oral cavity clerk sarah camille concepcion. outline introduction embryology anatomy physiology...

ORAL CAVITY

Clerk Sarah Camille Concepcion

OUTLINE

• 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 devtLOWER LIP• Fusion of mandibular prominences• 4th week of fetal devt

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

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

ANATOMY

PARTS/SUB-UNITS

• 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 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

• 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

HYOGLOSSUS

GENIO- GLOSSUS

GENIOHYOID

MYLOHYOID

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

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 arterySensory innervation• greater and lesser palatine nerves from V2

SALIVARY GLANDS

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

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.

• 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

• 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

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

• 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

CLEFT LIP AND PALATE

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

• 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

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 infection-common 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 cystb. Eruption cystc. Gingival cyst of the newbornd. Radicular cyste. 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 cystb. Nasopalatine or incisive canal cyst c. Palatal cyst of newborn infantsd. Dermoid and epidermoid cyst e. Submental or geniohyoid dermoid cystf. Retention cyst

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

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

• 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

• Hunter’s glossitis• Fissured tongue• Angioedema• Fixed drug eruption

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

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