b.

Hard Palate (highly keratinized)

○ Lining/Reflecting Mucosa
- Protective lining
- A covering of soft palate, vestibular
surface of the tongue, cheeks and
tonsils (firmly attached)
- Alveolar mucosa , vestibular mucosa,
mucosa of the floor of the mouth,
sulcular mucosa (loosely attached to
underlying bone or muscle)
○ Specialized/Sensory Mucosa
- Found in the dorsum of tongue
- Rough and irregular
- Papillae: taste buds; filiform,
ORAL MEDICINE, DIAGNOSIS AND fungiform, vallate and foliate
TREATMENT PLANNING
➢ Oral Medicine GENERAL CONSIDERATIONS IN DIAGNOSING
● Area of special competence concerned ORAL MUCOSAL LESIONS
with the health and diseases involving the ● Age and Gender
oral and paraoral structures ○ Primary herpetic gingivostomatitis (infants)
○ Jaws, salivary glands, oral mucosa
● Involves management and diagnosis of
facial pain and (TMD)
➢ Oral Diagnosis
● The practice of determining all problems
inside and outside of the mouth by using
scientific knowledge to determine the
relationship between them, and thereby
helping to make the right decisions
regarding treatment based on the findings
in hand. ○ Desquamative gingivitis (women)
○ Proper charting to get the right
diagnosis
○ Diagnosis is part of the holistic of the
patient

● Location Of The Lesion

○ Gingiva (ANUG)

STOMATOLOGY
● The study of the mouth
● Focus on Oral Mucosal Lesion
● 3 Types of Oral Mucosa:
○ Masticatory Mucosa
- Bound to bone, rough, does not
stretch
○ Tongue - benign migratory glossitis
a. Gingiva
 - Sometimes it’s an allergic reaction
from salty, spicy, sour; flaky
appearance
● Symptomatology
○ Presence or absence of pain
● Method of onset
○ Associated with stress, menstruation,
smoking
● History of occurrence
○ Primary or recurrent
- Recurrent herpes labialis
○ Non-recurrent
- Traumatic ulcers, necrotizing
sialometaplasia
● Length of time the lesion is present
○ Self-limiting or prolonged
● Number of lesion
○ Single
○ Multiple
● Clinical appearance of lesion
○ Symptomatology: presence or absence of
pain
○ Clinical appearance - most important
CLASSIFICATION OF ORAL MUCOSAL LESION
➢ According to clinical appearance
1. Lesion extending below the surface
● Erosion
○ Describes a soft tissue lesion in
which the epithelium above the
basal cell layer is denuded.
○ Moist, slightly depressed resulting
from a broken vesicle or traume
○ Healing rarely results in scarring
- Pemphigus and erosive
lichen planus are disease
that produce mucocutaneous
erossions
○ The lesion is in the epithelium
above the basal layer wherein it is
denuded
● Ulcer
○ Uncovered wound of cutaneous
or mucosal tissue that exhibits
gradual tissue disintegration and
necrosis
○ Extended deeper than erosions
○ From beyond basal layer of
epithelium into the dermis
○ Scarring may follow healing of an
ulcer
○ May result from trauma, aphthous
stomatitis or viral infection
(herpes simplex)
○ Usually painful and often require
topical drug therapy for effective
management
● Fissure
○ A normal/abnormal linear cleft in
the epidermis that affect the lips
and perioral tissues
 ○ Fissured tongue
2. Lesions extending above the surface
● Papule
○ Superficial, elevated solid lesion
<1 cm in diameter
○ May be of any color and may be
attached by a stalk or firm basses
○ Often represent a slow growing
lesion
● Plaque
○ A flat, solid, raised area >1 cm in
diameter
○ Essentially superficial but may
extend deeper into the dermis
than papules
○ Edges may be sloped
○ Sometimes surface keratin
proliferates
○ Example: Lichen planus
● Wheal
○ An edematous papule or plaque
that results from acute
extravasation of serum into the
upper dermis
○ Generally pale, red, pruritic and of
short duration
○ May be seen after insect bite,
allergic reaction to food or
mechanical irritation
(dermatographia)
● Vesicle
○ Circumscribed, fluid-filled
elevation in the epidermis that is
less than 1 cm in diameter
○ The fluid of a vesicle generally
consist of lymph or serum but
may contain blood
○ Thin epithelial lining eventually
breaks down → ulcer and eschar
○ Common in herpes simplex virus
(HSV) infections
● Bullae/Bulla
○ Vesicle exceed 1 cm
○ Develops from the accumulation
of fluid in the epidermal-dermal
junction or a split in the epidermis
○ Represents a more severe
disease than do conditions
associated with vesicles
 3. Lesions that are even or flat with the
surface
● Macule
○ Neither elevated nor depressed
○ May be of any size
○ Usually reserves for lesions 1 cm
or smaller

● Patch
● Pustule ○ Well circumscribed
○ Circumscribed elevation filled with ○ Larger than macule
purulent exudate resulting from ○ Differentiate from surrounding
infection epidermis by color, texture or both
○ <1 cm in diameter ○ Example: Focal argyrosis
○ May be preceded by a
vesicle/papule
○ Creamy white/yellowish
○ Often associated with epidermal
pore

● Purpura
○ Flat lesion
○ Reddish to purple → caused by
blood from vessels leaking into
subcutaneous tissue
○ Lesions do not blanch when
pressed
○ Pustules within the mouth is
● Ecchymosis
represented by a pointing
○ Sharply circumscribed blood
abscess or parulis
pigments
○ Herpes zoster: also produce
○ Larger than 1 cm
pustules → ulceration = PAIN
○ Large purpuric lesion
● Scar
● Petechiae
○ Permanent mark/cicatrix
○ Purpuric lesions 1-2 mm in
remaining after wound heals
diameter (or <1 cm)
○ Indicates a disruption in the
integrity of epidermis and dermis
and healing of epithelium with
collagen connective tissue
○ May result from surgery, burn or
trauma

4. Lesions which may be raised or flat

● Nodule
 ○ Solid mass of tissue that extends
zoster Pemphigoid
deeper into the dermis - HFMD
○ Usually detected by palpation - Herpangina
○ Example: irritation fibroma - Masles

1. VIRAL
A. HERPES SIMPLEX INFECTION (HSV1)
● Tumor
○ Indicates a solid mass of tissue
>1 cm in diameter that has
dimension of depth
○ Often used to denote a neoplasm
which can be benign or malignant
● Cyst
○ Epithelium-lined mass located in
the dermis, subcutaneous tissue
or bone
○ Results from entrapment of
epithelium/remnants of epithelium
that grow to produce a cavity
○ Example: Gingival cyst
● Etiology:
○ Physical contact with an individual
infected with Herpes simplex virus for
a seronegative individual
○ Low titer of protective antibody to HSV
○ Immunocompromised
● Clinical Feature
○ Age: most infections occur during
childhood and subclinically for adult
○ Incubation Period: several days to 2
weeks after exposure
● Symptomatology: systemic signs and
symptoms (e.g. fever, malaisses, artralgia,
anorexia, headache, and cervical
lymphadenopathy)
● Duration: self limited (1 week to 10 days)
● Acyclovir and analogs may control virus
200-400 mg 5X a day for 7 days
○ Must use early to be effective
○ Symptomatic care
● Location: vesiculoulcerative eruption
(primary gingivostomatitis) which typically
occurs in the oral and perioral tissues

I. VESICULOBULLOUS LESIONS
● Group of diseases characterized by the
appearance of vesicles and bullae in ● Secondary herpes Simplex Virus infection
oral cavity and skin are seen at the vermilion border of the lips
(cold sores or fever blisters), palate, or
fingers (herpetic whitlow)

VESICULOBULLOUS
VIRAL IMMUNOLOGIC HEREDITARY

- Herpes - Pemphigus - Epidermolysis ● Mode of Transmission: Saliva, genital

simplex vulgaris Bullosa secretions
Infection - Mucous
- Varicella Membrane ○ Primary: primary herpetic
and herpes - Bullous gingivostomatitis
 ○ Secondary: perio-oral crusted lesions ● Herpes Zoster or Shingles
(cold sores) ○ Clinical Features:
⤷ Intra-oral regular hallow ulcers ⤷ Age: adults
affecting the keratinized mucosa ⤷ Symptomatology: several days of
● Management: prodromal symptoms of pain,
○ Acyclovir 200 mg five times/day for 7 paresthesia of involved
days dermatome, well-delineated
○ Valacyclovir 2g once daily for 7 days unilateral maculo-papular rash
○ Supportive care including pain control, appear that become vesicular,
nutritional support, and adequate pustular and then ulcerative
hydration ○ Well-delineated unilateral
○ ***Lesions heal without scar formation maculopapular rash
B. VARICELLA-ZOSTER INFECTION
● Etiology: Varicella zoster virus
○ Primary: varicella or chickenpox
○ Secondary: herpes zoster or shingles
● Similarities of HSV and VZV
○ Structure
○ The ability to remain quiescent in a
○ Location:
sensory ganglia for indefinite period
⤷ Trigeminal Nerve involvement:
after a primary infection
unilateral oral, facial, and ocular
○ Cutaneous or mucosal
lesions
vesiculoulcerative eruption following
⤷ Facial and Auditory nerve
reactivation of latent virus
involvement: facial paralysis,
● Varicella or Chickenpox
accompanied by vesssssciless of
○ Clinical Features: transmission is via
the ipsilateral external ear,
inhalation of contaminated droplets or
tinnitus, deafness and vertigo
direct contact
(Ramsay Hunt Syndrome)
⤷ Age: common in children
● Ramsay hunt Syndrome
⤷ Incubation Period: 2 weeks
○ Symptoms consist of:
⤷ Symptomatology: fever, chills,
⤷ Facial paralysis
malaise, headache, pruritic
⤷ Ear pain
vesiculobullous eruption that
⤷ Vertigo
becomes pustular and eventually
⤷ Ringing in the ears (tinnitus)
ulcerates
⤷ Blistering rash on the ear on one
○ Intense pruritic skin lesion of different
side of the face
stages that heals with scar formation
○ Occurs more commonly; in people
with weakened immune systems,
such as elderly.

○ Location: vesicular eruption of trunk

and head and neck occurring in crops
○ Duration: 2-3 weeks (self limiting)
○ Complications may include:
encephalitis, pneumonitis, and
inflammation of other organs, fetal
abnormalities, and severe and ○ Research has shown that prompt
protracted cases for medically treatment with antiviral medications
compromised patients lessen the symptoms and improve
○ Treatment: symptomatic treatment recovery
 ○ Corticosteroids such as prednisone ○ Incubation period: 4-7 days
may be used, and scopolamine or ○ Symptomatology: systemic signs and
antihistamines such as meclizine symptoms (e.g. low grade fever,
(Antivert) will reduce vertigo and malaise, lymphadenopathy, and sore
tinnitus. mouth)
○ The symptoms will resolve over time, ⤷ Pain from oral lesions which
but some hearing loss and/or facial starts asss vesicles that will
paralysis may be permanent. rupture to from ulcers covered by
○ Duration: several weeks (self limiting) a yellow fibrinous membrane
but maybe protracted for surrounded by erythematous halo
immunocompromised patients ○ Multiple maculopapular lesions on the
○ Complications: feet and toes
⤷ Secondary infection of ulcers,
postherpetic neuralgia, motor
paralysis, ocular inflammation
○ Treatment:
⤷ Supportive therapy
⤷ Acyclovir (800mg 5x per day for
7-10 days) and analogs
● Location:
(vidarabine, human leukocyte
○ Anywhere in the mouth )palate,
interferon)
tongue, buccal mucosa)
⤷ Postherpetic Pain: analgesics, P
inhibitor (capsaicin)
○ Mode of transmission: saliva, airborne
droplets
⤷ Primary: varicella or “chickenpox”
may present with oral ulcers
⤷ Secondary: herpes zoster or
“shingles”, unilateral intraoral
ulcers
○ Management:
⤷ Acyclovir 800mg 5 times/day for
7-10 days
⤷ Valacyclovir 1,000 mg TID 7-10
days
⤷ Famciclovir 500mg TID for 7-10
days

○ Hand and fingers

C. HAND-FOOT AND MOUTH DISEASE

● Etiology:
○ Highly contagious viral infection
caused by Coxackie Type A16
○ Airborne spread or fecal oral
contamination
○ Epidemic and endemic proportion
● Clinical features:
○ Age: children below 5 years of age
● Duration: self limited (1 to 2 weeks)
● Treatment: symptomatic care and bland
mouth rinses (sodium bicarbonate in warm
water)
D. HERPANGINA
 ● Etiology: highly contagious viral infection ○ Koplo’s spots (small erythematous
caused by Coxackie Type A1-6, A8, A10, macules with white necrotic centers at
A22, B3 the buccal mucosa) precedes the skin
○ Thru contaminated saliva and rash (that starts from the head and
contaminated feces neck to the trunk and extremities) by
○ Endemic outbreaks typically in 1-2 days
summer and early autumn
● Clinical features:
○ Age: children > adult; adult caught it
from children
○ Symptomatology: systemic signs and
symptoms (e.g. malaise dysphagia,
low grade fever and sore throat)

● Skin rash (that starts from the head and

neck to the trunk and extremities)

● Mild to moderate pain from oral lesions

which starts as vesicles that will rupture to
from ulcers
● Location: bilateral eruption on the soft
palate, faucial pillars, and tonsils with a
diffuser erythematous pharyngitis

● Complications: encephalitis and

● Duration: self limited (less than a week) thrombocytopenic purpura, secondary
● Treatment: symptomatic care usually not infection may develop as otitis media or
required pneumonia
○ Once antibodies are formed post ● Duration: self limited
infection-immunity develops ● Treatment: supportive therapy of bed rest,
E. MEASLES (RUBEOLA) fluidss, adequate diet, and analgesics
● Etiology: High contagious Measles virus F.
○ Airborne droplets through the 2.
respiratory tract
○ Seasonally appears in winter and IMMUNOLOGIC
spring ● Vesiculobullous
● Clinical features:
○ Age: children Viral Immunologic Hereditary
○ Incubation period: 7-10 days > Herpes > Pemphigus
● Symptomatology: simplex vulgaris
○ Systemic signs and symptoms (fever, infection > Mucous
malaise, coryza, conjunctivitis, > Varicella and membrane
photophobia, and cough) herpes zoster pemphigoid
> HFMD > Bullous
> Herpangina pemphigoid
> Measles

VESICULOBULLOUS DISEASES: ANTIGENIC

TARGETS
MIDTERMS:
4. Associated with an ill-fitting lower denture

WHITE DIGITALISM (WHITE-YELLOW

REACTIVE LESIONS)
1. Focal hyperkeratosis
2. White lesions associated with smokeless
tobacco
● Clinical features:
3. Nicotine Stomatitis
○ Chronic cheek or lip chewing may result in
4. Hairy leukoplakia
opacification (keratinization) of the
5. Hairy tongue
affected area. Chewing on edentulous
6. Dentifrice-associated slough
alveolar ridges produces the same effect.
● Histopathology:
FOCAL HYPERKERATOSIS
○ Microscopically, hyperkeratosis is noted
● Is defined as the excessive formation of
without dysplastic change. A few chronic
tenaciously attached keratin in the mouth,
inflammatory cells may be seen in the
which can result from friction. This results in a
subjacent connective tissue but take note
hyperkeratotic white lesion that is analogous to
that epithelial maturation pattern is
a callus on the skin.
otherwise normal.
● Etiology:
● Differential Diagnosis
○ An oral habit of cheek biting, cheek
1) Leukoplakia
chewing, tongue thrusting and chronic
2) Lichen planus
rubbing or friction against an oral mucosal
surface Leukoplakia Lichen Planus
○ Maxillary and mandibular alveolar ridges
1. Caused by cheek chewing

2. Related to tongue-thrusting habit

● Diagnosis:
○ Careful history taking and examination
○ Biopsy
○ Use of 2x2 inch gauze
● Treatment and prognosis:
○ Discontinue the causative habit,
○ Offending tooth or denture should be
3. Caused by chronic rubbing of the lip against smoothed
teeth ○ No malignant potential exists

WHITE LESIONS ASSOCIATED WITH

SMOKELESS TOBACCO
● The development of oral mucosal white
patches or white folds surrounding the area
where tobacco is held.
● Labial and buccal vestibules.
● Used in different regions
 1) Prevalent in the United States: especially
in southern and western states.
2) Sweden: in the form of snus.
3) In regions such as Indian subcontinent
and southeast Asia: other smokeless
tobaccos used are much more
carcinogenic due to the preparations
containing a higher pH.
● Etiology:
○ A link between smokeless tobacco and
white tissue changes has been
documented and has a causal
relationship.
○ Smokeless tobacco-induced alterations in
tissues are thought to be a response to
tobacco constituents.
○ pH of snuff: ranges between 8.2 and 9.3
● Clinical Features:
○ Granular to wrinkled hyperkeratotic
appearance.
○ In advanced cases, a heavy, folded
character may be seen.
○ Immediate area where the tobacco is
habitually placed.
○ Mucobuccal fold of the mandible in the
incisor or the molar region.
○ Generally painless and asymptomatic.
● Histopathology:
○ Slight to moderate parakeratosis, often in
the form of spires or chevrons.
○ Superficial epithelium may demonstrate
vacuolization or edema.
○ Occasionally, epithelial dysplasia may
develop in these lesions.
● Differential diagnosis:
○ Hairy leukoplakia: lateral margins of
tongue
○ Smokeless tobacco induced lesions: area
where tobacco is habitually placed
Hairy leukoplakia Smokeless tobacco
induced lesions
● Main cause:
○ Snuff or shredded tobacco
● Treatment and prognosis:
○ Discontinuation of smokeless tobacco use,
○ Biopsy on persistent lesions
○ Long period of exposure to smokeless
tobacco increases the risk of
transformation to verrucous or squamous
cell carcinoma
● Tobacco influence:
○ Stained teeth,
○ Esthetics
○ Halitos
○ Tar
○ Nicotine
○ Carbon monoxide
● According to tobacco atlas
○ Asia and Australia = 57% tobacco
consumers in 2009
○ Within Asia, 16% are filipino smokers
● Smoking can also cause other systemic
conditions like
○ Disruption of normal lung function
(hemoglobin + CO = carboxyhemoglobin)
a 15% decrease normal oxygen levels
○ Coronary heart disease
○ Thrombosis of coronary
○ Cancer
○ bronchitis
NICOTINE STOMATITIS
● Is a lesion that appears on the smoker’s hard
or soft palate. The white patches represent
inflamed ducts of the minor mucous glands,
whereas the raised red dots represent inflamed
ducts of the major mucous glands. The surface
is frequently rough, giving the impression that
the palate is cooked.
● Nicotine and stomatitis are related because
smoking can cause a condition known as
nicotine stomatitis.
● Nicotine stomatitis is different from other forms
of stomatitis since it mostly affects just the
upper palate of the mouth and is caused
primarily by heavy smoking.
● Year after year, the number of men and women
who smoke increases. Nicotine is extracted
from tobacco during the smoking (inhalation) or
chewing process.
● Nicotine is bonded to the organic acids
inherent in the native plant’s leaves, and even
if the leaves are gradually dried, the nicotine
remains.
● Alkaloids are mediators present in tobacco
leaves that are crucial for the cigarette’s
effects. Nicotine, anabasine, myosmine, and
other chemicals found in tobacco leaves
include alkaloids.
● Nicotine is a highly poisonous alkaloid ● Etiology:
molecule found in tobacco. ○ Associated with local or systemic
● Etiology: immunosuppression (especially AIDS and
○ Nicotine stomatitis, often known as organ transplantation)
smoker’s palate, is a reaction on the roof ○ Represents an opportunistic infection by
of the mouth produced by excessive heat Epstein-Barr virus
in the mouth, which is most commonly ○ Found mainly in human immunodeficiency
induced by smoking. Nicotinic stomatitis, virus (HIV)-infected individuals
nicotina stomatitis, and smoker’s keratosis ○ Hematologic malignancy
are some of the other names for it. ○ Long-term use of systemic or topical
○ The development of hyperkeratosis and corticosteroids
acanthosis of the palatal epithelium is a ● Clinical features (oral manifestation):
defining hallmark of nicotine stomatitis, ○ Most commonly seen on lateral tongue,
inflammation of subepithelial connective often bilateral (but may also be unilateral)
tissue and mucosal glands that is mild, ○ Asymptomatic white lesion
spotty and chronic. The excretory ducts ○ papillary , filiform, corrugated lesion or flat
have squamous metaplasia. Although and plaque like architecture
smoking tobacco products causes nicotine ○ May occur before or after the diagnosis of
stomatitis, it is rarely associated with AIDS
dysplastic or neoplastic alterations. It has ○ May be secondarily infected by Candida
the same potential for neoplasia as normal albicans
hard and soft palate. Individuals who
reverse smoke are an exception to this
concept.
○ Nicotine stomatitis appears as a reddish
zone at first then gradually changes to a
whitish, swollen and fissured appearance.
There are numerous small salivary glands
on the palate. They swell and the orifices
become more evident, resulting in a
mottled white and red appearance to the
tissue.
● Treatment and prognosis:
○ Stop or to discontinue tobacco habit
○ Observe and examine all mucosal sites
○ Little risk of malignant transformation in
palate, except for “reverse smokers”
○ The only definitive treatment is smoking
cessation

HAIRY LEUKOPLAKIA
● An unusual white lesion along the lateral
margins of the tongue, predominantly in gay
men
● Occurs relatively soon after HIV
seroconversion, typically before AIDS

● Histopathology:
 ○ Found in the nuclei of upper level
keratinocytes
○ Viral inclusions and/or peripheral
displacement of chromatin with a resultant
smudgy nucleus
○ Hyperparakeratotic surfacer, often with the
formation of keratotic surface irregularities
and ridges.
○ C. Albicans hyphae are often seen
extending into the superficial epithelial cell
layers
○ Ballooning degeneration and perinuclear
clearing beneath the surface, within the
spinous cell layer
○ General paucity of subepithelial
inflammatory cells
○ Scant langerhans cells
○ In situ hybridization: nuclear inclusions
and basophilic homogenization
● Differential diagnosis:
○ Idiopathic leukoplakia
○ Frictional hyperkeratosis (tongue chewing)
○ Leukoplakia associated with tobacco use
○ Other entities that might be considered
are: lichen planus, lupus erythematosus,
and hyperplastic candidiasis
● Treatment and prognosis: ● Etiology:
○ None, unless cosmetically objectionable ○ The cause is obscure
○ Antiviral and antiretroviral agents likely to ● Possible initiating factors:
cause lesion to regress ○ Use of broad-spectrum antibiotics,
○ Responses to: systemic corticosteroids, hydrogen
- Acyclovir peroxide
- Ganciclovir ○ Intense smoking
- Famciclovir ○ Head and neck therapeutic radiation
- Tretinoin ○ Oxygenating mouth rinses
- Podophyllum ○ Hematopoietic stem cell transplantation
○ Note: with return of lesions often noted on ● Clinical features:
discontinuation of therapy. ○ Overgrowth of filiform papillae and
- Lesions usually improve or resolve chromogenic microorganisms
with improvement in the patients’ ○ Brown, white, green, or pink, yellow, black
immune system ○ Dense hair-like mat formed
○ Usually asymptomatic
HAIRY TONGUE ○ More frequently in men and primarily in
● Is a condition wherein there is an abnormal persons older than age 30 years.
elongation of filiform papillae on the dorsal
surface of the tongue of variable color that
gives it a hair-like appearance

● Histopathology:
○ Elongated filiform papillae over the dorsum
of the tongue, with surface contamination
by clusters of microorganisms and fungi.
○ Mildly inflamed lamina propria
○ Debris accumulation
● Differential diagnosis:
○ Because the clinical features of this lesion
are usually quite characteristic,
confirmation by biopsy is not necessary.
Differential Diagnosis
Stained normal ➮ Food coloring exposure
tongue ➮ Does not appear hairy
➮ Prompt return to normal
with cleaning
Oral hairy ➮ Tongue appears hairy
leukoplakia with white lesions
➮ Occurs most commonly
in
immunocompromised
patients
➮ May involve both dorsal
and ventral surface of
the tongue, including
buccal mucosa and
gingiva
Pigmented ➮ It is rare
fungiform papillae ➮ Fungiform instead of
of the tongue filiform
➮ Lateral aspects and
apex of the tongue are
more involved than the
dorsum
Acanthosis ➮ Multiple small brown or
nigricans black fine papillary
lesions
➮ Lip involvement
➮ Associated with
underlying malignant
disease
● Treatment and prognosis:
○ It is a temporary and harmless condition
● Possible treatment:
○ Brushing with mixture of sodium
bicarbonate (baking soda) in water oir
gentle once daily scraping of the dorsum
of the tongue may be beneficial
○ Discontinuing agents of possible etiologic
factors, such as antibiotic or oxygenating
mouth rinses
○ Brushing the tongue and maintaining
fastidious oral in individuals who have
undergone radiotherapy with resultant
xerostomia and altered bacterial flora.
DENTIFRICE-ASSOCIATED SLOUGH
● In vulnerable people, dentifrices and some
drugs may induce oral mucosal slough
● In a 50-years-old lady, an uncommon kind of
oral desquamation manifested as grayish-white
gelatinous membranes on the floor of the
mouth, lips, vestibules, and gingiva
● Relatively common phenomenon that has been
associated with the use of several different
brands of toothpaste.
● Etiology:
○ Chemical burn: because of the usage of
several toothpaste brands
○ Caused by a synthetic dentifrice detergent
(foaming agents) and exacerbated by the
patient’s use of drugs with anti sialic action
○ Related to the use of essential oil -
containing mouth rinses
● Histopathology:
○ Ia: epithelial desquamation in alveolar
mucosa
○ Ib: parallel sheets of flattened surface
layers corresponding to normal gingival
stratified squamous epithelium
 ○ 2b: at greater magnification, cells exhibited exaggerated cases, whitish cast with
good maturation with round/elliptical to surface textural changes, including
flattened nuclei of the superficial cells. wrinkling or corrugation may be seen. With
○ A superficial layer of stratified squamous stretching of the buccal mucosa, the
epithelium with degenerative opaque changes dissipate.
characteristics. Histologically, there is
evidence of a widening of the stratum
corneum of the epithelium due to the loss
of the surface integrity. It was possible to
collect a grayish-white membrane on the
buccal mucosa.
● Differential diagnosis:
○ Oral mucosal peeling management should
consider differential diagnosis with oral
desquamative lesions, particularly
desquamative gingivitis, with a guided
clinical interview together with pathological
confirmation while discouraging the use of
the product responsible for OMP.
● Treatment and prognosis:
○ Change toothpaste; resolves with a switch
to another, blander toothpaste or
mouthrinse
● Histopathology:
○ In leukoedema, the epithelium is
WHITE-YELLOW LESIONS
parakeratotic and acanthotic, with marked
(HEREDITARY-CONGENITAL)
intracellular edema spinous cells. The
1. Leukoedema
enlarged epithelial cells have small,
2. White sponge nevus
pyknotic (condensed) nuclei in optically
3. Hereditary benign intraepithelial dyskeratosis
clear cytoplasm.
4. Follicular keratosis
● Differential diagnosis:
○ White sponge nevus, hereditary benign
LEUKOEDEMA
intraepithelial dyskeratosis, the response
● Definition and Etiology:
to chronic cheek biting, and lichen planus
○ Leukoedema is a generalized mild
all may show clinical similarities to
opacification of the buccal mucosa that is
leukoedema. Microscopic features can
common enough to be regarded as a
differentiate these lesions.
variation of normal. It can be identified in a
● Treatment and prognosis:
large proportion of the population. To date,
○ Treatment is not necessary because the
the cause of leukoedema has not been
changes are innocuous and no malignant
established.
potential exists. If the diagnosis is in
○ Smoking
doubt, a biopsy should be performed.
○ Chewing tobacco
○ Alcohol ingestion
WHITE SPONGE NEVUS
○ Bacterial infection
● Definition and Etiology:
○ Salivary conditions
○ White sponge nevus (WSN) is an
○ Electrochemical interactions
autosomal-dominant inherited condition
○ Cannabis
that is due to point mutations for genes
● Clinical features:
coding for keratin 4 and/or 13. It affects
○ Usually discovered as an incidental
oral mucosa bilaterally and symmetrically,
finding. It is asymptomatic and
and treatment is generally not required.
symmetrically distributed in the buccal
● Clinical features:
mucosa and to a lesser extent over the
○ White sponge nevus (WSN) presents as
labial mucosa. It appears as a gray-white,
an asymptomatic, folded, white lesion that
diffuse, filmy, or milky surface alteration. In
 may affect several mucosal sites. Lesions
tend to be thickened and have a spongy
consistency. The presentation intraorally is
almost always bilateral and symmetric and
usually appears early in life, typically
before puberty. The characteristic clinical
manifestations of this particular form of
keratosis are usually best observed on the
buccal mucosa, although other areas such
as the tongue and vestibular mucosa may
also be involved. The conjunctival mucosa
is usually spared, but mucosa of the
esophagus, anus, vulva, and vagina may
be affected. Skin is not affected because,
unlike mucosa, skin does not contain
keratins 4 and 13.
● Histopathology:
○ Microscopically, the epithelium is greatly
thickened, with marked spongiosis,
acanthosis, and parakeratosis. Within the
stratum spinosum, marked hydropic or
clear cell change may be noted, often
beginning in the parabasal region and
extending very close to the surface.
Perinuclear eosinophilic condensation of
cytoplasm is characteristic of prickle cells
in WSN. It is often possible to see columns
of parakeratin extending from the spinous
layer to the surface.
● Differential diagnosis:
○ The differential diagnosis includes
hereditary benign epithelial dyskeratosis,
lichen planus, lichenoid drug reaction,
lupus erythematosus (LE), cheek chewing,
and possibly candidiasis. Once tissue
diagnosis is confirmed, no additional
biopsies are necessary.
● Treatment and prognosis:
○ No treatment is necessary for this
condition because it is asymptomatic and
benign.
HEREDITARY BENIGN INTRAEPITHELIAL
DYSKERATOSIS
● Definition and etiology:
○ Also known as Witkop disease or
Witkop-von Sallmann syndrome
○ Is a hereditary, autosomal dominant,
duplication of chromosome 4q35
○ A rare, genetic, superficial corneal
dystrophy disease characterized by white,
elevated, epithelial plaques located on the
bulbar conjunctiva and oral mucosa,
associated with dilated, hyperemic,
conjunctival blood vessels, observed
mainly in Haliwa-Saponi Native American
descendents.
● Clinical features:
○ Early onset of bulbar conjunctivitis,
conjunctival plaques at the corneal limbus,
and oral white lesions.
○ Preceding the bulbar conjunctivitis are
foamy gelatinous plaques that represent
the ocular counterpart of the oral mucosal
lesions.
○ Oral lesions consist of soft, asymptomatic,
white folds and plaques of spongy
mucosa..
○ Oral lesions are generally detected within
the first year of life, with a gradual
increase in extent until mid-adolescence.
● Histopathology:
○ Epithelial hyperplasia and acanthosis are
present with intracellular edema.
○ Dyskeratotic elements in the superficial
half of the epithelium
● Differential diagnosis:
○ Idiopathic leukoplakia
○ Chemical/thermal burn
○ Chronic low-grade trauma (morsicatio)
○ Lichen planus
○ Lupus erythematosus
● Treatment and prognosis:
○ No treatment is necessary for this
condition because it is asymptomatic and
benign.
FOLLICULAR KERATOSIS
● Definition and etiology:
○ Also known as Darier’s disease
○ Autosomal-dominant disorder (ATP2A2
gene)
○ The ATP2A2, also known as
sarcoplasmic/endoplasmic reticulum
calcium ATPase 2
● Clinical features:
○ 6 and 20 years
○ Has a predilection for the skin, with 13% of
patients demonstrating oral lesions.
 ○ Skin manifestations are characterized by
small, skin colored papular lesions,
symmetrically distributed over the face,
trunk, and intertriginous areas.
○ The papules eventually coalesce and feel
greasy because of excessive keratin
production
○ Lesions may also occur in a zosteriform
pattern
○ Lesions may also occur in a zosteriform
pattern
○ Fingernail changes may include fragility,
splintering, and subungual keratosis.
○ Lesions typically appear as small, whitish
papules, producing an overall cobblestone
appearance.
○ Papules range from 2 to 3 mm in diameter
and may become coalescent
● Histopathology:
○ Oral lesions closely resemble cutaneous
lesions. Features include:
1) Formation of suprabasal lacunae
(clefts) containing acantholytic
epithelial cells,
2) Basal layer proliferation immediately
below and adjacent to the lacunae or
clefts
3) Formation of vertical clefts that show
a lining of parakeratotic and
dyskeratotic cells, and
4) The presence of specific benign
dyskeratotic cells, called corps ronds
and grains.
● DIfferential diagnosis:
○ Acne vulgaris
○ Seborrheic dermatitis
○ Acanthosis nigricans
○ Confluent reticulate papillomatosis
○ Prurigo pigmentosa
○ Reticulate erythematomucinous syndrome
● Treatment and prognosis:
○ The treatment goals:
- Enhance the look of the skin lesions,
- Alleviate symptoms, and
- Prevent or treat infective
consequences
○ Although topical corticosteroids and the
vitamin A analog retinoic acid have been
used successfully, long-term therapy is
rarely tolerated
○ Oral retinoids have been the most
effective medical treatment for Darier
disease
IDIOPATHIC LESIONS
1. Idiopathic leukoplakia
2. Geographic tongue
3. Lichen planus
4. Lupus erythematosus
IDIOPATHIC LEUKOPLAKIA
● White patch or plaque of oral mucosa
● Cannot be rubbed off and cannot be
characterized clinically as any other disease
● Precancerous lesion
● Etiologically related to the used of tobacco,
may regress after discontinuation of tobacco
use
● Alcohol abuse, trauma, and C. albicans
infection and nutritional factors
● Iron deficiency anemia, and development of
sideropenic dysphagia (Plummer-Vinson or
Paterson-Kelly syndrome)
● Clinical features:
○ Middle-aged and older populations
○ Common sites: tongue to the mandibular
mucosa and the buccal mucosa
○ Less involved sites: the palate, maxillary
ridge and lower lip; floor of the mouth and
retromolar
○ Vague whiteness on a base of uninflamed,
normal-appearing tissue to a definitive
white, thickened, leathery, fissured,
verrucous (wartlike) lesion.
○ Red zones; speckled leukoplakia
(erythroleukoplakia)
○ Lesions may be soft, smooth, or finely
granular. Other lesions may be roughened,
nodular, or indurated.

● Histopathology:
○ Dysplasia: microscopic features
- Epithelial architecture
🢒 Drop-shaped epithelial ridges
🢒 Basal cell crowding
🢒 Irregular stratification
🢒 Reduced-intercellular adhesion
- Cytologic atypia
🢒 Pleomorphic-hyperchromatic,
smudgy, angular
🢒 Increased nuclear-cytoplasmic
ratios
🢒 Increased and abnormal mitoses
Idiopathic leukoplakia diagnosed as moderate
dysplasia
Idiopathic leukoplakia diagnosed as severe
dysplasia
Idiopathic leukoplakia diagnosed as
hyperkeratosis
● Differential diagnosis:
○ Pseudomembrane, a fungus colony or
debris
○ Hereditary conditions, cheek chewing,
lichen planus, and lupus erythematosus
(LE)
○ Fractional or tobacco-associated
hyperkeratosis
○ Hairy leukoplakia and geographic tongue
○ Clinically suspicious areas are red,
ulcerated or indurated areas
● Treatment and prognosis:
○ Periodic examination and re-biopsy of new
suspicious areas of leukoplakia
○ Use of topical agents has not proved
effective
○ Scalpel excision, cryosurgery,
electrosurgery, and laser surgery
○ Grafting procedures after surgery
○ Mandatory follow ups and repeated biopsy
GEOGRAPHIC TONGUE
● Definition and etiology:
○ Erythema migrans and benign migratory
glossitis
○ Highly linked to fissured tongue
○ Inversely linked to cigarette smoking
○ Emotional stress may help the procedure
in a few patients
 ○ Psoriasis, seborrheic dermatitis, Reiter’s
syndrome, adn atopy are only a few of the
illness that have been linked to geographic
tongue

● Differential diagnosis:
○ Useful for diagnosis
○ A biopsy is rarely required
○ Clinical differential diagnosis may include
candidiasis, leukoplakia, lichen planus and
● Clinical features:
lupus erythematosus
○ Women > men
○ Common in children, nonsmokers, and
people who are allergic or atopic
○ Presence of atrophic patches surrounded
by raised keratotic edges
○ Desquamated area appear red and may
be slightly sensitive
○ Pattern shifts throughout days or weeks
appearing to migrate across the dorsum of
the tongue
○ Geographic tongue and fissured tongue
have been found to have a strong link
○ The significance is unknown, but
symptoms may be more common when
● Treatment and prognosis:
fissured tongue is present presumably
○ Self-limiting and asymptomatic
because of secondary fungal infection in
○ Does not require treatment
the base of the fissure
○ Treatment is empirical
● Histopathology:
○ Using a mouthwash composed of sodium
○ The filiform papillae-atrophic
bicarbonate in the water
○ Lesion’s edges show hyperkeratosis and
○ Mucolytic agent: reduces the membrane
acanthosis
that is present on the surface of the
○ Keratin loss corresponds to the circinate
tongue
erythematous patches, as well as
○ Topical steroids: antifungal agents
intraepithelial neutrophils and lymphocytes
○ Reassuring the patient that this condition
○ Leukocytes are found near the surface of
is benign and does not indicate a more
a microabscess
serious condition can help reduce anxiety
○ Lamina propria - inflammatory cell
infiltration consisting of neutrophils,
LICHEN PLANUS
lymphocytes and plasma cells can be
● Etiology and definition:
detected
○ Bilateral white lesions, occasionally with
○ Histologic appearance resembles
associated ulcers
psoriasis
○ Cause:
○ No clinical relationship between
- Unknown; may be precipitated by
geographic tongue and cutaneous
stress; basal keratinocyte destruction
psoriasis
by T cells
● Clinical features:
○ Bilateral white striae (Whickham’s);
asymptomatic except when erosions are
present
○ Seen in middle age; buccal mucosa most
commonly affected, with lesions
occasionally on tongue, gingiva and palate
○ 5 P’s:
- Planar
- Polygonal
- Plaque/Papular
- Purpler
- Pruritic
● Histopathology:
○ The microscopic criteria: hyperkeratosis,
basal layer vacuolization with apoptotic
keratinocytes and a lymph phagocytic
infiltrate at the epithelium-connective
tissue interface
○ The epithelium undergoes gradual
remodeling, resulting in reduced thickness
and occasionally a sawtooth rete ridge
pattern
● These colloid, or civatte, bodies are seen in
other conditions such as drug reactions,
contact hypersensitivity, LE, and some
nonspecific inflammatory reactions
● Direct immunofluorescence demonstrates the
presence of fibrinogen in the basement
membrane zone in 90% to 100% of the cases.
Although immunoglobulins and complement
factors may be found as well, they are far less
common
● Differential diagnosis:
○ Other diseases with a multifocal bilateral
presentation that should be included in a
clinical differential diagnosis are lichenoid
drug reaction, lupus erythematosus (LE),
white sponge nevus, hairy leukoplakia,
cheek chewing, graft-versus-host disease,
and candidiasis
○ Idiopathic leukoplakia and squamous cell
carcinoma might be considered when
lesions are plaque-like. Erosive or atrophic
lichen planus affecting the attached
gingiva must be differentiated from
cicatricial pemphigoid, pemphigus
vulgaris, chronic LE, contact
hypersensitivity and chronic candidiasis.
● Treatment and prognosis:
○ Although oral lichen planus generally
cannot be cured, some drugs can provide
satisfactory control. Corticosteroids are the
single most useful group of drugs in the
management of lichen planus.
LUPUS ERYTHEMATOSUS
● Etiology and definition:
○ Multi-system inflammatory immune
disease
○ Autoantibodies found in the serum or in
tissue, bound to antigens, have been
identified against various cellular antigens
in the nucleus and the cytoplasm
○ Positive reactions noted in the antinuclear
antibody (ANA) and LE cell tests
○ Circulating in serum are antigen-antibody
complexes that mediate disease in many
organ systems
○ Caused by both genetic and
environmental
● Clinical features:
○ Discoid Lupus Erythematosus
- Seen in middle age
 - More in women
- Oral and vermilion lesions are
commonly seen, with the company of
cutaneous lesions
○ Systemic Lupus Erythematosus
- Mild skin and mucosal lesions
- Numerous autoantibodies directed
against nuclear and cytoplasmic
antigens
- Can cause lesions in nearly any
tissue, resulting in a wide variety of
clinical signs and symptoms
● Histopathology:
○ DLE
- Basal cell destruction
- Hyperkeratosis
- Epithelial atrophy
- Lymphocytic infiltration (subepithelial
and perivascular distribution)
- Vascular dilation with edema of the
submucosa
- Basal keratinocytes are a primary
target in mucous membranes
○ SLE
- Inflammatory cell infiltrates are less
intense and more diffuse
- The epithelial lesions are
hyperproliferative
- Positive for cytokeratin markers CK ⅚
and fibrinoid necrosis
- Direct immunofluorescence testing of
skin and mucosal lesions shows
granular-linear deposits of
immunoglobulins (lgG, IgM, IgA),
complement (C3), and fibrinogen
along the basement membrane zone
in a majority of patients
● Differential diagnosis:
○ Resembles erosive lichen planus
○ Delicate and subtle than Wickham’s striae
of lichen planus
○ Characteristic radiation from a central
focus
○ Erythematous gingival lupus may be
confused with mucous membrane
pemphigoid, erythematous lichen planus,
erythematous candidiasis, and contact
hypersensitivity.
● Treatment and prognosis:
○ DLE
- Topical corticosteroids
- Intraorally-high potency ointments
- Refractory cases-antimalarials or
sulfones
○ SLE
- Systemic steroids
- The prednisone dose may be
combined with immunosuppressive
agents for their therapeutic and
steroids-sparing effects
- Antimalarials and nonsteroidal
antiinflammatory drugs may help
control this disease.
NON-MELANOCYSTIC LESION
1. Amalgam tattoo
2. Drug-induced pigmentation
3. Heavy-metal pigmentations
4. Black hairy tongue
AMALGAM TATTOO
● Amalgam tattoo, orr focal argyrosis, is an
iatrogenic lesion that follows traumatic soft
tissue implantation of amalgam particles or
passive transfer by chronic friction of mucosa
against an amalgam restoration
● Etiology:
○ It is brought by the production of an
aerosol of amalgam that becomes
impregnated in the tissues
○ The formation of soluble silver compounds
may be involved in soft deposits

● Clinical features:
○ These lesions would be expected in the
soft tissues contiguous with teeth restored
with amalgam alloy
○ Asymptomatic gray-pigmented macule
found in gingiva, tongue, palate, or buccal
mucosa adjacent to amalgam restoration
○ May be seen radiographically if particles
are large
○ No associated inflammation
○ It is a common condition
● Histopathology:
○ Microscopically, the silver amalgam stains
collagen and eclectic fibers, typically
imparting them with a appears to be black
or golden brown color. Few lymphocytes
and macrophages are present, except in
cases in which particles are relatively
large. Multinucleated foreign body giant
cells containing amalgam particles may be
seen.
● Differential diagnosis:
○ Similarity to melanin-producing lesions. In
a gingival or a palatal location, separation
from nevi
○ Early melanoma is mandatory
○ Persistent gray appearance would help to
separate amalgam tattoo from melanoma
● Treatment and prognosis:
○ Amalgam tattoos are completely benign
that do not typically change in size, color,
or shape. It does not require any treatment
○ It may be removed. If not removed, it will
remain in your mouth permanently.
DRUG-INDUCED PIGMENTATION
● Etiology:
○ Several drugs can cause pigmentation
from antimalarials to antiretrovirals
○ Tetracycline-associated pigmentation
prolonged high doses of minocycline
● Drugs that may produce pigmentation of the
oral tissues:
○ Aminoquinolines (e.g. chloroquine)
○ Cyclophosphamide
○ Amiodarone
○ Zidovudine (azidothymidine [AZT])
○ Quinacrine
○ Clofazimine
○ Heavy metal - containing compounds
 HEAVY METAL PIGMENTATION
● Pathologic
● Exogenous pigmentation
● It is the result of increased levels of heavy
metals in the blood that causes oral mucosal
discoloration
● The most common cause is for treatment of
syphilis
● Etiology:
○ Increased levels of heavy metals in the
blood represent a known cause of oral
mucosal discoloration
○ Lead, bismuth, mercury, silver, arsenic and
gold ingestion
● Clinical features:
○ Deposited heavy metal in the skin and oral
mucosa given color black to gray
Bismuth line of gingiva Lead line of gingiva

● Histopathologic features: Bismuth pigmentation Argyria

○ Non-inflamed palatal mucosa with
pigment-containing histiocytes in the
mucous membrane
○ Immunohistochemically, both hemosiderin
and melanin were detected
● Differential diagnosis:
1) Addison disease
2) Peutz-jeghers syndrome
Addison disease Peutz-jeghers syndrome

Acrodynia

● Treatment:
○ Drug substitution
○ Limiting sun exposure
○ Topical treatment
○ Laser treatment
● Types of heavy metal: ○ Electrosurgery: a use of high frequency
1) Bismuth pigmentation electrical energy is needed
- Blue-black pigment due to bismuth
sulfide formation
2) Argyria
- A rare skin condition (if silver builds
up)
- It can turn your skin, eyes, internal
organs, nails and gums a blue-gray ○ Cryosurgery: gingiva is freezed with
color different material such a liquid nitrogen
3) Acrodynia
- Rare disorder caused due to chronic
mercury poisoning
● Histopathologic features:
○ Gingival pigmentation is presented as a
diffuse deep purplish discoloration or as
irregularly shaped brown and light brown
strands. It results from melanin granules,
which are produced by melanoblasts.
○ Melanin, a non-hemoglobin-derived brown
pigment, is the most common of the
endogenous pigments and is produced by ○ Lasers: one of the effective pleasant and
melanocytes. reliable technique
● Differential diagnosis:
○ The pigmentation of a heavy metal oral
lesion appears as a blue-black line along
the gingival margin and seems to be
proportional to the amount of gingival
inflammation
● Treatment and prognosis:
○ Scalpel surgical technique: surgically
removed using a scalpel
○ Radiosurgery: most advanced form of
electro-surgery. It removes the soft tissue.

BLACK HAIRY TONGUE

○ Bur abrasion method: a specific type of
● A black hairy tongue is a harmless dental
bur is used
ailment that causes the tongue to appear dark
and furry. A deposit of dead skin cells on the
many small projections (papillae) on the
surface of the tongue that contain taste buds
causes the characteristic appearance.
Bacteria, yeast, tobacco, food and other items
 can readily capture and discolor these papillae,
which are longer than typical.
● Etiology:
○ An overgrowth of dead skin cells causes
extension of the papillae and coloring from
bacteria, yeast, food, tobacco, or other
substances in the mouth, resulting in a
black hairy tongue.
○ When projections on the tongue called
papillae grow longer because they don’t
shed dead skin cells like they should, the
outcome is a black hairy tongue. This
gives the tongue a hairy appearance.
○ Discoloration can occur when debris,
germs or other organisms gather on the
papillae.
● Clinical features:
○ Filiform papillae can reach a length of 18
mm, giving then a “hairy” look
○ The tongue discolored, usually brown or
black, but other colors such as brown,
yellow and green have also been reported
○ The back of the tongue is frequently
impacted, whereas the tip and sides are
normally unaffected
○ It is normally asymptomatic, and the
primary issue is that it is unattractive
○ Patients may have a burning or itching
feeling on their tongue, nausea or halitosis
on occasion (bad breath)
● Histopathology:
○ Histopathology shows hyperkeratosis of
the filiform papillae, overgrowth of bacteria
and yeast, and non-specific inflammation.
● Differential diagnosis:
○ Coated tongue
- White, brown, black, yellow
discoloration of the dorsal tongue
without prominent elongation of the
filiform papillae
○ Oral hairy leukoplakia
- Only included in differential diagnosis
due to similarity of terminology
- Most often presents as furrowed white
plaque on lateral tongue
- Associated with Epstein-Barr virus
Coated tongue Oral hairy leukoplakia
● Treatment and prognosis:
○ Elimination of triggers and routine
brushing of the dorsum of the tongue with
a toothbrush
○ Topical keratolytic such as urea and
retinoic acid
○ Elimination of offending/contributing
agents such as tobacco and medications
○ Mechanical debridement with a tongue
scraper or toothbrush
○ If the precipitating factor was antibiotics,
the tongue returns to normal after the
antibiotics therapy is discontinued
○ If the patient has xerostomia, therapies to
increase saliva are of benefit
○ Patients who have candidiasis associated
with hairy tongue requires antifungal
therapy
RBB MELANOCYTIC LESIONS
1. Ethnic pigmentation
2. Smoking-associated melanosis
3. Peutz-jeghers syndrome
4. Addison’s disease
5. Melanocytic nevus
MELANOCYTIC LESIONS
● Melanocytes are melanin-producing cells that
have their embryological origin in the neural
 crest that migrate to epithelial surfaces where
they reside among basal epithelial cells
● They are found throughout the oral mucosa but
usually go unnoticed microscopically because
of their relatively low level of pigment
production
● They range from brown to balck, depending on
the amount of melanin produced and the depth
of the pigment relative to the surface.
PHYSIOLOGIC (ETHNIC) PIGMENTATION
● Etiology:
○ It also refers to the normal biology
dictating the type and amount of melanin
synthesized and the genetically and
embryologically determined patterns of
pigmentation, which occur by definition in
the absence of inherited or acquired
disorders of pigmentation
● Clinical features:
○ The most common site is the gingiva. The
pigmentation can vary from brown to balck
and may be symmetrical and
asymmetrical.
● Histopathology:
○ Physiologic pigmentation is not due to
increased melanocytes but instead
melanin production. Melanin is found
within surrounding basal keratinocytes and
subjacent connective tissue macrophages
(termed melanophages)
● Differential diagnosis:
○ A clinical differential diagnosis would
include smoking-associated melanosis,
peutz-jeghers syndrome, addison’s
disease and melanoma. Although
physiologic pigmentation is usually
clinically diagnostic, a biopsy may be
justified if clinical features are atypical.
● Treatment:
○ No treatment needed.
● All patients except people with albinism have
some degree of physiologic melanin
distribution throughout the epidermis.
● Physiologic pigmentation develops during the
first two decades of life but may not come to
the patients’ notice until later.
SMOKING-ASSOCIATED MELANOSIS
● Etiology:
○ Abnormal melanin pigmentation of oral
mucosa has been linked to cigarette
smoking, termed smoking-associated
melanosis or smoker’s melanosis.
● Clinical features:
○ The anterior labial gingiva is the region
most typically affected, where brownish
color can vary from subtle to obvious.
● Histopathology:
○ Melanocytes show increased melanin
production, as evidenced by pigmentation
of adjacent basal keratinocytes.
● Differential diagnosis:
○ Other entities to consider before a
definitive diagnosis is established are
physiologic pigmentation, diffuse
melanoacanthoma, peutz-jeghers
syndrome, addison’s disease, other
systemic drugs and melanoma.
● Treatment:
○ With cessation of smoking, improvement
can be expected over the course of
months to a few years. Smoker’s
melanosis appears to be of little clinical
significance.
PEUTZ-JEGHERS SYNDROME ● Treatment:
● Etiology: ○ There is no treatment
○ Is an inherited disorder distinguished by ○ Only consultations are offered
hamartomatous polyposis syndromes that
involve the growth of multiple polyps in the
gastrointestinal tract.
● STK/LKB1 gene:
○ Was identified in 1998
○ Located in chromosome 19
○ 50%
○ Parent to offspring
○ Produce serine/threonine kinase 11
enzymes
● History:
○ 1895
- Dr. J.T. Connor
○ 1921
- Dr. Jan Peutz
- Harrisburg family (dutch family)
○ 1949 ADDISON’S DISEASE
- Syndrome was defined by Dr. Harold ● Etiology:
Jeghers ○ Adrenal gland infection (tuberculosis),
- Dr. Harold Jeghers autoimmune disease, or idiopathic causes
○ 1954 may all cause Addison’s disease. As part
- Dr. Andre Bruwer named the of a negative feedback system, pituitary
syndrome as Peutz-Jeghers adrenocorticotropic hormone (ACTH) and
syndrome (PJS) a byproduct g2 melanocyte-stimulating
○ 1957 hormone (MSH) rise in response to
- Horelleno decreased cortisol production by the
● Clinical features: adrenals. Both ACTH and MSH
○ Dark hyperpigmentation are flat, blue-gray overproduction stimulate melanocytes,
to brown spots 1-5mm in size. resulting in diffuse pigmentation of the
Development of hamartomatous polyps. skin. With generalized pigmentation, oral
Obstruction and.or intussusception of the freckles and larger melanotic macules
small bowel. Gastrointestinal bleeding, appear.
anemia and stomach pain.
● Histopathology:
○ Microscopically, the Peutz-Jeghers polyps
are characterized by extensive
smooth-muscle proliferation with an
elongated, arborized pattern of polyp
formation.
○ Pathologically, PJS are characterized by
small intestine polyps in relation with a
definite pattern of skin and mucosal
macular melanin deposition.
○ The histopathology of PJS-associated
gastric polyps can be similar to
hyperplastic gastric polyps
● Differential diagnosis:
○ Laughier-Hunziker syndrome (LHS)
○ A fixed drug reaction
○ A normal feature especially in African
Americans

FINALS
ORAL DIAGNOSIS
● The identification of a disease by an
investigation of the signs and symptoms
● Signs: something that is observed
● Symptoms: only felt by the patients
DIFFERENTIAL DIAGNOSIS
● The determination, by systematic comparison
and contrast of symptoms, of the one of
several diseases from which a patient is
suffering.
ORAL DIAGNOSIS DEALS WITH:
1. Fundamentals of the interview
2. Principles and procedures of clinical exam
3. Methods of identifying oral diseases
4. Rationale for oral therapy
SCOPE OF ORAL DIAGNOSIS
● Efficient discipline for collection of material
necessary to make a diagnosis
● 2 major factors in selecting level of diagnostic
effect
○ ?
TYPES OF EXAMINATION
1. Thorough Complete Examination
● Utilizing all the skills of interviewing,
physical exam and supplemental
diagnostic exam
2. Screening Type of Exam
● of the practical aspects of reduced time, costs,
3. Emergency or Limited type of Exam
● Necessary for the diagnosis and mgmt of
acute and emergency conditions
4. Periodic Health Maintenance Exam
● Necessarily includes a complet
COMPLETE EXAMINATION
1) Case History
● Patients chief complaint, present illness,
past history and systems review
● Questionnaires:
○ Intended to elicit symptoms that may
indicate disease processes in the
various systems of the body
● Where circumstances do not permit
extensive history taking by the dentist, a
questionnaire to be completed by the
patient should be used, provided that the
dentist elaborates on the positive and
significant negative answers to the
questions on the questionnaire
● In order that the questionnaire not be
HEALTH QUESTIONNAIRES
● Should obtain certain vital statistics about the
patients such as the name, age, height, weight,
occupation, marital status and the name of the
patient's physician.
○ Introductory statements should be made
on how the questionnaire is answered,
and some reassurance that the answers to
the questions will be held
2) Clinical Examination
a. General appraisal of the patient
b. Detailed oral examination
c. Supplementary examination and special
test when indicated
3) Diagnosis
a. Summary of the nature of the abnormality,
its etiology and significance
b. Prognosis
4) Treatment Plan
a. Ideal
b. Alternate
SCREENING EXAM
● Will point out the necessity for ore thorough
examination
● Attempts to compromise between a complete
examination and a less extensive one because
and skill involved in a shorter type of
examination
● Scope must necessarily be determined
1) Chief complaints: an apparently well
patient may or may not have a significant
complaint, byt the chance to express one
should be given
2) Health questionnaire
3) Selected radiographs
4) Gross appraisal for decay, missing and
filled teeth
5) General appraisal of the gingiva for
alteration of color and form
6) Gross appraisal of the soft tissues for the
presence of lesions
7) Brief appraisal of oral hygiene
 8) Brief appraisal of occlusion
SCREENING TYPE OF EXAMINATION MAY BE
USED:
1. To indicate gross disease in broad surveys
EMERGENCY OR INCOMPLETE EXAMINATION
● This type of examination is limited to those
procedures that obviously appear related to the
complaint of the patient
● History will consist solely of the time of
occurence the manner in which the accident
occured, presence or absence of associated
signs and symptoms, and presence or
absence of systemic disease of immediate
importance to therapy.
○ The emphasis is placed upon the
evaluation
TREATMENT PLANNING
● Patients goals and desires
○ Patients modifiers
● Dentist goals and desires
○ Dentist modifiers
- Knowledge
- Technical; skills
- Treatment planning philosophy
PHASES OF TREATMENT PLAN
● Sorting treatment into phases helps the
clinician organize the plan and improves the
overall prognosis of the case
● Patients often comprehend a complicated
treatment plan more easily when it is
separated into segments
5 GENERAL CATEGORIES OF PHASING
● Systemic phase
● Acute phase
● Disease control phase
● Definitive treatment phase
● Maintenance care phase
SYSTEMIC PHASE
● Involves a thorough evaluation of the patient's
health history and any procedures necessary
to manage the patient’s general and
psychological health before or during dental
treatment.
● May include consultation with other health
providers, antibiotic prophylaxis, stress and
fear management, avoidance of certain
medications and products (e.g., latex)
ACUTE PHASE
● Resolve any symptomatic problems with which
a patient may present
● Common complaints include
○ Pain,
○ Swelling
○ Infection
○ Broken teeth
○ Missing restorations
● Dentist may choose to prescribe medications
to control pain and infection
● **Acute phase procedures are often provided
before a comprehensive treatment plan is
created.
● Possible acute phase treatments include
○ Extractions
○ Endodontic therapy
○ Initial periodontal therapy
○ Placement of provisional (temporary) or
permanent restorations, and
 ○ Repair of prostheses

DISEASE CONTROL PHASE

● Goal:
○ Control active and disease and infection
○ Stop occlusal and esthetic deterioration
○ Manage ang risk factors that cause oral
problems
● Common procedures include:
○ Oral hygiene instruction
○ Scaling and root planning
○ Caries risk assessment and prevention
○ Endodontic therapy
○ Extraction of hopeless teeth
○ Operative treatment to eradicate dental
caries

DEFINITIVE TREATMENT PLANNING

●