in the tonsillar area. or an erythematous and edematous patch involving the throat. tonsillar
area. and uvula. Burning is the initial symplom. followed by
increased salivary viscosity and halitosis. Other oral manifestations include the following; painful. discrete ulcerations
of the oral mucosa: fiery red and tender gingiva with or
without necrosis of the interdental papilla; tongue ulceration: and glossodynia. Penicillin G. tetracycline, and ceftriaxone regimens have been used effectively to treat this condition. C. /rochomads may also cause a sore, "lumpy"
throat. mild pharyngitis, and tonsillar inflammation with
pustule fonnatiOfi. TIle treatment of choice is tetracycline.

Infectious Mononucleosis (Figs. 46-5 and 46-61

Infectious mononucleosis is a relatively benign lymphocytic infection characterized by fatigue, fever. malaise.

'02

pharyngitis, stomatitis. and occasional jaundice.

commonly caused by the Epslein Barr virus
chieOy in adolescents and young adults. This d
low contagiousness and transmission is proba _
exchange of virus-contaminated saliva during deqt
Oral lesions are often the earliest manif~
infectious mononucleosis. Multipk red palatal
located at the junction of the hard and soft palate ........or
ing (he first few weeks of infection. These I~
brown and fade after 7 to 10 days. Acute u1cerati\'t
tis. pharyngeal ulcerations, and erythematous n
tonsillitis are frequently encountered during (he
of the infection. Bilateral posterior cervical 1),,,,,,",_
thy is a consistent finding. Blood analysis re\eal~
lymphocytosis. atypical lymphocytes. and the
heterophile antibodies. Trealment is supper:
includes bed rest. soft diet. analgesics. and
Recovery usually occurs within I 102 montM.
SyphJlls IFigs. 46-7 and 46-S1 Syphilis is a
disease caused by an anaerobic spirochete, Trt'po.........
lidum. The haJlmark of primary oral syphilis u.
painful chancre. which represents a granulomatolb..,c;.
to vascular obliteration. Chancres may affect a:rry
tissue; however. the lips are the most com
involvement, followed by the tongue. palate.
tonsillar areas. Oral syphilis is usually obsened
adult males.
The syphilitic chancre initially appears as a
that elevates, enlarges. erodes, and becomes ul=_.
lesion is usually punched-out. indurated, 2 to 3 em ",;:~
(er. and without a red inflammatory border. The ..
covered by a yellowish, highly infectious serous ..."". ."
Palatal erythema or an asymptomatic. reddish ulca
the initial lesion. along with swollen, non-tender. ""..
riorcervicallymph nodes. Chancres typically penIk
4 weeks and heal spontaneously, which may caU!t -::::lO:to erroneously believe thai no treatment is n~
latent period of 4 weeks to 6 months, the sec~
syphilis appears in which the patient rna)
headaches. lacrimation, nasal discharge. sore """"'..
generalized arthralgia. together with lymphade
vation of temperature, and weight loss. A painless..
rical. nonpruritic skin rash with notable maculo-"",..",,
mar-plantar eruptions soon follows. Concurrent ora
of secondary syphilis appear as oval red macules, 1*""'::;:'
lis, or isolated or multiple mucous patches (paID""
low highly infectious ulcers surrounded by an ery
halo). The borders often are irregular and re=....
tracks." Tertiary syphilis occurs in infected paos--.
years after OOl1treatment of secondary syphilis. It
Iy characterized by palatal perforation and neurolop.
toms. Parenteral penicillin G remains the drug of,",r==JIo:
treating all stages of syphilis.

,=

,=

SEXUALLY RElATED AND INFECTIOUS CONDmONS

~t;

46-1. Traumatic ulcer of the lIngual frenum

Dr James COttone,

Fig. 46-2. Condyloma acuminatum of the lingual

frenum. (Courtesy Dr Marden J\lder)

r'9 46-3. Herpes type-II Induced tonsillitis.

esy Dr James Cottonel

Fig. 46-4. Herpes type II-induced pharyngitis.

;<:;: 46-5. Pdk'ral pe1ect'l<ile: infectious

nomucleosis. iCoJ'lesy Dr Gez~ Te-f'zhaunyl

Fig. 46-6. ExudatIVe tomlI!IUS. same patient W1m

46-7. SyphilitIC chancre of primary syphilis; labla'

)ure ICounesy Drs laurie Cohen and JOhn COKe)

jCourtesy Dr James CotlOne)

infectious mononucleosis as rn Fig 46-5 {Courtesy

Dr Geza TerezhalmyJ

Fig. 46-8. Snail track mucous patch of se<ondary

syphilis. (Courtesy Drs laurie Cohen and John Coke!

103

HIV INFECTION AND AIDS

Acquired immune deficiency syndrome (AIDS) is a
communicable disease caused by the human immunodeficiency virus (HIV. HTLV.III) first reported by the Centers
for Disease Control in 1981. The virus is harbored in the
blood. tears. saliva. breastmilk. spinal fluid. vaginal secretions and seminal fluid of infected persons and is predominantly spread by sexual contact, by blood or blood products. or perinalally. Infeclion may resuil by exposure to the
virus through participation in high risk activities such as
sharing needles willi intravenous drug users; having unprotected sexual activity involving exchange of infected bodily
fluids; being a recipient of infected blood or blood products; or being accidentally exposed to infected materials.
Individuals infected with HIV. as determined by seroconversion. usually manifest persistent generalized lymphadenopathy (PeL) followed by AIDS-Related Complex
(ARq, which is characterized by lymphadenopathy. weight
loss, fever. dial'Thea. fatigue, skin anergy. oral candidias~s.
hairy leukoplakia. and herpes virus recrudescence. Progressive changes in immune regulation caused by T-cell lymphopenia and reduced helper T-cell (OKT4/LEU3a) function
results in full-blown AIDS, characterized by opponunistic
infections and susceptibility 10 cenain fonns of cancer. At
present there is no curative treatmem available for AIDS, and
infected persons eventually succumb to the disease.
The oral manifestations of HIV infection are often
numerous and concurrent. Recognition of the oral features
associated with HIV infection should warrant patient referral to a physician.

Oral Bacterial Infections fFigs. 47-' and 47-4)

Oral bacterial infections in patients infected with HIV usually involve the periodontal tissues. Examples of these
infections include acute necrotizing ulcerative gingivitis
(ANUG). HIVgingivitis, and HI V-periodontitis.
ANUG is common in HIV-infected patients. It is char- .
acterized by sudden onset of fiery red. swollen. painful,
bleeding gingiva and a fetor oris. The interdental papillae
appear "punched-out." ulcerated. and covered by a grayish
necrotic slough. Treatment involves debridement alone or
combined with metronidazole therapy if constitutional
signs such as fever, malaise, and anorexia are present.
HIV gingivitis is characterized by chronic gingival erythema that occurs equally in the maxilla and mandible
despite the absence of apparem local factors. Initially.
small. red. punctate. muhifocal petechiae of the attached
gingiva appear. which later fonn noncoalescing. distinctive red linear bands of the marginal and auached gingiva.
Spontaneous gingival bleeding and lack of response to
conventional therapy are common. The etiology is uncer+
tain. but it has been proposed that immune defects, in par+
ticular PMN abnonnalities. may playa role.

104

~""';;;~;

HIV periodontitis is an extremely rapid

process that produces a loss of periodontal an.
in days. It initially manifests in the amerior
sues. radiates to the posterior areas with time.
distinct propensity for occurence in the incisor
teeth. This bacterial infection is characterized
spontaneous gingival bleeding. interdental ..,,..~
and cratering. gingival edema and intense eT)~
gingival recession. extremely rapid and irregm.
(up to 10 mm in 6 months). delayed wound
spread to adjacent mucosa. Aggressive peri""_~
sures are required to limit this disease.
In the HIV-infecled patient. bacterial flora
the oral cavity can be found. The most COlTlllXa
bacteria are respiratory and colifonn flora.
t

-01_

often produce diffuse. erythematous. and ulcera:d.

of the tongue that results in symptoms of
Antibiotics are effective. but overgrowth of,,",""';"
isms may occur as a result.

Oral Fungal Infections 'Figs. 47-5 ane

Candidiasis, in a variety of clinical presen.w....
most common infection of the mouth affecting dIr
surfaces of patients with AIDS. and is often thr. ~::::~:
manifestation. Candidal infections are usuall) .:
nature and may appear red. white. flat. raised. or
Any oral mucosal surface may be infected. -:=-:,;~:
palate, tongue. and buccal mucosa are the lDOSI
sites. Symptoms of infection may include mild
burning. or altered taste. Types of candidiasis ~:~:::
domembranous candidiasis. erythematous (a
didiasis, hyperplastic candidiasis. and angular
Pseudomembranous candidiasis is charaac=;;
creamy white plaques that upon scraping reveal.!
or bleeding mucosal surface. A KOH-stained SlDeZ'
gal culture reveals the typical morphology of C''''''....
cans. The erythematous or atrophic fonn clin'
as a diffuse red area, usually located on the ~
tongue. At this location the condition is associ3tCd
loss of filifonn papillae and is tenned "medim
glossitis." A diffuse. erythematous contact I
sponding in size and shape to the tongue lesK.
apparent on the palate. Chronic hyperplastic c:::~~:
late stage of candidal infection, clinically appean.
white keratotic plaques on the buccal mUCOR.
plaques cannOl be wiped off.
Topical antifungal agents are almost alwa)'-s ......_
the treatment of oral candidiasis; however. me __0::.."'"
may be chronic and recurrent, and may be pmh.;;
esophageal candidiasis. Infrequent oral fUn,!g~21~:~::-
associated with AIDS are geotrichosis and his:

INFECTION AND AIDS

.: 7-1. ?'Uncned-out Interdental paPillae of

19 ulceratIVe gingIVItis; Hlv-posrnve patient.

Fig. 47-2. Pun<hed-oullrlterdemal papillae of

necrotizing uicerc'lllve glnglVl(ls, o;ame HIV-poSlllve patient

as In Fig 471

"
.'3. ~on<ontlnuous linear red band of HIV
Counesy Dr MlChaef VillI

; ~7-5. Median rhomboid

~e patient. ~Courtesy Dr

glossitis In <In HIVEd Heslop)

-r; 41-7. Acute pseudomembranous

Qindidiasis In a pauent WIth AIDS.

,,

Fig. 47-4. RadlographlC \Ildence or rapid bone loss;

bottom r ms liIken 6 months after lOP films; HIV
penodontl[l$

Fig. 47-6. Atrophic undidi..sls

i'!(

posrenor extent

of pal.?l' overlYing the glosS'lIS seen

(Cour.:esy Dr Ed Heslop)

'n

Fig 47-5

Fig. 47-8. Acute pseudomembranous

undidia,!, In same AIDS patl{'nt as In Fig 47-]

105

HIV INFECTION AND AIDS

Oral Viral Infections IFigs. 48-1 through 48-61
Herpes viruses (herpes simplex, varicella zoster, cytomegalovirus. and Epstein-Barr) figure prominently in oral disease in the AIDS patient. Herpes simplex virus (HSV)
infections usually appear on the lips as herpes labialis or
within the mouth on keratinized epithelium as recurrent
intraoral herpes. The recurrent infection forms smalL round
vesicles that rapidly erupt. leaving shallow yellow ulcers
bordered by a red halo. Coalescence of adjacent vesicles
into large ulcers is common. Unlike patients with normal
immune funclion. patients with AIDS may have herpetic
infections on mucosal surfaces lypically ascribed to aphthous stomatitis such as the tongue and buccal mucosa.
HSV recurrences are often more frequent. more persistent.
and more severe in patients infected with HIV.
Varicella zoster virus (VZV) recrudesces more frequently in HIV-infected persons than in the ordinary
population. The clinical appearance is similar in both
groups, but the prognosis is worse for patients with
immune suppression. VZV produces multiple vesicles
commonly located on the trunk or face thai are usually
self-limiting and unilateral. Cephalic vesicles are found
along a branch of the trigeminal nerve. either extraorally or
intraorally. Vesicle eruption, coalescence. ulcer formation.
and scabbing are characteristic of the condition. Deep searing pain is the premiere symptom. which may persist as
post-herpetic neuralgia. Therapy with acyclovir is sometimes used in an attempt to accelerate healing and to mitigate symptoms.
The prevalence of C}'tomegalovirus (CMV) approaches
l(}()% in HIV-positive homosexual males and approximately
10% in children with AIDS. The virus has a predilection for
salivary tissue and can be recovered from the saliva of persons infected with HIV. Inflammatory changes associated
with CMV and HIV-infection include unilateral and bilateral
parotid gland swelling and xerostomia.
Oral manifestations of human papilloma virus (HPV)
are frequently found in persons infected with HIV. So far,
over 65 serotypes of HPV have been identified. A variety
of mucocutaneous lesions are HPV-induced, including
squamous papilloma. verruca vulgaris, focal epithelial
hyperplasia (Heck's disease). and condyloma acuminatum.
The condyloma acuminatum, or venereal wart, usually
appears as a small, soft, pink to dirty gray. exophytic
growth that has a cauliflower-like surface. These lesions are
often multiple and recurrent, and coalesce to form large.
sessile, pebbly growths. Condyloma acuminata can be
found on any mucosal surface. particularly the ventral
tongue. gingiva, labial mucosa. and palate. Transmission is

106

most likely by direct contact resulting in contagioa:l

from anal or genital sites, or by self-inoculation. "Ii
consists of local excision together with simultanelXil
cation of all lesions of infected partners.
Hairy leukoplakia is a raised. corrugated. poart,
cated white lesion on the lateral border of the tongue.
associated with the Epstein-Barr virus and HIV.
Early lesions appear as discrete, white, vertican~
plaques on the lateral borders of the longue thai ~
bilateral, whereas older lesions may cover the eOla
and dorsal surface of the tongue and extend onto . .
mucosa and palate. The lesions are asymptomatic.
rubbed off, and often are of esthetic concern to ~
Histologically one sees hyperkeratotic hairlike ~
koliocytosis, minimal inflammation, and candidal .
Histopathologic confirmation of hairy leukoplakia II
tant, because the diagnosis predicts the devel"",,,,,..
AIDS within 80% of those affected in I to 3 yean.
Oral Malignancies {Figs. 48-7 and 48-81 No...:;;
sarcoma is the most common malignancy assoc'
HIV infection. It is a tumor of vascular prolife
affects the cutaneous as well as the mucosal tissue. ology is unknown. but viral factors (possibly eM\
ated with angiogenesis have been suggested.
mately 20% of all AIDS patients are affected: the
lence is about 30% in HI V-infected homosexual rI1IIIIa.
Kaposi's sarcoma is characterized by three stages.. _",~,
the malignancy is an asymptomatic red macule.
enlarges into a red-blue plaque. Advanced lesions
lobulated, blue-violet nodules that ulcerate and cao_,,The hard palate at the lateral areas is the mosl COllUDlill
tion, followed by the gingiva and buccal mucosa.
the lesions are multifocal, uncomfortable, and esthe
pleasing. Treatment is palliative. utilizing radiatioo
and chemotherapy. Clinically similar-appearing l~
can be ruled out by biopsy are erythroplakia. heman_
purpura. and atrophic candidiasis.
Non-Hodgkins B-cel! lymphoma and squa
carcinoma are associated with H1V infection. p
a result of abnormal immune surveillance which
enhanced neoplastic proliferation. Non-Hodgkim.
phoma often appears as a diffuse. rapidly prolifi
purplish mass of the palatal-retromolar compleL
mous cell carcinoma is most frequently found as a
white or ulcerated lesion on the lateral border
tongue. Many of the usual co-factors. such as
age, alcohol abuse, and poor oral hygiene. are
HJV-infected persons.

fn=_

lV INFECTION AND AIDS

If:.

48-1. Per51stent recurrent herpes labialis In <In

- :.positive patient. (Courtesy Dr Jerry Cioffi)

Fig. 48-2. Recurrent herpes simplex In a pallent

with AIDS.

_~,;;a;,,

r
~8-3. Un~lC!'al palatal ulcerauons of herpes
aest:e'r ran HIV'positlve patient. (Courtesy Dr
'1eg.i1rd)

"

Fig. 48-4. PapdlOma-vlrus-induced condyloma

acumin..ta In a HIV.positive patient.

48-5. White corrugated patches; hairy

Fig. 48-6. H.dry leukoplakia; XJmc pdtlent dS In Fig

oplakla in an HIV.posltlye patient.

48-5

C8-7. Early purple macule and mature purpliSh

:~ Kaposls saKoma In an AIDS patient.
5-, Dr \o1lCheal HUbef)

Fig. 48-8. Noduiar non-Hodgkins lymphoma In a

patient With AIDS. (Courtesy Dr George Kaugro)

101

EVIATIONS
TION

ENGLISH

LATIN DERIVATIVE

at pleasure

ad libitium

before meals

ante cibum

after meals

post cibum

water

aqua

a day. daily

dies

\Nice a day

bis in die

three times a day

rer in die

four times a day

quater in die

hour

hora

at bedtime

hora somni

every hour

quaque hara

every three hours

quaque tertia hora

every four hours

quaque quarta hara

every six hours

quaque sexta hara

do not repeat

non repetatur

as needed

pro re nata

immediately

statim

label

signetur

with

cum

drops

guttae

tablet

tabella

capsule

capsula

every day

quaque die

"'

Appendix II

THERAPEUTIC PROTOCOLS
ESICS

ANALGESICS

ENT RATIONALE:
relief of the symptoms of mild to
pain associated with oral

,":::te
.3

ns.

Acetaminophen Tylenol 325 mg

Rx

AspIrin 325 mg. Butalbnal 50 mg.

Caffiene 40 mg
Fiorinal rabs <!) (Sandoz)

Disp.:

40 Tablets

5ig:

Take I to 2 tablets q.4 h. p.r.n. pain.

Rx

Dihydrocodeine bitarrrate 16 mg.

Aspirin 356.4 mg. caffeine 30 mg
Synalgos-DC<!> Capsules (Wyeth)

Oisp.:

40 Tablets

5i9:

Take I to 2 tablets q.4 h. p.r.n. pain.

Rx

Oxycodone HCI 5 mg.

Acetaminophen 325 mg

McNeil)

Tylenol<!> 325 mg (McNeill

100 Tablets
Take 2 rabIes q.4 h. p.r.n. pain not to

exceed 12 tabs in 24 hours.

Acelylsallcytic I\cid
Bayer Asp.nn<!> 325 mg (Glenbrook)

100 TClblets

Take 2 tablets q,4 h. p.r.n. pain.

Percocet Tablets {Dupont)

Ibuprofen
'.Iotrln<!> 400 mg IUpjohn/

Disp.:

25 Tablets

51g:

Take I tablet q.4 h. p.r.n. pain.

laO Tablets

Take 2 tablets q.4 h. p.r.n. pain.

Rx

Oxycodone He! 4.5 mg. Oxycodone

Terephthalate 0.38 mg. Aspirin 325
Percodan/!) Tablets /Dupont)

aproxen

mg

Disp.:

25 Tablets

Sig:

Take I CClblet q.4 h. p.r.n. pain.

Rx
Acetaminophen with Codeine 30 mg
Tylenol with Codeine No.3 <!) Tablets
McNeil PharmJ

Meperidine Hel 50 mg,

Promethazine HCI 25 mg
Mepergan Fonis CapSUles /Wyeth)

Disp.:

25 Tabrets

30 Tablets

5ig:

Take I tablet q.4 to 6 h. p.r.n. pain.

Rx
AspIrin with Codeine 30 mg
Empirin with Codeine No.3 (!) Tablets
Burroughs WelJcome)

Hydrocodone bitartrate 5 mg,

Acetaminophen 500 mg
Lonab<!> 5 Tablets IRussl

Disp:

30 Tablets

30 Tablets

5ig:

Take I tablet q.4 h. p.r.n. pain.

aprosyn~ 375mg

/Synrexl

50 Tablets
Take 2 tablets t.i.d. p.r.n. pain.

T. e 2 lablets q.4 h. p.r.n. pain.

ake 2 tablets q.4 h. p.r.n. pain.

115

Appendix II

THERAPEUTIC PROTOCOLS
ANTIHISTAMINES

TOPICAL CORTICOSTEROIDS

TREATMENT RATIONALE:
For the relief of the symptoms of anxiety
and anxiety~related skin eruptions.

TREATMENT RATIONALE:
For adjunctive treatment and temporal')'
relief of symptoms associated with ora
inflammatory and ulcerative lesions.

Rx

HydroxyzIne
Atarax lXl 25 mg Tablets IRoerigl

Disp.:

50 Tablets

5ig:

Take 2 lablets q.i.d. p.r.n.

Rx

Diphenhydramine hydrochloride
Benadryl<l!> 25 mg fWarner-tilmbertJ

Disp.:

25 Tablets

5i9:

Take I tablet q.i.d.

116

Rx

Beramethasone valerate ointrne"'T

0.1 % Vallsone l!:l fScheringJ

Disp.:

15 gm (45 gm) tube

5ig:

Apply w mouth sores after

bedtime.

Rx

Fluocinonide gel
0.05% tide>< <I!> (Symex)

Disp.:

15 gm 130 gm/ tube

5ig:

Apply to mouth sores after meats

bedtime.

Rx

Hydrocortisone acetate oinunen;.

05% Orabase HCA <I!> (COlgale-h:

Disp.:

5 gm tube

5i9:

Apply to oral lesions after mealS

bedtime.

Rx

Triamcinolone acewnide oinrl'TleT

0.1% Kenalog in Orabase<!!> 15ql.o::I::

Disp.:

5 gm tube

5i9:

Apply to ulcerated area after meats"

at bedtime.

Rx

Dexamethasone elixir
Decadron <!l O.S/Sml IMerck-Shc:r:r
Oohme/

Disp.:

100 mJ bortle.

5ig:

Rinse with I teaspoonful q.l.d

minutes then expectorate.

meas:

~;;:

Appendix II

THERAPEUTIC PROTOCOLS
UNOSUPPRESSIVE AGENTS

ORAL ANTIMICROBIAL RINSES

JMENT RATIONALE:

TREATMENT RATIONALE:
To reduce the pathogenic microbial flora
often associated with the inflammatory
signs of oral disease.

.ard'junetive treatment and temporary

of symptoms associated with severe
f1ammatory and ulcerative lesions.
Prednisone
Medro/ 4 mg Dasepak 2/ s rUpjahn)

Rx

Chlorhexidine gluconate
0.12% Peridex Oral Rinse (Procter &
Gamb/e)

Disp.:

480 ml bortle

Sig:

Swish J teaspoonful for I minute then

expectorate. Peform twice daily
morning and evening after rooth
brushing. Avoid earrng or drinking for
30 minutes.

Rx

Tetracycline HCf
Tetracyn 250 mg (Pfizer/

Disp.:

40 Capsules

Sig:

Dissolve 1 capsule in 1 teaspoon of

warm water. then swish the solution for
3-5 minutes and swallow. Repeat q.i.d.

Rx

Tetracycline HCI
Achromycin V /25 mg/5m/ (Leder/e)

Disp.:

60 mr la/so available in 16 fI oz)

Sig:

Rinse with 2 teaspoonsful for 3 minutes

and swallow. Repeat q.i.d.

I dosepak 12/ t.3bs)

Take graduated daily doses according
to the manufacturerS directions listed

on the dosepak.

Prednisone I 0 mg
36 Tablets

Take 1 tab t.i.d. for 10 days. then

diminish dose by I tab every 2 days for

the next 4 days.

Azathiopnne
Imuran <!!> SO mg (Burroughs WellcomeJ
30 Tablets

Take a single dose of 50 mg once daily.

(Patients nor improved in '2 weeks mClY
be refractory to this drug).

-:..~~: Chronic immunosuppression with

~
ne increases the risk of neoplasia.
prescribing this drug should be familiar
nsk as well as the serious mutagenic

"'ematologic consequences to both men

oomer1.

117

Appendix II

THERAPEUTIC PROTOCOLS
FLUORIDE THERAPY

TOPICAL ORAL ANESTHETICS

TREATMENT RATIONALE:

TREATMENT RATIONALE:

To prevent dental caries in susceptible

patients.

Relief of the symptoms associated

minor irritations of the mouth.

Rx

Stannous ftuonde 0.4%

Rx

Disp.:

4.3 ft

519:

Apply 5 to 10 drops in a carrier and

place carrier on teeth daily for 5
minutes.

Ol

Rx

Oral ftuorlde
0.125 mg Luride l per drop
ICa/gateHayt)

Disp.:

60 ml bertIe with dropper

Sig:

Apply 2 drops per day" IBirth to 2 years)

Apply 4 drops per day" 12 to 3 years)
Apply B drops per day" 13 to 12 years)
"in the mouth of the child

DiphenhydramIne HCI
Benadryl elixir' 2.5 mg/5 rn
Davis}

Disp.:

4 ft Ol

Sig:

Rinse with 1 tablespoon a.c. an::

pain.

Rx

Benadf}'l <!l elixir /2.5 mg/5'" Davis) and Kaapectate <I!lIUPJO'Y'

mixture by volume

Disp.:

4 fJ 02 of each, mIx equal parts

51 9:

Rinse wirh I rablespoon for 2 ........... a.c. and p.r.n. pain.

Rx

lidocaine HCI
2% Xylocaine viscous soluoon -

Disp.:

4 fI

Sig:

Rinse with I teaspoon a.c. and p rpain. Expectorate after rinsing.

Rx

Orabase with Benzocaine IColga:rHayti

Disp.:

5 gm 115 gm)

Sig:

Apply to affected area a.c. and p

pain.

Ol

r..,

Appendix II

THERAPEUTIC PROTOCOLS
XIETY AGENTS
TMENT RATIONALE:
the management and shortterm relief
symptoms of anxiety.
Chlordiazepoxide
LJbrium III 10 mg {Rochel

20 Tablets

NUTRIENT DEFICIENCY THERAPY

TREATMENT RATIONALE:

To replace deficient nutrients necessary for

homeostasis.

Rx

Ferrous sulfate 250 mg

Disp.:

100 Tablets

5i9:

Take I tablet t.i.d. for I month, then

r'-assess patient'> hemoglobin.

Rx

Folic acid 0.4 mg

Disp.:

30 Tablets

5i9:

Take I tablet daily for I month, then

re-assess patients folic acid level. .,.

Take I tablet twice daily.

Diazepam.
Valium 5 mg IRoche)

20 Tablets
Take I tablet 2-3 times daily. and J
tablet , hour before dental

appoIntments
AlpraxoJam
)(.;nax 025 mg [UpJOhn)
20 Tablets
Take I tablet twice daily.

*Caution: Medical supervision is advised.

Rx

Water soluble bioflavinoids 200 mg

with ascorbIC acid 200 mg
Peridin-e lID 400 mg (Beutlich)

Disp.:

100 Tablets

51 9:

Take I tablet t.i.d. for 2

weeks.

Busprrone
Buspar 5 mg {Mead JohnsonJ
20 Tablets
Take 1 tablet twice daily.

119

Appendix II

THERAPEUTIC PROTOCOLS
ANTIHISTAMINES

SALIVA SUBSTITUTE

TREATMENT RATIONALE:
To reduce the effects of histamine-mediated
hypersensitivity and temporary relief of the
symptoms associated with minor oral
irritations.

TREATMENT RATIONALE:
For the relief of a dry mouth.

Rx

Carboxymethyl cellulose 0.5%

solution.

Rx

Disp.:

8 fI 02

51g:

Use as a rinse p.r.n.

Rx

Moi-stir l8:l (Kingswood)

Disp.:

120 ml with pump spray

51 9:

Use as a rinse p.r.n.

Rx

Xerolube <!l> (Scherer)

Disp.:

180 ml with pump spray

5i9:

Use as a rinse p.r.n.

Phenylpropanolamine HCI 25 mg and

Brompheniramlne Maleate HCI 4 mg
Dimerapp <!l> (Roblnsl

Rx

Salivart (!!) (Westport PharmJ

Disp.:

40 Tablets

Disp.:

75 ml with pump spray

519:

Tak.e I tablet q.4 h. as needed.

519:

Use as a rinse p.r.n.

Rx

Terfenadine
Sefdane 60 mg (Merrell Dow)

Oisp.:

30 Tablets

51 9:

Tak.e 1 tablet twice a day.

Rx

Astemizole
Hismanal (!l 10 mg (Janssen)

Oisp:

25 Tablets

519:

Take I tablet once a day.

Diphenhydramine HCI
8enadryl <!l> 25 mg (Parke-Davis)

Disp.:

40 Tablets

5ig:

Take I tablet every 6 hours as needed.

Rx

Brompheniramine Maleate Hel

Dimetane <ID 4 mg (Robins)

Disp.:

40 Tablets

51 9:

Take 1 or 2 tablets every 6 hours as

needed.

Rx

120

--

Appendix II

THERAPEUTIC PROTOCOLS
UNGAL THERAPY
~TMENT RATIONALE:

ANTIFUNGAL THERAPY

Rx

NystatIn ointment
Mycost.3tin ointment 100,000 I.U.
ISquibb!

Disp.:

15 gm (30 gml tube

Si9:

Apply liberally to affected area 4 to 6

times daily.

Rx

Nys[CItin-neomycrn sulfate-gramrcidintriamcinolone acetamide

TreS"'tin IRugby)

Disp.:

15 gm 130, 60 gml tube

Si9:

Apply liberally to affected area 3 to 4

times daily.

Sninate pathogenic fungal organisms

, iO

reestablish the normal oral flora.

Nystatin vaginal tablets
Nil,,,,, II!> I 00,000 W.ILederle!

90 Tablets
DIssolve , tablet as a lozenge 5 rimes
dally for I4 consecutIVe days.

Remove denturef5) jf applicable.

Clorrimazole
Mycelex Troches 10 mg (Miles Pharm)
60 Tablets
DIssolve I tablet as a lozenge 5 times
dally for 14 consecutIVe days.

Remove denture/5J jf applicable.

ANTIVlRAL THERAPY
TREATMENT RATIONALE:
To prevent and/or treat oral herpetic
infections.

Kewconazole
Mzera! (g) 200 mg (Janssen PharmJ

Rx

Acyclovir ointment
5% Zovirax @ (Burroughs WelicomeJ

14 Tablets

Disp.:

15gm

Sig:

Apply ta oral lesions with a conon tip

applicator 6 times a day.

Note:

Treatrnenr should begin during the

earty /prodromal! stage of the recurrence.

Rx

Acyclovir
Zovirax 200 mg (Burroughs Wet/come)

Disp.:

50 CapSUles

S;9:

I capsule q.4.h. for 5 to 10 days.

Remove denture(s/ if applicable.

Note:

Treatmenr should begin during the

early stage of the recurrence In the
immunosuppressed patient

Nystatin topical powder

Mycosratin (B) ropical powder
100,000 W. ISquibb)

Rx

Llysine
Enisyl 500 mg (Person & Covey)

15 gm squeeze bottle

Disp.:

100 Tablets

Apply liberally to tissue side of clean

denrure p.e. Soak the clean denture in a
suspension of I teaspoon of powder
and 8 oz. of water over night

Sig:

Take 4 tablets q.4.h. until symptoms

subside.

Note:

Treatment should begin during the

early stage of the recurrence.

Take 1 tablet daily for 2 weeks.

Nystatin
Mycostatln Pastilles (!I 200.000 U
fSquibb!
60 Tablets
Dissolve 1 pastille in mouth 4 times daily
as a lozenge for 14 consecutive days.

121

Appendix II

THERAPEUTIC PROTOCOLS
SEDATIVElHYPNOTICS

ANTIBIOTIC THERAPY

TREATMENT RATIONALE:
To produce a "sleep-like" state for the
effective management of an oral disease or
condition.

TREATMENT RATIONALE:
To eliminate pathogenic bacterial
organisms that cause oral infection..
Rx

Phenoxymethyl PeniCillIn
Penicillin V 500 mg Tablets

Disp.:

40 Tabs

51 9:

Take 2 tablets immediately eTC

tab q.6 h. 1 hour before I1'lea$..

Flurazepam
Dalmane I 5 mg (Roche)

Rx

PeniCllhn V Porassium lIqUId

PeniCillin VK liquid 125 mgI5

Disp.:

30 Tablets

Disp.:

200ml

519:

Take) tablet h.s.

51 9:

Child should tClke ! teaspoorT:

Rx

Temazepam
ResOnl ~ I 5 mg (sandoz)

Rx

Amoxicillin
Amoxil 500 mg /Beecharr'

Disp.:

30 Tablets

Disp.:

40 Tabs

51 9:

Take 1 tablet h.s.

51 9:

Take I 500 mg tablet q.8 h

Rx

Chloral hydrate
Noctec 500 mgt 5 ml ISquibb)

Rx

OlcloxaciUin Sodium
Dynapen II!> 500 mg ISnstol

Disp.:

I pim

Disp.:

40 Tabs

5i9:

Take 1 teaspoon before bedtime or 30

minutes before surgery.

51 9:

Take 1 500 mg tablet q.8 h

Note:

For penicillinase-resistant lnfec:xr

Rx

Trimethopnm 80 mg and
Surfamethox.3zole 400 mg
&:lctrim /Rochel

Disp.:

40 Tabs

5ig:

Take

Note:

For infections involving Esche'c""

Hemophilus influenzae, Kl
Enrerobaaer species.

Rx

Triazolam
HalClon 0.25 mg /Upjohn)

Disp.:

30 Tablets

5i9:

Take 1 tablet h.s.

Rx

122

tablet q.12 h.

Appendix II

THERAPEUTIC PROTOCOLS

Metronidazole
Flagyl 500 mg 15earlel

40 Tabs

ANTIBIOTIC THERAPY - BACTERIAL

ENDOCARDITIS PROPHYLAXIS
TREATMENT RATIONALE:
To prevent bacterial endocarditis in

patients with rheumatic, congenital, or

Take 2 tablets immediately then 1 tablet

q.6 h. until gone.

other acquired valvular heart disease who

are undergoing dental procedures.

For a febrile patient with acute

necrotizing ulcerative gingivitis involving
anaerobic bacteria.

Rx

Amoxicillin, 500 mg

Disp.:

9 tabs (4.5 grams)

5;9:

Take 6 tabs (3 g). orally! hr before

dental procedure. then 1,5 9 6 hr after
the initial dose.

Note:

Standard regimen for the prevention of

bacterial endocarditis in adults and
children> 66 Ibs; (30 kg)

Rx

Amoxieillin. 250 mg

Disp.:

By weight

Sig:

Take 50 mg/kg. orally. 1hr before dental

treatment, followed by half the original
dose 6 hr after the original dose.

Note:

Standard regimen for the prevention of

infective endocarditis in children < 66 Ibs
(30 kg). The following weight ranges may
also be used for the initial pediatric dose
of amoxicillin < 15kg, 750 mg; 15 to 30
kg. 1500 mg; and> 30 kg. 3000 mg.

Rx

Erythromycin"- ethylsuccinate. 400 mg

Disp.:

3 Tabs

Sig:

Take 2 tabs orally, 2 hr before dental

treatment, followed by half the original
dose 6 hr after the initial loading dose.

Erythromycin ethyJsuccinare 400

EEl 400 mg (Abbott!

56 Tabs
Take I 400 mg tablet q.6 h. Continue
for 7 days.
Tetracycline Hel
Achromycin V 250 mg (Lederle)

56 Tabs
Take

tablet q.i.d. Continue for 7 days.

Cephalexin
Keflex 250 mg (Distal
.

...

56 Tabs
Take 2 tablets q,6 h. Continue for 7

days.

CTERIAL ENDOCARDITIS
PHYLAXIS
Clindamycin
By weight
J0

mg/kg I hr prior to dental treatment,

followed by half the original dose 6 hr
after the initial loading dose
For the prevention of infective
endocarditis in children allergic to
penicillins

OR

Rx

Clindamycin, ) 50 mg

Disp.:

3 Tabs

Sig:

Take 2 tabs orally. I hr before dental

treatment, followed by half the original
dose 6 hr after the initial loading dose.

Note:

For patients allergic to penicillin.

~erences in absorption and bio-availability require changes in dosing vvhen using different fams of erythromycin.

123

Appendix II

THERAPEUTIC PROTOCOLS
ANTIBIOTIC THERAPY - BACTERIAL
ENDOCARDITIS PROPHYLAXIS
HIGH RISK PROTOCOL - ADULT

ANTIBIOTIC THERAPY - BA
ENDOCARDITIS PROPHYLAXIS
HIGH RISK PROTOCOL - CHILD

Rx

Ampicillin

Rx

AmpICillin

Disp.:

2g

Disp.:

By weight

519:

2 9 1M or IV 30 min prior to dental

treatment.

Sig:

50 mglkg 1M or IV 30 mIn pncl'"

dental treatment

PLUS

PLUS

Rx

Gentamycin

Disp.:

Byweighr

Si9:

1.5 mg/kg 1M or IV 30 min prior to

dental treatment

THEN

Rx

Gentamycin

Disp.:

By weight

51 9:

2 mg/kg 1M or IV 30 min prlOf

treatment

1.5 g. AmoxicjIJjn. orally 6 hr ilfter

Initial dose

THEN
One haff the initial dose 6 tv Be'"

OR

The parenteral regimen may be

repeated 6 hr after initial dose
Note:

Note:

For maximum protection agaInst

bacterial endocarditis in adults at risk.

For prevention of bacterial endal:m::=

in children under 66 lbs {30 kg

ALTERNATIVE INTRAVENOUS
REGIMEN - ADULT

ALTERNATIVE INTRAVENOUS
REGIMEN - CHILD

Rx

Vancomycin
Vancocin fUlly) in parenteral solution

Rx

Vancomycin
Vancocin (LJllyJ in parental SClksUa"1

Disp.:

Ig

Disp.:

By weight

Si9:

Slowly administer I g over I hr

intravenously beginning I hr prior to
dental procedure.

51 9:

20 mg/kg IV given slowly ""'"

beginning I hr prior to dental
procedure

Note:

For prevention of bacterial endocarditis

in penicillin-allergic. high-risk adult
patients undergoing dental procedures.

Note:

For prevention of bacterial enooc...;

in penicillin.allergic. high-risk cr
undergoing dental procedures

124

III

TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

LESIONS

ease
's granules

Age

Sex

Any

M-F

Any

-..skatio
.-..curum

..._ ..u c white

M-F

Melanoderms

"""'''',e keratosis Elderly

Treatment
None reqUIred

White wiJI/Y line of vilf}'Ing length located on

Eliminate
buccal mucosa. bilaterally lesionS are
bruxism and
nomender. smooth to palpatJon. and do nO[
clenching.
rub off Variable onset; per<;lsts With oral h.3bits.

Graytsh-lNtllle patch of variable size located OIl buccal None reqUired

mucoSCl Ibllaterally). labial mucoSCl, and soft palate,
LeSions Clfe nontender. smooth to palpatiOn Clnd
dlSClppear when the mucosa is stretched
Leukoedema becomes more evident WIth
Increasing age

M-F

Eliminate
AsymmeUlc white plaque located on buccal
mucosa and labial mucosa. often blaterally,
(heft!
lesions are nonleoder. rough to palpaoon. and
~p chewing
peel slighrty when rubbed. YanabIe onset perstStS habit.
WIth cheek Of lip biting habtt

M-F

Solitary or confluent rc'llSed while plaques that

None required
rTlCly appear on buccal mucosa. labial mucosa.
alveolar ndge. floor of the mouth. ancllor soft
palate, lesions are nontender; rough to palpation,
and do f'IO( rub off Onset at blrth. perSists for I.fe

M-F

White surface slough (eschar) usually located on Eliminate

the less-keratinized alveolar mucosa Palilte
irritant,
common for food -burns- lesions are tender to
topical
palpation i1nd rub off leaving a raw or bleeding
anesthetics
surface. Onset within hours of trauma; regression and
in I to 2 weeKs
analgesicS.

lesions

oplakla

Clinical Characteristics
VhlItlsh-yeUow granules clustered In plaques
located on buccal mucosa (bllaterallyl. labial
mucosa. retrOfllCllar pad. lip. auached gingIVa.
tongue. and frenum lesJons are nonteoder.
rough to palpation. and do flO{ rub off 0"lSet
after puI:lel'ty. ~ for ~fe

Any

Mba buccalis Any

oedema

Race!
Ethnicity

21 (MFJ

Any

White patch tNt VClrit's in size, hOmOgeneity, and BiOpsy and

texture High fisk lOCations include tlocr of the
histologic
mouth, vemral tongue. lateral tongue. and
examinatIOn
uvulo-paJatal complex_ lesions do not rub off
Close
and usually are nontender. Onset occur<; after
follow-up
prOlOnged contae[ WIth an indUCing agent
mandatory.
persists as long as the InduCing agent is present.
WhIte pebbly CIrcular patches localed on upper
Use filtered
and lower Nps lkiSSlng 1es1Of1S1, Keraloses are
Clgarmes.
firm. non!ender; and do not rub off Onset II"l
conjunctIOn WIth a PfOlOnged clQ<lrette smoking ,mo""'9
habit perSISIS WIth habit.
BIopsy If
lesion
becomes
ulcerated or
Indurated.

"'"00

127

Appendix III

GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

WHITE LESIONS

Disease

Age

Sex

Race!
Ethnlcity

Nicotine
stomatitis

40-70

Any

Snuff dipper):
patch

Verrucous
c.ardnom.a

Teenage and
adult

Over 60

Any

Clinical Characteristics
White cobblestoned papules located on hard
palate. exCluding the anterior third. Papules
have red centers. are nontender. and do not
rub off. Onset is vanable to degree of smolong.
lesIons are long-standir19.

Corrugated whitlsh-yellow patch lOCated on

rrucobuccal fold, most prominent unilaterally.
Patch IS rough. nonlender and does nol rub
off. long-standing habit precedes lesion, patch
persists with continuation of habit.

128

lsee Red and/or RedMlhite Lesions)

..,.

"""'
"
...,..

Papuloncx.lular whilJsh-red mas.s located on buccal

mucosa. a~r ridge, gtngNa Lesion is firm
nomendef; rough to palpation, and does not
rub off. Long..standir19 tobacco habit precedes
onset lesion enlarges unless treated.

Squ.amous cell
c.arclnom.a

Sroc

~~?~.

t""e"I

"'

DE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

USIONS

Disease

Age

Sex

Clinical Characteristics

Race!

Treatment

Ethnicity
Purpura

M-f

My

Red spot or palCh consistlf"IQ of extravasated

blood

mat onsetS soon after uaurna

El,mInate
under~ng

Le'irDnS do not blanch upon diascopy and size

problem
varies /petechlae < ecchymosis < hematoma).
Petechiae common on soft palate; other purpurae
typically occur on buccal/labial mucosa, depending
on SIte at whICh blood IXJOIs LesIOrn fade awcry

v.icosity

~mbus

ngloma

""'" 55

""'" 30

ChildadOleSCent

M-f

Reddlsh-purple papule or nodule located on

None
venual tongue. lip. or labial mucosa. lesions are
necessary
asymptomatic and blanch upon diaSCOpy.
Surgery for
Varicosities increase in size and number with
esthetics.
increasing age and are persistent

Red to blue-purple nodule kxated on labial

SurgICal
mucosa, lip. or tongue. leslOl1S are firm and
rerTlCl'laJ and
may be render 10 palpatiOn. OnSet after traumatic histologiC
bleed, lesion is diascopy negatIVe and persists
examination.
until treatment. OCcasionally thrombi will
jf persistent or
spontaneously regress
symptomatic.

Red (0 purple. soft smooth-surfaced or

multtnodular exophytIC mass located on dorsal
tongue. buccal mucosa. or glnglVa lesions are
diascopy positive. Onset early in life; perSistS until
treated. OCcasionally hemangiomas will
spontaneously regress.

If present Since
youth. no
funaJonal
disability, and
no changes in
size. shape. or
color; no
ueatment IS

necessary.
OCherwJse.
surgery/
histologic
e.<affi.

Post-puberty

M-f

MJltlfocal red macules located on palms. fingen. None reqUired.

nail beds. face. neck. conJunctIVa. nasal septum. Monitor for
lips. tongue. hard palate. and gingIVa. LesJOns
hefTlO(rhage
are present at birth. become more Visible at
and/or
puberty. and increase in number with age.
anemia
Telangiectasias lack cenual pulsation. blanch
upon dIaSCopy. and If they rupture severe
bleedJOg may result

Birth

M-f

Syndrome associated WIth seizures. mental deficits. None reqUired.

gyriform calCifications, and a red to purple flat or Elective
slightly raised facial hemangioma. Vascular lesion surgery for
often affects lips. IabiaVbuccal mucosa. gingiva
esthetics
along branches of trigeminal flefVe. Abnormal
()(a1 enlargements may be concurrent.

~sls

2MS and

JOUComa

over 60

"'ifteditary

-.onhaglc
jectasla

e-weMr
tyftdrome

.Jewish.
AsymptOfTla!JC red macule of mucocutaneous
Mediterranean structures that enlarges and becomes raised
or HIVinfected and then darkens in color. Advanced lesions
are red--blue-violet nodules !hat ulcerate and
cause pain. The hard palate. gingIVa. and
buccal mucosa are the most common oral
Iocaoom.

PalliatIVE'.
conSisting
of radiation
therapy. laser
surgery.
chen'lOtherapy.

"'.

combinatIOn
thereof

129

Appendix III

GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

RED AND REDIWHITE LESIONS

Disease
Erythroplakia

Age

Sex

Race/
Ethnicity

Over 50

M>F

Any

Erythroleukoplakia Over 50
& speckled
erythroplakia

Squamous cell
carcinoma

Over 50

21 M:F

Any

Any

Clinical Characteristics
Red pi.l[ch of vanable size located on any oral
mucosal site. High risk areas Include floor of the
mouth, soft palate--retromolar trigone, I<Jter<'li
border of tongue. Erythropl<1kias do not rub off
and are usually asymptomatic. Lesions onset
after prolonged contact with carcinogens,
duration is varl<1ble. Regression IS rare.
Red pi.ltch with multiple foci of white. Nontender.
do not rub off, often superficially Infected With
candida. Common locations include lateral
tongue, buccal mucosa, soft pal."te, and floor
of the mouth. Onset after prolonged exposure
to carcinogens Regression unlikely even If
inducing agent IS removed.
Red, red/white, or ulcer commonly located on
lateral tongue, ventral lOngue, oropharynx,
floor of the mouth, gingiva, buccal mucosa,
or lip. Carcinoma often asymptomatic until It
becomes large, indurated, or ulcerated. Onset
after prOlonged exposure to carcinogens.
Persistence results in metastasis, usually
apparent as painless, firm, matted, fixed
lymph nodes

.....

.........
c.a.

""
" "
"""'
CJc

c
""}G

Lichen planus

Over 40

Any

Purple, polygonal, pruritic papules on flexor

surfaces of skin: occasionally finger nails are
affected, Intraoral lesions are often symptomatk:
and consist of white linear papules, reddish,
patches and ulcerated regions of mucosa. Metted
surfaces are often bilateral. Most common
locations include buccal mucosa, tongue, lips,
palate, gingiva, and the floor of the mouth.
Lesions onset with stress; persist for many years
with periods of remission and exacerb<1tion,

Electrogalvanic
white lesion

Over 30

Any

Reddish-white patches that resemble lichen pl<1nus . . " . , .

located on buccal mucosa adjacent to metalliC
restorations Lesions do not rub off and are
usually tender or cause a burning sensation
eli&>
Onset after weeks to years of exposure to metallIC ca..sn;
restoration; duration is variable depending on
">
rt:SCOR
the persistence of the allergen.

Lupus
erythematosus

Over 40

Any

Reddish butterfly rash on bridge of nose, MaculoT".,...

papular eruption with atrophic central areas rnaj
involve the lower lip, buccal mucosa, tongue and =uc;;
palate. Intraoral lesions invariably have red and
white radiating lines emanating from the lesion
Lesions do not rub off, but are tender to palpatIOn.
Onset often after acute sun exfXlsure, Lesions
persiSt and require drug treatment.

,....-

'"'

130

~ixlll

GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

AND REDlWHrTE LESIONS

Disease

Age

l.ichenold &

Adult

pus-llke
'*Y9 eruption

c.ndldl~sis

Sex

Race/"
EthnlcJty

Clinical Characteristics

Treatment

Red-white patches that resemble lichen planus

and lUpus Often the lesions are atrophic or
ukerated Centrally. Buccal mucosa, bilaterally.
is the most common site. Onset is variable and
may be weeKs or years after an allergic medication
IS begun. Regression occurs when the offending
drug is eliminated.

Withdraw
offending
drug and
substiMe

Variable appearance: white curds. red patches,

white patches with red margins. Any oral soft
tissue 5lte is susceptible: hoI.Yever; the attaChed
gingiva is rarefy affected. Onset is often
coincident with neutropenia,
and/or immune suppression.
lesions persist until adequate
anufungal therapy is provided

MUfungai

medication,

_apy

Eliminate
diabetes,

en""

crinopathy,
immune-

suppression.

13.

Appendix III

GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

PIGMENTED LESIONS

Disease

Age

Me'anoplakJ41

Sex

Race!
Ethnicity

M-F

Melanoderrns

Clinical Characteristics
GeneralIZed C()flStant daI'k patch located on
attached gIngIVa and buccal mucosa
PIgmentation vanes from light brown to dart
brown and IS often drffuse. cuMllnear.
asymp!Omauc. and does not rub off
Melanoplaklo3 pl"esent at bKth and pefSlSts fOf fe

Tanoo

Teenagers
adults

M-F

Ephelis

Any

M-F

Smoke,~

Older adult

M-F

DIffuse brown patch of several centlfnetE!fs. lJSl.0I

on posteric:N' buccal mucosa and soft palate
HIStory of heavy tobacco s~ng precedes
development of the lesion. Features may
decrease with discontinuation of the habit
Melanosis is asymptomatIC and nonpalpable

O,al melanotic
m.-eule

25 - 45

Slight male
predilectIOn

Asymptomatic brown [0 black macule usuali)'

IocClted on Io\rver lip near mldlrne, also OC~
on palate. buccal mucosa. and gingIVa Onsel
IS posHnnammatory and (he lSIon perSIstS UJ"Iti
treatment.

Nevus

Any

Any

Melanoma

25-60

caucasians.

Amalgam !attoo IS the most common type of

Intraotal tattoo Appears as a blue-black macule
on gingIVa, edentulous ndge. vestibule. palate.
or buccal mucosa. RadiographS may demonstrate
radiopaque foci. lesions are asymptomatic, do
nOl blanch. and persist for life.

Ughtskinned
persons

melanosis

especially
IIghl-skinned

proons

1J2

''''''''

Ught to dark brown macule !hat appears on facial

skin. elC(remities. or lip following sun elCposure
Ephelides are Initially small but may enlarge ana
coalesce lesions are nontender Clnd do not bW'lCt'
or rub off

Nevi are highly variable in appearance. They r'T'la'r E.""""

be pink. blue, brown, or black. but do not l:lIanc1' =XC!I!t
upon diascopy They usually appear as a blursn
~~~'-=
or brownIsh smooth-surfaced papule JocatecJ Clf'I I!
the palate. Other common Sites Include the tu::ca
mucosa. face, neck. and trunk_ Many lestOns are
present at birth. They increase in size and ~
WIth Increased age.

Panless. slightly raISed plaque (l( patCh that has

multiple colors. especially foci of brown. black.
gray. Of red. Indefined marglfls. sate(I:le lesions
and InftammatOl)' borders are charaeterrstIC
They are usually located on maxillary alveolar
ndge, palate, antenor gingJYc'l. and Iablal rrucosa
30% aflse from pre-exJsting plgmenlaUOl'lS A
recent change In size. Shape. or cOlOr IS
particularly ominous.

.te:lpendiX III

GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

ENTED LESIONS

Disease

Age

Sex

Race!

Clinical Characteristics

Treatment

Ethnlclty
-.-utz:.J~hers

syndrome

Child.
young adult

Multiple, asymptomatiC melanotic oval macules.

Oral: none
prominently located on the skin of the palmarl
required.
plantar surfaces of the hands and feet around
Gastrothe eyes, nose, mouth. lips. and perineum.
intestinal
IntraoraUy. brown dIscoloratIOns occur on the
evaluation
buccal mucosa. labial mucosa, and glnglVCl.
and geneoc
lesions do not Increase in siZe, but cutaneous
counseling
lesions often fade WIth age; mucosal pigmentatJO/l
persists for life, Colickly intestinal symptoms are
prObable

Diffuse inuaoral hypermelanotre palC~ occunng Sy5temK

in conjunction Wllh bronzing of the skin,
corticosteroids.
especiaily of the knuckies, elbows, and palmar
creases. Patches are nontender. nonraised, and
vanable In shape. The buccal mucosa and glnQiva
are most commonty affected. Onset of the disorder
is insidious and associated with adrenal gland
hypofunction. Patlenl may complain of
gClstrointestlnal symptoms and fatigue.

Adu'

Blue-black linear pigmentation of marginal

gingrva, prominemty viewed along arJterior
gingiva. Spotty gray macules may be apparent
on buccal mucosa, Neuralgic symptoms,
headache, hypersalivation are common.
Argyria: blue-gray skln pigmentation. especially
In sun-exposed areas.

Terminate
exposure {O
heavy metal.
medical
referral.
Oral lesions
require no
treatment.

13'

AppendIx 1/1

GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

PAPULES AND NODULES

Disease

Age

Sex

Race!
Ethnicity

Clinical CharacteristIcs

Retrocuspid

Child.
young adult

M-F

N1y

Smooth-surfaced pink papule, 1 to 4 mm In

diameter, located on the lingual attached gJngM!I
apical to the marginal gingiva of the mandibular
cuspds. These papuJes appear early In life. are
often found bilaterally, and regress as the paoert'
ages. The rerrocuspid papilla IS firm to paJpaoon.
asymptomatIC. and nonhemorrhaglC

Any

Welkircumscribed, soft, fluctuant yellO'NiSh

swelling that ranges in size from a f~
millimeters up to I cm, Common locations for
this nontender cyst include the lateral neck JUS[
anterior 10 the sterno-cleidomastoid muscle. tIoor
of the mou!h. lingual frenum, and ventral tongue
lesion onsets dUring chrldhood or adolescence
and persists until ueatment.

Any

Torus: bony hard nodule or mulnnodular mass

located on !he palate at the midline. or
mandibular lingual afveolar ridge. Exostosis
.nos

bony hard nodule, often multiple. located on

buccal/labial alveolar ridge. Osteoma: bony hard
nodule located adjacent to the jaWS. often
embedded In soft ossue /oJ1 3 !}'PeS 0( Ieslons
are firm. asympwmauc lunless uaumatizedl.
slow gr'O'Nlng. and Ion9"standing. Osteomas
have !he greatest growth polenClaL

papilla

LymphoepitheJial Child.
cyst
young adult

Torus, exostosis,

!\dult

and osteoma

fibroma

Mult

Upoma

Ovec 30

Upoflbrorna

134

Ovec 30

M-F

M-f

T",-",==

...,..,,==

Jrrltation fibroma: smoo[h.surfaced, pink. firm.

symmetric papule or nodule that anses at a Site
of chronic irritation, such as the buccal mucosa.
labial mucosa, and tongue. The gingwa is the
most common location for the peripheral odont~
genic fibroma. Both Jesioru; have sessile bases.
are nontender. and nonhemorThagJC

""""'"

Welkircumscribed. smooth-surfaced. domeshaped, yellowish to pink nodule commonly

located on buccal mucosa. lip. tongue. floor
of the mouth, soft palate. or mucobuccal fold
lesion is Slightly doughy upon palpation and
groINS Slowly.

""""'"

Welkll"cumscribed, smooth--surfaced, domeshaped. ptnkish nodule commonly located on

buccal Of labia, mucosa. lesion IS painless.
movable. and rather firm. Slow grcrwth and
persistence are characteristic.

""""'"
""""l'
twa

boo<So

-9'~

'"'QDIMdix III

IDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

'llt'PULES AND NODULES

Disease

Age

Sex

Race!

Clinlca' Characteristics

'h'eatment

Ethnlclty
Tlo1umo1tlc
ftflIroma

~ro'ibroma

Any

Over 25

Childhood

M-f

Small. slightly raised, firm, pressure-sensitrve papule Excisional

that is commonly located in the mandibuiar
biopsy and
mueobuccal fOld near the mental foramen,
histologic
facial to mandibular IncisorS, Nnguaf retromolar
eJlamrnatlon,
regions, and ventral tongue VisualizatIOn of the If lesiOn recurs
lesion may be difficult if the neuroma is subjacent COrticosteroid
to normal-appearing mucosa, Palpation elicits
injections may
an 'electric shock' sensation. Onset occurs
be effective.
subsequent to trauma; lesions persist until treated

Firm pink: nodules that Clre often deep-seated.

These rumors are loCated in skm. bones. Q(
lI1tTaoraIIy - buccal mucosa, tongue, CJ( lips
lesions are nontendef but movable. Contll1l..JE"d
enlargement can lead to defCJ(mity Multiple
lesions and slon pigmentations are associated
with von Recklinghausen'S disease
lneurofibromatosis).

ExcisionaJ
biopsy.
histologIC
eJlammtion
and fOllO'vv-up
fOf malignant
transformation
In cases of

neurofibromatosis

P;apllloma

30s

llIBTuColI vulgaris Chlldh/xld

young adult

Condyloma

M-f

20 - 45

Childhood.
adolescent

M-f

~mlnolltum

phollnglomi!l

Small. pink:. pebbly, slow grO'Ning papule located

on LMJIa. soft palate, longue, frenum. lips.
buccal mucosa. CJ( gingiva The base IS pedunculated and welKircumscribed. whereas the
surface is most often rough to palpatIon,

Excisional
biopsy and
histok>glC
examination.

Rough. VoIhitis~nk: papule located on the skin of Excisional

the hands. and perilablally on the lips, labial
biopsy and
and buccal m..x:osa, and attaehed gingiva. Lesions histologic
are skwgro..ving and have a sessile base.
examination.
Verrucae may regress spontaneously or spread to
adjaCent mucocutaneous surfaces.

Small, plnk-to<lirty gray papule With rough,

papillary surface that resembles a cauliflO'Ner.
Base of COndyloma is sessile and the borders are
raised and rounded Lesions occur in multiples
and onset rapidly folfONing rnoculation from
affecled sexual partner. Most common location IS
genitalia. labial mucosa. labial commissure,
anached gingrva. and soft palate. lesions can
spread and coalesce into extensive clu'ilers

Excisional
biopsy and
histologiC
examination.

Soft. compreSSible. pinkish-white swelling that

Surgical
may be superficial or deep-seated. Superficial
excision;
lesiOns resemble papillomas; deep-seated lesiOns depending on
cause diffuse enlargement. lymphangiomas
size and
may occur In neck IcystK: hygroma). dorsallocation.
lateral tongue. lip. or labial rruc:O$Cl. long-standing
surgery may
lesions can cause functional problems or regress
require
g""",,,1
spontaneously.
anesthel:JC

135

Appendix III

GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

VESICULOBUUOUS DISEASES

DIsease

Age

Sex

Race!

ClinIcal Characteristics

Ethnlclty
Primary
Infant Child,
herpetic:
young adult
glng Ivostomatltls

Multiple vesICles that rupture, coalesce. and f(l(lTl

ulcers of the tip. buccal and labial mucosa.
gingiva. palate. and tongue. Ulcers are painful
and initially are small, yellOW. and have red

M-F

inflammatOf)' borders. Onset is rapid. several days

after contaCt WIth person haroorrng the virus
lesiOnS persiS! for 12 to 20 dayS

Recurrent herpes
simplex

Herpangina

Adult

Child.

MUltiple small vesiCles that rupture and ulcerale

These lesiOns occur repeatedly at same site,
usually the lip. hard palate. and attached glngN<l
Onset is rapid; preceded by prodromal bumlng
or tingling, Duration is 5 to 12 days. Heals
spontClneously.

M-F

D.ter 55,

My

M-F

over 35 in HIV+

Hand-foot
and-movth
disease

Child.

young adult

Allergic reactions
JmmecUate

Any

Vesicles on skin and face that after rupturing

resemble a "deo.v drop_' Intraorally ulcers may
be seen on soft palale. buccal mucosa. and
rrMJcobuccal fold. Skin lesions crust over and
heal with 5Gl{ formation. CondltJOn otten
accompanied by chills. fever nasophal)'fl9ltJi.
and malaise. Spontaneous healing
occurs in 7 to 10 days.
Unilateral vesicular and pustular eruptions that
develop over I to 3 days. lesions occur along
dermatomes and especially along the trigeminal
nerve tract. lesions are vesicular. uicerative.
intensely paInful and commonly affect me lip.
tongue and buccal mucosa extendIng up
to the mIdline Neuralgia may persist after healing

M-F

:~:~:
~

Crops of mUltiple small yellO'Nish ulcers that ocas

on palm and sole of hand and foot. Inuaorally
the tongue.hard palate, buccal and labial
mucosa are affected. Total number of lesions may
approach 100. Healing occurs spontaneous~ IJ1
about 10 days.
Red swellings or wheals that occur perioral~ or en ~
lips. buccal mucosa. gingiva. lips, and tongue
~
Contact wim allergen usually precedes epISOde
by a f(W ITllnutes to hours. warrnd1. tenseness.

and itchiness are concurrent L.esions regress If the

allergen is withdrawn.

136

(J'

rrMJltiple discrete .shallovol ulcers lesions have

etythematouS border and arE' bmlled to anlenor
pillars. soft palate. lMJIa. and tonsils. PharyngltlS.
headache. fever; and lymphadenitis are often
concurrent. lesiOns heal spontaneously Within
1 to 2 weeks.

Child

Herpes zoster

::~~

light gray paprllary vesicles that rupture formtng

M-F

youngaduJt

Chicken pox

~ndixlII

GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

VESICULOBUUOUS DISEASES

Age

Disease
Allergic reKtJons
delayed

Erythema
m"ltJforme

Sex

Any

Race!
Ethnicity
Any

Clinical Characteristics

Itct erythemal:ous lesions tllat may eventuaty

ulcerate May occur on any cutaneous or
mucocutaneous surface. IntraOl"alty me lips,
gingiva, alveolar mlJCOsa. tongue. and palate
are affected. Erythema develops slowty over 24
to 48 hours Fissuring and ulceration may result.

Young adult

My

Treatment
""gen;
"""""'
"
corueo
steroids.

Skin - rilrget lesions. Oral- hemorrhagic crust of the Topical

lipS: painful ulcerations of me tongue. buccal
mucosa. Attached gingiva rarety affected.
Headache. kJv.J-grade fever; and previous
resplratory infection often precedes lesions.

analgesics.
antipyretics.
flUIds.
cO!1icosteroids.
amibioocs to
prevent

>e<onda<y
infeclJOn

Slight
SteYens.Johnson Child.
syndrome
young adult preference

Skln - target lesions. Eye - conJunctivitis. Genital- Topical

balanitis. Oral - hemorrhagic crust of the lips:
analgesics.
painful ulcerations and weeping bullae of the
antipyretics,
tongue. buccal mucosa, Attached gingiva rarely fluids.
affected. Stevens-Johnson syndrome is the
corricofulminant form of erythema mu/tlforme.
steroids.
Eating and swallO'Nlng often are impaired.
antibiotics to

for males

"'''''''''
>e<onda'Y
infection.
hospitalitauon

Pemphigi"s
v"lgarJs

30-50

M-f

light skinned

persons. Jev.nsh

"'"
""""persons

a.nlgn mucous
Membrane

pemphigoid

Over 50

2:1 F:M

Multiple skin and mucosal bullae !hat ruptUre.

hemorrhage. and cruSt lesions tend to recur
In the same area. have cIrcular or serpiginous
borders. and tend to spread to adjacent areas.
Nikorsky sign positIVe. CO/lapsed bullae is a
common sign. Dehydration can occur if
lesions are extensive.

Medical
referral.
sy'itemic
steroids.
and oral
topical
steroids.

Bullae on skin folds. ingUinal and abdominal areas. Oral topical

Corneal lesions can lead to scarring. Bullae often steroids.
are hemorrhagic and persist fOf days then
Medical
desquamate. lesions occur on the gingIVa. palate referral and
and buccal mucosa.
systemic
steroids
rf severe; rule
out cOl"neal
involvement
and
internal
malignancy.

137

Appendix III

GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

ULCERATIVE LESIONS

Disease

Age

Sex

Race!

Cllnlca' Characteristics

Ethnlcity
Traumatic ulcer

My

SymPCOrrt.:lliC. yellow-gray ulcer of variable SIze

and shape, depending on IndUClrlg agent_
Ulcers are often depressed and usually oval 111
shape with erythematous border Commonly
located on labial and buccal mucosa. tongue at
the borders. and hard palate Duration is I to

2 weekS.

Recurrent
aphthous
stomatitis

Young adult

Srnau yellowlsh oval ulcer WIth red border. Icxat:eo ~:;~;=

on movable non-keraClnlled mucosa. COfm'lC:W1
:
SItes Il1Clude labial mucosa. buccal mucosa. tIoc.Ir ::::of the mauCh. longue. and occ.asK>nally soft palCtt aJ...Ir:
UlCers are lender and may be associated WIth a
tender ~ph node lesions onset raptdly and
disappear in 10 10 14 days without
SG3f tormaoon

Pseudoaphthous
ulcer

25 - 50

DepresSed yellowish round<lv'ar ulCer located on

movable nOr'l-kerarinlzed mucosa. Common SItes
include labial mucosa, buccal mucosa, floor of
the mouth, tongue, and occasionally soft: palate
Tongue may demonstrate atrophied papillae
Ulcers are tender, onset during deficiency state
and disappear with replacement therapy within

20 days.

;~~~~
':;s_
::oc:il

...
2

,e~

Major aphthous Young <tdult

stomatitis

138

Asymmetric unilateral ulcer with necrotic and

depressed center. Ulcers have a red inflammatory
border and are extremely painful. located on soft
palate. consillar fauces. labial mucosa, buccal
mucosa, tongue: may extend onto attached
gingiva. Rapid onset. Underlying tissue is often
destroyed. lesions heal In 15 to 30 days with scar
forrrt.:ltion. Recurrences are common.

~=::~

.ac:oendix III

DE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS

RATIVE LESiONS

Disease

Age

Sex

("petirorm

20,

20-30

3: I (MF)

~e,atlon

Chemo-

ttwraPMItlc
ulcer

OIer 50

15to30and
older adult

ClinIcal CharacteristIcs

Treatment

Multiple pmhead-$ized yellOWIsh ulcer$located on Tetracycline

movable non-keratinlzecl mucog, Common $ite$ rime<;.
include anterior tip of tongue. labial mucog. and
floor of the mouth No ve<;icle formatIon. Ulcers are
painful and may be associated WIth several tender
lymph nodes le$ions ome( rapldly and dlo;appear
in 10 [0 14 day!: WIthout $car formatIOn.

Asian,
Eye - conjunctivitis. irins; Genital - ulcers; Oral Mediterranean,
painful aphthc:ll.5-1ike ulcers on labial and buccal
Anglo
mucosa. S1un - maculopapular r.Nl and nodular
eruptIOnS. Oral ulcers are often an initial Sign of
the disea$e onset. Mhritis and gastrointestinal
complaints may be concurrent. Recurrences,
exacerbations. and reml$$iom are likely.

Topical and

systemic
steroids

Asymptomaoc, cobblestoned ulcer that usually

BiOpsy.
occurs on dorsum of tongue, or labial
histologic.
commi$sure. Cervical lymphadenopathy and
examination.
primary respiratory complaint often is concurrent. Tuberculosis Onset of oral disease fol~ lung Infection of
streptomycin
$everal weeks to monthS duraDon Oral ulcer
and isoniazid.
may per$i$t for months to years If underlying
~
disease not treated.
AlI~delCil B.

Sr"any'omatovs Older adult

"Ice,
'nlbercYlosls.
plasmosisl

SqlUlmous cell
urdnoma

Race!
Ethnlclty

2:1 MF

M-F

Nonpalnful yeUovvish ulcer WIth red indurated

bc:lrders commonly located on pasterll)( third
of the lateral border of tongue. Vffiual tongue.
lips. and floor of the mouth. AssoclCltec! features
may nclude numbness, leukoplakia,
erythroplakia. induration. fixation. fungation.
and lymphadenopathy. Caronoma has a sk:rw'
~ and is often notICed after a recent Increase
In sIZe

Surgery.
rachaoon

IrregUlar ulcerations of the lips, labial and buccal

mucoo;a. tongue. and pal<lte. Red inflammatory
border is often IackJOg. Hemorrhage is likely
when ulcers are deeply situated. lesions are
extremely palnful and usually ~ffilt mastication
and swallQlNing. Onset during second week of
chemotherapy. Secondary infection with oral
microorganisms is likely.

Antimicrobial
rinses to
prevent
seconda<y
infeeoon.
Topical
anesthetiCS,
IV fluids.

therapy,
and/or
chemotherapy.

1J9

Appendix IV

SELF-ASSESSMENT QUIZ
1. fFig. 49-)) This soft tissue swelling was observed on
the gingiva of a 7-monch-old infant. The infant's mother
sCates that during the past several days the lesion has slowly
increased in size. Aspiration yielded a straw-colored fluid.
This lesion is most likely a:
A. congenital epulis of the newborn
B. congenitallymphangioma
C. mucous retention phenomenon
D. gingival eruption cyst
E. traumatic hyperplasia

6. 'Fig. 49-5) This raised soft tissue leslm

~~~~
the patient"s lower lip. In the central region 01
appears translucem. Palpation reveals the I~
and fluctuant. The differential diagnosis for
should include:
lympangioma
hemangioma
varix
D. mucocele
E. all of the above

A.
B.
C.

7_ ,Fig. 49-5) The most likely diagnosis

of"'o===-

A. Iympangioma

B. hemangioma
2. (Fig. 49-2) This dome-shaped papule on the ventral
surface of the tongue is soft and fluctuant. Although the
lesion is painless. the lesion occasionally fluctuates in size.
A history of trauma was confinned. The most likely diagnosis for this lesion is a(n):
A. fibroma
B. lymphoepithelial cyst
C. mucous retention phenomenon
D. accessory salivary gland tumor
E. bulla of pemphigoid

3. 'Fig. 49-31 A 34-year-old man who is a member of the

wind section of the symphony arrives at the dental clinic for
evaluation of a sore lump on his palate. He states that he
was unaware of the swelling until 4 days ago, when the
reed of his clarinet contacted the lesion. Palpation reveals
the mass to be very finn. This patient most likely has a(n):
A.
B.
C.
D.
E.

periapical abscess
incisive canal cySt
necrotizing sialometaplasia
adenocarcinoma of the palate
traumatic ulcer of the palatal torus

4. 'Fig. 49-41 A healthy 9-year-old male appears at the

dental clinic with this soft tissue mass. It has been present
for 3 weeks. but has progressively increased in size. The
patient claims that moderate bleeding occurs every time he
brushes. so he has avoided brushing that area for the last
several days. All the adjacent teeth are asymptomatic and
test vital. Periapical radiographs of the area reveal no abnormalities. This lesion shows features of malignancy.
A. troe

B. false

C.

vanx

D. mucocele

8. (Fig. 49-6) A 45-year-old woman appe3Ba

clinic with this pink: smooth-surfaced papuk_ II

diameter and is linn and nonfluccam. 11le ...

~~':.::.~"~~:
present for several years and has slowl) IflCleasot
The lesion is most likely a(n):
irritation fibroma
peripheral odontogenic fibroma
C. parulis
D. pyogenic granuloma
E. lipoma
A.
B.

9. (Fig. 49-7) This asymptomalic speclkd ~ _ . . , .

patch of the tongue was found in an el~
admitted to heavy alcohol and tobacco au.e n "",.
was aware of the lesion's presence but \10m :~::~
the duration. The lesion was finn 10 palpanca
likely diagnosis of this lesion is:
A.
B.
C.
D.
E.

an accessory salivary gland tumor

traumatic erythema
candidiasis
squamous cell carcinoma
lichen planus

10. (Fig. 4981 This asymptomalic le~.~:.:~~::

ered in a 45-year-old woman who has had jo
removed from her trunk over the last se\
tenn that best describes this lesion is:
A.
B.
C.
D.

macule
papule
plaque
patch

5. (Fig. 49-4) The most likely diagnosis for the lesion

described in question 4 is:

11. (Fig. 49...a) The most likely diagnosn

A.
B.
C.
D.
E.

A. melanoplakia
B. melanotic macule
C. blue nevus
D. intramucosal nevus
E. malignant melanoma

irritation fibroma
peripheral odontogenic fibroma
peripheral giant cell granuloma
peripheral fibroma with ossification
pyogenic granuloma

142

=11I
~-.

Fig. 49-1. COUrtesy Dr Barney Olsen

Fig. 49-2.

Fig. 49-3.

Fig. 49-4.

Fig. 49-5. Courtesy Dr Nancy Manuch

Fig. 49-6. Courtesy Dr CUI1 Lundeen

Fig. 49-7. Courtesy Dr.James COUonE'

Fig. 49-8. Courtesy Dr Mcnear VIti

143

Appendix IV

SELF-ASSESSMENT QUIZ
12. IFig. 50-11 A 66-year-old man presents 10 the dental
clinic complaining of pain associated with Ihese lesions on
his tongue. He states that the lesions cropped up overnight
and the discomfort he is experiencing is limiting his abiliIy to swallow. Although the patient has had a history of
intraoral ulcerations. he says thai he has neyer before had
one in this location. The most likely diagnosis for this condition i~:
A.
B.
C.
D.
E.

recurrent herpes simplex

aphthous stomatitis
traumatic ulceration
herpangina
pemphigoid

13. (Fig. 50-2) This ulcer appeared 8 days ago in a 31year-old homosexual man following a yacation in the
Carribean. He claims that the lesion began as a vesicle. but
enlarged oyer the last seyeral days. and is now quile
painful. The regional lymph nodes on that side are tender
10 palpation. This lesion is most likely a:
A.
B.
C.
D.
E.

traumatic ulcer
recurrent aphlhous ulcer
re<:urrent herpetic ulcer
syphilitic ulcer
granulomatous ulcer

14. (Fig. 50-31 Two months 3fter you treated the patient
in Figure. 50-2 he returns to the dental clinic for an operatiye appointment. Your examination reveals scauered white
plaques on the lateral border of the tongue and persistent
anterior and posterior cervical lymphadenopathy. A low
grade fever is also concurrent. This patient demonstrales
clinical features most consistent with:
A.
B.
C.
D.
E.

lichen planus
lupus erythematosus
infectious mononucleosis
syphilis
HIV infection

15. {Fig.50-3) The condition affecting Ihis patient's

tongue is most likely:
A.
B.
C.
D.
E.

coated tongue
hairy tongue
hairy leukoplakia
leukoplakia
erythroleukoplakia

16. {Fig. 5041 A 34-year-old H1V-posilive man appears

at the dental clinic complaining of a burning tongue.
Clinical examination reveals an isolated area on the dorsal
surface of the tongue that is red and denuded. Bacterial and
fungal cultures are obtained. Forty-eight hours later the fun-

144

gal cultures are reponed to be negathe: lite ~::::~~

tures are positive for gastrointestinal flora. Tbe
causali\'e organism is:
A. Escherichia coli
B. Strepw("(x'cus mlllans

C. S,reprococclis I'iridans
D. Actinomyces I'iscnms
E. Treponema pallidum

\\.oman~~p<~....-~~~~

17. fFig. 50-51 This 28-year-old

dental clinic with the chief complailll of a
tion in my mouth and throat:' She has no
plaint of dryness. Review of her medical hi~
recent upper respiratory infection which ",as ~
l4-day course of amoxicillin. Imraorally one fi
::~~
red patches on buccal mucosa. soft palate. ar:d
pharyngeal wall that are tender to palpation. ThM~
is most likely:
A.
B.
C.
D.
E.

lichen planus
pemphigoid
pemphigus
acute atrophic candidiasis
chronic atrophic candidiasis

18. (Fig. 50-61 These linear white plaques \\oCR

ered in a 50-year-old woman during a routine ~
ination. The patient claims she has been under
stress lately because of family problems. The ~-::~
asymptomatic and do not rub off. The most Iil..t.
sis is:
A.
B.
C.
D.
E.

lupus erythematosus
lichen planus
candidiasis
frictional keratosis
none of the above

19.IFig. 50-11 A 45-year-old black woman appe:r

dental clinic with a swelling of the palate thai has
ly enlarging over the past severnl months. 1lle Iesit'.
less but finn to palpation. The condition is most
A.
B.
C.
D.
E.

periodontal abscess
palatal abscess
palatal torus
pleomorphic adenoma
malignant accessory salivary gland tUrTl(W

20. fFig. 50-81 This 53-year-old woman camedenial clinic because of burning, painful gingi\a. .
sional biopsy was performed, and during the initial _ _m:
Ihe gingiva began to slough. The biopsy report i'-:~:
thai the epithelium was separating from the lamma
below the basal cell layer. The most likely diagnosu
A.
B.
C.
D.
E.

pemphigus
pemphigoid
lichen planus
lupus erythematosus
erythema multifonne

Fig. SO-I.

Fig. S0-2. Courtesy Dr

Fig. S0-3. COUrtesy Dr WilCheaI VII

Fig. SG-4. Courtesy Dr Sol SIlverman

Fig. SO-So

Fig. SG-6.

Fig. SO-7.

Fig. 50-8. Courtesy Dr Nancy M<!ntlch

\1Ic:heal Vitt

145

Appendix V

GLOSSARY
-\bdomen: That pan of the body lying between the thorax
(chest) and pelvis.

Anomal.v: Deviation from normal.

Anorexia: A lack or loss of appetite for food.

-\cute: Having severe symptoms and a short course.

Anterior: Located toward the front (opposite of posferior).
-\drenal gland: A small endocrine gland located near the
kidney that secretes endogenous glucocorticosteroids.
\\ihich conlrol digestive metabolism; mineralocorticoids.
lo'h.ich connol sodium and potassium balance: sex hormones: and catecholamines (epinephrine and norepinephrine). which aller bloext pressure and hean function.

Antibiotic: A chemical compound that inhibits the growth

or replication of certain forms of life. especially
pathogenic organisms such as bacteria or fungi.
Antibiotics are classified as either bioslatic or biocidal.

.\drenalectomy: Surgical removal of the adrenal gland.

Antibiotic sensilivily: Testing a suspected organism to see

if if is sensitive to destruction by one or more specific
antibiOlics.

.\Junctional: Not functioning or working.

"genesis: Complete absence of a structure or pan of a
structure due to an absence of the tissue of origin in me
embryo.

.\IDS: Acronym for Acquired Immune Deficiency

Syndrome. reserved for patients infected with HJV
(Human Immunodeficiency Virus). It also refers to the
tenninal stage of the disease.
.\..Ilergen: A substance capable of inducing hypersensitivity or an allergic reaction.
.\malgam: An alloy used to restore teeth. composed mainly of silver and mercury.

Antibody: A protein produced in the body in response to

stimulation by an antigen. Antibodies react specifically
10 anligens in an auempt to neutr.dize these foreign substances.
Antigen: A substance, usually a protein. that is recognized
as foreign by the body's immune system and stimulates
formation of a specific antibody to the antigen.
Antipyretic: A drug or substance used for the relief of
fever.
Aplasia: Absence of an organ or organ part due to failure
of development of Ihe embryonic tissue of origin.
Arthralgia: Pain in one or more joints.

-\melogenesis: The formation of the enamel portion of the

toom.
.\mputation: Strictly. this term refers to the removal of a
limb such as an ann or of an appendage such as a finger.
With reference to a neuroma, however, amputation means
a tumor of nerve tissue due to the severing of a nerve.
-Ulalgesic: A drug or substance used for the relief of pain.
.\.nalogous: Having similar properties.
"naplastic: Pertaining to adult cells that have changed
irreversibly toward more primitive cell types. Such
changes ure often malignant.
.\.nergy: A total loss of reactivity to specific antigens.

Aspiration: 1lle withdrawal of fluid, usually into a syringe.

Asymptomatic: A lack of symptoms or complaints by the
patient.
Atherosclerosis: A condition consisting of degeneration
and hardening of the walls of arteries due to fat deposition.
Atopy: Hypersensitivity or allergy due to hereditary
influences.
Atrophic: A normally developed tissue that has decreased
in size.
Atypical: Pertaining to a deviation from the normal or typical state.

"ngioma: A tumor made up of blood or lymph vessels.

.\.nodontia: Congenital condition in which all the teeth fail
to develop.

Autoinoculation: To inoculate with a pathogen such as a

virus from one's own body. An example would be to
spread herpes from your own mouth or lips to your finger.
149

Appendix V

GLOSSARY
Autosomal dominant: The uppearun<.:e in offspring of one of
two mUlually antagonistic fealures in association with one
of the 22 pairs of chromosomes in humans Ihat is not concerned with sexual determination.
Bacterial plaque: A collection of bacteria. growing in a
deposit of material on the surface of a tooth. that is
capable of causing disease.
Bilateral: On bOlh sides of Ihe body.
Biopsy: Excision of living tissue for the purpose of examination by a pathologist.

Cirrhosis: A chronic disease of the liver charactimJElo<

degenerative changes in the liver cells. the de""'....,.
connective lissue. and other changes. The resuh
the liver cells .'Stop functioning and Ihe flov. of
through the liver decreases. There are man) ""_.,,,
cirrhosis. including infection. toxic subst~
chronic alcohol abuse.
Cla\'icle: The collar bone. connecting the shoulder
(scapula) to the chest bone (sternum).
Coagulation: The process of cloning. usuall) of
Cloning is the natural means by which a patiea
bleeding when a vessel has been severed.

Bosselated: Covered with bosses or bumps.

Bruxism: A habit related to stress or a sleep disorder.
characterized by grinding one's leelh.
Bulimia: An ealing disorder characterized by frequent periods of excessive food consumption followed by the
purging of the ingested food by vomiting and/or the use
of laxatives.
Bulla: A circumscribed, fluid..-containing, elevated lesion
of the skin more than I crn in diameter.
Carcinogen: An agent thai induces cancer.
Carcinoma: A malignant growth made up of epithelial
cells that are capable of infillration and metastasis.
Carcinoma is a specific form of cancer.

Collagen: A protein present in the connective 1Issar:

body.
Coloboma: A developmental defect Ihal may affen
ous pans of the eye, characterized by a mlssJn~ I*'"
the structure affected. For example. a coloboma
lower eyelid means a missing pan of the lower~.....
Commissure: The junction of the upper and lo\o\tt
the comer of the mouth.

_.,.or.

Complement: A series of enzymatic proteins in

serum that. in the presence of a specific sensitiza.
destroy bacteria and other cells. CI through C9 aK'
nine components of complement that combme
antigen-antibody complex to produce lysis.
Concretion: A hardened mass such as calculus.

Cellulitis: A spreading. diffuse. edematous, and sometimes

suppuT1uive (pus-producing) inflammation in cellular tissues.
Cervical lymphadenopathy: Abnormally large lymph
nodes in the neck, often caused by lymphocyte replication in response to a disease state.
Chemotaxis: Taxis or movement in response to chemical
stimulation.
Chemotherapy: Treatment by chemical substances Ihal
have a specific effect on the microorganisms causing
the disease. This term is usually reserved for the treatment of cancer wilh the use of drugs, thai inhibit rapidly
reproducing cells. Side effects are possible.
Chronic: Persisting over a long time: when applied to a
disease, chronic means that there has been little change
or extremely slow progression over a long period.

150

Concurrent: One or more conditions. events, or fi_"'~

occurring at the same time.
Congenital: Present at. or existing from the time of
Constitutional symptoms: Symptoms affecling die
body, such as fever, malaise, anorexia. nausea..
lethargy.
Cornified: A process whereby a tissue has beuxue
or has thickened its outer coating.
Culture: The propagation of an organism in a .........
conducive to growth.
Cyst: A pathologic epithelium-lined cavity. us
taining fluid or semisolid material.
Cytologic: Pertaining 10 the scientific study of celh..

C~lOpathic:

Pertaining 10 or chamclerized by palhologic

changes in cells.

mesoderm and Ihe innermost layer is the endodenn.

EClOdennal structureil include the skin, hair, nails, oral
mucous membrane, and the enamel of the teeth.

Debilitation: The process of becoming weakened.

Dt'Ciduous tooth: The primary denlition. or baby leeth.
The normal number is 20.

EClopic: Located in an abnonnal place. The ectopic tissue

or slruclure mayor may nm be nonnal.
Edema: Abnormal amounts of fluid in the intercellular
spaces. resulting in visible swelling.

Deglutition: The process of taking a substance through the

mouth and throat into the esophagus. Deglutition is a
stage of swallowing.

Emanate: To gi"e off or flow away from.

Dehydration: The removal of water from a substance.

Prolonged fever and diarrhea cau~e dehydrotion.

EmbrJonic: Pertaining to the earliest stage of development of an organism.

Dtntallamina: 'The embryonk: tissue of origin of the teeth.

Encephalitis: Inflanunation of the brain.

Oe\'elopmenlal: Pertaining to growth to full sir'c or maturity.

Endocrinopathy: A disease or abnormal stale of an

endocrine gland.

Diascopy: The examination of tissue under pressure

through a transparenl medium. For example suspected
,ascular lesions are examined by pressing a glass slide
over an abnormality to see if the reddish tissue turns
white. Since blood flows through vascular lesions. pressure causes them to tum white. thus helping to confirm
the diagnosis.
Distal: Farlhest from a point of reference. In dentistry,
distal describes the surface farthest from the midline of
lhe patient.

Endodermal: Pertaining to the innermost of the three

primitive genn layers of an embryo. Endodennal structures include the epithelium of the pharynx. respiratory
tract (except the nose), and the digestive tract.
Epistaxis: Bleeding from the nose.
Epilhelium: The cellular makeup of skin and mucous
membranes.
Epulis: A nodular of lUmerous enlargement of the gingiva.

Dorsal: Directed toward or siluated on the back surface

(opposite of venlml).
Dysplasia: An abnormality of developmenl characlerized
by the loss of normal cellular architecture.
Dysplastic: Penaining to an abnormality of development.
This term is often used 10 describe the appearance of
abnormal. premalignant cells under the microscope. The
cells begin to lose their normal maturation pattern. and
have abnormally shaped, hyperchromatic nuclei.
O~'spnea:

Erosion: The wearing away of teeth through Ihe aClion of

chemical substances, or a denudation of epithelium
above the basal cell layer.
Eruption: An emergence from beneath a surface. For teelh.
eruption means Iheir growlh imo Ihe oral cavity: it may
also refer 10 the development of skin lesions.
Er)'themalous: Characterized by a redness of the tissue
due to engorgement of the capillaries in the region.
El),thematous lesions blanch on diascopy.

Labored or difficult breathing.

Ecchymoses: Large reddish-blue areas caused by the

escape of blood into Ihe tissues, commonly referred to
as a bruise. Ecchymoses do not blanch on diascopy.
Ecosystem: The interaction of living organisms and nonliving elements in a defined area.
Ectodermal: Pertaining to the outennost of the three primitive genn layers of an embryo. The middle layer is the

Erythroplastic: Characterized by a reddish appearance.

This tenn implies abnormal tissue proliferation in the
reddish area.
Eschar: A slough of epithelium oflen caused by disease.
trauma. or chemical bum.
Esthetic: Penaining 10 the appearance of oral or dental
structures or the pleasing effect of dental restorations or
procedures.
151

Appendix V

GLOSSARY
Etiolog)': The cause or causes of a disease. or the study
lhereof.
E"erted: Folded or turned outward.
Exacerbation: An increase in severity.

Frenum: A fold of mucous membr:me that I

movement of an organ or organ pan. For e\
lingual frenum limits longue movement. and the
frenuli limit lip movements.

Exanlhematic: Characterized by the development of an

eruption or rash.

Frontal bone: This bone fonns the pan of the

sisting mainly of thc forehead. The frontal bone
sponds to the fronl pan of the skull and conwn.. _
space called lhe frontal sinus.

Excisionul biopsy: To completely remove a mass of tissue

for the purpose of scientific analysis.

Furcal: Pertaining to or associated with lhe pan of a

rooted tooth where the roolS join the crown.

Exophytic: An outwardly growing lesion.

Ganglion: A collection of cell bodies of neurons ou...~

the central nervous system. A ganglion is esse
terminal through which many peripheral cireui
neet with !he central nervous syStem.

Extensor surface: Since the anns and legs can be extended or tensed by the appropriate extensor or tensor muscles, the anlerior surface is referred to as the extensor
surface and the posterior surface is referred to as the
tensor surface.
Extirpate: To completely remove or eradicale.
Extremity: A limb of the body. for example an ann or leg.
Exudate: Material that has escaped from blood vessels
into tissue or onto the surface of a tissue, usually
because of inflammation.

Gastroenterologist: A medical specialist whose fi

disorders of the stomach and intcstine,
Gastrointestinal: Penaining to the stomach and in
Genetic counselling: A form of patient counsell "'which the transmission of inherited traits is disc
Gingivectomy: Surgical removal of gingival tissue.

Fascial plane: Spaces between adjacenl bundles of fascia thaI

cover muscles. Infection often spreads along these planes.

Glaucoma: A disease of the eye charaCteriZN

increased intraocular pressure. This condition is
asymplomatic and, if not recognized or treated.
blindness.

Fenestration: A perforation or opening in a tissue.

Glossal: Pertaining 10 or associated with the lOngue.

Fetor oris: An unpleasant or abnormal odor emanating

from !he oral cavity.

Glucose: A form of sugar that is the most imponant

hydrate in the body's metabolism.

Field Cancerization: Malignant growths occurring in

mulliple sites of the oral cavity. Oflen the oral tissues
have been exposed to a carcinogen for a long time.

Glucosuria: The presence of an abnonnal quantit> 0(

case in the urine. A sign of diabetes mellitus.

Factitial: Self-induced. as in factitial injury.

Fissure: A narrow slit or clef!.

Fluctuant: Strictly. this tenn describes a palpated, wavelike motion that is felt in a fluid-containing lesion. In
this text, lhe teon is frequently used to describe a soft.
readily yielding mass on palpation.

Granulomatous: Penaining to a well-defined area th:a

developed as a reaction to the presence of living orp
isms or a foreign body. The tissue consists primaru,
histiocytes.
Gravid: Pregnllnt.
Halitosis: An unpleasant odor of the brellth or expired __

Fontanelle: One of several soft spots on the skull of

infants and children where the bones of the skull have
not yet completely united. In these areas the brain is
covered only by a membrane beneath the skin.

152

Hamartoma: A tumor-like nodule consisting of a ml

of normal tissue usually present in an organ but ell
in an unusual arrangement and/or an unusual site.

Hapten: An incomplete allergen. When combined with

another substance to fonn a molecule. a hapten may
stimulate a hypersensitivity or allergic reaction.

Hyperdontia: A condition or circumstance characteri7..ed

by one or more extra. or supemumemry teeth.
Hyperemia: 1lle presence of excess blood in a tissue area.

Hematopoietic: Penaining to the production of blood or of

lts constituent elements. Hematopoiesis is the main
funclion of the bone marrow.
Hematoma: A large ecchymosis or bruise caused by the
escape of blood into the tissues. Hematomas are blue on
the skin and red on the mucous membranes. As hematomas resolve they may tum brown. green. or yellow_
Hematuria: The presence of blood in the urine.
Hemihypertrophy: The presence of hypertrophy on one
side only of a tissue or organ. For e:r;:ample. in facial
hemihypertrophy one half of the face is visibly larger
than the other.
Hemoglobin: The Iron-contammg pigment of the red
blood cells. Its function is to carry o:r;:ygen to the tissues.
One of the causes of anemia is a deficiency of iron.
causing patients to look pale and feel tired.
Hemolysis: Generally speaking. this tenn refers (0 the disintegration of elements in the blood. A common fonn of
hemolysis occurs during anemia and involves lysis or
the dissolution of red blood cells.
Hemorrhage: Bleeding: the escape of blood from a severed blood vessel.
Hemostasis: The stoppage of blood flow. This can occur
naturally by dOlling or anificially by the application of
pressure or the placement of sutures.
Hereditary: Transmined or transmissible from parent to
offspring: detennined genetically.
Hiatal hernia: Protrusion of any structure through the hiatus of the diaphragm. Affected patients are prone to
indigestion.
Histiocyte: A large phagocytic cell from the reticuloendothelial system. The reticuloendothelial system is a network made up of all of the phagocytic cells in the body.
which include macrophages, Kupffer cells in the liver.
and the microglia of the brain.
Histology: The microscopic study of the structure and
form of the various tissues making up a living organism.

Hyperglycemia: The presence of excessive sugar or glucose in the bloodstream.

Hypermenorrhea: Excessive uterine bleeding of unusually long duration at regular intervals.
Hyperorthokeratosis: Keralin is the outermost layer of
epithelium as seen under the microscope and is seen in
TWO forms: onhokeratin and parakeratin. Orthokeratin
has no visible nuclei wilhin the outer layer. whereas in
parakeratin nuclei are present. HyperoTlhokeratosis is
the presence of excess onhokeratin.
Hyperplasia: An increase in the size of a tissue or organ
due to an increase in the /lumber of constituent cells.
Hypersensitivity: Generally this term means an abnonnal
sensitivity to a stimulus of any kind. The term. ho\\ever.
is often used with specific reference to some form of
allergic response.
Hypertension: High blood pressure.
Hypertrophy: An increase in the s;:e of a tissue or organ
due to an increase in the size of constituent cells.
Hypocalcifteation: Less than normal amount of calcificalioo.
Hypodontia: The congenital absence of one or several
teeth as a result of agenesis.
Hypoplasia: Incomplete development of a tissue or organ:
a tissue reduced in size because of a decreased number
of constituent cells.
Hypopyon: Pus in the anterior chamber of the eye.
Hypotension: Low blood pressure.
Ileum: The distal or tenninal portion of the small intestine.
ending at the cecum. which is a blind pouch fonning the
proximal or firsl pan of Ihe large intestine.
Ilium: The lateral or flaring part of the pelvic bone, otherwise known as the hip.
Incisional biopsy: The removal of a portion of suspected
abnormal tissue for microscopic study.

153

Appendix V

GLOSSARY
Incisive papilla: A slightly ele\'ated papule of nonnaltissue on the palate in the midline immediately posterior to
the central incisors. lmmedi<ltcly beneath this ~tructure
lies the incisive canal.
Induralion: Characterized by being hard; an abnonnally
hard ponion of a tissue with respect to the surrounding
similar tissue: often u~ed to describe the feel of locally
invasive m<llignam tissue on p<llpation.

Lamina propria: The layer of conneclive tissue- _ _'"

ately beneath the epithelium of the oral mucosa.
Laryngeal: Pertaining 10 the larynx. which is a pan: 01
airway. It is located between the pharynx at the ""'.....
the oral cavity and the trachea at the beginnlOl
lungs. The larynx contains the vocal cords. ~hida
audible sounds.
Lateral: Pertaining to or situated at the side.

Infant: A human baby from binh to two years of age.

Infarct: A localized area of ischemic necrosis resulting from a
blockage of the anerial supply or the \'cnous drainage of tissue. Ischemic necrosis is dead tissue resulting from an inad~
equ<lte blood supply. An example is <l hean anack, which is
an infarct of heart muscle.
Insulin: A protein hormone secreted by the islands of
Langerhans of the pancreas; insulin deficiency produces
hyperglycemia. otherwise known as diabetes mellitus.
Invaginate: To fold and grow within. in the manner of a
lX'uch.
Iris: TIle iris is the pan of the eye which is blue. grey. green
or brown. It is a muscular tissue and its function is to
constrict and dilate the pupil. The pupil is the black portion in the middle of the iris that allows light into the eye.
Iritis: Innammation of the iris which is often caused by
viral infection or rheumatoid disease. The main symptom of iritis is photophobia (aversion to light).
lS4:hemia: A deficiency of blood to a lxxIy pan. usually due
to constriction or blockage of <l blood vessel.
Kaposi's sarcoma: A malignant tumor of vascular tissue.
Once rare in the Americas, it is now seen frequently in
patients with AIDS. 1be lesions are red-purple in appearance and may be seen anywhere on the skin. especially on
the face and in the oral cavity.
Keratinization: The formation of microscopic fibrils of
keratin in the keratinocytes (keratin-fonning cells). In
the oral cavity the tenn is used to describe changes in the
outer layer of the epithelium.
Keratotic: A condition of the skin characterized by the
presence of horny growths. On the oral mucous membrane. keratotic tissue usually looks white; the term
implies a lhickening of the outer layer of the oral
epilhelium.

154

Leptomeninges: The two more delicate componenb

meninges. the pia mater and the arachnoid.
Lesion: A site of slructural or functional change ill
tissues that is produced by disease or injury.
Leukoplakia: A white patch thai cannOI be rubbed , , - that does not clinically represent any olher condu-.
Lipid: Fat or fany: a naturally occurring subsrantt
up of fatty acids.
Lobulated: Made up of lobules. which are smaller
sions of lobes. Many structures are divided IIlto
and lobules. such as the brain. lung. and sali\ at) p-*Some pathologic lesions are described as Job......
when the lesion is divided into smaller pans.
Lymphadenitis: Innammation of lymph nodes g:<D"'~
resulting in enlargement and tenderness.
L:,.mphoblastic: Pertaining to a cell of the lympboc:!1&
series: the lerm implies proliferation. Lymphoblmzic
one of the forms of leukemic cancer of the ~hltr
cells characterized by the presence of malignant ~
phoblflsts or immature lymphocytes.
Lymph()(~'le:

A variety of leukocyte or white blood that is important to Ihe immune reponse and that
in lhe lymph nodes. Lymphocytes can be large or
and are round. nongranular. and classified as eilher TB-lymphocytes.

Macrocheilia: Abnormally large lips.

Macrodontia: Teeth that are considerably larger than I10mIIl
Macule: A spot or stain on the skin or mucous ~
that is neither raised nor depressed. Some exampks
macules include cafe au lait spots. hyperemia. ery~
petechiae. ecchymoses. purpura. oral melanotic ~
and many others illustrated in !his atlas.

\lalaise: A conslitutional symptom thai describes a feeling

of uneasiness. discomfort. or indisposition.
\Ialignant: A neoplastic growth that is OOt usually encapsulaled. grows rapidly. and can readily metastasize.
\laSlication: Chewing.

M)'elogenous leukemia: Leukemia is cancer of the white

blood cells: in this instance the predominating leukocytes. or while blood cells. are myeloid or granular
(polymorphonuclear leukocytes).
Nasophar)'ngitis: Inflammation of the nasopharynx which
is the back of Ihe nasal complex and upper throat. Sore
throat. posl-nasal drip. and fever are common signs.

\ledial: Sirualed toward the midline (opposite of lateral).

\Ielena: Darkened or black feces that are due to the presence of blood pigments: a sign of intestinal bleeding.
:\Ieningitis: Inflamm3lion of the meninges. which are Ihe
three membranes covering the brain and spinal cord (Ihe
dura mater. arachnoid. and pia maier). Meningitis pro
duces both mOlar and mental signs such as difficulty in
walking and confusion.

Neocapillary: New growth of capillaries. which are the

smallest blood vessels and connect small arterioles to
small venules.
Necrosis: The death of a cell as a resull of injury or dis-

me.
Neoplasia: Characlerized by the presence of new and
unconlrolJed cellular growth.

\lesenchymal: The meshwork of embryonic cOllnective lis

sue in the mesoderm that gives rise 10 the connective tissue of the body. blood vessels. and lymph vessels.

Neoplasm: A mass of newly formed tissue: a tumor.

\lesial: Toward the front. anterior. or midline. The mesial

surface of teeth is the side of the tooth closest to the midline. The five surfaces of teeth are mesial. distal.
occlusal or incisal. labial or facial. and lingual or palatal.

Neuropathy: Any abnOnllality of nerve tissue.

\Ielastasize: To spread or travel from one pan of the body

to anOlher: a tenn usually reserved to descri~ the
pread of malignant tumors.
\licrodontia: Teeth Ihat are considerably smaller than
normal.
\tineralized: Characteri7..ed by the deposition of mineral.
often calcium and other organic salts in a tissue. The
term "calcified" is used when the mineral content is
known 10 be calcium. whereas the term "minemlized" is
more general and does not specify the exact nature of
the mineral.
\Ionoc)'tic leukemia: Leukemia is cancer of the white
blood cells: in this instance the predominating leukoc)tes. or white blood cells. are monocytes.
\Iorpholog)': Descriptive of shape. form. or structure. or
lhe science thereof.

Neurogenic: Originaling in or from nerve tissue.

Neutrophil: A medium-sized white blood cell with a nucleus

consisting of three 10 five lobes and a cytoplasm containing
small granules: one of a group of white blood cells called
granulocytes. the others being eosinophils and basophils.
Neutrophils make up about 65% of the while blood cells in
normal blood. Also known as polymorphOlluciear leukoC)1e. PMN.or"poly."
Neutrophil chemotaxis: Taxis or movement of neulTophils
in response to chemical substances or agents.
Ne\'us: A small tumor of the skin containing aggregations
or theques of nevus cells: a mole. It may be flat or elevated, pigmented or non-pigmented. and mayor may
not contain hair.
Nodule: A circumscribed. usually solid lesion having the
dimension of depth. Nodules are less Ihan I em in
diameter.
Noncaseating: A lissue-degeneralive process that forms a
dry. shapeless mass resembling cheese.
Occipital bone: One of the bones that make up the skull; a
thick bone at the back of the head.

\Iucopurulent: Consisting of bOlh mucous and pus.

\Iutagenesis: The induction of genetic mutation.

Oligodontia: Presence of fewer than the normal number of

teeth.

155

Appendix V

GLOSSARY
Oncugenic: C.pable of cau~ing tumor fannation.
Opportunistic microorganism: Microorganisms Inat usually aren't pathogenic. but become '>0 under certain circuml>lanccs. such as an environment allcrcd by the
aClion of antibioticl> or long term steroid therapy.
Opportuni~tic microorganisms C<luse opportunistic
infeclion~.

Organism: Any viable life foml. sucn as animals. plants.

and microorganisms. including bacleria. fungi. and
,iruses.
Otorhinolaryngologist: An car. nose. and tnroat specialist.
Palliati\'e: Treatment or the relief of symptoms. nOlthe
cause of a condition.

Pedunculated:
ils base.

tissue mass originating b) a

S1

Periapical: Pertaining to or localed at the ape... I

of a tOOlh.
Perirurcal: Pertaining to or located at the furcum
tooth: below the eEJ where the roots fuse togelhtt'
Perilabial: Pertaining to the region around or near Ibt
Perineum: The lower surface of the trunk: \\'hen a""..."
is lying down with legs spread apart. the perineum
area from thc base of the spine to the anal region
genital area and. finally. to Ihe crest of the mons pI'L
Perioral: In the proximity or or around the oral

ca\l~

Pallor: Paleness of the skin or mucous membrane; an

absence of a healthy color. This sign often accompanies
constitutional symptoms and anemia.

Periorbital: In the pro:;:imity of or around the orbit....

is the bony socket of the eye.

Palpate: To feel with the fingers or hand.

Peripheral: Pertaining to the outer part. such

or margin.

I'apule: A small mass. without the dimension of depth.

thai is smaller than I cm in diameler. When described as
pedunculated. a papule is on a stalk: when described as
sessile. a papule is anached at its base and does not
have a stalk.

Permanent denlition: Succedaneous (adult) tceth....

follow Ihe primary lecth. Since there are no replanments for the pennanent teeth. they musl last a Ii~
There are 32 pennanent teelh.

Parturition: The delivery of the fetus from the 11100her: to

give birth.

Petechiae: Liule red spots. ranging in size from pm

to several millimeters in diameter. Petechiae con,
extravasated blood.

Patch: Similar to a macule but larger: a large stain or

spot. usually neilher raised or depressed. which may be
textured.

Physiologic: Refers to nonnal body function (oppos,ltt

pathologic).

Palent: The condilion of being open: this ternl is often

applied to ducts. vessels. and passages to indicate thai
they are not blocked.
Pat hognornonic: Uniquely distinctive of a specific disease
or condition: usually consists of signs or findings Ihal
when present and recognized. enable the diagnosis to be
made.

l\.)

tht ec5!"c

Pilocarpine: A drug used to stimulate salivary flo\\, or

produce constriction of the pupil of the eye.
Plaque: An area with a flat surface and raised edges.
Platelet: One of the elements found in circulating blood..
plalelet has a circular or disk-like shape and is s
hence Ihe tenn platelet. Platelets aid in blood coa
tion and clot retractioo.

Pathologic: Pertaining to or caused by disease.

Polydipsia: Excessive thirst. A sign of disease.
Pathosis: An abnonnal stale or condition.
Pol~'poid:

Parietal bone: One of the bones that makes up the skull:

there is one parietal bone on each side of the skull,
fonning Ihe skull's tOp and upper sides.

156

A polyp-like protruding growlh with a base tha

equaJ in diameter to the surface of the mucosal lesion.

Pol}'uria: Excessive amounts of urine. A sign of diseast

Posterior: Directed toward or situated at the back (oppotte of anterior).

Primar~

mar)

tooth: Deciduous (baby) tooth; there are 20 priteeth.

Prognathism: A developmental deformily of the mandible

that causes it to protrude abnormally.
Pruritis: Itching.

Relinopath)': A disease or abnormality of the retina of the

eye. The retina cannot be seen without special instruments. and is thai pan of the eye which receives and
transmits visual information coming in from the pupil
and lens onto the brain via the optic nerve.
Renal Failure: Inability of the kidneys to function properly. A patient whose kidneys fail completely will die
without renal dialysis or a kidney transplant. One of the
causes of kidney failure is prolonged hypertension (high
blood pressure).

~udoh~'phae:

Long. filamentous foons that can be seen

under the microscope when Cal/dida albicafls. a fungal
microorganism. assumes its pathogenic form.

Pulse: A patient's heartbeat. as felt through palpation of a

blood vessel.

Punctate: Spotted: characterized by small points or punctures.

Purpuric: Pertaining to purpura. which are large bruises
consisting of blood extravasated into the tissues.
Bruises are bluish-purple in color.
hrulent: Containing pus.
P1lstule: A well-circumscribed. pus-containing lesion. usu
ally less than I cm in diameter.
QuaJitati,'e: Of or pertaining to quality: descriptive information ahoUl what something looks and feels like.
Quantitalh'e: Of or pertaining to quantity: descriptive
Information ahout how much of something there is or
how big something is.

Sarcoma: A malignant growth of cells of embryonic connective tissue origin. This condition is highly capable of
infiltration and metastasis.
Sarcomatous: Pertaining to sarcoma. which is a malignant
tumor of mesenchymal tissue origin.
Scar: A mark or cicatrix remaining after the healing of a
wound or other morbid process.
Sclera: The strong outer tunic of the eye. or whites of the
eyes. When the sclera turns blue or yellow. it is a sign of
systemic abnormality.
Sepsis: A morbid state resulting from the presence of
pathogenic microorganisms. usually in the bloodstream.
Sepficemia: The presence of pathogenic bacteria in the
blood.

Sequestration: Abnormal separation of a pan from the

whole. such as when a piece of hone sequestrates from
the mandible because of osteomyelitis: the act of isolating a patient.
Serpiginous: Chamcterized by a wavy or undulating margin.

Radiation: In dentistry. electromagnetic energy or x-rays

transmitted through space. Radiation also means divergence from a common center: one of the properties of xrays is that. like a beam of light. they diverge from their
source.

Serum: The watery nuid remaining after coagulation of

the blood. If clolled blood is left long enough. the clot
shrinks and the fibrinogen is depleted. the remaining
fluid is the serum.

Ibdiolherapy: Radiation therapy: the use of radiation from

"arious sources to lreal or cure malignant disorders.

Sessile: Auached to a surface on a broad base: does not

have a stalk.

RecrudeS4:ence: Recurrence of signs and symptoms of a

disease after temporary abatement.

Sign: An objective finding or observation made by the

examiner of which the patient may be unaware or does
not complain.

dractory:

01 readily responsive to treatment.

Rtmission: Improvement or abatement of the symptoms of

a disease: the period during which symptoms abate.

Sinus: An airspace inside the skull. such as the maxillary

sinus: an abnonnal channel. fistula. or tract allowing the
escape of pus.

157

Appendix V

GLOSSARY
Supernumerary: In excess of the regular number.

within the heart or blood vessels from conSlllueDb

the circulating blood. Patients prone to the formauc.
thrombi are placed on anticoagulant therapy.

Splenic: Of or penaining to the spleen. which is tl struclUre

in the upper left abdomen juSt behind and under the stom
ach. TIle spleen contains the largest collection of reticuloendothelial cells in the whole body; its functions include
blood fonnation, blood storage, and blood fihr.llion.

Tooth bud: The embryonic tissue of origin of tht

tooth buds develop from the more primitive tiss~ at
dental lamina.

Sponlaneous: Occurring unaided or without apparent

cause; voluntary.

Torus: A bony nodule on the hard palate or on the- 11 .::

aspect of the premolars.

Superficial: Located on or near the surface.

Tourniquet test: When pressure is applied to the

vessels of the upper ann. using a blood pressure etdf_ .a
bleeding tendency is detected when petechiae de"
in the region.

Symptom: A manifestation of disease of which the patient

is usually aware and frequently complains.
S)'ndrome: A combination of signs and symploms occurring
commonly enough to constitute a distinct clinical entity.

Transient: TemporMy: of short duration.

Translucent: Somewhat penetrable by rays of light.

Taurodont: A malformed multirooted tOOlh characterized

by an allered crown-to-root ratio. the crown being of
oonnallenglh, the roots being abnonnally shon. and the
pulp chamber being abnormally large.
Telangiectasia: The formation of capillaries near the surface of a tissue. Telangiectasia may be a sign of hereditary disorder, alcohol abuse, or malignancy in the region.
Template bleeding time: The amount of time necessary
for bleeding to stop. following a skin incision of consistent length and depth.
Texture: Pertains to the characteristics of Ihe surface of an
area or lesion. Some descriptions of texture are as follows: smooth, rough. lumpy. and vegetative. The tiny
bumps on the surface of a wan cause it to have a vegetative texture.
Therapeutic: Of or penaining to therapy or ttealmCnt; beneficial. Therapy has as its goal the elimination or control
of a disease or olher abnormal state.

Trauma: A wound or injury; damage produced

external force.

b~

Trismus: Tonic contraction of the muscles of maslieatM&

commonly referred to as lockjaw. Trismus is cau:.ed
oral infections. salivary gland infections. tetanus. u..rna and encephalitis.
Trunk: The main pan of the body. to which the limbs ~
attached. The trunk consists of the thorax and abdorne-..
and contains all of the internal organs. This term 1 a.b.;
used to describe the main part of a nerve or blood \-essd..
Tumor: A solid. raised mass that is larger than I em ..
diameter and has the dimension of depth. This teon
describes a mass consisting of neopla~tic cells.
Ulcer: Loss of surface tissue due to a sloughing of necroo.:
inflammatory tissue; the defect extends into the UJ1dcr.
lying lamina propria.
Unilateral: Affecting only one side of the body.

Thorax: That part of the body between the neck and

abdomen. enclosed by the spine. ribs. and sternum. In
the vernacular. the thorax is referred to as the chest.
The main contents of the thorax are the hean and lungs.
Thrombophlebitis: The development of venous th.rombi in
the presence of inflammatory changes in the vessel wall.
Thrombosis: Formation of thrombi within the lumen of
the hean or a blood vessel. A lumen is the space within
a passage: a thrombus is a solid mass that can fonn

158

Uremia: A toxic condition caused by the accumulation

nitrogenous substances in the blood that are no~
eliminated in the urine.
Urticaria: A vascular reaction of the skin charactenzed
the appearance of slightly elevated patches that art
either more red or paler than the surrounding
Unicaria is also known as hives. and may be caused
allergy. excitement. or exercise. These patches ~
sometimes intensely itchy.

\asoconstriction: To diminish the diameter or caliber of a

blood vessel.

a feeling of dizziness or that one's surroundings are

spinning or moving.

'mlral: Directed toward or situated on the belly surface

(opposite of dorsal).

Vesicle: A well-defined lesion of the skin and mucous

membranes that resembles a sac. contains fluid. and is
less than 1 em in diameter.

'ennilion: That part of the lip which has a naturally pinkish red color and is exposed to the extraoral environment. The vennilion contains neither sweat glands nor
3CCessory salivary glands.
\~milion

border: The mucocutaneous margin of the lip.

Visceral: Pertaining to body organs.

Viscous: Thick or sticky.

\ermilionectomy: Surgical removal of the vennilion border of the lip.

Wheal: A localized area of edema on the skin. Usually the

area is raised. smooth-surfaced and is often very itchy.

\e-rtigo: An unpleasant sensation characterized mainly by

Xerostomia: Dry mouth.

159