oral medicine/oral pathology

lecture given 8/19/2026

pathology

the study of diseases

histopathology

the stidy of stained slides

pathosis

individual disease entity

pathoses

multiple disease entities

pediatric dentist / general dentist

recognizes normal vs abnormal, refers when necessary, sometimes performs biopsies

oral and maxillofacial radiologists

the expert in diagnosis via imaging

oral and maxillofacial pathologist

the expert in diagnosis via histopathology, sometimes performs biopsies

oral medicine

the expert in diagnosis via lab tests, treating with medicine, performs biopsies

oral and maxillofacial surgery

the expert in treating with surgery, performs biopsies

periodontist

performs biopsies

orofacial pain

the expert in pain and sensory disturbances

epstein pearls

benign keratin filled cysts from epithelium entrapped during fusion of the palatal shelves

along the midpalatal raphe (midline of hard palate)

1-3mm firm white-yellow nodules, single or in clusters

asymptomatic

present in 60-85% of newborns

self-resolve in weeks

epstein pearls

bohn nodules

keratin filled cysts, remnants of odontogenic epithelium/mucous gland origin

buccal/linugal gingival (alveolar) surfaces and palate away from the raphe

small symptomatic white nodules

rupture spontaneously within weeks to months

bohn nodules

gingival cysts of the newborn / dental lamina cysts

inclusion cysts from epithelial remnants of the dental lamina during tooth development

crest of the alveolar ridge, usually anterior maxilla

small (1-3mm) whitish/translucent cystic nodules, often mutliple

asymptomatic

self resolve

gingival cysts of the newborn / dental lamina cysts

eruption cyst

soft tissue dentigerous type cyst, dental follicle separates from the crown of an erupting tooth

overlying the erupting primary tooth (mandibular alveolar ridge common)

dome shaped bluish/translucent swelling

may become an eruption hematoma

can impair feeding/latching

usually self resolves as tooth erupts, surgical marsupialization/excison if feeding interference or pain

eruption cyst

congenital epulis (neumann tumor/congenital granular cell tumor)

rare benign tumor, likely mesenchymal origin

granular cell histology, distinict from adult granular cell tumor (S100-negative)

anterior maxillary alveolar ridge > mandible

pedunculated, smooth, mucosal colored mass

female predominance (~8:1)

large lesions impair feeding/rarely breathing

surgical excision (curative, no recurrence, no dentition change)

small asymptomatic lesions may be observed, some spontaneous resolution noted

congenital epulis (neumann tumor/congenital granular cell tumor)

melanotic neuroectodermal tumor of infancy (MNTI)

rare neural crest-derived, benign but locally aggressive pigmented tumor

anterior maxilla most common (~60%), then skull, mandible

infants <1 yr

rapid enlarging expansile pigmented mass

osteolytic with tooth displacement on imaging, can mimic an eruption cyst

MRI/CT + complete surgical excision/enucleation

can disrupt tooth development

melanotic neuroectodermal tumor of infancy (MNTI)

natal and neonatal teeth

~all are mandibular central incisors (<10% supernumerary)

often mobile with hypoplastic enamel/poor root formation

retain if stable, extract if excessively mobile (aspiration risk) or supernumerary

radiograph to distiguish primary vs supernumerary

may cause breast trauma during feeding- can smooth, cover with composite, use breast shield, switch to formula, or extract

natal teeth

present at birth

neonatal teeth

erupt within first 30 days

natal / neonatal teeth

riga fede disease

insensitivity to pain

benign traumatic ulceration of oral mucosa from repetitive rubbing against primary teeth in infants

typical presentation- healthy infant (6-15 mo), ulceration of ventral tongue (can become firm scar tissue), coincides with tooth erutpion, responds to conservative treatment (smoothing tooth edges, protective barriers)

red flag for extensive RFD- involves both lip and tongue, fails to respond to treatment, suspect underlying pain insensitivity syndrome

riga fede disease

autism spectrum disorder- self injurious behavior

affects 26-50% of individuals with ASD

pain paradox- many individuals show pain hypersensitvity not indifference, pain perception is highly variable, variability relates to perceptual noise rather than consistently elevated thresholds

oral manifestations- biting lips, tongue, buccal mucosa, hands, self extraction of teeth, mouthing objects causing mucosal trauma, higher rates of dental trauma and bruxism

SIB in ASD is often a response to pain or distress elsewhere

what can cause oral ulcerations?

recurrent aphthous stomatitis (RAS)

periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis (PFAPA) syndrome

inflammatory bowel disease (IBD)

celiac disease

hand, foot, mouth disease

herpangina

erythema multiforme (EM)

reactive infectious mucocutaneous eruption (RIME)

cyclic neutropenia

herpes simplex virus (HSV)

minor recurrent aphthous stomatitis

80% of cases

<1cm

located on nonkeratinized mucosa

lasts 7-10 days, no scar

major recurrent aphthous stomatitis

10-15% of cases

>1cm

located on lips, oropharynx, soft palate

lasts >4 weeks, often scars

herpetiform recurrent aphthous stomatitis

5-10% of cases

mutliple 0.1-0.3cm

located on nonkeratinized mucosa

lasts 7-14 days, no scar

what is the clinical appearance of all recurrent aphthous stomatitis lesions?

painful round/oval ulcer with gray-white fibrin base and erythematous halo

recurrent aphthous stomatitis

what is the pathophysiology of recurrent aphthous stomatitis?

mostly idiopathic but can be related to underlying systemic conditions

mutlifactorial T cell mediated immune dysregulated disease

children with affected parents have 90% chance of developing

underlying systemic conditions: celiac disease, behcet disease, IBD, iron deficiency anemia, cyclic neutropenia, PFAPA syndrome

periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis (PFAPA) syndrome

most common periodic fever syndrome in children, particularly in non-mediterranean populations

usually manifest before age 5

clusters in families → autosomal dominant inheritance

hallmark: remarkably regular periodicity- typically ever 3-8 weeks (mean 28 days/4 weeks), parents can often anticipate the next episode

each episode is characterized by- high fever (39-41 C) lasting 3-7 days, pharyngitis (most frequent symptom, ~89% of pts), cervical adenitis, apthous stomatitis

key clinical recognition points: between episodes completely well with normal growth and development, episodes abort dramatically with a single dose of corticosteroids, negative infectious workup during episodes, elevated CRP and mild leukocytosis during attacks, normal between episodes

pathophysiology- innate immune dysregulation, RAS-PFAPA-Behcet spectrum all have shared susceptibility loci, 10-30% of adult behcet’s disease patients may have had PFAPA-like sypmtoms in childhood

periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis (PFAPA) syndrome

inflammatory bowel disease (IBD)

crohn disease (patchy in small and large bowel) and ulcerative colitis (uniform colon) - increasingly common in children and adolescents

25% diagnosed before the age of 20

primarily affects the intestinal tract

up to 50% of ped pts with IBD present with oral manifestations

oral manifestations can appear before GI symptoms by months or years

what are the oral manifestations that are highly specific for IBD (particularly crohn disease)?

indurated mucosal tags

cobblestoning

deep linear ulcerations with vertical fissures

lip swelling with vertical fissures

mucogingivitis

what are the oral manifestations that are highly suspicious for IBD?

pyostomatitis vegetans- snail track pustules, more specific for UC, considered virtually pathognomonic for IBD when present

what are the oral manifestations that are non specific for IBD (occur in both CD and UC)?

aphthous stomatitis- most common oral manifestations

angular chelitis- more common in UC

atrophic glossitis

periodontitis

oral manifestations of IBD

celiac disease

chronic immune-mediated systemic disorder caused by ingestion of gluten found in wheat, rye, and barley

affects approx 1% of children- up to 90% of pts are undiagnosed

GI: diarrhea, bloating, weight loss, abdominal pain

oral symptoms may be the only presenting symptoms in some pts

symmetric enamel defects + ulcers are highly suspcious, esp with any growth concerns or family history

what are the key oral manifestations of celiac disease?

oral ulcerations, dental enamel defects, delayed dental eruption, hyposalivation, atrophic glossitis and geographic tongue, oral dysesthesia/glossodynia, angular chelitis- related to iron and vitamin B deficiencies

why is it important for celiac disease to be diagnosed early?

initiation of gluten free diet may prevent progression of oral manifestions

established enamel damage is irreversible

oral manifestions of celiac disease

hand, foot, and mouth disease

common, highly contagious viral illness- predominantly affects children <5 yr

causative agents- coxsackievirus A16, A6, A10, enterovirus 71

transmission- fecal oral, oral oral, respiratory droplets

seasonality- spring to fall outbreaks

incubation is 3-6 days, self limited illness resolving in 7-10 days

clinical presentations of hand, foot, and mouth disease

prodrome- low grade fever, malaise

oral enanthem- painful vesicles → shallow ulcers on buccal mucosa, tongue, hard palate

cutaneous exanthem- paulovesicular rash on palms, soles, may involve buttocks, knees, elbows

delayed sequelae (weeks later)- onychomdesis (nail shedding), beau’s lines, palmoplantar desquamation

hand, foot, and mouth disease

how can you distinguish hand, foot, and mouth disease from herpangina? (characteristics of HFMD)

anterior oral ulcerations- buccal mucosa, tongue, lips

skin rash on hands, feet, and buttocks

causative agents- same enteroviruses (CVA16, CVA6, EV71)

how can you distinguish hand, foot, and mouth disease from herpangina? (characteristics of herpangina)

posterior oral ulcerations- soft palate, uvula, tonsils, pharyngeal folds

no skin rash

causative agents- same enteroviruses (CVA16, CVA6, EV71)

CVA6 associated hand, foot, and mouth disease can present with…

more extensive and atypical features

more extensive vesicobullous eruptions

widespread distribution beyond hands/feets

eczema coxsackium (localizes to atopic dermatitis areas)

high fevers, more severe pain

more common in adults

hand, foot, and mouth disease

erythema multiforme (EM)

acute, immune mediated mucocutaneous reaction

mean age in children is 5.6 yr

EM minor- skin only

EM major- skin and mucosal involvement

self limiting, long term sequelae rare

triggers- infecitons are the primary triggers (unlike SJS which is drug induced), HSV 17.9%, mycoplasma pneumoniae 15.7%, drugs 24.1%, vaccines 3.2% overall (most common trigger in infants)

recurrent EM: 61% HSV- associated

how can you distinguish EM vs RIME (reactive infectious mucocutaneous eruption)? (EM symptoms)

raised target lesions (3 rings)

prominent, acral distribution on skin

variable on mucosa (minor none, major > 2 sites)

HSV ~70% common trigger

young adults

how can you distinguish EM vs RIME (reactive infectious mucocutaneous eruption)? (RIME symptoms)

prominent mucositis

minimal or absent on skin

always prominent on mucosa (oral, ocular, genital)

mycoplasma, other respiratory pathogens are common trigger

children/adolescents

oral and cutaneous lesions of erythema multiforme?

hallmark target lesions with 3 concentric zones

symmetric acral distribution (hands, feet, extensor surfaces)

fixed lesions > 7 days

spread centripetally

oral cavity = most commonly affected mucosal site

vesicles → painful, irregular erosions

non-keratinized mucosa- lips, buccal mucosa, ventral tongue

hemorrhagic crusting of vermilion border

gingiva typically spared (distinguishes from primary HSV)

resolves in 2-3 weeks without scarring

erythema multiforme

cyclic neutropenia

rare autosomal dominant hematologic disorder

usually diagnosed within first year of life

characterized by ~21 day cycles of severe neutropenia (ANC <200/uL) lasting 3-6 days

cycle length can range from 14-36 days in ~30% of pts

pts are completely well between episodes

during neutropenic nadir (lowest time)- recurrent fever, aphthous ulcers, gingivitis, pharyngitis, skin infections

more severe in children than adults

what are the oral manifestations of cyclic neutropenia?

>60% experience oral ulcerations, gingivitis, tooth abscesses >5 times/year

ulcers appear at predictable ~21-day interval

severe, progressive periodontal disease disproportionate to age/hygiene

permanent tooth loss from chronic gingivitis, recurrent abscesses, and alveolar bone loss in adolescence/young adulthood is common

cyclic neutropenia

primary herpes simplex virus (acute herpetic gingivostomatitis)

HSV1 » HSV2

6 mo to 5 yrs

cervical LAD, chills, fever of 101-103F, nausea, anorexia, irritability

oral manifestations- severe pain, pinhead vesicles, collapse and coalesce into an ulcer, keratinized tissue

lasts 5 days to 2 weeks

primary herpes simplex virus (acute herpetic gingivostomatitis)

secondary (recurrent herpes simplex virus; herpes labialis)

site of primary inoculation or adjacent

herpes labialis = cold sore = fever blister (15-45% of US)

prodrome: itching, tingling, warmth, erythema (6-24 hrs)

vesicles rupture and crust within 2 days- highly transmissible when vesicles rupture- avoid manipulation until scabbed

secondary (recurrent herpes simplex virus; herpes labialis)

soft tissue masses

mucocele

ranula

fibroma

squamous papilloma

verruca vulgaris

multifocal epithelial hyperplasia

pyogenic granuloma

peripheral ossifying fibroma

peripheral giant cell granuloma

juvenile spongiotic papillary gingival hyperplasia

leukemia

mucocele

extravasation pseudocyst from trauma to a minor salivary gland duct, no epithelial lining

lower lip most common

soft, dome shaped, bluish-to-translucent swelling, fluctuates in size

surgical excision to muscle layer (remove associated gland)

what is this, and why is the lesion blueish?

mucocele

tyndall effect

ranula

mucocele of the sublingual gland

floor of the mouth- lateral to midline

plunging- submandibular/cervical swelling (herniates through mylohyoid into neck)

soft bluish translucent floor of mouth swelling; can enlarge and impair feeding/speech

treatment must address the sublingual gland- marsupialization, sublingual gland excision, untreated lesions may become plunging ranulas

ranula

fibroma (irritation/traumatic fibroma & giant cell fibroma)

reactive fibrous hyperplasia from chronic mucosal trauma (traumatic/irritation fibroma)

buccal mucosa at line of occlusion, lateral tongue, lips

giant cell fibroma is a distinct variant not clearly linked to irritation

giant cell fibroma favors tongue, gingiva, alveolar mucoas (retrocuspid papilla)

firm, smooth, sessile or pedunculated, pink asymptomatic nodule

giant cell fibroma may be papillary/bosselated

conservative surgical excision; remove the source of trauma

fibroma (irritation/traumatic fibroma & giant cell fibroma)

squamous papilloma

benign HPV associated epithelial neoplasm (HPV6/11)

in infants consider caregiver- fetal/neonatal transmission, in older children autoinoculation

soft palate/uvula, tongue, lips, gingiva

solitary, soft, exophytic, pink to white cauliflower/finger like front surface

usually 1cm, painless

simple surgical excision (curvative), recurrence uncommon

squamous papilloma

verruca vulgaris (oral wart)

HPV driven (commonly HPV2 and 57) benign hyperkeratotic lesion

often autoinoculated from skin warts (finger sucking, nail biting)

keratinized surfaces- labial mucosa, anterior tongue, gingiva, hard palate

painless, white, papillary/verrucous hyperkeratotic papule, may be multiple, more heavily keratinized than squamous papilloma

excision or destructive therapy (cryotherapy, cautery, laser), look for and treat concurrent skin warts

verruca vulgaris (oral wart)

multifocal epithelial hyperplasia (heck disease)

benign HPV-driven epithelial proliferation (HPV13 and 32), transmitted via salivary contact, strong genetic/familial predisposition

2-13 yrs

female predominance (~4:1- 5:1)

endemic in indigenous populations (native americans, central/south americans, inuit/yupik)

immunosuppression/HIV and low SES

labial mucosa, buccal mucosa, and tongue

multiple soft, painless, sessile papules/nodules 1-10mm, pink to mucosa-colored (occasionally whitish), papulonodular or papillomatous, may coalesce into plaques, usually asymptomatic

often non- spontaneous regression (mean 18 mo)

treat for cosmetic/functional/traumatic reasons via excision, cryotherapy, CO2 laser, or topical agents

multifocal epithelial hyperplasia (heck disease)

pyogenic granuloma (lobular capillary hemangioma)

reactive vascular proliferation (not pyogenic, not granulomatous)

triggered by trauma/irritation/hormones

gingiva » lips, tongue, buccal mucosa

rapidly growing, friable red/purple papule or nodule that bleeds easily, may ulcerate

excision with removal of irritant- laser, sclerotherapy, cryotherapy, and topical timolol in children, recurrence ~0-15%

pyogenic granuloma (lobular capillary hemangioma)

peripheral ossifying fibroma (POF)

reactive gingival lesion with fibroblastic proliferation and mineralization (bone/cementum) product

thought to arise from periodontal ligament

may represent maturation of a PG

gingiva exclusively, typically interdental papilla, anterior maxilla common

peaks in adolescents/young adults

firm, sessile or pedunculated gingival nodule, pink to red, may ulcerate

excision down to periosteum/PDL with scaling of adjacent teeth; recurrence higher than the other Ps if base is not fully removed

peripheral ossifying fibroma (POF)

peripheral giant cell granuloma (PGCG)

reactive lesion of multinucleated giant cells arising from periosteum/PDL, often after local trauma

gingiva/alveolar ridge only (anterior to molars), can occur on edentulous ridge

red to bluish purple, sometimes ilcerated gingival nodule

may cause superficial cupping bone resorption

must exclude a brown tumor of hyperparathyroidism if multiple/recurrent

excision to the periosteum with removal of local irritants

peripheral giant cell granuloma (PGCG)

parulis

nodule of inflamed granulation tissue at the mucosal opening of a draining sinus tract from an underlying odontogenic infection

attached/alveolar gingiva or vestibular mucosa overlying ot apical to the offending tooth

small yellow-red papule/nodule that may intermittently discharge pus and recur

often relatively painless once draining

pulpectomy/pulpotomy or extraction of the offending tooth

parulis

localized juvenile spongiotic gingival hyperplasia

distinct benign reactive inflammatory gingival lesion- not plaque induced

anterior maxillary (labial) gingiva, usually unifocal

mean age ~13-16 yr

slight female predominance

bright red, well demarcated, finely granular/papillary enlargement, bleeds easily

persists despite excellent oral hygiene and debridement

surgical excision is most common (cryotherapy/laser alternatives), recurrence can occur

localized juvenile spongiotic gingival hyperplasia

leukemia

most common pediatric malignancy

oral changes result from direct leukemic infiltration and/or marrow failure (thrombocytopenia, neutropenia)

may be the first presenting sign

gingiva » palate, tongue, buccal mucosa

diffused boggy gingival enlargement (begins at interdental papillae), spontaneous gingival bleeding, petechiae, mucosal pallor, ulceration

systemic signs: fever, fatigue, lymphadenopathy, hepatosplenomegaly

non-plaque gingival enlargement with bleeding in a child warrants urgent CBC and hematology referral

leukemia

vascular and lymphatic pathoses

hemangioma

lymphatic malformation

hemangioma

positive on diascopy

require doppler US prior to excision- high flow v low flow

congenital hemangioma- RICH, PICH, NICH

infantile hemangioma- rapidly grows, plateaus, then involutes by school age

hemangioma

infantile hemangioma

most common benign vascular tumor of infancy, from endothelial cell proliferation

usually not present at birth (a pale macule/telangiectatic patch may herald it)

rapid proliferation over the first 1-3 mos, then slow involution over years

lips, buccal mucosa, and tongue

associated with female sex, prematurity, low birth weight

bright red superficial (strawberry) or bluish deep component

most need only observation/reassurance- medical management with oral propranolol, topical timolol or laser/surgery for residual changes

infantile hemangioma

lymphatic malformation (microcystic lymphangioma / macrocystic cystic hygroma)

low flow congenital vascular malformation of maldeveloped lymphatic channels

not a tumor and does not involute

childre <2yr, ~50% present at birth

~75% in head/neck, oral cavity, oropharynx, and tongue commonly involved

large lesions cause macroglossia, airway obstruction, and dysphagia

mucosal microcystic lesions = clusters of clear or dark purple frog egg vesicles that leak chyle or blood

classified macrocystic (>1-2cm), microcystic (<1-2cm), or mixed

complications- intralesional bleeding, infection, sudden enlargement

doppler ultrasound, MRI

multidisciplinary and individualized- observation (spontaneous regression is possible, mainly macrocystic), sclerotherapy, surgical resection/debulking, CO2 laser, systemic sirolimus (mTOR inhibitor) alpelisib (PI3K inhibitor)

lymphatic malformation (microcystic lymphangioma / macrocystic cystic hygroma)

both are macro