Exam 1 - Oral Path

How is the formation of the oral and maxillofacial region described?

A complex process

What occurs during development of the oral and maxillofacial region?

Tissues develop and merge

How do oral clefts develop?

Result from disruption of the orchestrated development and merger of tissue processes

Medial nasal processes

Merge with each other to form central part of the upper lip

• Occurs during weeks 6 and 7

Maxillary processes

• From 1^st pharyngeal arch

• Merge with nasal prominences to form lateral portions of the upper lip

• Occurs during weeks 6 and 7

Primary Palate

• Only hard palate

• Formed from the merging of medial nasal processes

• Forms the intermaxillary segment

• Gives rise to premaxilla (triangular bone bearing the four incisors)

Secondary Palate

• 90% hard and soft palates

• Formed from merging of maxillary processes from 1^st pharyngeal arch

Components of the Intermaxillary Segment

1. Labial: Philtrum

2. Upper jaw: carries four incisors

3. Palatal: forms primary triangular palate

Palatal shelves

• Medial projections of maxillary processes

• Growth toward one another

• Fusion of palatal shelves begins by week 8 in a cranio-caudal direction

• Simultaneous fusion with primary palate and nasal septum

When does complete fusion of the palatal shelves occur?

Week 12

What is the cause of cleft lip?

Defective fusion of medial nasal processes with maxillary process

What is the consequence of a failure of the palatal shelves to fuse?

Cleft palate

Incidence of Cleft Lip And/Or Palate

• Cleft lip and cleft palate together

• Either Cleft palate or Cleft lip separately

Causes of Syndromic Clefts

1. Single-gene syndromes

   • Autosomal dominant

   • Autosomal recessive

   • X-linked inherited

2. Chromosomal anomalies

3. Idiopathic

 Do oral clefts follow a simple Mendelian inheritance pattern?

No, they have heterogeneous causes

What are the three contributing factors to oral clefts?

Heterogenous causes:

• Major genes

• Minor genes

• Environmental factors

Causes of Oral Clefts

• Genes

• Environmental factors

• Maternal alcoholism

• Maternal tobacco use

• Anticonvulsant therapy

Lateral facial cleft

• Lack of fusion of the maxillary and mandibular processes

• From the commissure to the ear

• Uncommon

What are lateral facial clefts associated with?

1. Accessory mandible

2. Absent parotid gland

3. Peripheral facial weakness

Oblique facial cleft (rare)

• Form upper lip to the eye

• Due to failure of fusion of lateral nasal process with the maxillary process

Median cleft of the upper lip

Due to failure of fusion of the medial nasal processes

Clefting

One of the most common major congenital defects

Cleft lip

More prevelant unilaterally

Complete Cleft Lip

• From the lip to the nostril

• Involves the alveolus

  • Usually between lateral incisor and the cuspid

  • tooth can be absent in the cleft area (especially the lateral incisor)

  • Supernumerary teeth may be seen

Incomplete CL

Nose not involved

Severity of Cleft Palates

Depends on structures involved:

• Hard and soft palates

• Only soft palate

Cleft (bifid) uvula

Less Severe Cleft Palate

Submucous Palatal Cleft

• Intact mucosa

• Defect of muscles of soft palate

• Frequent notch in bone along posterior margin of hard palate

• Bluish midline discoloration

• Best identified by palpation with blunt instrument

• Can be associated with cleft uvula

Key features of Pierre Robin Sequence (or anomalad)

1. Cleft palate: palatal shelves fail to fuse

2. Mandibular micrognatia: constraint of mandibular growth in utero

3. Glossoptosis → airway obstruction due to posterior displacement of tongue (tongue fails to descend)

Can Pierre Robin sequence be isolated?

Yes, it may be isolated or occur with other syndromes/anomalies

What clinical difficulty is common in Pierre Robin sequence?

Respiratory difficulty, especially in the supine position → can cause asphyxia

Treatment of orofacial clefts

Mutlidisciplinary approach:

• Pediatrician

• Oral and maxillofacial surgeon

• Otolaryngologist

• Plastic surgeon

• Pediatric dentist

• Orthodontist

• Prosthodontist

• Speech pathologist

• Geneticist

Leukodema

• Common oral mucosa condition

• Considered an anatomical variation

• Unknown cause

• More prevalent in African Americans

• More common and severe in smokers

• Less pronounced with smoking cessation

• Benign condition

Clinical Manifestations of Leukoedema

• Mucosa appearance:

  • Diffuse, gray-white, milky, opalescent

  • Folded surface with wrinkles or whitish streaks

  • Lesions do not rub off

• Distribution:

  • Typically bilateral in oral mucosa

  • May extend to labial mucosa

  • Can involve floor of mouth

Diagnosis of Leukoedema

White appearance diminishes or disappears with eversion of the cheek

Differentials of Leukoedema

• Leukoplakia

• Candidiasis

• Lichen planus

Ankyloglossia

• Developmental condition

• Characterized by a short and thick lingual frenum

• Leads to limitation of tongue movement

• More common in neonates

Clinical Manifestations of Ankyloglossia (Mild cases)

Little clinical significance

Clinical Manifestations of Ankyloglossia (Severe cases)

• Fusion of tongue to floor of mouth

• Possible fusion of frenum to tip of tongue

• Slight clefting of tongue tip

• Speech difficulties (usually minor)

Treatment of Ankyloglossia

• Mild cases: no treatment necessary

• Frenotomy: for infants with specific breast-feeding problems

• Frenuloplasty: postponed until 4–5 years old in children

  • Indicated in children and adults with functional or periodontal difficulties → increases tongue mobility

Fissured Tongue (Scrotal Tongue)

• Relatively common

• Multiple grooves or fissures on the dorsal lingual surface

• Cause: unknown

• Contributing factors: age & environment

Clinical Features of Fissured Tongue

• Multiple grooves or furrows

• Severe cases:

  • Numerous fissures covering entire dorsal surface

  • Tongue papillae divided into multiple separate “islands” (associated with geographic tongue)

• Symptoms:

  • Usually asymptomatic

Treatment of Fissured Tongue

• Benign condition → no treatment needed

• Prophylaxis: prevent accumulation of debris → encourage patients to brush the tongue

Varicosities

• Abnormally dilated, tortuous veins

• Rare in children, common in elderly

• Associations:

  • Leg varicosities ↔ tongue varicosities

  • Smoking

  • Cardiovascular disease

Most common type of Varicosities

Sublingual varix

Clinical manifestations of Varicosities

• Multiple lesions

• Purple papules (elevated)

• Located on ventral & lateral borders of tongue

• Symptoms:

  • Usually asymptomatic

  • Thrombosis may occur

Solitary Varices

• Less common than sublingual varices

• Locations:

  • Lips

  • Buccal mucosa

• Often noticed after thrombosis

• Thrombosed varix:

  • Firm

  • Nontender

  • Blue-purple nodule (isolated)

Treatment of Varicosities

• Asymptomatic cases: no treatment required

• Solitary varices: surgical removal (laser treatment)

Exostoses

• Benign bony protuberances arising from cortical plate

• Location: jaws frequently affected → related to stresses from teeth function

• Best-known forms:

  • Torus palatinus

  • Torus mandibularis

Clinical Manifestations of Exostoses

• More frequent in adults

• Buccal exostoses:

  • Bilateral row of bony nodules

  • Located on facial aspect of maxillary and/or mandibular alveolar ridge

• Symptoms:

  • Usually asymptomatic

  • Surface mucosa may ulcerate

Clinical Manifestations of Palatal Exostoses

• Location: Lingual aspect of maxillary tuberosities

• Bilateral or unilateral

• More common in males

• Patients with buccal or palatal exostoses may also present palatal or mandibular tori

Cyst

• Pathologic cavity

• Filled with fluid

• Lined by epithelium

• Many developmental cyst are considered fissural cysts

• Slow increase in size

Palatal Cysts of the Newborn

• Prevalence: mostly in neonates

• Appearance: White or yellow-white papules

• Location:

  • Often along midline

  • Near junction of soft and hard palate

• Lesion pattern: Single or clusters (2–6 lesions)

• Symptoms: Asymptomatic

• Treatment:

  • No treatment necessary

  • Self-healing

Nasolabial Cyst

Location: Upper lip, lateral to midline

Clinical Manifestations of Nasolabial Cyst

• Swelling of upper lip, lateral to midline

• Elevation of the ala of the nose

• Obliteration of the maxillary mucolabial fold

• Pain: uncommon, occurs if secondary infection develops

• Rupture: may occur → drains into oral or nasal cavities

Treatment and Prognosis of Nasolabial Cyst

• Complete surgical excision

• Recurrence is rare

Nasopalatine duct cyst

Most common nonodontogenic cyst of the oral cavity

Clinical Manifestations of Nasopalatine Duct Cyst

• Swelling of anterior palate

• Drainage

• Pain

• Many cases are asymptomatic

• Discovered on routine radiographs

Radiographic Features of Nasopalatine Duct Cyst

Appearance:

• Well-circumscribed radiolucency

• Located in or near midline of anterior maxilla

• Between apices of central incisors

Shape:

• Usually oval or round

• May appear as inverted pear shape

Borders: sclerotic margins commonly present

Treatment & Prognosis of Nasopalatine Duct Cyst

Treatment:

• Surgical enucleation

• Biopsy recommended

Prognosis:

• Recurrence is rare

• Malignant transformation is very rare

Thyroglossal Duct Cyst

• Remnant of epithelium from the thyroglossal tract

• Develops classically in the midline

• Often adjacent to the hyoid bone

Clinical Manifestations of Thyroglossal Duct Cyst

• Midline swelling

• Painless in most cases

• Movable and fluctuant

• Complications:

  • Secondary infections may occur

  • If located at the base of the tongue, can cause laryngeal obstruction

Treatment of Thyroglossal Duct Cyst

Sistrunk procedure → complete removal of:

• Cyst

• Midline segment of hyoid bone

• Portion of muscular tissue along the thyroglossal tract

Environmental Alterations of Teeth

• Developmental tooth defects

• Post-developmental structure loss

• Discolorations of teeth

• Localized disturbances in eruption

Environmental Effects on Tooth Development

• Ameloblasts (cells forming enamel) are highly sensitive

• External stimuli → significantly alter enamel structure

• Severity of defect is directly proportional to intensity/duration of factors

• Two categories of factors:

  • Systemic

  • Local

Does enamel remodel after its initial formation?

• No enamel does not remodel (unique to enamel)

• Abnormalities of enamel development remain permanently etched on the tooth surface

What are the 3 major steps in enamel development?

1. Matrix formation – proteins are laid down

2. Mineralization – minerals deposited, most original proteins removed

3. Maturation – final mineralization and removal of protein remnants

Effects of time on enamel defects

• Timing of ameloblastic damage impacts location and appearance of enamel defect

• Final enamel is a record of insults received during tooth development

• Position of enamel in permanent tooth provides rough estimate of time of damage

What are the two main classifications of enamel defects?

• Hypoplasia: quantitative defect

• Opacities: qualitative defect

What characterizes enamel hypoplasia?

Pits, grooves, or larger areas of missing enamel

What characterizes enamel opacities?

• Diffuse or demarcated defects

• Enamel thickness is normal

• Appear as variations in translucency

Diffuse opacities

Increased white opacities without clear boundaries from normal enamel

Demarcated opacities

• Areas with decreased translucence and increased opacity

• Sharp boundary with adjacent enamel

• Porosity determines color (white, cream, yellow, or brown)

Environmental Enamel Hypoplasia

• Cause: Systemic influences during tooth development

• Characteristic pattern:

  • Rows of pits or diminished enamel

  • Bilateral and symmetrical enamel loss

  • Defects’ location corresponds to developmental stage of affected teeth

Turner Hypoplasia

• Pattern of enamel defects in permanent teeth

• Cause: Periapical inflammatory disease of the overlying deciduous tooth

• Usually affects only one tooth (“Turner tooth”)

• Determinants: timing & severity of insult → appearance of defect

• Most frequent: Permanent bicuspids → close relation with overlying deciduous molars

• Less frequent: Anterior teeth → crown formation usually complete before apical inflammation develops in caries-resistant anterior deciduous teeth

Clinical signs of Turner Tooth

• Extensive enamel hypoplasia

• Lack of significant enamel

• Irregular dentin surface

Turner tooth

• Cause: Traumatic injuries to deciduous teeth

• Most affected: maxillary central incisors

Factors determining degree of damage of permanent teeth

1 Stage of tooth development

2. Length of time infection is not treated

3. Virulence of microorganisms

4. Host resistance to infection

Molar-Incisor Hypomineralization

• Hypomineralization affecting one or more molars

• Appearance of enamel:

  • White, yellow, or brown areas

  • Sharp demarcation with normal enamel

• Yellow/brown enamel:

  • Increased porosity

  • Posteruptive enamel loss

• Incisor involvement correlates with number of molars affected

Clinical consequences of molar-incisor hypomineralization

• High dental sensitivity

• Difficulties with oral hygiene

• Higher caries risk

• Problems with dental anesthesia

Syphilis hypoplasia

Rare nowadays:

• Hutchinson teeth (anterior teeth)

• Mulbery teeth (posterior teeth)

Hutchinson teeth

• Affects anterior teeth

• Crowns shaped like straight-edge screwdrivers

• Greatest circumference at middle one-third of crown

Mulberry molars

• Affects posterior teeth

• Constricted occlusal tables → bumpy surface of mulberries

Treatment & Prognosis of Hypoplasia

Most cases: No treatment required

1. Dental microabrasion → effective for most dental fluorosis cases

2. Treatment of caries where present

3. Cosmetic approaches:

   • Acid-etched composite resin restorations

   • Labial veneers

   • Full crowns

Post-Developmental Tooth Structure Loss

• Tooth structure is lost after formation

• Common causes: caries & traumatic fractures

Causes of Post-Developmental Destruction of Enamel Surface of the Crown

• Abrasion

• Attrition

• Erosion

• Abfraction

Causes of Post-Developmental Destruction of Root (dentin/cementum surfaces)

• External resorption

• Internal resorption

Tooth wear (Tooth surface loss)

• Physiologic

  • Normal process

  • Age dependent

• Pathologic

  • Functional problems

  • Esthetic concerns

  • Dental sensitivity issues

Causes of tooth wear

Multifactorial: combination of more than 2 factors

• Attrition

• Abrasion

• Erosion

• Abfraction

Attrition

• Loss of tooth structure due to tooth-to-tooth contact during occlusion and mastication

• Some degree is normal

• Pathologic attrition:

  • Functional problems

  • Esthetic concerns

• Factors that accelerate tooth destruction:

  • Poor-quality or absent enamel

  • Premature contacts (edge-to-edge occlusion)

  • Intraoral abrasives, erosion, and grinding habits

Clinical Manifestations of Attrition

• Teeth affected: Both deciduous and permanent

• Affects predominantly opposed dental surfaces in contact

• Most frequent locations: Incisal and occlusal surfaces

• Characteristic finding: Large, flat, shiny wear facets

• Loss of interproximal contact points: due to vertical movement of teeth → leads to shortening of arch length

• Pulp exposure and dentin sensitivity are rare

  • Slow tooth structure loss allows for apposition of reparative secondary dentin within pulp cavity

Abrasion

• Wearing away of tooth structure or restoration due to mechanical action of an external agent

• Most common cause: Inadequate tooth brushing

  • Abrasive toothpaste

  • Heavy pressure

  • Horizontal brushing stroke

• Other causes:

  • Pencils

  • Toothpicks etc

Clinical Manifestation of Abrasion

• Toothbrush abrasion:

  • Horizontal cervical notches on buccal surface of exposed radicular cementum & dentin

  • Well-defined margins

  • Smooth, hard surface

• If acid is present: lesions become rounded & shallower

• Other manifestations: rounded or V-shaped notches on incisal edges of anterior teeth → associated causes:

  • Thread biting

  • Use of pipes or bobby pins

Erosion

• Loss of tooth structure caused by a nonbacterial chemical process

• Also called dental corrosion

• Causes:

  • Chelating agents (primary cause)

  • Acidic agents

  • Involuntary or voluntary regurgiation (eating disorders)

Clinical Manifestations of Erosion

• Not correlated with functional wear patterns

• Loss usually linked to known abrasives (dietary/chemical sources)

• Areas most affected (not protected by serous secretions)

  • Anterior maxillary teeth: facial (buccal) & palatal surfaces

  • Mandibular posterior teeth: facial (buccal) & occlusal surfaces

Cupped Lesion

• Classic pattern of dental erosion

• Central depression of dentin surrounded by elevated enamel

• Seen on:

  • Occlusal cusp tips

  • Incisal edges

  • Marginal ridges

Erosion of Posterior Teeth

• Findings:

  • Extensive loss of occlusal surface

  • Edges of metallic restorations stand above tooth structure

• Progression:

  • Rapid dentin destruction

  • Concave depression of dentin

  • Surrounded by elevated rim of enamel

Erosion of buccal cusps

• Loss of entire buccal cusps

• Replacement by ski slope-like depressions from lingual cusp to buccal cementoenamel junction

Erosion of palatal surfaces

• Palatal surfaces affected

• Exposed dentin with a concave surface showing peripheral white line of enamel

Area-Specific Causes of Erosion

• Facial surfaces of maxillary anterior teeth: dietary sources of acids

• Incisal portion of anterior teeth (both arches): environmental sources (suggested)

• Palatal surfaces of maxillary anterior teeth + occlusal surfaces of posterior teeth (both arches): regurgitation of gastric secretions