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Transcript of ORAL CAVITY Clerk Sarah Camille Concepcion. OUTLINE INTRODUCTION EMBRYOLOGY ANATOMY PHYSIOLOGY...
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ORAL CAVITY
Clerk Sarah Camille Concepcion
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OUTLINE
• INTRODUCTION• EMBRYOLOGY• ANATOMY• PHYSIOLOGY• DISEASES
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ORAL CAVITY
BOUNDARY: Vermilion border of the lips to junction of hard and soft palate and circumvallate papillae (tongue)
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EMBRYOLOGY
• Derived from the embryonic foregut• Stomoduem
– Primitive mouth that forms the topographic center of the developing face
– Fusion of ectoderm & endoderm
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EMBRYOLOGY OF ORAL CAVITY
UPPER LIP• Fusion of medial frontonasal and lateral
maxillary prominences • 6th-8th week of fetal devtLOWER LIP• Fusion of mandibular prominences• 4th week of fetal devt
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EMBRYOLOGY OF ORAL CAVITY
CHEEK• Formed by the buccinator muscleSALIVARY GLANDS• Develop from stomadeal ectoderm by
ingrowth of oral epithelium into underlying mesenchyme
• Starts at a 6 weeks AOG
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EMBRYOLOGY OF ORAL CAVITY
TONGUE• from lingual swellings and tuberculum impar• ~4 weeks AOGPALATE• Fusion of primary and secondary plates• 12th week AOGMANDIBLE• Membranous ossification of Meckel’s cartilage• 4 ½ weeks AOG
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ANATOMY
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PARTS/SUB-UNITS
• Lips• Buccal mucosa• Alveolar ridges• Anterior 2/3 of the tongue• Retromolar trigone• Floor of the mouth• Hard palate
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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
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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
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LIPS & CHEEK
• Cheeks– Muscular framework formed by buccinator– Bichat fat pad (buccal fat pad)– Innervated by branches of the facial nerve
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MUSCLES OF MASTICAITON
• Masseter muscle• Temporalis muscle• Medial and lateral pterygoid muscles
• Supplied by mandibular nerve (third division of the trigeminal nerve)
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TEETH
Infants: 2 I, 1 C, 2M Adults: 2 I, 1C, 2PM, 3M
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TEETH
Deciduous Age (mo) Permanent Age
(years)Medial incisors Lateral incisors First molar CanineSecond molar
79
1518
20-24
1st molarMedial incisorsLateral incisors1st premolarCanine2nd premolar2nd molar3rd molar
66-78-9
10-1110.5-11.5
11-1212-1317-25
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• 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
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SURFACE ANATOMY
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SURFACE ANATOMY
• Divisions: apex, body, and base • Terminal sulcus• Papillae
– Filiform, fungiform, foliate, vallate• Foramen cecum• Frenulum lingua
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Extrinsic muscles (CNXII)
STYLOGLOSSUS
HYOGLOSSUS
GENIO- GLOSSUS
GENIOHYOID
MYLOHYOID
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Intrinsic muscles (CNXII)A) VERTICAL M. - FIBERS SUP & INF - FLATTEN & BROADEN TONGUE
B) TRANSVERSE M. - FIBERS HORIZONTAL - NARROW TONGUE
C) LONGITUDINAL M. - FIBERS ANT-POST. - SHORTEN TONGUE
CORONAL SECTION
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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
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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
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Vascular supply• ascending palatine branch of the facial arterySensory innervation• greater and lesser palatine nerves from V2
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SALIVARY GLANDS
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PAROTID SUBMANDIBULAR SUBLINGUALStensen’s Wharton’s Rivinus’
Lateral to upper 2nd molar
midline floor of mouth adjacent to lingual frenulum
multiple orifices draining into floor of
mouth or into submandibular duct
Serous Serous and mucous Serous and mucousSupplies 1/3 saliva
in resting stateSupplies 2/3 saliva
in resting stateSupplies 2/3 saliva in stimulated state
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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
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SALIVA
1500 mL/day; pH 6.2-7.4– 99.5% water – 0.5% organic/inorganic solids.
• Na – 10 mEq/L• K – 26 mEq/L• Cl – 10 mEq/L• HCO3 – 30 mEqlL• glycoprotein and amylase
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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
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• 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 syndromesTX: Surgery
MICROGNATHIA
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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
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PROGNATHISM
• Enlargement or anterior placement of lower jaw
TX: Surgery
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MALOCCLUSION
• Disturbed development of face and jaws
• Underdevelopment of maxilla or mandible or overdevelopment of mandible
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MACROGLOSSIA
• Enlarged tongue that may result in abnormal speech
• Due to increase in amount of tissue
• Most are due to lymphangioma or hemangiolymphoma
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MEDIAN RHOMBOID GLOSSITIS
• Smooth to nodular, elevated or depressed area of void papillae
• No treatment required
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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
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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
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CLEFT LIP AND PALATE
Unilateral incomplete
Unilateral complete
Bilateral complete
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• 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
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• 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
CLEFT LIP AND PALATE
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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”
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LICHEN PLANUS
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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.
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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
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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
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• 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: Herpes simplex virus
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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
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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
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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
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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
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Bacterial and fungal infections
• oral floor abscess• lingual abscess• candidiasis
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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
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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
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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
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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
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CANDIDIASIS
• Angular cheilosis
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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
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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.)
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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
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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
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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
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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
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DENTAL CARIES
• Bacterial infection-common sequel to caries
Sequelae:Pulpitis (acute or chronic)
Acute alveolar abscess
Dental granuloma
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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.
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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
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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.
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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.
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Categories
• Odontogenic cyst- proliferation cystic degeneration of odontogenic epithelium
a. Dentigerous cystb. Eruption cystc. Gingival cyst of the newbornd. Radicular cyste. Keratocyst
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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 cystb. Nasopalatine or incisive canal cyst c. Palatal cyst of newborn infantsd. Dermoid and epidermoid cyst e. Submental or geniohyoid dermoid cystf. Retention cyst
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Cysts of the Jaws and Oral Floor
• Odontogenic CystsDentigerous Cyst
Asymptomaticoccassionally pain or swellingfirm hard mass appears
as if missing a tooth usually involve unerupted
mandibular third molars
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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
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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
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Cysts of the Jaws and Oral Floor
Radicular Cyst Nevoid Basal Cell Carcinoma Syndrome
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Cysts of the Jaws and Oral Floor
• Nonodontogenic and Fissural Cysts Nasopalatine or Incisive Canal Cyst Nasoalveolar Cyst
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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
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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.
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EPIDERMOID CYST
• Epidermoid cyst-absence of skin
appendages microscopically
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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
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Superficial tongue lesions
• Hunter’s glossitis• Fissured tongue• Angioedema• Fixed drug eruption
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HUNTER’S GLOSSITIS
• 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
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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
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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
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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.
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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
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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
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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
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Tumors of the Lips and Oral Cavity
• Benign tumors• Precancerous lesions• Malignant tumors
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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
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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)
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a Papilloma of the uvula.b The bulge in the palate is caused by a pleomorphic adenoma arising from the palatal salivary glands.
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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
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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
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PRECANCEROUS LESIONS: BOWEN’S DISEASE
• a chronic inflammatory disease caused by an intraepidermal carcinoma
• Rare• morphologic features are similar to those of leukoplakia
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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
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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.
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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
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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
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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
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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
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– 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
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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.
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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%
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SQUAMOUS CELL CARCINOMA
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