Ludwig’s Angina is a rapidly progressive, bilateral cellulitis of the submandibular, submental, and sublingual spaces, often without initial abscess formation.
It is life-threatening due to potential airway obstruction and mediastinal spread.
Named after Wilhelm Friedrich von Ludwig (German surgeon, 1790–1865).
🔸 Submental Space
Boundaries:
Roof: Mylohyoid muscle
Floor: Deep cervical fascia, platysma, superficial fascia, skin
Lateral: Anterior belly of digastric
Posterior: Submandibular space
Contents: Lymph nodes, anterior jugular vein
Infection Source: Mandibular incisors
🔸 Sublingual Space
Boundaries:
Superior: Mucosa of floor of mouth
Inferior: Mylohyoid muscle
Posterior: Hyoid bone
Anterior/Lateral: Inner mandibular body
Medial: Geniohyoid, genioglossus, styloglossus
Infection Source: Mandibular premolars and first molars
🔸 Submandibular Space
Boundaries:
Superior: Mylohyoid muscle, mandible
Inferior: Digastric muscle (anterior and posterior bellies)
Lateral: Platysma, deep cervical fascia, skin
Medial: Mylohyoid, hyoglossus, styloglossus
Posterior: Hyoid bone
Anterior: Submental space
Infection Source: Mandibular second and third molars
Odontogenic (75–90%): Dental caries, extractions, poor hygiene
Trauma: Lacerations, puncture wounds of floor of mouth
Secondary infections: Oral malignancy, sialadenitis
Systemic compromise:
Diabetes mellitus
HIV/AIDS
Chemotherapy
Transplant recipients
Aplastic anemia
Glomerulonephritis
Swelling:
Bilateral “wooden” induration in submandibular, submental, sublingual spaces
Skin is tense, pits and blanches on pressure
“Double chin” appearance
Tongue displacement:
Elevation and posterior displacement
Leads to dysphagia, odynophagia, dysphonia, cyanosis
Voice changes:
“Hot potato voice” due to laryngeal edema
Systemic signs:
High-grade fever, malaise, leukocytosis, body aches
Septicemia risk
Airway compromise:
Dyspnea in supine position
Thumb sign on lateral neck radiograph (epiglottic swelling)
Spread:
Masticator space
Parapharyngeal space
Retropharyngeal and mediastinal spaces (late stages)
Modality
Purpose
Panoramic X-ray (OPG)
Identifies odontogenic source
Lateral neck radiograph
Detects soft tissue swelling, tracheal deviation
Ultrasound
Differentiates cellulitis vs. abscess; no radiation
CT Scan
Gold standard for extent, staging, and airway evaluation
Blood tests
CBC, CRP, cultures
FNAC
Confirms abscess if suspected
Angioneurotic edema
Cellulitis
Lingual carcinoma
Lymphadenitis
Peritonsillar abscess
Salivary gland abscess
Sublingual hematoma
🔸 Goals
Secure airway
Control infection
Drain abscesses
Support nutrition and hydration
Technique
Notes
Fibre-optic nasotracheal intubation
Preferred; less invasive
Tracheostomy
Gold standard; risks: mediastinal spread, tracheal stenosis
Cricothyroidotomy
Emergency alternative; lower mediastinal risk
Blind nasal intubation (BNI)
Discouraged due to trauma and low success
IV access and fluid resuscitation
Empirical IV antibiotics, tailored to cultures:
Penicillin + β-lactamase inhibitor
Cephalosporins (2nd–4th gen)
Metronidazole for anaerobes
Steroids: May reduce edema
Analgesics and antipyretics
🔸 Incision & Drainage Principles (Topazian & Goldberg)
Incise in healthy skin, not at fluctuance
Use natural skin folds
Place incisions in dependent positions
Blunt dissection preferred
Insert drains; remove when output is minimal
🔸 Incision Sites
Bilateral submandibular incisions
Midline submental incision
~3–4 cm below mandibular angle, parallel to inferior border
Monitor airway and vitals
Nasogastric feeding if needed
Pain control and oral hygiene
Follow-up imaging for complications
Excellent with early diagnosis and intervention
Delayed treatment → airway obstruction, mediastinitis, sepsis, death
L – Laryngeal edema
U – Unerupted molars
D – Drooling
W – Wooden swelling
I – Infection (odontogenic)
G – Glossal elevation
S – Surgical drainage
Maxilla: Largest midfacial bone; forms orbit, nasal cavity, and hard palate.
Processes:
Frontal: Connects to forehead.
Zygomatic: Joins cheekbone.
Alveolar: Holds upper teeth.
Palatine: Forms roof of mouth.
Bone Composition:
Cancellous bone: Spongy, absorbs shock.
Compact bone: Hard outer layer, provides strength.
Facial Buttresses: Bone pillars that absorb and transmit force.
Vertical: Nasomaxillary, zygomaticomaxillary, pterygomaxillary.
Horizontal: Frontal bar, orbital rims, alveolar ridges, mandible border.
Le Fort I (Low-level fracture):
Horizontal fracture above teeth roots.
Separates upper jaw from midface.
Guérin fracture: Alternate name.
Often missed due to subtle signs.
Le Fort II (Pyramidal fracture):
Starts at nasal bridge, spreads downward.
Involves nasal bones, orbital rim, maxillary sinus.
Causes swelling, bruising, nasal flattening.
Dish-face deformity: Flattened midface.
Pseudotelecanthus: Eyes appear wide-set due to nasal swelling.
Le Fort III (Craniofacial dysjunction):
Complete separation of midface from skull.
Involves eye sockets, zygomatic arches.
Leads to full facial mobility, raccoon eyes, vision issues.
Enophthalmos: Sunken eyeball.
Diplopia: Double vision.
Le Fort IV:
Extension of Le Fort II/III into skull base.
May cause CSF leak (cerebrospinal fluid from nose).
Marciani’s Modification:
Adds subtypes to Le Fort fractures.
Accounts for mixed and complex patterns.
Le Fort I:
Swollen upper lip and cheek.
Bruising in mouth (buccal sulcus).
Guerin’s sign: Palatal bruising near greater palatine foramen.
Anterior open bite: Front teeth don’t meet.
Cracked pot sound: Hollow percussion sound.
Palatal fractures: Seen in 8–15%, may be sagittal or parasagittal.
Le Fort II:
Ballooning of midface.
Bilateral eye swelling, bruising (subconjunctival hemorrhage).
Depressed nasal bridge.
Nosebleeds (epistaxis), speech issues, CSF leak.
Infraorbital paresthesia: Numbness below eyes.
Le Fort III:
Severe swelling, raccoon eyes.
Entire midface mobile.
Vision problems: diplopia, enophthalmos, blindness.
Frontozygomatic tenderness: Pain at cheekbone-forehead junction.
CT Scan: Best imaging; shows coronal, axial, and 3D views.
Plain Radiographs:
Water’s view: Maxillary sinuses.
Caldwell view: Frontal sinuses.
Lateral view: Side profile.
Submentovertex view: Zygomatic arches.
Timing of Surgery
Immediate: For stable patients needing urgent repair.
Delayed (7–14 days): Allows swelling to reduce.
Too late: Risk of poor healing due to fibrosis.
Surgical Approaches
Le Fort I:
Transoral vestibular incision: Inside upper lip.
Crestal incision: Along gum line in edentulous patients.
Le Fort II & III:
Coronal incision: Across scalp.
Sinusoidal/saw-tooth incision: Modified coronal.
Subciliary/mid-eyelid/transconjunctival: Access to infraorbital rim; risk of scarring or ectropion (eyelid droop).
Reduction Techniques
Manual manipulation: For loose fractures.
Rowe’s Williams forceps: For impacted bones.
Hayton-Williams forceps: For palatal splits.
Fixation Methods
Indirect:
Suspension wires: Hold bones in place.
MMF (Maxillomandibular fixation): Jaw wiring for 4–6 weeks.
Direct:
Miniplates (1.3–2.0 mm): Metal plates for bone stabilization.
Transosseous wiring: Wire through bone holes.
Titanium mesh: For shattered bones.
Bone grafts: Replace missing bone.
Positioning: Upright to reduce swelling.
Avoid nose-blowing: Prevent orbital emphysema (air in eye socket).
Medications:
Nasal sprays, antibiotics, painkillers, steroids.
Avoid aspirin/NSAIDs (increase bleeding risk).
Wound Care:
Remove stitches in 5 days.
Use ice packs, sun protection.
Diet:
Soft food after healing.
Liquid diet during MMF.
Oral Hygiene:
Soft toothbrush, antiseptic rinses.
Eye Exercises: Prevent muscle imbalance and double vision.
Early
Heavy bleeding.
Airway blockage.
Infection.
CSF leak.
Blindness.
Late
Palpable hardware.
Non-union or malunion.
Plate exposure.
Lacrimal obstruction: Tear duct blockage.
V2 anesthesia: Numbness in cheek/upper lip.
Devitalized teeth.
Diplopia, enophthalmos, orbital misalignment.
Facial changes, nasal blockage, malocclusion.
A benign but locally invasive tumor of odontogenic (tooth-forming) epithelial origin.
Composed of proliferating odontogenic epithelium within a fibrous connective tissue stroma.
Unknown, but possible contributing factors include:
Trauma or inflammation
Oral infections
Tooth extractions or jaw injuries
Irritation from erupting third molars
Exact origin is uncertain; may arise from:
Epithelial rests of Serres or Malassez (remnants of tooth development)
Epithelial lining of odontogenic cysts, especially dentigerous cysts
Directly from oral epithelium
Conventional solid or multicystic – 94% of cases
Unicystic (mural) – 5%
Peripheral (extraosseous) – 1%
Most common epithelial odontogenic tumor
Accounts for 1% of all oral tumors
Mandible is affected more than maxilla (85% vs. 15%)
In mandible:
70% in molar–ramus area
20% in premolar area
10% in incisor region
In maxilla:
Usually in posterior region
Age group: Most common in 4th and 5th decades, but can occur in children or elderly
Early Stage:
Slow-growing and asymptomatic
Advanced Stage:
Expansion of cortical bone plates
Thinning and erosion of bone (egg shell crackling)
Invasion into soft tissues
Visible swelling causing facial asymmetry
May appear as solid, cystic, or mixed lesion
Dental signs:
Loosening or tipping of teeth
Involvement of inferior alveolar nerve
Draining sinuses
Unhealed extraction sockets with granulation tissue
Bleeding, trismus (jaw stiffness), and other dental complaints
Maxillary Ameloblastoma:
Nasal obstruction is often the first symptom
Can be potentially lethal due to:
Thin bone structure
Proximity to nasal cavity, sinuses, orbit, pharynx, and skull base
These factors also make complete surgical removal difficult
Osteolytic lesion (bone-destroying)
Appears as:
Unilocular (single cavity) or multilocular (multiple cavities) radiolucency
Honeycomb pattern: small loculations
Soap bubble pattern: large loculations
May show:
Expansion or destruction of cortical bone
Associated unerupted tooth (resembles dentigerous cyst)
Root resorption of adjacent teeth
Maxillary lesions often appear as monocystic cavities
Main Types:
Follicular ameloblastoma:
Resembles enamel organ
Has peripheral tall columnar cells (ameloblast-like) and central stellate reticulum-like cells
Plexiform ameloblastoma:
Epithelium forms a network of strands and cords
Same cell layers as follicular type
Variants of Follicular Type:
Cystic
Basal cell
Acanthomatous
Desmoplastic
Other odontogenic tumors:
Ameloblastic fibroma
Odontogenic myxoma
Non-odontogenic tumors:
Central giant cell granuloma
Aneurysmal bone cyst
Odontogenic cysts:
Dentigerous cyst
Odontogenic keratocyst
General Principles:
Treatment depends on site, size, and nature of the tumor
Ranges from conservative curettage to radical resection
Curettage:
Scraping out the tumor
Least preferred due to high recurrence
Tumor cells often extend beyond visible margins
En-block Resection:
Removal of tumor with a rim of healthy bone
Maintains jaw continuity
Effective for conventional ameloblastoma
Tumor invades cancellous bone, but rarely the compact bone’s haversian system
Segmental Resection:
Removal of a segment of jaw (e.g., hemimaxillectomy or hemimandibulectomy)
Most effective with lowest recurrence rates
Arises from the wall of a dentigerous cyst
Second most common pericoronal radiolucency
Can occur in other locations, not always linked to teeth
Represents 5% of all ameloblastomas
Affects younger patients (2nd–3rd decades)
Common in mandibular third molar region
May be associated with other cysts (radicular, primordial, residual, globulomaxillary)
Clinical Features:
Asymptomatic early on
Detected via routine radiographs
Slow enlargement, non-tender swelling
Bone destruction may cause soft areas on palpation
Radiographic Signs:
Haziness and thinning of radiopaque rim
Tumor invades cyst capsule and bone trabeculae
Management:
Before surgery, distinguish between unicystic and conventional types
During surgery:
Enucleate cyst
If mural mass found, mark it for pathology
If tumor has not penetrated basement membrane, no further surgery
If penetration is confirmed, perform curettage or bone removal
Regular follow-up is essential
Originates from:
Basal layer of oral epithelium
Extraosseous epithelial rests of Serres
Commonly affects gingiva and alveolar mucosa
More frequent in mandible than maxilla
Microscopically resembles acanthomatous basal cell carcinoma
Management: Simple excision
Behavior: Less aggressive than intraosseous types
Ossify: To turn into bone or bony tissue.
Fibroma: Benign fibrous tumor of connective tissue.
Ossifying Fibroma: A rare, benign fibro-osseous neoplasm of the jaw where normal bone is replaced by fibrous tissue and calcified products (bone, cementum, or both).
🦴 Common Sites
Mandible (especially below premolars/molars) > Maxilla.
Other craniofacial bones: Periorbital, ethmoid, sphenoid, temporal.
Origin: Odontogenic or periodontal ligament.
Central: Bone.
Peripheral: Gum.
HRPT2 gene mutation (tumor suppressor gene).
Triggers:
Trauma
Tooth extraction
Periodontal disease
Congenital impaired bone maturation
Swelling, deformity, teeth displacement
Slow-growing, wide age range
Female predilection
Small lesions: Asymptomatic, found radiographically.
Large lesions: Painless swelling of bone.
Well-defined, unilocular
May be radiolucent or show varying radiopacity
Root divergence, resorption
Large lesions: Downward bowing of mandibular cortex
Not encapsulated but well-demarcated
Fibrous tissue with mineralized material
Connective tissue: Collagen, fibroblasts, mitotic figures
Mineralized material: Bony trabeculae, cementum
Helps distinguish from fibrous dysplasia (more uniform bone pattern)
Condition
Key Feature
Fibrous dysplasia
Uniform bone pattern
Cemento-osseous dysplasia
Reactive, not neoplastic
Adenomatoid odontogenic tumor
Contains duct-like structures
Giant cell granuloma
Multinucleated giant cells
Calcifying odontogenic cyst
Ghost cells
Calcifying epithelial odontogenic tumor
Liesegang rings
Osteogenic sarcoma
Malignant, aggressive
Surgical resection, may require bone grafting
Good prognosis, rare recurrence
No malignant transformation
Benign gum swelling, common in teenagers/young adults
Origin: Periodontal ligament
F:M = 2:1
Sessile/pedunculated, red or mucosal-colored, painless, hard
Common site: Interdental papilla, maxillary incisor/canine region
Radiograph: Superficial bone erosion
Histology: Connective tissue, increased cellularity, calcifications (bone, cementum, dystrophic)
Treatment: Surgical excision or tooth extraction
Aggressive variant, 79% diagnosed before age 15
Equal gender distribution
Origin: Periodontal ligament
85% in facial bones, 12% calvarium, 3% extracranial
Mandible involved in 10%
Well circumscribed, locally aggressive, may disrupt cortex and adjacent structures
Subtypes:
🧱 Trabecular JOF (Desmo-osteoblastoma)
Children/adolescents
Maxilla > Mandible
Rapid bone expansion
May cause nasal obstruction, epistaxis
⚪ Psammomatoid JOF
More common than trabecular
Found in sinonasal/orbital bones
Psammoma-like ossicles
Symptoms: Proptosis, blindness, nasal obstruction, ptosis, ocular mobility issues
Aggressive behavior
Roy Eversol et al., Head Neck Pathol, 2008.
Neville BW et al., Oral and Maxillofacial Pathology.
Definition & Nature
Also called cemento-ossifying fibroma or cementifying fibroma.
A true neoplasm (tumor) with significant growth potential.
Composed of highly cellular fibrous tissue with varying amounts of abnormal bone or cementum-like material.
Previously classified separately based on dominant calcified material:
Bone-dominant: Ossifying fibroma.
Cementum-dominant: Cementifying fibroma.
Now grouped under cemento-ossifying fibroma due to similar microscopic appearance.
Juvenile Ossifying Fibroma
Aggressive variant occurring in the first two decades of life.
Rapid growth and potential for significant deformity.
Affects a wide age range, most common in 3rd–4th decades.
Female predilection.
Mandible is more commonly affected than maxilla.
Most common site: premolar–molar region.
Maxillary lesions often involve the antrum (sinus area).
Tooth displacement may be an early sign.
Small lesions: Asymptomatic, found on radiographs.
Large lesions: Painless jaw swelling, facial asymmetry, possible deformity.
Pain and paraesthesia (numbness) are rare.
Usually solitary, but multiple lesions may occur in rare cases or as part of hyperparathyroidism-jaw tumor syndrome.
Location
Found exclusively in facial bones, most commonly:
Mandible: Below premolars/molars, above inferior alveolar canal.
Maxilla: Canine fossa and zygomatic arch.
Periphery
Well-defined borders.
May have a thin radiolucent line (fibrous capsule).
Surrounding bone may show sclerotic border (dense bone reaction).
Internal Structure
Mixed radiolucent–radiopaque appearance.
Depends on type and amount of calcified material:
Bone-like: Wispy (cotton tuft) or flocculant (snowflake) pattern.
Cementum-like: Solid, amorphous radiopacities called cementicles.
Some lesions may appear mostly radiolucent with minimal calcification.
Effect on Surrounding Structures
Tooth displacement, inferior alveolar canal shift, and cortical bone expansion.
Outer cortical plate is thinned but remains intact.
Lamina dura (tooth socket lining) often missing.
Root resorption may occur.
In maxilla, lesion expands walls outward but maintains a bony partition between tumor and sinus.
Fibrous dysplasia
Periapical cemental dysplasia
Calcifying odontogenic cyst
Calcifying epithelial odontogenic tumor (Pindborg tumor)
Adenomatoid odontogenic tumor
Osteogenic sarcoma
Surgical enucleation or resection.
Large lesions: May require bone grafting.
Recurrence is uncommon after complete removal.
Good prognosis, no known risk of malignancy.
Most common fibro-osseous lesion.
Occurs in tooth-bearing areas of the jaws.
Not a neoplasm—considered a reactive or dysplastic process.
Classified into three types based on location and extent:
Focal
Periapical
Florid
Clinical Features
Involves a single site, usually posterior mandible.
90% of cases in females, mean age: 41 years.
Most common in American Blacks, followed by East Asians and Whites.
Asymptomatic, found on routine radiographs.
Lesion size: <1.5 cm.
Clinical Features
Affects periapical region of anterior mandible.
May be solitary or multiple, often bilateral.
Strong female predilection (10:1 to 14:1).
70% of cases in Black patients.
Age range: 30–50 years.
Associated teeth are vital (not infected or dead).
Radiographic Features
Epicenter at tooth apex or apical third.
Well-defined periphery, often with:
Radiolucent border
Surrounding sclerotic bone reaction
Shape: Round, oval, or irregular.
Effect on Surrounding Structures
Lamina dura is lost.
Periodontal ligament (PDL) space may appear widened or unclear.
Hypercementosis (excess cementum on roots) may occur.
No jaw expansion in small lesions.
Larger lesions may cause mild expansion with intact cortex.
Internal Structure – 3 Stages
Early Stage:
Bone replaced by fibrous tissue.
Appears as radiolucency at apex.
Mixed Stage:
Radiopaque material appears in radiolucent area.
Composed of cementum or abnormal bone.
May form cementicles (small calcified bodies).
Mature Stage:
Entire lesion becomes radiopaque.
Surrounded by a radiolucent margin.
May contain simple bone cysts.
Periapical rarefying osteitis (early stage)
Benign cementoblastoma (mixed/mature stage)
Odontoma
Diagnosis based on clinical and radiographic features.
No treatment required unless complications arise.
Biopsy risk: Poor vascularity may lead to secondary infection.
In cases of alveolar ridge atrophy, cementum may reach mucosa and cause ulceration under dentures.
If exposed, cementum must be surgically removed to prevent osteomyelitis.
Clinical Features
Multifocal involvement, not limited to anterior mandible.
Affects Black females, typically middle-aged to older adults.
Often bilateral and symmetrical.
May involve all four quadrants.
Usually asymptomatic, but may cause:
Dull pain
Sinus tract formation
Exposure of yellowish avascular bone
Jaw expansion
Radiographic Features
Bilateral lesions in both jaws.
Epicenter: Apical to teeth, usually posterior to cuspids.
In mandible: Above inferior alveolar canal.
Periphery
Well-defined, with sclerotic border.
Soft tissue capsule may be absent in mature lesions.
Effect on Surrounding Structures
Inferior alveolar canal may be displaced downward.
Maxillary sinus floor may be pushed upward.
Buccal and lingual cortical plates may expand.
Hypercementosis may fuse tooth roots with lesion.
Internal Structure
Varies from mixed radiolucent–radiopaque to fully radiopaque.
May show:
Cotton wool appearance: Small, fluffy opacities.
Amorphous calcifications: Irregular dense areas.
Simple bone cysts: Radiolucent areas that may enlarge or fill with dysplastic tissue.
Paget’s disease
Chronic sclerosing osteomyelitis
Secondary osteomyelitis
No treatment needed unless complications occur.
Emphasize oral hygiene to prevent infection.
Avoid odontogenic infections.
If denture pressure causes mucosal breakdown, exposed cementum must be removed surgically.
In severe cases, large areas of cementum may be removed, leaving minimal bone for prosthetics.
A developmental, tumor-like bone condition.
Characterized by replacement of normal bone with fibrous connective tissue and irregular bony trabeculae.
Often affects one side of the bone more than the other.
Two types:
Monostotic: Involves a single bone.
Polyostotic: Involves multiple bones.
Common in children and young adults.
75% of cases occur before age 30, especially between 3–15 years.
Polyostotic form often presents by age 10.
Affects males and females equally.
Non-hereditary, sporadic condition.
Caused by postzygotic mutation in the GNAS I gene (chromosome 20).
Mutation affects stem cells that become bone, skin pigment cells, and endocrine cells.
Severity depends on timing of mutation:
Early embryonic mutation → widespread bone involvement.
Later embryonic mutation → multiple bone lesions.
Postnatal mutation → single bone affected.
Often asymptomatic.
May present with:
Bone pain
Swelling
Bone deformity
Fractures
Skin pigmentation (café-au-lait spots)
Endocrine disturbances
Monostotic Fibrous Dysplasia
Involves one bone; accounts for 80–85% of cases.
Maxilla is more commonly affected than mandible.
Mandible is strictly monostotic.
Presents as painless swelling.
Maxillary lesions may extend to sphenoid, zygoma, occiput.
Polyostotic Fibrous Dysplasia
Involves two or more bones; 20–30% of cases.
Can affect up to 75% of the skeleton.
Common sites: femur, tibia, skull, facial bones, pelvis, ribs, spine, clavicle.
Often presents with café-au-lait pigmentation.
May be associated with endocrine disorders:
Sexual precocity
Pituitary adenoma
Hyperthyroidism
A form of polyostotic fibrous dysplasia.
Features:
Café-au-lait spots
Multiple endocrinopathies
Sexual precocity (especially in girls)
Menstrual bleeding in infancy
Breast and pubic hair development by age 4
Classic appearance: “ground-glass” opacity
Caused by disorganized, poorly calcified bone trabeculae.
Increased trabeculation → mottled, opaque appearance.
Tooth roots may be displaced or separated.
Bone replaced by fibrous tissue with irregular woven bone.
Trabeculae are immature, curved, and not lined by osteoblasts.
No capsule; blends into surrounding bone.
Usually no treatment needed—lesions often stabilize after puberty.
Surgical decompression for severe mass effect.
Bisphosphonates may reduce pain and fracture risk.
Radiation therapy is contraindicated due to risk of bone sarcoma.
Prognosis is generally good, but worse in:
Young patients
Polyostotic cases
Bone deformity
Fractures
Vision or hearing loss
Arthritis
Rare malignant transformation (e.g., osteosarcoma)
Ossifying fibroma
Ameloblastoma
Ameloblastic fibroma
Osteosarcoma
Hyperparathyroidism
A developmental odontogenic cyst that forms around the crown of an unerupted or impacted tooth.
Originates from fluid accumulation between the reduced enamel epithelium and the enamel surface.
The cyst is attached at the cementoenamel junction (CEJ) and encloses the crown within its lumen.
Also known as:
Follicular cyst
Pericoronal cyst
Second most common jaw cyst (after radicular cyst); accounts for ~20% of epithelial-lined jaw cysts.
Most common developmental odontogenic cyst.
Age: Typically seen between 10–30 years.
Slight male predilection.
More common in Whites than Blacks.
Mandible (67%) more affected than maxilla (33%).
Common sites:
Mandibular third molars
Maxillary canines
Maxillary third molars
Mandibular second premolars
Rare in deciduous teeth, but may occur due to inflammation from non-vital primary teeth.
May be associated with supernumerary teeth, odontomas, or syndromes like:
Cleidocranial dysplasia
Maroteaux-Lamy syndrome
Developmental Origin
Pressure from erupting tooth → venous obstruction → serum transudation.
Increased hydrostatic pressure separates the follicle from the crown.
Inflammatory Origin
Periapical inflammation from a non-vital primary tooth may affect the underlying permanent tooth germ, leading to cyst formation.
Small cysts: Asymptomatic; discovered on routine radiographs or when investigating delayed eruption.
Large cysts:
Painless jaw swelling
Facial asymmetry
Smooth, hard prominence
Eggshell crackling: Thin bone overlying cyst gives a brittle sound on palpation.
May interfere with dentures or cause ill-fitting prosthetics.
Infected cysts:
Pain, swelling, pus discharge.
Infection may spread from adjacent periapical or periodontal lesions.
Tooth displacement:
Teeth may be pushed into unusual positions (e.g., third molars into mandibular border or ramus; maxillary teeth into sinus or orbit floor).
Unilocular radiolucency associated with crown of unerupted tooth.
Well-defined, corticated borders unless infected.
Types of cyst-to-crown relationships:
Central (coronal): Crown projects symmetrically into cyst.
Lateral: Cyst grows along one side of crown/root.
Circumferential: Cyst surrounds crown and extends along root.
Root resorption of adjacent teeth may occur.
Tooth displacement can be significant.
Size criteria: Radiolucency >5 mm around crown suggests cyst; 3–4 mm may be a hyperplastic follicle.
Radiographic mimics: OKC, ameloblastoma, adenomatoid odontogenic tumor, ameloblastic fibroma.
Non-inflamed Cyst
Lining: 2–4 layers of non-keratinized stratified squamous epithelium.
Flat epithelium-connective tissue interface.
May resemble reduced enamel epithelium.
Connective tissue: Loosely arranged, rich in glycosaminoglycans.
May contain odontogenic epithelial rests.
Inflamed Cyst
Thickened fibrous wall, infiltrated by chronic inflammatory cells.
Epithelium may show:
Hyperplasia
Rete ridges
Squamous metaplasia
Keratinization (must be differentiated from OKC)
May contain:
Mucous cells
Ciliated columnar cells
Sebaceous cells
These reflect the multipotential nature of odontogenic epithelium.
Radiological:
Orthopantomogram (OPG): First-line imaging.
CT scan: For large or complex lesions.
Laboratory:
FNAC: May show straw-colored fluid.
Biopsy: For definitive diagnosis.
Odontogenic keratocyst (OKC)
Ameloblastoma
Adenomatoid odontogenic tumor
Ameloblastic fibroma
Periapical cyst
Osteoclastoma
Hyperplastic dental follicle
Small Cysts
Aspiration + incisional biopsy
Enucleation with or without tooth removal
If tooth eruption is possible:
Leave tooth in place
Remove part of cyst wall
May require orthodontic assistance
In children: Attempt to preserve tooth if root formation is complete
Large Cysts
Marsupialization:
Creates a surgical window to decompress cyst
Reduces bone defect size
Allows tooth eruption or facilitates later enucleation
Preferred in children or when tooth preservation is desired
Excellent with complete removal.
Recurrence is rare.
Tooth eruption may occur post-treatment, especially in younger patients.
Neoplastic transformation:
Ameloblastoma
Squamous cell carcinoma
Mucoepidermoid carcinoma (from mucous cells in cyst lining)
“A Silent Menace May Strike”
A = Ameloblastoma
S = Squamous cell carcinoma
M = Mucoepidermoid carcinoma
S = Secondary infection
Most commonly fractured facial bone due to its exposed position.
Can occur during trauma or as a complication of dental procedures.
Two broad categories:
Fractures without significant tissue loss.
Fractures with comminution and extensive tissue damage.
Mandible: U-shaped body with two rami.
Key landmarks: condylar process, coronoid process, mental foramen, mandibular foramen.
Muscles:
Elevators: masseter, temporalis, medial pterygoid.
Depressors: lateral pterygoid, digastric, mylohyoid, geniohyoid.
Nerves: mandibular nerve (CN V3), inferior alveolar nerve, mental nerve.
Blood supply: internal maxillary artery, inferior alveolar artery, mental artery.
By type:
Simple: closed, linear.
Compound: communicates with oral cavity or skin.
Comminuted: fragmented bone.
Pathological: due to diseased bone.
By site:
Condyle, coronoid, ramus, angle, body, parasymphysis, symphysis, dentoalveolar.
By cause:
Direct trauma, indirect trauma, muscular contraction.
Road traffic accidents.
Interpersonal violence.
Sports injuries.
Industrial trauma.
Falls.
Sudden muscular contraction (e.g., temporalis causing coronoid fracture).
Mandible accounts for ~61% of facial fractures.
Most common sites:
Body and subcondylar region.
Angle, dentoalveolar, ramus, symphysis, coronoid (less frequent).
Influenced by geography, social trends, legislation, and seasons.
General signs:
Swelling, pain, drooling, tenderness.
Bony discontinuity, lacerations.
Limited mouth opening, ecchymosis.
Displaced or fractured teeth, bleeding.
Site-specific signs:
Body: step deformity, lip paraesthesia, hemorrhage.
Symphysis/parasymphysis: sublingual hematoma, tongue control loss.
Angle: posterior gag, occlusion issues, molar step deformity.
Condyle:
Unilateral: TMJ swelling, ear bleeding, deviation on opening.
Bilateral: anterior open bite, restricted movement.
Coronoid: trismus, tragus tenderness, protrusion.
Extraoral radiographs:
Oblique lateral, posterior-anterior, reverse Towne’s.
Intraoral radiographs:
Periapical, occlusal.
Desirable imaging:
Panoramic tomography, CT scan.
Initial care:
Airway protection.
Soft tissue repair.
Pain and infection control.
Nutrition support.
Definitive treatment:
Reduction:
Open: surgical exposure.
Closed: non-surgical.
Immobilization:
Rigid: plates, screws.
Non-rigid: splints, wiring.
Primary healing:
No callus formation.
Requires rigid fixation and minimal gap.
Heals via contact or gap remodeling.
Secondary healing:
Callus formation.
Occurs with mobility at fracture site.
Progresses through hematoma → granulation → cartilage → bone.
Risks:
Infection via periodontal membrane.
Pulp necrosis.
Pre-existing pathology.
Indications for removal:
Absolute:
Root fracture, dislocation, periapical infection, infected fracture line, pericoronitis.
Relative:
Non-functional teeth, advanced caries or periodontal disease, delayed presentation.
Management of retained teeth:
Radiographic assessment.
Antibiotics.
Splinting if mobile.
Endodontic therapy if pulp exposed.
Extraction if infection develops.
Depends on:
Fracture site.
Retained teeth.
Patient age.
Infection status.
Example:
Angle fracture in young adult: 3 weeks.
Add 1 week for retained tooth or symphysis fracture.
Add 1–2 weeks if age ≥ 40.
Subtract 1 week for children.
Without intermaxillary fixation:
Compression plates, mini plates, lag screws.
With intermaxillary fixation:
Arch bars, eyelet wiring, cap splints.
Combined methods:
Transosseous wiring, bone clamps, external pin fixation.
Indications:
Favorable, non-displaced fractures.
Pediatric cases.
Condylar fractures.
Advantages:
Low cost, short procedure, local anesthesia possible.
Disadvantages:
Less stability, hygiene challenges, TMJ complications.
Techniques:
Arch bars, Ivy loops, Essig wire, IM screws, splints.
Indications:
Unfavorable or unstable fractures.
Edentulous mandible with displacement.
Delayed cases with soft tissue interposition.
Can be used for rigid or non-rigid fixation.
Children:
Resilient bone, high tooth-to-bone ratio.
Consider growth potential and dentition stage.
Edentulous patients:
Reduced blood supply and healing capacity.
Use gunning splints, bone plates, wiring.
Infection, malunion, non-union.
TMJ ankylosis, nerve damage.
Displaced teeth, periodontal issues.
Limited mouth opening, scar formation.
Causes include poor technique, inadequate immobilization, soft tissue interposition.
Second most common oral neoplasm after squamous cell carcinoma.
Major glands (parotid, submandibular, sublingual): 80–85% of cases
Of these, 75–80% are benign.
Minor glands (palate, lips, buccal mucosa): 15–20%
Only 50–55% are benign.
Parotid gland: Most common site overall; majority are benign pleomorphic adenomas.
Palate: Most common site for minor gland tumors.
Children: Most common malignancy is mucoepidermoid carcinoma.
Sublingual gland tumors: Rare but most likely to be malignant.
🟢 Benign Tumors
Mixed Tumor: Pleomorphic adenoma
Monomorphic Adenomas:
Basal cell adenoma (solid, tubular, trabecular, membranous)
Canalicular adenoma
Myoepithelioma
Oncocytoma
Warthin’s tumor (papillary cystadenoma lymphomatosum)
Sebaceous adenoma
Ductal Papillomas:
Sialadenoma papilliferum
Inverted ductal papilloma
Intraductal papilloma
🔴 Malignant Tumors
Low-grade: Mucoepidermoid carcinoma (low), polymorphous low-grade adenocarcinoma, acinic cell carcinoma, clear cell carcinoma, basal cell adenocarcinoma
Intermediate-grade: Mucoepidermoid carcinoma (intermediate), epimyoepithelial carcinoma, sebaceous adenocarcinoma
High-grade: Mucoepidermoid carcinoma (high), adenoid cystic carcinoma, carcinoma ex-pleomorphic adenoma, salivary duct carcinoma, squamous cell carcinoma, oncocytic adenocarcinoma
⭐ Pleomorphic Adenoma
Most common benign tumor of salivary glands
Origin: ductal + myoepithelial cells
Sites: parotid (60–70%), submandibular (40–60%), minor glands (40–70%)
Age: 30–50 years; M:F = 3:2
Clinical: Painless, slow-growing, firm, mobile → becomes nodular
Pathology:
Gross: Well-encapsulated, tan-white, glossy
Microscopy: Ductal + myoepithelial cells, variable glandular patterns, no mitoses
Treatment: Surgical excision with margin; avoid enucleation
Prognosis: >95% cure rate; 5% risk of malignant transformation
⭐ Canalicular Adenoma
Site: Upper lip (81%), buccal mucosa
Age: 7th decade; F:M = 1.2–1.8:1
Clinical: Slow-growing, painless, bluish or normal mucosa, may mimic mucocele
Pathology:
Gross: Encapsulated or circumscribed, pink-tan, cystic spaces
Microscopy: Bilayered cords (“party wall”), papillary projections, vascular stroma
Treatment: Local excision
Prognosis: Excellent; recurrence rare
⭐ Myoepithelioma
Site: Parotid > minor glands > submandibular
Age: Median 53 years; both genders
Clinical: Painless, circumscribed mass
Pathology:
Microscopy: Spindle or plasmacytoid cells; S-100, actin, cytokeratin positive
Treatment: Conservative excision or superficial parotidectomy
Prognosis: Excellent
⭐ Warthin’s Tumor
Site: Tail of parotid gland
Age: 6th decade; M:F = 7:1
Clinical: Soft, painless swelling
Pathology: Papillary epithelial projections + lymphoid stroma with germinal centers
Treatment: Simple surgical excision
Prognosis: Excellent
Histology: Double-layered ductal epithelium, oncocytic appearance, inflammatory infiltrate
Treatment: Conservative excision
Prognosis: Recurrence rare
🔺 Mucoepidermoid Carcinoma
Most common salivary malignancy
Sites: Parotid (60–90%), palate
Clinical:
Low-grade: Painless, slow-growing
High-grade: Rapid growth, ulceration, facial palsy
Pathology:
Low-grade: Mucinous fluid, encapsulated
High-grade: Solid, invasive; few mucinous cells
Treatment:
Low-grade: Superficial parotidectomy
High-grade: Total parotidectomy ± nerve resection, neck dissection, radiation
Prognosis:
Low-grade: 95% survival
High-grade: ~40% survival; 60% recurrence/metastasis
🔺 Acinic Cell Carcinoma
Site: Parotid (90–95%), submandibular
Age: 5th decade; more common in women
Clinical: Slow-growing, sometimes painful; bilateral in 3%
Pathology: Acinar-like cells + clear cells; lymphocytic infiltration
Treatment: Superficial parotidectomy or gland removal
Prognosis: 50% survival at 20 years
🔺 Adenoid Cystic Carcinoma
Site: Submandibular + minor glands (50%)
Age: 5th decade; M = F
Clinical: Firm mass, pain, facial palsy, mucosal ulceration, bone invasion
Pathology: Small cuboidal cells, pseudocystic spaces, dense chromatin
Treatment: Wide excision ± radiation; chemotherapy limited
Prognosis:
5-year survival: ~70%
15-year survival: ~10%
High recurrence (16–85%)
🔺 Polymorphous Low-Grade Adenocarcinoma
Site: Minor glands (palate)
Age: 50–70 years
Clinical: Firm, non-ulcerated, painless swelling
Pathology: Uniform cells, perineural invasion, trabecular cords
Treatment: Wide excision; neck dissection if nodes involved
Prognosis: Excellent; ~10% recurrence
80% of parotid tumors are benign
80% of those are pleomorphic adenomas
80% of pleomorphic adenomas occur in parotid
80% of parotid pleomorphic adenomas are in superficial lobe
80% of untreated pleomorphic adenomas remain benign