developmental anomalies of oral cavity

7/25/2019 Developmental Anomalies of Oral Cavity

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DEVELOPMENTAL ANOMALIES OF ORAL CAVITY

ORAL TORI CLEFT LIP/PALATE OTHETorus palatinus

Nodular or lobular bony growth in the midline of the

hard palate

Surgical removal if for maxillary denture construction

Midline bony growth in the palate.

Commonly seen in adults

Harmless

Torus mandibularis Bony growths on the lingual aspect of mandible in the

region of the premolars

If indicated, do surgery

Congenital malformation that is usually gets noticed

when the child is already a teenager or during adulthood

when they get fitted for dentures.

We just drill or burn these to flatten out the area.

A common problem is that it is prone to trauma when

they eat because the MUCOSA IS THINNED OUT.

Just reassure patient. No surgical corrections are done

because these are bony overgrowths. Patient may only

have problems with their dentures, with the denture

edge causing trauma.

These bony overgrowths can be seen in mandible as well

(at medial, lateral or vestibular side of mandible). But

most commonly seen at the palate. Upon palpation, you

feel something hard, just reassure the patient that it is an

oral torus. However, sometimes, you can also have

tumors that are cystic so you have to rule out salivary

gland tumors. But if it really is Bony, then that is torus

subdivided into PARTIAL AND COMPLETE CLEFT LIP

They could occur in isolation (cleft lip only) or they could go together as cleft lip and palate .

Complete cleft lip and palate

– if it goes beyond the area of nostril, involving the nasal cavity

Incomplete cleft lip and palate

– if it doesnt involve nasal cavity or it didnt go beyond incisive foramen and only involves secondary palate

Cleft lip could be unilateral or bilateral

– More commonly occurs in the left but it could also occur in the right

Cleft lip and palate is usually genetic

– If one of the parents has this, their child would have a 70-80% chance of having it as well.

– There IS FAILURE OF FUSION OF THE NASOMAXILLARY CREST AND BUCCOPHARYNGEAL CREST during the embryonic

period

When do we correct cleft LIP? We use the rule of 10s for cleft lip.

– 10 weeks old

– 10 g/dL Hemoglobin

– 10 pounds

– WBC not more than 10,000 (in somebooks, but not a major consideration)

For, surgical correction of cleft PALATE, it is done before 2 years old, before onset of speech.

Cleft palate can be:

– incomplete cleft of the primary palate (rare).

–

bilateral cleft of primary palate – complete (bilateral or unilateral) cleft involving both primary and secondary palate

Incomplete cleft of secondary palate

– If only soft palate is involved, and not the hard palate

Sometimes patients with cleft lip and palate could also have bifid uvula (submucosal cleft)

– Patients with bifid uvula will also have speech abnormalities such as nasal thwang

Patients with cleft palate will also have middle ear infections because of the muscles involved in the palate - the tensor vela

palatini and levator vela palatini. So you need to assess hearing

May involve only the vermilion border of the upper lip or may extend to involve the nostril and the hard and soft palates

50% of all maxillofacial clefts: Combination of cleft lip and cleft palate comprises

25% of all maxillofacial clefts: Isolated cleft lip or cleft palate is only

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Cleft lip, with or without

cleft palate

Isolated cleft lip Isolated cleft palate Cleft uvula

o 1 per 1000 births

o Increasing incidence

o High incidence in

Orientals, low in

blacks

o Unilateral or bilateral

o If unilateral, L>R

o If with cleft palate, usually

BILATERAL

o Cleft lip-cleft palate is

more common in MALES

o 30% have associated

congenital anomalies

o More common in

females, Orientals

o Incomplete form of cleft

palate

o 1 per 80 whites, high

among American Indians

Otitis media is almost universal in infants under 2 yrs with unrepaired clefts

Angular as compared to linear incisions are preferred. In bilateral clefts, lip closure is accomplished in two stages

Bridge flap technique (von Langenbeck)

Pedicle flap technique (Veau)

o Lengthening of soft palate is accomplished using the “push-back procedure”

Velopharyngeal closure

o is important for speech and deglutition and blowing, if not achieved, foods and liquids may be directed into the

nasopharynx during deglutition. Evaluation of velopharyngeal closure is through speech itself

o

Associated developmental anomalies:

o Facial clefts

o Acrocephalosyndactyly (Apert Syndrome)

– turribrachycephaly associated with syndactryly of the hands and feet

o

Craniofacial Dysostosis (Crouzon syndrome) – underdevelopment or flattening of the middle of the face associated with relative mandibular prognathism and a

beaklike nose. Maxillary teeth are crowded, arch is V- shaped. Exophthalmos is a constant feature. It is Autosomal

dominant.

– Mandibulofacial Dysostosis (Treacher Collins Syndrome)

– autosomal dominant. Characterized by anomalies of the eye, abnormalities of the external and middle ears and hypoplasia

of the mandible and malar bones



CYSTS OF JAW/ORAL CAVITY

ODONTOGENIC CYST

A cyst is a cavity lined with epithelium. It is od ontogenic if it comes from dental lamina, primary involving the teeth.

DENTIGEROUS CYST ERUPTION CYST GINGIVAL AND PALATAL CYST OF

NEWBORN

RADICULAR CYST NEOVID BASAL CELL

SYNDROM

o associated with unerupted tooth

o Surrounds the crown of an unerupted

tooth of either the regular (95%) or

the supernumerary dentition.

o Arises through alteration of the

reduced enamel epithelium after thecrown has been completely formed.

o Usually solitary. Suspect Nevoid Basal

Cell Carcinoma Syndrome if multiple.

Usually involves the ff teeth:

Mandibular third molar

Maxillary canine

Maxillary third molar

Second mandibular

premolar

o Uncommon type of dentigerous

cyst associated with erupting

deciduous or rarely permanent

teeth.

o Accumulation of tissue fluid or

blood in a dilated follicular space

about the crown of an erupting

tooth.

o White to yellowish white and

with inclusion cysts.

o Become superficial and usually

rupture in the first few weeks of

life.

o

Degeneration of dental lamina

remnants.

o Most common oral cyst

o Inflammatory in origin

o Apical granuloma (mass of

inflammatory tissue) contains

epithelial rests of Malassez which

coalesce and become cystic

o Often symptomless

o Involves dental caries

o We request dental x-rays (panoramic)

to visualize cysts involving the roots

of teeth

o Treatment is surgical

o Removal of carious tooth if it is a

radicular cyst

o Multiple keratocysts

multiple cutaneous n

cell carcinomas and n

skeletal and other an

o Autosomal dominant

NON-ODONTOGENIC CYST

noted along the incisive canal or embryonal fissure

INCISIVE CANAL CYST NASOALVEOLAR CYST DERMOID AND EPIDERMOID CYST RETENTION CYST

Closed, epithelium-lined intrabony sac

Called cyst of the palatine papilla if

below the incisive foramen

Usually present in 4

thto 6

th

decade of life

Painless unless infected

Often manifest with enlargement

of the palate

Klestadt’s cyst

Probably arising from epithelial rests located at the junction

of the globular, lateral nasal, and maxillary processes

Situated in the attachment of the ala of the naris

Not located within bone

May cause enough facial swelling to obliterate the

nasolabial fold on the involved side

Attached to the nasal mucosa

Clearly demonstrated with the use of an radiopaque dye

Developmental cyst lined by epidermis and cutaneous

appendages

Incorporation of ectoderm at the time of closure of

embryonic fissures during the third to fourth week in

utero

Commonly arise in the floor of the mouth

Commonly originate above the mylohyoid muscle

May cause elevation and displacement of the tongue

Rupture of a duct of a minor sali

Occurs most often on the mucos

lower lip

Cyst of Blandin-Nuhn – ventral s

of the tongue

Ranula – involves the sublingual

MOST COMMON

Usually brought about by traum

sang patient. There is blockage

gland, leading to extravasation

the salivary gland, then there wi

cyst

Treatment is excision



DISORDERS OF THE ORAL MUCOSA

LICHEN PLANUS APHTHOUS ULCER PYOGENIC GRANULOMA ERYTHEMA MULTIFORME CANDI

Thickened white patch which can occur

anywhere in the oral mucosa

Premalignant lesions

Can appear in the buccal mucosa if the

patient is a smoker

Always perform biopsy if you see this in

your patient

Appear on buccal mucosa, tongue,gingiva, and lips

May precede appearance of

cutaneous lesions by several years

Wickham’s Striae – fine

lacework of white reticular

hyperkeratotic papules

On tongue, begins in posterior area

and spread anteriorly

Asymptomatic, metallic taste

Common condition

Small, round, or ovoid lesions with a circumscribed

margin, erythematous halos and yellow or gray

floors.

Recurrent

Can occur solitary or multiple lesions

If recurrent and solitary but in different places, it can

be inflammatory; has multifactorial causes

if it occurs in the same place and doesn’t disappear,

rule out malignancy by doing biopsy

Recurrent Aphthous Stomatitis

Unknown etiology but maybe Pleomorphic

transitional L for of alpha-hemolytic strep.

Definitely not viral

Recurrent, maybe autoimmune

Ulcer is covered by grayish white fibrinous

exudate and surrounded by a bright red halo

Lasts for one to two weeks and heals without

scarring

Xylocaine and Tetracycline may offer relief

Tumor of pregnancy”

Benign, rapidly growing vascular mass

noted in the oral cavity

Usually seen in the interdental papillae,

most likely odontogenic

Occurs in 5% of pregnant women

Would usually complain of bleeding

Treatment is antibiotics and surgical

removal

Acute, recurrent, self-limited

eruption of the skin and

mucus membranes

Probably a hypersensitivity reaction

Mucus membranes and joints

may be involved in severe cases

Steven Johnson Syndrome (toxic,

acute, febrile course) Precipitating factors: viral

disorders especially herpes

simplex and mycoplasma, drugs

especially sulfonamides

Neonatal moni

present on the

postpartum da

Therapeutic us

antibiotics incr

incidence of ca

infections

Superficial mon

– inflamed “wh

Denture stoma

swelling, sensit

pain of the ora

membrane at p

denture contac

Treat with: Imp

hygiene, nutrit

(especially iron

Causes

Bacterial

– Acute necrotizing ulcerative

gingivostomatitis

– Streptococcal

– Oral tuberculosis

– Gonococcal

– Stomatitis

– Syphilis

Fungal

– Oral Candidiasis

Histoplasmosis

Viral Infections

–

Herpes simplex

– Recurrent herpes simplex



DISEASES OF OROPHARYNX

ACUTE TONSILLITIS PERITONSILLAR CELLULITIS AND ABSCESS ACUTE PHARYNGITIS

Inflammatory reaction of the tonsils which can be secondary to

a bacterial/ viral infection

Etiologic agents

– B-hemolytic streptococcus (most common)

– Staphylococcus

– Pulmonitis diplococcus

– Hemophilus influenzae

–

Adenoviruses

– Rhinoviruses

– Herpes simplex

Symptoms

– Fever

– General body malaise

– Odynophagia

– Dysphagia

– Otalgia - referred pain

Sign

– Bilateral hypertrophied tonsils

– (+/-) pus - pus in exudative tonsillitis

–

(+) tender lymph nodes

– You can differentiate this from pharyngitis with the

congestion of pharynx without tonsillar enlargement or

tender lymph nodes. Same treatment as pharyngitis.

Most common cause is beta hemolytic strep group A

There is general inflammation and swelling of the tonsil tissue with an

accumulation of leukocytes, dead epithelial cells and pathologic

bacteria

Treated with bed rest, adequate fluid intake and a light diet

Three glassfuls of gargling warm solutions every two hours

o Isotonic saline solution and sodium perborate powder

o Penicillin is drug of choice

Recurrent tonsillitis involving the adjacent areas

seen in older children with history of tonsillar infection, not seen

in children of younger ages

Always presents with odynophagia, dysphagia and speech

abnormalities (sweet, este hot potato voice)

Etiology

Infections of the tonsil proceed to diffuse cellulitis that couldlead to peritonsillar abscess

May occur rapid or late

Unilateral and more common in older children and young

adults

Symptoms: marked dysphagia, pain referred to the ear in the

involved site, increased salivation, fever, drooling

Symptoms

Swelling interferes with articulation and speech is difficult

Inspection is difficult due inability to open mouth

Tonsil may appear normal as it is pushed medially and swelling

develops lateral to tonsil

Palpation – distinguishes an abscess from cellulitis

Pathophysiology

Suppurative infiltration occurs most often in supratonsillar fossa

Causes edema of soft palate and displacement of uvula across

midline ( inflammatory processes push the uvula to the

contralateral side)

Swelling extends to adjacent soft tissues, causing painful

swallowing

Bacteriology

Throat cultures are ineffective

Culture of the actual abscess is ideal through aspiration

More common bacteria – Streptoccocus pyogenes; less common

– Staph. aureus

Treatment

Surgical incision and drainage or needle aspiration technique

Strep, pneumococci and influenza bacillus

Hyperemia first then edema and increased

Vesicles suggest herpes

Dryness or scratchiness of the throat

Headache

Fever

Pharyngeal wall is reddened and may haveappearance and a coating of mucoid secret

Treat with antibiotics and warm irrigation



DEEP NECK SPACE INFECTION

Etiology

1. Dental infection

2. Tonsillar and peritonsillar infection

3. Trauma of upper aerodigestive tract - iatrogenic on esophagoscopy on removal of foreign bodies

4. Retropharyngeal lymphadenitis

5. Pott’s disease

6. Sialadenitis

7. Bezold’s abscess

8.

Infection of congenital cyst and fistula

9. Intravenous drug abuse

PARAPHARYNGEAL SPACE INFECTION Most common cause: Peritonsillar infection

may present as such, except that there is trismus

There is swelling at the lateral area of the buccal mucosa

Patients usually have history of recurrent tonsillitis

There is unilateral enlargement of the tonsils

Patients come to your clinic with a hot potato voice

These patients need to be admitted and started on IV antibiotics because they are at risk for airway obstruction

Typical finding

• Trismus - limitation in opening of the mouth, less than two finger wide, if more than two fingers it is different

• Angle mandible swelling

•

Medial displacement of lateral pharyngeal wall

• Can present as upper airway obstruction so advise patient for admission to start antibiotics and assess for airway patency (tracheostomy for eme



Treatment

Evaluate and maintain airway & fluid hydration

Parenteral antibiotic high dose 24-48 hrs.

If not improve, consider surgical drainage - prophylactic tracheostomy

Pharyngomaxillary (Parapharyngeal) Space Infection

Marked trismus

Neck becomes swollen near the angle of the mandible

Complications include Septic thrombophlebitis, hemorrhage from erosion of t he internal carotid artery

SUBMANDIBULAR SPACE INFECTION

Most common cause: Dental caries

Anterior teeth and first molar: infection enter sublingual space

Second and third molar: infection enter submaxillary space

–

If it involves the swelling of the whole submandibular space, it can be bilateral leading to Ludwig’s angina

LUDWIG’S ANGINA Clinical features

Start unilateral and progress bilaterally

Induration of submandibular region and floor of mouth (severe cellulitis)

Tongue thrust posteriorly and superiorly (cause airway obstruction; do standby tracheostomy because you cannot do intraoral intubation)

Drooling, odynophagia, trismus, fever

No purulence(due to no time to develop) - more of cellulitis; very rigid if palpated like wood

Usually with history of tooth extraction

Treatment

Early stage (unilateral, mild swelling and edema)

– IV antibiotic, extraction of infected tooth

Advance stage (bilateral swelling, dysphagia with drooling)

– Early airway intervention

– Surgical drainage (submandibular incision and IV

antibiotics)

Cellulitis or phlegmonous inflammation of the superior compartment of the suprahyoid space Forces the tongue upward and posteriorly causing airway obstruction

Usually a result of infection of dental origin



RETROPHARYNGEAL SPACE INFECTION

Request for soft tissue lateral x-ray of

the neck ,

at level of C2 and C7

Only lymph nodes are located in this area

Most common case is Koch’s infection

Patients would usually come to you with dysphagia, odynophagia and drooling

and when you check the throat, the tonsils are not enlarged and there will be

trismus

Clinical features

In children

– Irritability, neck rigidity, fever, drooling, muffled cry, airway

compromise, stridor (rapid onset)

In adult

–

Fever, sore throat, odynophagia, neck tenderness, dyspnea

Lateral neck film

– C2 > 7 mm both children and adult

– C7 > 14 mm in children, 22 mm in adult

Chest film

– Detection of mediastinitis

Most common cause:

In children

– Retropharyngeal lymphadenitis , infections (Pott’s dise

In adults

– Regional trauma and endoscopic procedure

Treatment

Admit patient– Complication can be mediastinitis

IV antibiotics

Airway

Irrigation and Drainage

Retropharyngeal abscess

Primarily in infants or children less than 2

Unexplained fever following an upper respiratory infection

Loss of appetite, change in speech, difficulty swallowing

Drain abscess, protect airway

MASTICATOR SPACE INFECTION Most common cause: Dental caries

Clinical features

– Extreme trismus with minimum facial swelling

Masseteric space (lateral compartment):

– Edema at ramus of mandible

Ptrygomandibular space (medial compartment):

–

Edema at retromolar trigone

request for CT scan of the neck, can be mistaken for tetanus

Masticator abscess

In close proximity to the pharyngomaxillary space

Involves the internal pterygoid muscle, masseter and ram

the mandible

Treated initially and vigorously with appropriate antibiotic

PARTOID SPACE INFECTION Most common cause: Bacterial retrograde from oral cavity

Clinical features:

High fever, weakness, marked swelling and tenderness of parotid gland,

fluctuation, pus at Stensen’s duct

Treatment : antibiotics and airway management

Parotitis

Acute suppurative parotitis – sudden onset of pain and swelling of

the parotid region usually cause by coagulase negative S. aureus.

Immediate treatment with IV antibiotics is necessary

Complications

Internal jugular vein thrombosis

Cavernous sinus thrombosis

Neurologic deficit

Osteomyelitis of the mandible

Osteomyelitis of the spine

Mediastinitis

Pulmonary edema

Pericarditis

Aspiration

SepsiS

developmental anomalies of oral cavity

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