Transcript ORAL CAVITY

ORAL CAVITY
Clerk Sarah Camille Concepcion
OUTLINE
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INTRODUCTION
EMBRYOLOGY
ANATOMY
PHYSIOLOGY
DISEASES
ORAL CAVITY
BOUNDARY: Vermilion border of the lips to junction of
hard and soft palate and circumvallate papillae (tongue)
EMBRYOLOGY
• Derived from the embryonic foregut
• Stomoduem
– Primitive mouth that forms the topographic
center of the developing face
– Fusion of ectoderm & endoderm
EMBRYOLOGY OF ORAL CAVITY
UPPER LIP
• Fusion of medial frontonasal and lateral
maxillary prominences
• 6th-8th week of fetal devt
LOWER LIP
• Fusion of mandibular prominences
• 4th week of fetal devt
EMBRYOLOGY OF ORAL CAVITY
CHEEK
• Formed by the buccinator muscle
SALIVARY GLANDS
• Develop from stomadeal ectoderm by
ingrowth of oral epithelium into underlying
mesenchyme
• Starts at a 6 weeks AOG
EMBRYOLOGY OF ORAL CAVITY
TONGUE
• from lingual swellings and tuberculum impar
• ~4 weeks AOG
PALATE
• Fusion of primary and secondary plates
• 12th week AOG
MANDIBLE
• Membranous ossification of Meckel’s cartilage
• 4 ½ weeks AOG
ANATOMY
PARTS/SUB-UNITS
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Lips
Buccal mucosa
Alveolar ridges
Anterior 2/3 of the tongue
Retromolar trigone
Floor of the mouth
Hard palate
LIPS & CHEEK
• Vermillion
– Red due to thin squamous epithelium
• Vestibule
– Region between internal mucosa of cheek and
teeth
• Orbicularis oris
– Foundation of lips and cheeks
LIPS & CHEEK
• Labial commissure
• Nasolabial fold
• Lips
– Supplied by superior and inferior labial arteries
– Drained by facial vein
– Innervated by infraorbital (upper lip) and mental
(lower lip) nerve
LIPS & CHEEK
• Cheeks
– Muscular framework formed by buccinator
– Bichat fat pad (buccal fat pad)
– Innervated by branches of the facial nerve
MUSCLES OF MASTICAITON
• Masseter muscle
• Temporalis muscle
• Medial and lateral pterygoid muscles
• Supplied by mandibular nerve (third division
of the trigeminal nerve)
TEETH
Infants: 2 I, 1 C, 2M
Adults: 2 I, 1C, 2PM, 3M
TEETH
Deciduous
Medial incisors
Lateral incisors
First molar
Canine
Second molar
Age
(mo)
7
9
15
18
20-24
Permanent
1st molar
Medial incisors
Lateral incisors
1st premolar
Canine
2nd premolar
2nd molar
3rd molar
Age
(years)
6
6-7
8-9
10-11
10.5-11.5
11-12
12-13
17-25
• Alveolar Ridge
– thickened ridge of bone that contains the tooth
sockets on bones that bear teeth
• Retromolar Trigone
– Area between the upper and lower posterior
molars
SURFACE ANATOMY
SURFACE ANATOMY
• Divisions: apex, body, and base
• Terminal sulcus
• Papillae
– Filiform, fungiform, foliate, vallate
• Foramen cecum
• Frenulum lingua
Extrinsic muscles (CNXII)
STYLOGLOSSUS
GENIOGLOSSUS
HYOGLOSSUS
GENIOHYOID
MYLOHYOID
Intrinsic muscles (CNXII)
A) VERTICAL M. - FIBERS SUP & INF - FLATTEN &
BROADEN TONGUE
CORONAL SECTION
C) LONGITUDINAL
M. - FIBERS ANTPOST. - SHORTEN
TONGUE
B) TRANSVERSE M. - FIBERS HORIZONTAL
- NARROW TONGUE
TONGUE
• Vascular supply: Lingual artery and vein
• Motor innervation: CN XII
• Sensory innervation:
– Anterior 2/3 – lingual nerve  chorda tympani
– Posterior 1/3 – CN IX
• Lymphatic drainage
• ipsilateral and contralateral submandibular
and submental lymph nodes
PALATE
HARD PALATE
• formed by palatine processes of the maxilla
anteriorly, incisive bone, and horizontal plates of
palatine bones posteriorly
SOFT PALATE
• Seals the oral cavity posteriorly
• tensor veli palatini, levator veli palatini,
palatoglossus, palatopharyngeus muscle
Vascular supply
• ascending palatine branch of the facial artery
Sensory innervation
• greater and lesser palatine nerves from V2
SALIVARY GLANDS
PAROTID
SUBMANDIBULAR
Stensen’s
Wharton’s
Lateral to upper 2nd
molar
Serous
Supplies 1/3 saliva
in resting state
Supplies 2/3 saliva
in stimulated state
SUBLINGUAL
Rivinus’
multiple orifices
midline floor of
draining into floor of
mouth adjacent to
mouth or into
lingual frenulum
submandibular duct
Serous and mucous Serous and mucous
Supplies 2/3 saliva
in resting state
PHYSIOLOGY
• Importance for food intake
– Mastication (teeth, tongue)
– Digestion (salivary enzymes)
– Taste (Gustatory, chemoreception)
– Swallowing (Hard and soft palate)
• Speech (phonation and articulation)
– Tongue, cheeks, lips
SALIVA
1500 mL/day; pH 6.2-7.4
– 99.5% water
– 0.5% organic/inorganic solids.
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Na – 10 mEq/L
K – 26 mEq/L
Cl – 10 mEq/L
HCO3 – 30 mEqlL
glycoprotein and amylase
ORAL TORI
- nodular or bony growth
• Torus Palatinus
– in the midline of hard palate
• Torus Mandibularis
– In the lingual aspect of the
mandible
TX: Surgery
MICROGNATHIA
• Congenital or acquired diminution in size of
the mandible
• Failure at the growth center of the condyle
• May be due to trauma
• Some associated with syndromes
TX: Surgery
ROBIN ANOMALY
• Triad:
– Cleft palate + Micrognathia + Glossoptosis
– Symmetric lack of mandibuilar growth prevents
adequate support of lingual musculature, allowing the
tongue to fall downward and backward
TX: mild case – keep the infant in prone position,
suspend head by stocking cap
severe – tongue tip sutured to anterior
mandible or lower lip
PROGNATHISM
• Enlargement or
anterior placement
of lower jaw
TX: Surgery
MALOCCLUSION
• Disturbed development
of face and jaws
• Underdevelopment of
maxilla or mandible or
overdevelopment of
mandible
MACROGLOSSIA
• Enlarged tongue that
may result in abnormal
speech
• Due to increase in
amount of tissue
• Most are due to
lymphangioma or
hemangiolymphoma
MEDIAN RHOMBOID GLOSSITIS
• Smooth to nodular,
elevated or depressed
area of void papillae
• No treatment required
LINGUAL THYROID
• Partial or complete
embryologic failure of the
thyroid gland to descend
from the foramen cecum
• No tx for small lesions
• Before surgery, make
certain that it is not the
only throid tissue in the
body
ANKYLOGLOSSIA
• Inability to elevate the tongue
tip above a line extending
through the commissures of a
congenitally short lingual
frenulum
• TX: frenulum clipped during
infancy in severe forms
CLEFT LIP AND PALATE
Unilateral
incomplete
Unilateral
complete
Bilateral
complete
CLEFT LIP AND PALATE
• Developmental anomaly of the embryonic head
– Genetic inheritance
– External influences: viral infections, placental oxygen
deficiency, intrauterine bleeding, exposure to ionizing
radiation
• Symptoms:
– Hypernasal speech (due to incomplete closure of the
nasopharynx)
– Recurrent middle ear effusions and inflammation resulting
from eustachian tube dysfunction
– Variable abnormalities of the nasal septum or in the shape of
the external nose
CLEFT LIP AND PALATE
• Diagnosis: palpation of the hard palate to detect
bony discontinuity
• Goals of surgery
– To achieve closure of the hard and soft palate.
– To provide soft palate sufficient length and
mobility.
• Treatment: lip/velum/palate repair, rhinoplasty,
speech promotion/therapy
• RULE OF 10
– 10 weeks, 10 pounds,10 g Hemoglobin
WHITE LESIONS OF THE ORAL
MUCOSA
• A change in color of the normally reddish oral
mucosa to white.
• One of the most frequently encountered oral
abnormalities.
• Leukoplakia-”white patch” that does not rub
away
• Frequently caused by increased retention and
production of keratin by mucosal stratified
squamous epithelium.
• Biopsy may demonstrate cytologic alterations and
may warrant consideration as “premalignant”
LICHEN PLANUS
LICHEN PLANUS
• present as fine lacework of white reticular keratotic
paules (wickham’s striae) and gray plaque like or
annular lesions on the dorsum of the tongue
• On the buccal mucosa, the lesions originate in the
posterior area and spread anteriorly.
• Generally asymptomatic although a metallic taste or
mild discomfort is common.
• Superficial erosions, bullous lesions, and deep,
chronic, painful, ulcerations occasionally occur.
Viral infections: Herpes simplex virus
• Etiology: HSV type 1 (cutaneous and oral-
mucosa strain)
• Transmission: contact or droplet infection
• Primary infection
– Usually acquired in early childhood
– Predominantly affects the oral mucosa as
herpetic gingivostomatitis (aphthous
stomatitis)
– Appearance of local lesions (bullae) on the
oral mucosa, preceded by fever and
lethargy consistent with a flulike infection,
accompanied by regional lymphadenitis
Viral infections: Herpes simplex virus
• Reactivation of HSV
– Occurs in response to
physical exertion, UV
radiation, febrile infection,
emotional stress, pregnancy
– Commonly manifested as
herpes labialis
– Site of predilection is
perioral region, especially
the mucocutaneous
junction of the lips
Viral infections: Herpes simplex virus
• Diagnosis: history & PE, classic giant cells by Tzanck
smear
• Complications
– Herpes impetiginatus - secondary bacterial
superinfection by S. aureus or streptococci
– Postherpetic exudative erythema multiforme –
skin lesions & typical ulcerative eruptions on the
mucous membranes of the mouth, lips, and
genitals
• Treatment: topical antiseptics to prevent
superinfection; acyclovir; 5-7days
Viral infections: Varicella-Zoster Virus
• Chicken pox
– Predominantly in children
– VZV Primary infection
– Symptoms
• skin rash consisting of erythematous papules
and thin-walled vesicles with watery contents,
covering the body but especially pronounced
on the head and trunk
Viral infections: Varicella-Zoster Virus
• aphtha-like vesicles appear on the oral mucosa
especially on the hard palate, buccal mucosa
and gingiva
• After the cutaneous lesions have healed, the virus
persists in the ganglion cells of sensory nerves
Viral infections:
Varicella-Zoster Virus
• Zoster
– Reinfection or reactivation of the virus in
response
to
various
provocative
mechanisms
– Segmental disease, with cutaneous and
mucosal lesions distributed alon a sensory
nerve segment and often accompanied by
systemic signs such as lethargy, fatigue, and
occasional neuralgiform pain in the
distribution of the affected nerve
Viral infections:
Varicella-Zoster Virus
– With involvement of the 2nd & 3rd dvisions of the
trigeminal nerve, aphthae or scalloped
ulcerations can be found on the buccal mucosa,
palate and body of the tongue
– Treatment
• 5-7 days acyclovir or famciclovir
• analgesics and anti-inflammatory drugs (esp.
carbamazepine)
• antibiotics may be indicated in elderly or
immunocompromised patients to prevent
superinfection
Bacterial and fungal infections
• oral floor abscess
• lingual abscess
• candidiasis
Oral Floor Abscess
• Inflammation usually originates from the lower
molars, sometimes from mucosal injuries in the oral
floor, leading to abscess formation in the tongue
muscles or connective-tissue spaces of the oral floor
• Can develop as a sign of impaired host resistance
• Symptoms:
– edematous expansion with a firm, erythematous
swelling in the submental to submandibular areas
– Difficulty swallowing and speaking
– high fever
Oral Floor Abscess
• Downward spread of infection: dyspnea with acute
respiratory distress or mediastinitis
• Imaging to define the extent of the oral floor
abscess: UTZ or CT scan
• Tx: incision & drainage of the abscess via intraoral
and transcervical route, concomitant antibiotic
therapy
Lingual abscess
• Infected overt or covert mucosal injuries to the tongue
• Dx: clinical appearance of the tongue
• Tx: surgical – incision and drainage of the abscess with
concomitant antibiotic therapy
CANDIDIASIS
• Etiologic agent — Candida albicans
• Newborns may be infected by mothers w candidiasis
of the vaginal tract
• Factors that promote infection:
– Age (infants, elderly)
– Hormonal status (diabetes, pregnancy)
– Heredity
– Local factors (edentulousness, ill-fitting dentures,
lowered body resistance)
– Extensive use of antibiotics
CANDIDIASIS
• Angular cheilosis
CANDIDIASIS
• Superficial monilial stomatitis
– Mild erythema with fine, whitish deposits to
diffuse, inflamed “white mouth”
– In infants, first changes appear on the anterior
dorsal third, edges, and ventral surfaces of the
toungue and later in the oral vestibule
– Lesions resemble snow-white, curdled milk, diffuse
pseudomembranes
CANDIDIASIS
– Denture stomatitis
• Swelling, sensitivity and pain at points of denture
contact
– Deep granulomatous candidiasis
• Treatment
– Improve oral hygeine and nutritional status
– Correct underlying disorder and irritating factor
– Oral nystatin susp., ointments, tablets.
– Clotrimazole troches (10mg q.i.d.)
HALITOSIS
• Fetor oris or bad breath
• Factors:
– Decreased salivary flow rate
– Mucosal dryness (antihistamines, Sjogren’s syndrome,
astringent mouthwashes)
– Poor oral hygiene (food remnants, unclean dentures)
– Odoriferous foods (garlic, onion, fatty diet)
– Periodontal disorders (periodontitis, nec ulcerative
gingivitis)
– Heavy smoking
HALITOSIS
• Rarely a systemic cause (disorder of respi sys,
acetone breath of DM, ammoniacal odor of
uremia)
• Treatment
— mouthwash only transient
— cause must be eliminated
RECURRENT APHTHOUS STOMATITIS
• Aphthae; cancer sores
• Mycoplasmas and pleomorphic transitional “L” form
of αhemolytic streptococci
• Ulcer is covered by grayish white fibrinous exudate
and surrounded by a bright red halo
DENTAL CARIES
• Disease of enamel,
dentin and cementum
• Demineralization of
calcified area with
cavity formation
• Areas:
-cervical portion of the
tooth
-interproximal surfaces
-pits and fissures
DENTAL CARIES
• Bacterial infectioncommon sequel to
caries
Sequelae:
Pulpitis (acute or
chronic)
Acute alveolar abscess
Dental granuloma
GINGIVITIS
• Inflammation of the gum tissue
• Irritated and swollen due to a plaque or calculus
(tartar) buildup along the gumline
• Red, puffy, bleeding gums indicate the presence of
gingivitis.
TOOTH DISCOLORATION WITH
TETRACYCLINES
• Yellow – gray; bright yellow; gray to brown or
darker discoloration of the teeth
• With or without hypoplasia of the enamel
• Occur during period of tooth formation
DISORDERS IN TOOTH ERUPTION
Baby Bottle Tooth Decay
• Baby Bottle Syndrome or Nursing Bottle Mouth
• Rapid decay of many or all the baby teeth of an
infant or child.
• Upper front teeth
• Frequent exposure of a child’s teeth for long
periods of time to liquid containing sugars.
• Liquid pools around the front teeth. During sleep,
the bacteria living in every baby’s mouth, turns
the milk sugar or other sugars to acid which
causes the decay.
TRUE CYSTS
• Cavity lined by epithelium
• May be situated entirely within soft tissue or
deep within bone or may lie on the bony
surface, producing a saucerization.
Categories
• Odontogenic cyst
- proliferation cystic degeneration of odontogenic epithelium
a. Dentigerous cyst
b. Eruption cyst
c. Gingival cyst of the newborn
d. Radicular cyst
e. Keratocyst
Categories
• Nonodontogenic and fissural cyst
- derived from epithelial remnants of the tissue covering the
embryonal processes that participate in the formation of the
face and jaws
a. nasoalveolar cyst
b. Nasopalatine or incisive canal cyst
c. Palatal cyst of newborn infants
d. Dermoid and epidermoid cyst
e. Submental or geniohyoid dermoid cyst
f. Retention cyst
Cysts of the Jaws and Oral Floor
• Odontogenic Cysts
Dentigerous Cyst
Asymptomatic
occassionally pain or swelling
firm hard mass appears
as if missing a tooth
usually involve unerupted
mandibular third molars
Cysts of the Jaws and Oral Floor
 Eruption Cyst
 common particularly with
premature eruption of teeth
 well demarcated
 directly over the crown on
an erupting tooth
 soft, fluctuant swelling of the
alveolar ridge
 blue to dark red due to blood
in the cystic fluid
Cysts of the Jaws and Oral Floor
 Gingival and Palatal Cyst of
Newborn Infants
 alveolar mucosa of themaxilla
 asymptomatic multiple or
solitary white nodules
 Epstein’s pearls occur on the
midline of the
hard palate
 Bohn’s nodules occur scattered
over the
hard palate near the border
with the soft palate
Cysts of the Jaws and Oral Floor
Radicular Cyst
Nevoid Basal Cell Carcinoma Syndrome
Cysts of the Jaws and Oral Floor
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Nonodontogenic and Fissural Cysts
Nasopalatine or Incisive Canal Cyst
Nasoalveolar Cyst
DERMOID CYST
• Cyst lined by epidermis and
cutaneous appendages
• Result of the incorporation
of the ectoderm during the
closure of embryonic
fissures (3rd-4th wk in utero)
• Commonly arise from floor
of the mouth
• Either median/midline or
lateral
• Evident between 12-25
years of age
DERMOID CYST
• Sublingual/Genioglossal cyst-causes elevation
and displacement of tongue
• Submental/Geniohyoid cyst-extends from the
mandible to hyoid bone (double chin). When
enlarged, it could cause a bulge in oral floor.
• Microscopic: keratinized squamous
epithelium. 1 or more skin appendages could
be present.
EPIDERMOID CYST
• Epidermoid cyst
-absence of skin
appendages
microscopically
RETENTION “CYST” (Mucocele)
• Result of the duct rupture of
a minor salivary gland.
• Occurs often on the mucosal
surface of the lower lip
• Cyst of Blandin-Nuhn-cyst is
on the ventral surface of the
tongue’s tip.
• Ranula- cyst is large and
involves sublingual salivary
gland
Superficial tongue lesions
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Hunter’s glossitis
Fissured tongue
Angioedema
Fixed drug eruption
HUNTER’S GLOSSITIS
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Atrophic glossitis
Atrophic inflammatory condition of the tongue base
An accompanying feature of pernicious anemia
Symptoms: burning of the tongue, dry mouth, and
altered sense of taste
• Tongue presents a typical smooth, shiny appearance
with partial atrophy of the filiform papillae
FISSURED TONGUE
• presence of numerous furrows on the
dorsal surface of the tongue
• a harmless hereditary condition that
affects approximately 10–15% of the
population
ANGIOEDEMA
• A transient, frequently pronounced vascular reaction
which, in the head and neck region, can lead to
swelling of the face, lips, tongue, and larynx
(anaphylactic or anaphylactoid reaction)
• drugs such as ASA and ACE inhibitors
• C1-esterase inhibitor (C1-INH) deficiency: less
common, may be hereditary or acquired
ANGIOEDEMA
• massive facial swelling: most pronounced in the
periorbital region but also affects the lips, tongue,
tongue base, and laryngeal area
• Massive tongue swelling: can cause acute
obstruction of the upper airways
• hereditary form: swelling of the extremities and
episodes of abdominal pain.
ANGIOEDEMA
• Tx: depends on the cause
– for angioedema not induced by a C1-INH
deficiency:
symptomatic
treatment
with
corticosteroids or epinephrine (especially in the
form of the disease induced by ACE inhibitors).
– for C1-INH deficiency, direct replacement with a
C1-inhibitor concentrate should be provided in
acutely life-threatening cases with swelling of the
tongue and larynx
FIXED DRUG ERUPTION
• delayed (type IV) allergic reaction
• occurs at the same cutaneous or mucosal sites (e.g.,
the extremities, soles of the feet, palms of the hands,
external genitalia, oral mucosa) following repeated
drug use
• superficial erosions that may resemble an HSV
infection due to their scalloped margins
FIXED DRUG ERUPTION
• may be induced by analgesics, anti-inflammatory
agents
(e.g.,
pyrazolone,
phenylbutazone,
phenazone), antibiotics (penicillin, tetracyclines,
erythromycin),
chemotherapeutic
agents,
sulfonamides, and by certain hypnotics (e.g.,
barbiturates) and laxatives (phenolphthalein)
• Treatment consists of avoiding the suspicious
substances
Tumors of the Lips and Oral Cavity
• Benign tumors
• Precancerous lesions
• Malignant tumors
BENIGN TUMORS OF THE LIPS AND
ORAL CAVITY
• can arise from all epithelial and mesenchymal tissues
in the head and neck region
• Papillomas, pleomorphic adenomas, various
mesenchymal tumors such as fibromas, lipomas,
rhabdomyomas, leiomyomas, and chondromas
• Treatment
– generally surgical
– Indicated for patients who describe symptoms and
in cases in which it is necessary to exclude a
malignant tumor
BENIGN TUMORS OF THE LIPS AND
ORAL CAVITY
• Hemangiomas and lymphangiomas
– high rate of spontaneous remission during the first
years of life: conventional surgical treatment or
laser surgery is advised only if the tumor persists
beyond that period, provided the patient does not
have serious symptoms such as dyspnea or
dysphagia that would necessitate earlier surgical
intervention
– Radiotherapy is no longer advocated for these
tumors due to the potential for adverse sequelae
(malignant transformation, growth disturbance)
a Papilloma of the uvula.
b The bulge in the palate is caused by a pleomorphic adenoma arising from the palatal
salivary glands.
PRECANCEROUS LESIONS:
LEUKOPLAKIA
• most common precancerous lesion of the lips and
oral cavity
• Many of these lesions are asymptomatic and are
detected incidentally
• Exogenous irritants such as denture pressure or
alcohol/nicotine abuse have been most strongly
implicated as causal factors
PRECANCEROUS LESIONS:
LEUKOPLAKIA
• morphologic resemblance to carcinoma in situ
and invasive carcinoma
• potential for malignant degeneration
• lesions should always be investigated by
biopsy
• Tx: complete surgical removal of the neoplasm
PRECANCEROUS LESIONS: BOWEN’S
DISEASE
• a chronic inflammatory disease caused by an intraepidermal
carcinoma
• Rare
• morphologic features are similar to those of leukoplakia
MALIGNANT TUMORS OF THE LIPS
• almost invariably squamous cell carcinomas
• most commonly affect the lower lips (approximately
90% of cases).
• occur predominantly in pipe smokers
• Prolonged, intense sun exposure is a cofactor
MALIGNANT TUMORS OF THE LIPS
• Sx: Early tumors often appear clinically as “intractable”
ulcerations in the vermilion border of the lip but may also
consist of large, exophytic lesions
• Dx: Whenever a tumor is suspected, a biopsy should be taken
to confirm the diagnosis.
• Differentials: keratoacanthoma; primary syphilis chancre ;
Basal cell carcinoma involves the vermilion border of the lip
only by secondary spread.
MALIGNANT TUMORS OF THE LIPS
• Treatment: surgical excision followed by a local
primary closure or plastic repair of the defect using
various reconstructive techniques (using regional flap
techniques)
• low rate of metastasis to regional lymph nodes, but a
neck dissection should be performed in patients with
category 2 or higher tumors
MALIGNANT TUMORS OF THE ORAL
CAVITY
• Squamous cell carcinomas predominate in the oral
mucosa
• variable in their clinical appearance
• Approximately 90% of patients have a long history of
nicotine and alcohol abuse
• nearly 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
MALIGNANT TUMORS OF THE ORAL
CAVITY
• Symptoms:
– vary with the location and extent of the tumor
– painful swallowing, blood-tinged saliva, and a fetid
breath odor
– Some tumors are completely asymptomatic
MALIGNANT TUMORS OF THE ORAL
CAVITY
• Diagnosis:
– Visual inspection can raise the suspicion of a malignant
neoplasm
– Bimanual palpation, since many tumors infiltrate deeper
tissues and the visual impression of superficial findings can
be misleading
– palpation of the regional cervical lymph nodes to exclude
metastases
– Imaging procedures (UTZ, CT, MRI)
• only for extensive masses, as many tumors
can be adequately evaluated clinically owing
to their exposed location
• with more advanced lesions, imaging is
valuable for defining the depth of tumor
infiltration and assessing the involvement of
adjacent structures (bone) and for excluding
regional cervical lymph-node metastases
MALIGNANT TUMORS OF THE ORAL
CAVITY
• Treatment:
– 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 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
may be considered as alternatives for T3 and T4 tumors.
MALIGNANT TUMORS OF THE ORAL
CAVITY
• Prognosis:
– Depends on the location and stage of the disease
– 5-year survival rate varies accordingly, ranging
from 0% to 80%
SQUAMOUS CELL CARCINOMA