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Lips and Oral Cavity
Emmanuel Samson, MD, FPSO-HNS July 2, 2015

So turn up the corners of your lips, part them and feel my *5th branchial arch is embedded between the 4th and the 6th so
fingertips trace the moment, fall forever. it is normally not seen.
~Vindicated, Dashboard Confessional

OUTLINE

I. Embryology
II. Conditions Associated with Embryologic Abnormalities
A. Pre-auricular Duct Cyst
B. Thyroglossal Duct Cyst
C. Branchial Cleft Cyst/ Fistula
D. Hemangioma
III. Basic Anatomy and Physiology of the Lips and Oral
Cavity
A. Anatomy
B. Physiology
IV. Methods of Examining the Lips and Oral Cavity
Pharyngeal arch structures
A. Visual Inspection
B. Palpation
C. Taste Testing CONDITIONS ASSOCIATED WITH EMBRYOLOGIC
D. Imaging Procedures ABNORMALITIES
V. Malformations of the Lips and Oral Cavity PRE-AURICULAR SINUS
A. Cleft Lip and Palate  usually an elevation before the ear and has a sinus. When
B. Rare Malformations Involving the Oral Cavity pressed yellow discharge can be seen
C. Other Malformations
VI. Diseases Associated with the Tongue
VII. Inflammations of the Lips and Oral Cavity
A. Viral Infections
B. Bacterial and Fungal Infections
C. Superficial Tongue Lesions
D. Angioedema
E. Immunologic Disease
VIII. Tumors of the Lips and Oral Cavity
A. Benign Tumors
B. Precancerous Lesions
C. Malignant Tumors

Pre-auricular sinus (maraming tao ang may ganito)

Italicized texts are lifted from 3A 2014 ENT trans
and Doc Samson’s ppt. The rest is from Probst’s THYROGLOSSAL DUCT CYST
Basic Otorhinolaryngology.

EMBRYOLOGY
 there are 5 pharyngeal arches: I, II, III, IV, and VI
o each contains skeletal, primitive artery, vein, and nerve
components
o pharyngeal arches develop into branchial arches

Thyroglossal duct cyst, a hyperemic anterior neck muscle

Epidemiology  75% of the cases are diagnosed before 5

y/o; most are diagnosed before 12 months
 malignancy = rare
Symptoms  Tense, firm, swelling in the midline of the
neck
Pharyngeal arch formation (ventral view) Diagnosis  by inspection and palpation → thyroglossal
duct cyst moves when the patient
Branchial swallows
Nerve Artery Skeleton
arches  Ultrasound
I Trigeminal Atrophy Mandible, o support diagnosis
incus, malleus o well circumscribed, elliptical, hypoechoic
II Facial Atrophy Stapes, portion or echo free mass with distal acoustic
of hyoid, enhancement
styloid Treatment  surgery through a transverse suprahyoid
ligament incision
III Glossopharyngeal External
carotid
IV Superior laryngeal Arch of
aorta
VI Recurrent Ductus
laryngeal arteriosus

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 Lips and Oral Cavity
BRANCHIAL CLEFT CYST/FISTULA
Branchial cleft cyst (left) and branchial cleft fistula (right)
Epidemiology  Branchial cleft cyst – manifested
between 15-25 y/o
o 4x more prevalent than branchial fistulas
 Branchial fistula – manifested
immediately after birth
 Malignancy is rare
Symptoms  Branchial cleft cysts → painless, tense
swelling in the carotid triangle between the
hyoid bone and sternocleidomastoid muscle
 Branchial fistulas → open externally at the
anterior border of the sternocleidomastoid
muscle and may be marked by a clear,
amber-colored discharge
Diagnosis  B Mode Ultrasound – homogenous, echo-
free masses with smooth margins located at
a typical site
Treatment  surgery
HEMANGIOMA
 a vascular formation
 belongs to the group of harmatomas (a malformation;
dysontogenetic growth of normally formed tissue)
 no proliferation of cells
 development of the tissues involved did not proceed
Hemangioma
Epidemiology  incidence = 10% during 1st year of life
 predominant in premature
 common in females
Symptoms  soft, reddish-purple swelling
 can occur anywhere in the body
Course  regress spontaneously (80%)
Diagnosis  B-mode ultrasound – defines the overall
extent of the lesion
 color duplex ultrasound
Special types  Kassabach-Merritt
o presence of typically large hemangioma in
which thrombotic processes lead to DIC
with consumption coagulopathy
o almost exclusive to small infants
 Blue rubber Bleb Nevus Syndrome
o autosomal dominant
o deep blue hemangiomas with a rubbery
consistency form on the integument and
persist without involution
BASIC ANATOMY AND PHYSIOLOGY OF THE LIPS AND
ORAL CAVITY
 Lips and the soft tissues of the cheek function as the outer
boundary of the oral vestibule and oral cavity
 forms the initial part of the digestive tract
 functions: food ingestion and speech production (developed
during the course of phylogenesis)
 TONGUE
o Body
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1.3
 within the oral cavity
 with the most number of taste receptors
o Base/Root
 forms the anterior boundary of the oropharynx
Anatomy of the lips, oral vestibule and oral cavity
ANATOMY
ORAL VESTIBULE
 boundaries
o Externally – lips and cheeks
o Internally – alveolar processes and teeth
o oral vestibule communicates with the oral cavity via a
space behind the last molar
o the oral cavity opens into the pharynx at the faucial
isthmus
LIPS AND CHEEKS
 formed largely by the mimetic muscles
 lined by nonkeratinized squamous epithelium
LIPS
 labial commissures at the corners of the mouth connect the
longer upper lip and shorter lower lip
 Nasolabial fold – an oblique sulcus that runs laterally and
inferiorly from the nasal alae separate the lips from the cheek
 lamina propria of the lips contains numerous seromucous
salivary glands (secretions from which drain into the oral
vestibule)
 orbicularis oris muscle forms the muscular foundation of
the lips
o shows the superficial and deep masticatory muscles, the
buccinator muscle, and the orbicularis oculi muscle
Blood supply  facial artery  superior and inferior
labial arteries  lips
Drainage  facial vein
o communicates with the orbital veins via
the angular vein above the upper lip
 infectious organisms can spread into the
cranial cavity via connections between the
orbital veins and cavernous plexus
Lymphatics  submandibular and submental lymph
nodes
 lymphogenous metastasis of malignant
tumors of the lips
Sensory  Upper Lip: infraorbital nerve
innervation  Lower lip: mental nerve
CHEEKS
 form the lateral boundaries of the oral vestibule
 contain small salivary glands in their mucosa
 Buccinator
o forms the muscular framework of the cheek
o mimetic muscle like orbicularis oris
o innervated by the branches of the facial nerve
 Bichat fat pad (buccal fat pad)
o between the buccinator muscle and the overlying
masseter muscle
o smooths cheek countour by filling in the depression at
the anterior border of the masseter muscle
 Masseter muscle
o located in the posterior part of the cheek, covers the
vertical ramus of the mandible and the mandibular angle
from the outside
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 Lips and Oral Cavity 1.3

o fibers run almost perpendicular to the buccinator PALATE

 excretory duct of the parotid gland runs through the HARD PALATE FORMATION
buccinator muscle and opens into the mucosa of the cheek Anterior  Palatine processes of the maxilla
opposite the upper second molar Posterior  Incisive bone
 Horizontal plates of the palatine
MASTICATORY MUSCLES bones
 Masseter muscle (posterior part of the cheek) PALATAL MUSCLES
 Temporalis muscle TENSOR  Form the framework of the soft
 Medial and lateral pterygoid muscles VELIPALATINI palate
 Supplied by the mandibular nerve (third division of the  Form the framework of the soft
trigeminal nerve) palate
LEVATOR
VELIPALATINI  Elevates the soft palate during
swallowing to keep food from
entering the nose
 Runs in the anterior faucial pillar
PALATOGLOSSUS
(palatoglossal arch)
 Muscle of the posterior faucial pillar
PALATOPHARYNGEUS
(palatopharyngeal arch)

 The palatal mucosa contains numerous salivary glands

(palatine glands).

PALATAL MUSCLES
ARTERY  Ascending palatine branch of the facial artery
The superficial & deep masticatory muscles, the buccinators SENSORY  Greater and lesser palatine nerves (from the
muscle, and the orbicularis oculi muscle NERVE second trigeminal nerve division)
MOTOR  Cranial nerves 9, 10, small degree of 5
TEETH NERVE  CN 9 and 10 deficits tend to restrict the mobility
 two sets of teeth of the soft palate, causing difficulties in
 the deciduous teeth are replaced by the permanent teeth swallowing; the uvula and faucial pillars deviate
 (8) of which occupy each half of the maxilla and mandible: toward the unaffected side, during phonation.
o 2 incisors
o 1 canine TONGUE AND ORAL FLOOR
o 2 premolars  the tongue is continuous anteriorly and laterally with the floor
o 3 molars of the mouth
 each tooth consists of a crown and a root that terminates at  Mylohyoid – forms the muscular foundation of the oral floor
the apex and stretches between anterior portions of the mandible
 Neck (cervix)  the sublingual folds and sublingual papillae can be
o area between the crown and root which protrudes from identified on both sides of the frenulum in the anterior part of
sockets (dental alveoli) in the alveolar processes of the the oral floor
maxilla and mandible
 Crown
o projects freely into the oral cavity and is covered
externally by enamel
 Pulp chamber (internally)contains:
o connective tissue
o nerve fibers
o blood vessels
o connected to the alveolus via the root canal
 Periodontium – collectively function as anchoring and
supporting structures, includes:
o cementum,
o bony alveolar wall
o gingival
 alveolar processes (in maxilla) – form the floor of the
maxillary sinuses
 roots of the 2nd premolar and 1st molar are very closely
related to the maxillary sinus
Intrinsic and extrinsic (genioglossus and geniohyoid) lingual
muscles. Geniohyoid muscles provides the muscular foundation of
Blood supply  Maxillary artery  Inferior alveolar the oral floor.
artery, anterior and posterior alveolar
arteries Maxilla and mandible  Main anatomical subdivisions of the tongue
Innervation  Branches of the maxillary nerve  upper o Apex
teeth o Body
 Branches of the mandibular nerve  o Base or root
lower teeth  Terminal sulcus
o v-shaped groove, separate the body from the base
ORAL CAVITY o tip of this groove is directed toward the tongue base and
 boundaries: is formed by the foramen cecum
Anterior  Alveolar ridge and teeth
Lateral
Superior  Hard and soft palate
Posterior  Faucial isthmus
o a narrow opening between the oral cavity and
pharynx and is bordered by the soft palate
with the uvula and by the dorsum of the
tongue at its junction with the tongue base

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 Lips and Oral Cavity 1.3
 Receives sensory supply from lingual
TERMINAL
nerve (from the third division of the
SULCUS
trigeminal nerve)
SENSATION TO  Glossopharyngeal and superior laryngeal
THE TONGUE nerves (from cranial nerve X)
BASE
 The chorda tympani (from cranial nerve
TASTE BUDS VII) in the anterior two-thirds of the
(SENSORY
tongue and the glossopharyngeal nerve
INNERVATION)
in the posterior third

 Developmentally, the tongue is derived from structures of the

first through fourth branchial arches.
 Paralysis of the Hypoglossal nerve maybe secondary to:
o to radical neck dissection
o surgery of the submandibular gland
o stroke (if there is presence of other cranial nerve deficits
manifests as slurring of speech or dysphagia
o rigid telescopes (larynx 70 degrees, 30 degrees, 0
The body and base of the tongue, superior aspect. degrees)
o flexible telescopes
 the mucosa of the tongue conatains numerous papillae,
which project from the surface of the tongue and give it its CN INNERVATING THE FUNCTION
characteristic roughness TONGUE
12: Hypoglossal Motor
FOUR TYPES OF PAPILLAE 9: Glossopharyngeal Sensory: Taste for posterior 1/3
FILIFORM 7: Facial (through Sensory: Taste for anterior 1/3
FUNGIFORM* less taste buds chorda tympani)
VALLATE* with most number of taste buds 5: Trigeminal (branches General sensation: touch, pain,
FOLIATE* with most number of taste buds to lingual nerve) position, temperature
*most important for taste perception
CENTRAL GUSTATORY PATHWAYS
 small numbers of taste buds also occur in other regions of the  all gustatory fibers converge centrally in the area of the
oral cavity and pharynx (e.g., the soft palate, the anterior
ipsilateral solitary tract
pillar, and the posterior wall of the oropharynx) o which ends at the solitary tract nucleus in the
 each taste bud consists of 30–80 elongated cells that
medulla oblongata;
extend superficially to the gustatory pore o there the signal is relayed to the second neuron
 the gustatory pore is located between the squamous
 although not yet fully understood, according to recent
epithelial cells and communicates with the oral cavity discoveries, the axons initially continue on to the medial
 the lingual tonsil is part of the collection of lymphoepithelial
parabrachial nucleus, where they synapse with the third
tissue known as Waldeyer’s ring neuron
 the fibers then travel via the dorsal trigeminothalamic
tract, some crossed but most uncrossed, to the thalamus
 the cortical taste areas themselves are located in the
lateral part of the postcentral gyrus and in the adjacent
insular cortex

Central Gustatory Pathway

Histology of the Tongue
PHYSIOLOGY
TONGUE AND ORAL CAVITY IMPORTANCE OF FOOD INTAKE
 Lingual and sublingual arteries (from  Lips – “acts as gateway”
ARTERY
the external carotid muscle)  Orbicularis oculi muscle closes  sealing the oral cavity
 (Lingual and sublingual veins)  facial during chewing and swallowing  prevent the spillage of food
VEIN
vein  internal jugular vein  deficiency of lip closure can cause eating difficulties as well as
 Ipsilateral and contralateral drooling from the corners of the mouth at rest
submandibular and submental lymph  the tongue has major functional importance as a
nodes  drain to the lymph nodes at the “multifunction organ” with both motor and sensory properties
LYMPHATIC  extrinsic muscles-are attached to the mandible & the hyoid or
junction of the facial and internal jugular
styloid process
veins (upper jugular lymph nodes) o project into the body of the tongue
**potential for contralateral lymphogenous o affect position and movement
spread of malignancy  Intrinsic tongue muscles (serve mainly to alter the shape
 Cranial nerves 5, 7, 9, 10; of the tongue) are composed of:
NERVE
 CN 12 (motor)

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 Lips and Oral Cavity 1.3

o Longitudinal
o Transverse
o Vertical fiber systems
 the tongue muscles :
o are extremely mobile and strong
o play an essential role in swallowing
o also influence the normal development of the maxilla and
the dentition
 the molars have the greatest importance in chewing
o because they are located closest to the insertion of the
masticatory muscles (which allows very high pressure to
be developed between their occlusive surfaces)

TASTE
 there are only four basic taste sensations: sweet, sour,
salty, and bitter
o *5th taste = UMAMI/MEATY (from Guyton and Hall
Medical Textbook of Medical Physiology, 12 th ed.)
 a combination of olfactory, thermal, mechanical, and sensory
impressions
Physical examination of the oral cavity. (a)Positions of the
patient and examiner. (b) The lips and cheeks are retracted from
IMPORTANCE UN PHONATION AND ARTICULATION the teeth and alveolar ridge with a tongue blade to inspect the
 Musculature of the lips  essential in phonation mucosa and assess the condition of the parotid duct orifice
 “Lingual articulation” controls the production of vowels, opposite the second upper molar. (c) The patient elevates the
tongue so that the examiner can evaluate the floor of the mouth
certain consonants, and palatal sounds
and the submandibular duct orifices. (d) The tongue is retracted
 through changes in the shape and position of the tongue with the blade so that the lateral oral floor can be examined.
 the oral cavity joins with the pharynx, nose, and paranasal
sinuses in forming the “supraglottic vocal tract,” which TECHNIQUES AND RATIONALE
plays a role in the coordination of vocal sounds
Retract the lips
 To inspect the mucosa
and cheeks from
METHODS OF EXMINING THE LIPS AND ORAL CAVITY  To assess the condition of the
the teeth and
 inspection of lips and oral cavity – essential part of every parotid duct orifice opposite the
alveolar ridge with
otolaryngologic examination second upper molar
a tongue blade (b)
 some problems that cannot be adequately investigated by Ask the patient
clinical examination alone (e.g. taste disturbances, tumors)  To evaluate the floor of the mouth
elevates tongue
may require additional diagnostic procedures (e.g. taste tests, and submandibular duct orifices
(c)
imaging studies) Retract the tongue
 Disturbances of taste  To examine the lateral oral floor
with the blade (d)
o rare but can be very distressful for the patient  To assess tongue mobility
o reversible in many cases, depending on the cause Ask the patient
o With hypoglossal nerve palsy,
stick out the
the tongue will deviate toward
CAUSES OF TASTE DISORDERS tongue
the affected side
CLASSIFICATION EXAMPLES  To assess the mobility of the soft
CONGENITAL  Aplasia of the taste buds Watch the soft palate
 Diabetes mellitus palate while the o With glossopharyngeal nerve
ENDOCRINE
 Hypothyroidism patient says "ah" palsy, the uvula and palatal arches
DISORDERS
 Adrenal insufficiency several times deviate toward the healthy side
 D-penicillamine (“backdrop sign”)
DRUG SIDE  Various lipid-lowering drugs
EFFECTS  ACE* inhibitors
 Antifungals
 Involvement of the chorda tympani
by facial nerve palsy
 Otitis media or previous middle ear
PERIPHERAL
surgery
NERVE LESIONS
 Involvement of cranial nerve IX by
tumors or fractures of the skull base
 Very rarely after sonsillectomy
RADIOTHERAPY  Radiation damage to the papillae
 Alcohol
EXOGENOUS
 Nicotine Left CN XII (a) and CN IX (b) palsy. (a) The tongue deviates
CHEMICAL AGENTS
 Mouthwashers toward the affected side when protruded. (b) The soft palate
CENTRAL TASTE  Head trauma deviates toward the healthy side during phonation.
DISORDERS  Carbon Monoxide poisoning
PARALYSIS OF THE HYPOGLOSSAL NERVE
 may be secondary to radical neck dissection, surgery of the
VISUAL INSPECTION
submandibular gland, and stroke (if there is presence of other
 inspection of the lips cranial nerve deficits
 removal of dentures before examination is started  manifests as slurring of speech or dysphagia
 examination of the oral cavity
o done with the aid of a tongue blade
PALPATION
o examiner holds instrument in the right hand
o examiner uses left hand to position and steady the  if inspection reveals questionable changes, the affected region
patient’s head or structure should next be palpated to better assess the
consistency and depth of the suspicious finding
 cervical lymph nodes should also be palpated

TASTE TESTING
 abnormalities of taste are classified as:
o Hypogeusia – diminished sense of taste
o Hypergeusia – increased sensitivity of taste
o Ageusia – absence of the sense of taste

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 Lips and Oral Cavity 1.3
 Hypernasal speech (rhinophonia aperta)
o due to incomplete closure of the nasopharynx

Symptoms
SUBJECTIVE TASTE TESTING
 Recurrent middle ear effusions and
CHEMOGUSTOMETRY inflammations
 aqueous solutions of glucose, NaCl, citric acid, and o resulting from eustachian tube dysfunction
quinine are applied to the tongue in various  Variable abnormalities of the nasal septum (septal
concentrations to test the threshold of taste perception deviation) or in the shape of the external nose
for the four basic qualities of sweet, salty, sour, and bitter

Diag-
nosis
 easy to perform but does not provide a high degree of  Examination: palpation of the hard palate to detect
reliability or reproducibility the bony discontinuity in that region.

ELECTROGUSTOMETRY  Requires close interdisciplinary teamwork among the

 procedure in which sensations are evoked by applying a pediatrician, otolaryngologist, maxillofacial
constant anodal current to the taste receptors of the surgeon, orthognathic surgeon, and
tongue phoniatrist.
 has methodologic advantages over chemogustometry:
o Provides better quantitative assessment of side-to-side
differences
o Provides more accurate localization of responses

Treatment
OBJECTIVE TASTE TESTING
 based on gustatory evoked potentials
 analogous to objective hearing and olfactory tests
 possible in principle but are very costly
 practiced only at large centers
 used mainly in examinations for disability assessment

IMAGING PROCEDURES
 since the anatomical structures of the oral cavity are easily
accessible:
o diagnosis can often be established by clinical
examination alone (inspection, palpation, biopsy, or
local excision of a suspected tumor) Basic treatment plan for cleft lip and palate
o imaging procedures tend to have a limited role in
diseases of the lips and oral cavity THEORIES OF CLEFT FORMATION
 however, there are various clinical situations (e.g. a  FUSION – non fusion of a pre-existing cleft in the fetus
tumor or extensive inflammatory process) in  PULSION – breakdown of developing upper lip of fetus
which a sectional imaging procedure can advance o due to: teratogenic drugs, viral infection (rubella)
the diagnosis  Theory of our mothers

ULTRASOUND
 only B-mode instruments are useful for ultrasound
examinations of oral floor and tongue
 real-time scanning is preferred
 transducers with an operating frequency in the 5-10MHz
range are used, depending on the desired penetration depth
and resolution
MALFORMATIONS OF THE LIPS AND ORAL CAVITY
 epithelial in origin
 based on a common teratogenic mechanism
EMBRYOLOGY
 6 weeks – pre-existing cleft n normal development
 9 weeks – can see if baby has cleft
 6 months and 1 week – closed
CLEFT LIP
 unilateral complete cleft of the lip
 incomplete cleft lip – cleft doesn’t extend to nasal cavity
 complete cleft lip – cleft reaches up to nasal cavity
 due to the failure of fusion of the maxillary and medial nasal
processes (formation of the primary plate)

CLEFT LIP AND PALATE CLEFT PALATE

 a condition in which two plates of the skull that form the
hard palate (roof of the mouth) are not completely joined
Epidem-

 Occur in various combinations.

iology

 the soft palate in these cases is cleft as well

 Incidence: 1 in 500 (among the most common
malformations)
1. Cleft lip and alveolar ridge
2. Cleft lip, alveolar ridge, and palate
3. Isolated cleft palate
o BIFID UVULA
 a very mild variant of the cleft palate
Classification
 in most cases, cleft lip is also present
 when cleft palate occurs, the uvula is usually split
o occurs due to the failure of fusion of the lateral palatine
processes, the nasal septum, and/or the median
palatine process (formation of the secondary plate)
 the hole in the roof of the mouth caused by a cleft connects
the mouth directly to the nasal cavity

COMORBID DEFORMITIES/ OTHER FEATURES

Characteristic appearance of a median
cleft in the uvula
 involves a developmental anomaly of the embryonic
Pathogenesis
ASSOCIATED WITH CLEFT LIP AND PALATE
 maloclussion
 flattening of the ala
 shortened columella (pango)
 malorientation/splaying of the teeth
 Velopharyngeal insufficiency (VPI)
o direct result of an open connection between the oral
cavity and nasal cavity
o because of the gap, air leaks into the nasal cavity →
hypernasal voice resonance and nasal emissions
 environmental influences may also cause or interact with

head genetics to produce oro-facial clefting

 genetic inheritance o seasonal causes (pesticide exposure)
 external influences o maternal diet and vitamin intake
o viral infections o retinoids (vitamin A)
o placental oxygen deficiency o anticonvulsant drugs, alcohol, cigarette use
o intrauterine bleeding o organic solvents
o exposure to ionizing radiation

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 Lips and Oral Cavity 1.3
o parental exposure to lead; illegal drugs (cocaine, crack TRANSVERSE FACIAL CLEFT
cocaine, heroin)  cleft cheek, macrostomia, lateral facial cleft
 causes:
RARE MALFORMATIONS INVOLVING THE ORAL CAVITY o failure of fusion of the maxillary and mandibular
MALFORMATIONS OF THE INTERMANDIBULAR FUSION processes
ZONE o failure of the buccal membrane to regress due to fusion
1. Dermoids of the tongue, oral floor, and mandible of the myoblasts
2. Superficial median neck clefts  marked by bilateral extension of the oral fissure due to lateral
3. Clefts of the lower lip, mandible, and tongue displacement of the commissure
 frequently associated with facial dysplasia and auricular
Illustrative case: Dermoid cyst of the oral floor dystopia

OTHER MALFORMATIONS
VERRUCA VULGARIS
 aka common wart
 benign skin lesion caused by HPV 2 and 4
 MOT: constant contact
o transmitted to the mouth by nail biting

Symptoms  2 mm white, cornified, well-delineated

embossed lesion on the lip
 small sessile, well-defined exophytic growth
with a cauliflower surface and white or normal
color
(a) The patient presents with a submental swelling and (b) a  oral lesions maybe single or multiple and are
tense bulging of the entire anterior and lateral oral floor. frequently found on the lips and palate
 can also be found in the fingers and hands
Treatment o surgical excision or cautery
o ASA (chemical excision)
*if veruccal warts are present on the lips, always check the
fingers if there is also presence of warts.

(c) A transverse ultrasound scan reveals displacement of the

oral-floor musculature by a cystic mass. d An axial T2-weighted
magnetic resonance image (MRI) defines the lateral extent of the
mass (arrows).

Verruca vulgaris on the hands and lips

GINGIVAL HYPERPLASIA
 excessive overgrowth of the gum tissue surrounding the teeth

(e) Coronal MRI (T1-weighted, postcontrast) demonstrates the

relationship of the mass to the musculature of the oral floor and
tongue, and (f) a sagittal T2-weighted image defines the
anteroposterior extent of the mass in the direction of the tongue
base. The streaky markings within the cystic mass are a motion
artifact due to swallowing. Gingival hyperplasia secondary to Dilantin intake

 Localized gingival hyperplasia

o can be due to constant irritation
 Generalized gingival hyperplasia
o hormonal (secondary to pregnancy)
o familial/congenital
Etiology

o secondary to prolonged therapy with Phenytoin or

Dilantin (anticonvulsant)
o systemic illness (e.g., leukemia)
 other drugs that can cause gingival hyperplasia:
Nifedipine and Cyclosporine
 other causes:
o scurvy
o acute myeloid leukemia
 can grow so much that it literally surrounds and often
Symp-
toms

(g) The lesion was surgically removed via the anterior oral cavity, covers the teeth
yielding a well-circumscribed, thin-walled mass loosely attached
 usually irregular and may or may not be associated
to the surrounding tissue and identified histologically as a
dermoid cyst. An important differential diagnosis is a dysgenetic
with bleeding
salivary-gland cyst (ranula), which also tends to occur in the
anterior oral floor.

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 Lips and Oral Cavity 1.3
 Gingivitis above the location of the mylohyoid
Diag-
nosis
o also causes swelling of the gums but not to the muscle’s attachment to the mandible
extent seen in this condition  in 90% of the cases, there is torus on both
the left and right sides, making this finding
an overwhelmingly bilateral condition
Treat-
ment

 surgical excision or cautery  size of the tori may fluctuate throughout life
 ASA (chemical excision) Treatment  if small, leave it as it is

LONG UVULA
GINGIVAL SARCOMA  the tip of the uvula touches the base of the tongue and cause
 aggressive tumor of the soft tissue irritation to the throat
 cancer of the connective and support tissue of the gingival  Tx: if asymptomatic – none

BIFID UVULA
 prevalence:
o males: 0.4/1000 population
o females: 0.0/1000 population
 can be a mild form of cleft palate

DISEASES ASSOCIATED WITH THE TONGUE

HERPES SIMPLEX
 blisters on the oral cavity and dorsum of the tongue which
eventually ruptures and heals after 2 weeks
 Tx: do not give antibiotics unless infected with bacteria

HAIRY TONGUE
Gingival sarcoma  outgrowth of mucosa or papilla
 triggered by fungal compounds
 usually seen in patients taking antibiotics for a prolonged
TORUS PALATINE period
 an exostosis protruding from the midline of the hard palate  Tx: stop antibiotics; practice good oral hygiene
o exostosis – a noncancerous growth on the surface of a bone,
usually with a cartilage cap, that is due to long-term irritation as
a result of osteoarthritis, infection or trauma
 well-localized bony outgrowth
 most common
o ~10% of the population have this

Hairy tongue

FISSURED OR SCROTAL TONGUE

 variant of normal appearance of the tongue
 prone to small food particle lodge → infection
Torus palatinus
 Tx: none
Symptoms  classical features: midline location, covered
with normal mucosa, bony hard to palpation
Treatment  if small and asymptomatic, leave it as it is
 if symptomatic causing ulceration → leave as it
is (3A 2014 ENT trans)

TORUS MANDIBULARIS
 second most common
 bony growth in the mandible along the surface nearest to the
tongue

Fissured tongue

LARGE TONGUE

Torus mandibularis

Epidemiology  prevalence ranges from 5-40%

 less common than torus palatine
Etiology  caused by several factors
 common in early adult life
 associated with bruxism
o bruxism – grinding or gnashing of the teeth
typically occurring during sleep (2D 2014 Psych
trans)
Symptoms  usually present near the premolars and Macroglossia

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 Lips and Oral Cavity 1.3
 Herpes impetiginatus
 may be part of a sinister disease o secondary bacterial superinfection by S. aureus or
 infant with a large tongue and petechiae on the head and streptococci
neck → hemangioma o frequently heals by scarring, in contrast to non-
 children with Down syndrome can also have enlarged superinfected cases
tongue

DEVIATED TONGUE
 usually appears as half-normal, half-atrophied
 same-side paralysis
o mass of the tongue is diminished on the same side of
paralysis
 causes of paralysis of the R hypoglossal nerve
o stroke
o iatrogenic – complication of submandibular gland

Complications
surgery

INFLAMMATIONS OF THE LIPS AND ORAL CAVITY Typical clinical appearance of bacterial superinfection in
VIRAL INFECTIONS herpes labialis

HERPES SIMPLEX VIRUS  Postherpetic exudative erythema multiforme

o characterized by skin lesions as well as typical
Epidem-

ulcerative eruptions on the mucus membranes of

iology

 85% to 90% of the adult population are seropositive

the mouth, lips and genitals
for HSV, particularly in urban areas

 HSV type 1: cutaneous and oral-mucosa strain

 HSV type 2: genital region
genesis
Patho-

 Mode of transmission (MOT):

o direct contact
o droplet infection
o occasionally through superficial skin injuries
 Primary infection:
o usually acquired in early childhood
Postherpetic exudative erythema multiforme
o predominantly affects the oral mucosa as
 herpes simplex labialis
Symptoms

herpetic gingivostomatitis (aphthous

o topical antiseptics to prevent superinfection
stomatitis)
Treatment

 Acyclovir
 flulike fever and lethargy → appearance of local
o severe herpes labialis
lesions (bullae) on the oral mucosa + regional
o administered topically as ointment or systemically
lymphadenitis
o generally continued for 5–7 days
 herpetic rhinitis (nasal mucosa involvement) in
o immunosuppressed patients may require a more
rare cases
prolonged course of treatment
 can occur in response to
o physical exertion
o UV radiation SEVERE FORMS OF HERPES SIMPLEX VIRUS
o febrile infection (HSV) INFECTION
o emotional stress  Pospichill-Feyrter aphthoid
o pregnancy o can occur in immunocompromised children or as a sequel
 most commonly manifested as herpes labialis to measles, rubella, or chickenpox
 site of predilection: o a comparable form of this disease occurs much less
o perioral region (mucocutaneous junction of the frequently in immunocompromised adults and especially
lips) in HIV-infected patients
 Herpetic meningoencephalitis
Reactivation

o mouth and nasal vestibule

o cheeks, earlobes, or eyelids o a dreaded complication of primary HSV infection in
children

THEORIES ON THE REACTIVATION OF HERPES SIMPLEX

VIRUS (HSV) INFECTION
1. Reinfection due to an exogenous cause
2. Endogenous reactivation of the virus
 precipitating factor may be the integrated viral DNA in
the host cells → often not detectable during latent
periods → able to induce the production of an active virus
 herpes virus persist asymptomatically in the spinal cord
→ activated by any number of provocative mechanisms
→ travel along sensory nerve fibers to corresponding
Herpes simplex labialis. Typical clinical appearance with
sites on the skin or mucosa
vesicles about the upper and lower lip.
 generally based on the history and clinical
examination VARICELLA–ZOSTER VIRUS
Diagnosis

 no need for viral culturing or costly methods of viral CHICKENPOX

identification (electron microscopy,  occurs predominantly in children and results from
immunofluorescence microscopy, PCR) primary infection with the varicella-zoster virus
 Tzanck smear – cytologic examination to  after the cutaneous lesions have healed, the virus
Pathogenesis

demonstrate classic giant cells persists in the ganglion cells of sensory nerves

ZOSTER
 occurs as a reinfection or results from reactivation of
the virus in response to various provocative
mechanisms
o UV radiation exposure, infectious diseases, or
weakened immune defenses (i.e. to
immunosuppressant therapy or HIV infection)
 Requires previous contact with the virus

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 Lips and Oral Cavity 1.3
CHICKENPOX
 skin rash (erythematous papules and thin-walled RECURRENT APHTHOUS STOMATITIS
vesicles with watery contents) covering the body but (Benign Aphthous Disorders, Cancer Sores, Recurrent
especially on the head and trunk Aphthous Ulcerations)
 aphtha-like vesicles: consistently appear on the oral  Aphthae: considered the most common
mucosa and especially on the hard palate, buccal inflammatory lesion of the oral mucosa

Epidem-
iology
mucosa, and gingiva  occur predominantly during the 2nd and 3rd decades
Symptoms

of life
ZOSTER  approximately 40% of case show a familial pattern
 segmental disease of occurrence
o with cutaneous and mucosal lesions distributed along
 still unclear

Etiology
a sensory nerve segment
o often accompanied systemic signs: lethargy, fatigue,  although viruses of the herpes group (varicella-
occasional neuralgiform pain in the distribution of the zoster virus, cytomegalovirus) have been identified
affected nerve in some cases
 involvement of 2nd and 3rd divisions of trigeminal nerve
 minor trauma
o aphthae or scalloped ulcerations can be found on the
 hormonal changes (e.g. premenstrual)

Predis-

factors
posing
buccal mucosa, palate, and body of the tongue
 concomitant GI disease
ZOSTER  emotional stress
 Acyclovir and Fanciclovir: 5-7 day course
Treatment

 iron, folic acid or vitamin B12 deficiency

 analgesics and anti-inflammatory drugs:
Carbamazapine  inflammatory, shallow mucosal ulcerations with
 antibiotics: may be indicated in elderly or slightly raised erythematous borders and a
immunocompromised patients to prevent superinfection tendency to recur
 adjuvant cortisone therapy: still controversial  3 clinical variants:
1. Minor aphthae (~80-90%)
HERPANGINA o Superficial , usually small (2-5mm) ulcerations
located in the anterior 1/3 of the oral cavity
o Heal without sccarring, usually in about 1
Epidem-

 predominantly affects young children but also occurs in

iology

week
adults
2. Major aphthae (~10%)
 often manifested in the spring and fall
o Significantly larger (>10mm) and deeper
ulcerations
o Heal with scarring in about 2-4 weeks
genesis

Symptoms
Patho-

 main: Group A Coxsackie virus

o Often accompanied by tender, enlarged
 less common: Group B Coxsackie virus
regional lymph nodes
 occasional: Retrovirus or Echovirus
3. Herpetiform aphthae (~5%)
 Very small aphthae showing a herpes-like
SYSTEMIC SYMPTOMS
arrangement
 fever  Mild systemic effects
 nalaise
 headache and muscle pain
 bullous eruptions surrounded by a red halo appear on
the oral mucosa, particularly affecting the anterior
faucial pillars, uvula and palatine tonsils
 the vesicles rupture in a few days, leaving behind
shallow ulcerations
Symptoms

 Bechet’s disease
o early differentiation is necessary for prognosis
and critical for proper diagnostic and therapeutic
management
Diagnosis

o accompanying symptoms: fever, lethargy, joint

pain, ocular signs, since severe oropharyngeal
symptoms in themselves can also occur with
Aphthous lesions on the anterior faucial pillar major aphthae
 herpes simplex
Diag-
nosis

 Gingivostomatitis (HSV): considerably more painful  herpangina

and runs a longer course  hand-foot-mouth disease
 symptomatic
 Purely symptomatic: anti-inflammatory agents or  frequent topical application of astringents
Treat-
ment

mouth rinses with chamomile (tincture of myrrh) or mouth rinses with special
Treatment

 The disease generally resolves in 14 days without pain-relieving electrolyte solutions (e.g. Hanks’
complications solution)
 deficits can be corrected by means of iron, folic
HAND-FOOT-MOUTH DISEASE acid and/or vitamin B12 replacement
Epidemiology  predominantly affects small children from 6  chronic recurrent lesions: topical application of
months to 5 years of age corticosteroid gel alternating with antiseptic mouth
Etiology  Coxsackie viruses rinses
Symptoms  small bullae typically appear simultaneously
on the palate, tongue, and gingiva as well INFLAMMATORY MUCOSAL LESIONS IN HIV INFECTION
as on the palms of the hands, fingers, toes  commonly observed in symptomatic HIV- infected patients
and soles of the feet but are not caused by the HIV itself but occur secondary as a
Treatment  symptomatic result of weakened host defenses
 generally resolves in 1-2 weeks without
complications A. Candidiasis
 caused by Candida albicans
 the most common infection seen in HIV(+) patients

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 Lips and Oral Cavity
Candidiasis
B. Viral Infections
 most common: HSV, VZV and CMV
Etiology
 CMV infection: has been identified as a potential
cofactor for the progression of HIV disease and tends
to affect patients with an advanced immune deficiency
 clinical features differ from those of the ordinary forms
of these viral infections
 characteristic morphologic signs (e.g. a herpes simplex
infection may have zoster-like manifestations)
 course of the diseases (markedly protracted in this
subset of patients and is associated with more severe
complaints)
Symptoms
CMV infection manifested by mucosal ulcerations with
grayish white plaques
 Acyclovir: HSV and VZV infections, but CMV is less
Treat-
ment
sensitive
 Ganciclovir: CMV infections
C. Oral Hairy Leukoplakia
 another disease that has been linked to HIV infections
since it is an initial description
Etiology
 the presence is basically considered pathognomonic for
an HIV infection
 today, it is believed to be caused by Epstein-Barr
virus
 marked by patchy, whitish, slightly raised lesions
occurring predominantly on the border of the
tongue
 less commonly, the mucosal lesions are found in other
regions of the oral cavity (buccal or lip mucosa, oral
floor, soft palate)
 painless course and dysphagia
 occurs only in cases with Candida superinfection
 despite their resemblance to leukoplakia, the lesions
Symptoms
have not been known to undergo malignant
transformation
Oral Hairy Leukoplakia
 local measures: topical application of Vitamin A acid
and/or podophyllin
Treat-
ment
 virostatics: should not be used d/t high incidence of
side effects and the likelihood that OHL will recur
within few days after the drugs are continued
D. Bacterial Infections
 HIV infected patients are also predisposed of the bacterial
infections of oral and pharyngeal mucosa
 they have an increased incidence:
o acute and subacute tonsillitis
o tuberculosis
o atypical mycobacterial infections
Transcribers: CARLOS, DELA ROSA, GNILO, LATONIO, LAURILLA
1.3
o syphilis (~50% of HIV infected patients test
seropositive for syphilis)
Ultrasound (B-mode) image of the tongue and oral floor. Normal
ultrasound anatomy of the oral floor. The transducer is placed
submentally, resulting in an upside-down monitor image
COMPUTED TOMOGRAPHY AND
MAGNETIC RESONANCE IMAGING
 more cost-intensive than ultrasound
 more invasive in cases where contrast media are used
 indications:
o pronounced inflammatory changes
o tumors with information on extent, depth of invasion,
and spread across the midline
 these 3 parameters are important in selecting
optimum treatment modality
 MRI – has superior soft-tissue discrimination compared to
computed tomography
 if an imaging procedure is performed for confirmation (esp. of
a suspected tumor), the examination should include the soft
tissues of the neck to check for regional lymph-node
metastases
BACTERIAL AND FUNGAL INFECTIONS
ORAL FLOOR ABSCESS (LUDWIG’S ANGINA)
Epidem-
 rare, can become potentially life-threatening if
iology
inflammatory process spreads to the deep cervical
soft tissues and mediastinum
 common: inflammation originates from the lower
Pathogenesis
molars
 less common: develops from mucosal injuries in the
oral floor, leading to abscess formation in the tongue
muscles or connective tissue spaces of the oral floor
 can also develop as a sign of impaired host resistance,
as in the case of diabetic or immunosuppressed
patients (esp. children)
 edematous expansion with a firm, erythematous
Symptoms and Diagnosis
swelling in the submental to submandibular areas
 difficulty swallowing and speaking muffled speech
 high fever
 downward spread of infection can lead to dyspnea
with acute respiratory distress, and descending
infection through the fascial compartments of the
neck can incite a life threatening mediastinitis
 imaging is necessary to define the extent of the oral
floor abcess (often this cannot be done by physical
examination alone due to local pain and induration)
 the principle options are ultrasonography and
computed tomography
 should include an abscess of the submandibular or
Differential
sublingual glands as well as actinomycosis, in which
Diagnosis
subcutaneous infection by Actinomyces israelli can
cause an indurating infiltration of the fatty tissue in
the oral floor region
 actinomycosis – less painful; tends to form an
external fistula
 treatment of choice: incision and drainage of the
abscess via the intraoral and transcervical route
Treat-
ment
 concomitant: antibiotic therapy should be appropriate
for a mixed spectrum of aerobic and anaerobic
organisms
Page 11 of 15
 Lips and Oral Cavity
LINGUAL ABSCESS
 the diagnosis is established unequivocally by the
clinical appearance of the tongue
 clinical examination reveals a tense, dorsal swelling
Diagnosis
Oral floor abscess
Treat-
ment
 surgical: incision and drainange of abscess with
concomitant antibiotic
SYPHILIS
 Although lesions of the oral and oropharyngeal mucosa can
occur in all stages of syphilis, the manifestations in the
primary and secondary stages are most important for the
differential diagnosis of mucosal lesions in these regions.
PRIMARY LESION
 begins about three weeks
 sites of predilection for extragenital primary lesions: perianal
region, oral cavity and oropharynx
 most commonly affected: lips, buccal mucosa, tonsil
(unilateral) and tongue
 primary chancre is painless and appears as an initially
papular lesion that gives way to an erosive or ulcerative
eruption
 concomitant regional lymphadenopathy (bubo) is frequently
present and is also painless
SECONDARY LESION
 begins about 6 weeks after the primary lesion appears, as
the disease becomes generalized due to hematogenous
spread of the micro-organisms
 most commonly affected sites: skin and mucous membranes
 the mucosal syphilids (mucous plaques) are a dangerous
source of infection, as they are teeming with infectious
organisms
 the syphilitic enanthema in the secondary stage typically
consists of patchy, reddish lesions on the hard and soft palate
and buccal mucosa
 an even more common finding is specific angina
 both palatine tonsils are inflamed and covered with grayish-
white coatings
o in contrast to the unilateral tonsillar changes in the
primary stage
 a sweetly fetid breath odor is also present
 malignant syphilis – severe form of secondary syphilis which
occurs predominantly in immunosuppressed and especially
HIV-infected patients
TERTIARY STAGE
 may develop within a period of 3–5 years
 lesions of the oral and oropharyngeal mucosae are less
common at this stage, but gummata (syphilitic granulomas)
are occasionally found on the soft palate and uvula and also
on the tonsil (unilateral).
 the tonsillar gumma appears as a sharply circumscribed ulcer
with a greasy coating on its base and may initially be
mistaken for a primary lesion, but the latter is almost always
associated with painless regional lymphadenopathy.
 interstitial glossitis is another, rare intraoral manifestation of
tertiary syphilis
Differential
Diagnosis
 If specific angina is suspected, ddx should include
diphtheria, in which the mucosal lesions spread to
involve the soft palate and uvula.
Transcribers: CARLOS, DELA ROSA, GNILO, LATONIO, LAURILLA
1.3
 Identification of the causative organism from
the primary lesion can be accomplished with dark-
field microscopy (only reliable test in primary stage)
 Serologic test such as T. pallidum hemagglutination
Dignosis
(TPHA) test or fluorescent treponemal antibody
absorption (FTA_ABS) test are not positive until 3
weeks after the infection is acquired.
 A good follow-up test is the cardiolipin
complement binding reaction (CBR), a modification of
the Wassermann reaction whose titers correlate with
the px response to therapy
 Penicillin G (600,000 IU daily for 14 days)- drug of
choice for all stages of the disease
Treat-
ment
 Erythromycin if allergic to penicillin
 Syphilis serology should be retested at the conclusion
of treatment
SUPERFICIAL TONGUE LESIONS
 may reflect systemic diseases and thus provide important
clues to the patient’s general state of health
HUNTER’S GLOSSITIS
 synonym: atrophic glossitis
 atrophic inflammatory condition of the tongue base
 an accompanying feature of pernicious anemia
 common symptoms: burning of the tongue, dry mouth, and
altered sense of taste
FISSURED TONGUE
 characterized by the presence of numerous furrows on the
dorsal surface of the tongue, is a harmless
 hereditary condition
Typical appearance, with conspicuous furrows in the dorsal
surface of tongue
GEOGRAPHIC TONGUE
 synonym: benign migratory glossitis
 marked by areas of desquamation of the filiform papillae on
the dorsal surface of the tongue
 affected areas are irregularly shaped but are clearly
demarcated relative to surrounding areas
 harmless; histologic exam shows signs of inflamm
 generally, the only symptom is occasional burning sensation
BLACK HAIRY TONGUE
(LINGUA VILLOSA NIGRA)
FEATURE
 spread to involve the soft palate and uvula.
PATHOGENESIS
 may result from failure of desquamation of the cornified
layers or an excessive formation rather
ETIOLOGY
 besides antibiotic and corticosteroid use, they mainly include
chronic mucosal irritation from oral/ hygiene procedureor
nicotine abuse as well as metabolic disorders
 (e.g., diabetes mellitus),
 vitamin deficiency, and wasting diseases
ANGIOEDEMA
 transient, frequently pronounced vascular reaction which, in
the head and neck region, can lead to swelling of the face,
lips, tongue, and larynx.
PATHOGENESIS
Page 12 of 15
 Lips and Oral Cavity 1.3
 occurs as one feature of an anaphylactic or anaphylactoid  Systemic corticosteroids
reaction  Immunosuppresants
 drugs such as acetylsalicylic acid and angiotensin-converting  Oral rinses with anti-inflammatory or anesthetic solutions are
enzyme (ACE) inhibitors- precipitate an attack most commonly recommended
 Bradykinin – major pathogenic role PROGNOSIS
MANIFESTATION  May lead to death within a period of months or years,
 massive facial swelling that is most pronounced in the secondary to sepsis or bronchopneumonia
periorbital region but also affects the lips, tongue, tongue
base, and laryngeal area BECHET’S DISEASE
 massive tongue swelling acute obstruction of the upper EPIDEMIOLOGY
airways  Occur predominantly in Mediterranean countrues
TREATMENT (Turkey) and Japan
 cause of the angioedema is a key factor in selecting the ETIOLOGY
appropriate treatment.
 Viral or Autoimmune
 symptomatic treatment with corticosteroids or epinephrine
(especially in the form of the disease induced by ACE DIAGNOSIS
inhibitors).  Criteria for Dx: 3 major features or 2 major plus 2 minor
 in the form that is induced by a C1-INH deficiency, direct features
replacement with a C1-inhibitor concentrate should be  Major features
provided in acutely life-threatening cases with swelling of the o oral aphthae
tongue and larynx. o aphthous genital ulcers
 antihistamines and cortisone preparations are of little or no o hypopyonirits
benefit in this form of angioedema  Minor features
o Polyarthritis
IMMUNOLOGIC DISEASE o GI sx
 vascular lesions
FIXED DRUG ERUPTION TREATMENT
Delayed (type IV) allergic reaction following repeated drug use  Corticosteroids
 Cytostatics and immunosuppresants
 Analgesics
 Oral mucosal lesions can be treated locally with mouth
 Anti-inflammatory agents (pyrazolone, phenylbutazone,
rinses (chamomile) or pyoktanin (2%)
ETtiology

phenazone)
 Antibiotics (penicillin, tetracyclines, erythromycin)
 Chemotherapeutic agents ERYTHEMA MULTIFORME (EM)
 Sulfonamides
 Hypnotics (barbiturates)
Epidem-
iology

 Laxatives (phenolphthalein)  Occur predominantly in Mediterranean countrues

(Turkey) and Japan
Symp-
toms

 superficial erosions that may resemble HSV infection

due to scalloped margins
 Multifactorial
o viral infection (HSV, Hepa B, Mumps, Measles)
Etiology

o bacteria (Strep, diphtheria or syphilis)

SYSTEMIC LUPUS ERYTHEMATOUS o drugs SE (sulfonamides, pyrazolone derivatives,
 Chronic inflammatory systemic disease of the vascular barbituates, penicillins, phenothiazines)
connective tissue with cutaneous involvement and potential o systemic diseases (polyarteritisnodosa, Wegener
involvement of almost all organs granulomatosis, SLE, lymphoma, carcinoma)
 Not fully understood  Minor form
 Familial 10% o bullae formation on oral mucosa, lips and later
Etiology

 Hormonal (estrogen) erosive lesions)

 Viral involvement  Major form
 UV radiation exposure, drugs (isoniazid, sulfonamide, o Steven-Johnson syndrome, erythematous areas
phenytoin and penicillamine) on extremeties and buttocks, conspicuous
Symptoms

 Oral involvement 40% mucosal erosions appear on lips, oral mucosa

Symptoms

 Edematous, erythematous areas, erosions, or ulceration and pharynx

by fibrinous exudate and located on hard palate, buccal o may also have ocular involvement:
mucosa and tongue, others (polyarthritis, serositis, renal conjunctivitis, keratitis, iritis or uveitis
involvement, central nervous system involvement,  Systemic sx
hematologic changes) o generalized weakness, headache,and high fever
DIAGNOSIS  Severe cases may develop cardiopulmonary
disorders ranging to renal failure or toxic circulatory
 Special laboratory tests are necessary
collapse.
 Due to painful oral involvment (may need
PEMPHIGUS VULGARIS parenteral nutrition)
 Mild
Treatment

ETIOLOGY
o rinsing with chamomile solution, local
 Uncertain
anesthetics
 Genetic disposition
 Severe
 UV radiation exposure; Drugs (phenylbutazone,
o corticosteroids are agents of choice accompanied
indomethacin, ibuprofen, tuberculostatic drug); coexist with
by broad-spectrum antibiotics to prevent
other autoimmune disease (Myasthenia Gravis)
superinfection; prophylaxis (acyclovir)
PATHOGENESIS
 Ab against adhesion proteins in the epidermis, detected in
LICHEN PLANUS
affected mucocutaneous areas and in the serum
ETIOLOGY
SYMPTOMS
 Unknown
 Show involvement of oral mucosa 50% with bullous eruptions
 Viral disease (Hepa B and C)
or saliva-macerated bullae that can make eating extremely
 Drugs (antimalarial medications, organ arsenic compounds
difficult.
and gold salts)
DIAGNOSIS
 May also be psychosomatic
 Immunologic detection of pemphigous Ab; elevated titers SYMPTOMS
correlate with exacerbation of sx.
TREATMENT

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 Lips and Oral Cavity 1.3
 Mucosal involvement 25-70%, common in oral mucosa and
vermillon border of lips TREATMENT
 Oral lesions typically appear as reticular white markings on  SURGICAL
mucosa of the cheek and tongue(Wickham’s phenomenon o Indication:
needs histologic differentiation from leukoplakia)  symptomatic patients
 Painful ulcerations may occur (erosice LP)  cases in which it is necessary to exclude a malignant
 Differentiate from lesions of pemphigus vulgaris, SLE and tumor
stage II syphilis.  Surgical treatment or laser surgery is advised in
TREATMENT hemangiomas and lymphangiomas only if:
 Antibiotics, tuberculostatics to antimalarial drugs o Tumor persists beyond the first year of life
 Corticosteroids are of symptomatic benefit o And the patient does not have serious symptoms such as
 Aromatic retinoid and isoretinoin are recommended for dyspnea or dysphagia that would necessitate earlier
mucosal lesions surgical intervention
 Oral rinses with anti-inflammatory and local anesthetic o Due to the high rate of spontaneous remission during the
solutions are recommended for very painful, erosive intraoral first years of life
lesions.
PROGNOSIS  RADIOLOGIC THERAPY:
 Oral mucosal lesions to persist for years, especially in the o No longer advocated due to potential for adverse sequelae
erosive form of the disease (malignant formation, growth disturbance)
 Since it is now believed that LP is a potentially premalignant
disease, regular; follow-ups are also essential. PRECANCEROUS LESIONS
 Most common precancerous lesion of the
BURNING MOUTH SYNDROME lips and oral cavity
 Most prevalent in postmenopausal women  Asymptomatic; detected incidentally
 Causal factors:
 Dentures
o Denture pressure
 Candidiasis
o Alcohol/nicotine abuse
 Geographic tongue
 Morphologically similar with carcinoma in
 Allergic mucosal reactions (sorbic acid,
Local situ and invasive carcinoma
zimtaldehyde, nicotinic acid)
 Potential for malignant degeneration
 Toxic mucosal reactions (nickel sulfate or
 Diagnosis: biopsy
mercury) LEUKOPLAKIA  Treatment: surgical removal
 Radiotherapy
Etiology

 Iron-deficiency anemia
 Vitamin B1, B2, B6, and B12 deficiency
 Folic acid deficiency
 Sjögren disease
Sys
 Menopause
 Diabetes mellitus
 Human immunodeficiency virus infection
 Drug side effects (ACE inhibitors)
 Depression
Psy  Cancerophobia  A chronic inflammatory disease caused
 Emotional stress BOWEN’S
by an intraepidermal carcinoma
 Burning sensation and other soreness in the oral cavity DISEASE OF
 rare
 Tongue is most commonly affected “burning tongue” THE ORAL
Symptoms

 similar to leukoplakia in morphologic

 May involve the hard palate, alveolar ridge (especially in MUCOSA
features
denture wearers), and other regions of the oral cavity
(buccal mucosa, oral floor, mucosal surfaces of the lips)
MALIGNANT TUMOR
 Concomitant xerostomia and dysgeusia are occasionally
SQUAMOUS CELL CARCINOMA (LIP)
reported.
 Affects the lower lip in 90% of the cases
 predominant in pipe smokers
TUMORS OF THE LIPS AND ORAL CAVITY
 cofactor: prolonged, intense sun exposure
BENIGN TUMORS
 Can arise from all epithelial and mesenchymal tissues in the
head and neck region but are relatively rare

EPITHELIAL  Papilloma
TUMOR  Pleomorphic adenoma
 Fibromas
 Lipomas
 Rhabdomyomas
MESENCHYMAL
 Leiomyomas
TUMOR
 Chondromas
 Hemangioma (congenital)  Early tumors often appear clinically as “intractable”
Symp-

 Lymphagioma (congenital) ulcerations in the vermilion border of the lip

toms

 May also consist of large, exophytic lesions

 If tumor is suspected, do a biopsy for confirmation
Differential

 Keratoacanthoma
Diagnosis

 Primary syphilis chancre

 Basal cell carcinoma
Involves the vermillion border of the lip only by
secondary spread

(L-R) Papilloma of the uvula, Pleomorphic adenoma of palatal

salivary gland

Transcribers: CARLOS, DELA ROSA, GNILO, LATONIO, LAURILLA Page 14 of 15

 Lips and Oral Cavity
 Treatment of choice: almost always surgical excision
followed by a local primary closure or plastic repair
of the defect using various reconstructive techniques
 Extensive tissue defects can be repaired using
regional flap techniques
 Neck dissection should be performed in patients with
category 2 or higher tumors even though lip
carcinomas have a low rate of lymph node
metastasis
Treatment
SQUAMOUS CELL CARCINOMA (ORAL CAVITY)
 90% of patients have a long history of nicotine and alcohol
abuse
 75% of malignant tumors form in the drainage area of the oral
cavity (i.e. the trough between the base of the alveolar ridge
and the border of the tongue)
The typical clinical appearance of squamous cell carcinoma of the
oral floor (a), buccal mucosa (b), and soft palate (c)
 Vary with the location and extent of the tumor
Symp-
 may consist of painful swallowing, blood-tinged saliva,
toms
and a fetid breath odor
 some are asymptomatic
 Visual Inspection
Can raise suspicion of malignancy
May be misleading
 Bimanual palpation
since many tumors infiltrate deeper tissues and the
visual impression of superficial findings can be
misleading
Diagnosis
Includes palpation of the regional cervical lymph
nodes to include metastases
 Imaging Procedure (UTZ, CT, MRI)
o generally necessary only for extensive masses and
advanced lesions
o defines the depth of the tumor infiltration
o assesses involvement of the adjacent structures
(bone)
 tool for excluding regional cervical lymph-node
metastases
Transcribers: CARLOS, DELA ROSA, GNILO, LATONIO, LAURILLA
1.3
 Treatment of choice: surgical removal of the primary
tumor
The resulting defect is either closed primarily or
reconstructed using pedicled flaps or
microvascular free transfers (e.g., a radial forearm
Treatment
flap)
A unilateral or bilateral neck dissection may be
necessary, depending on the location and T
category of the primary tumor
 Radiation to the tumor site and lymph areas is
frequently indicated following surgery
 Primary radiotherapy or combined radiochemotherapy
alternatives for T3 and T4 tumors
PROGNOSIS
 Depends on the location and stage of the disease
 Five-year survival rate varies accordingly, ranging from 0%
to 80 %
T classification of malignant tumors of the lip, oral
cavity, and oropharynx
T1 ≤ 2 cm
T2 > 2 cm and < 4cm
T3 ≥ 4 cm but still superficial
Tumor of any size that invades deeper structures
T4
(e.g. bone)
HIV-RELATED MALIGNANT TUMORS (ORAL CAVITY)
With a disproportionately high incidence of malignant tumors
because of weak immune status
 20% of affected homosexual and bisexual
men
 less than 5% occur in HIV-infected
individual from other risk groups
 has a variable appearance, depending on its
location in the oral cavity
 Hard palate – site of predilection
KAPOSI
SARCOMA
Kaposi sarcoma of the tongue
B-CELL  Smaller percentage of HIV patients have
LYMPHOMA this kind of malignant tumor
QUIZ
1. Site in the nasal cavity which is the usual source of
epistaxis? –Kiesselbach’s plexus
2. CT scan view usually ordered for? –Coronal scan plane
3. Differentiate between a turbinate and a polyp
Turbinate – with pain; Polyp – no pain (Please refer to
ENT trans 1.1 for other answers)
4. -5. Give 2 structures visualized during anterior
rhinoscopy. –Middle and anterior turbinates
6. Stones in the nasal cavity. - Rhinolith
7. CASE: colds usually in the morning (non-verbatim).
–Allergic rhinitis
8. Common complication after septorhinoplasty. –Septal
perforation
9. A locally aggressive benign tumor that inverts into the
surface epithelium. –Inverted papilloma
10. Meaning of FESS – Functional Endoscopic Sinus
Surgery
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