Oral lesions - lecture 4 Flashcards
cancer of oral cavity associated with what?
ulcers or masses that don’t heal
how do tongue and lip cancers present?
as exophytic (outward growth) or ulcerative lesions
what should be biopsied?
Persistent papules, plaques, erosions, or ulcers
what accounts for 80% of squamous cell carcinoma of head and neck? (HINT: 2)
use of tobacco and ETOH
aphthous stomatitis also called?
canker sore
what is aphthous stomatitis?
- Painful oral lesions
- Sometimes genital
- Repeated development
where is aphthous stomatitis most common?
Middle East and south asia
what is the most common acute oral lesion?
aphthous stomatitis
when do you first develop aphthous stomatitis and when does it wane?
first develop during adolescence and wanes with increasing age
classification of aphthous stomatitis
simple (mikulicz) & complex
simple (mikulicz) aphthous stomatitis
- Several episodes per year
- One to several lesions
- Lasting up to 14 days
- Limited to oral mucosa
- Most common form of disease
complex aphthous stomatitis
- Oral and genital
- More numerous lesions
- Larger than 1 cm
- Takes 4-6 weeks to resolve
- So frequent that patients almost always have them
which canker sore is seen only on the oral mucosa?
simple (mikulicz) aphthous stomatitis
which canker sore is seen on oral mucosa and genital?
complex aphthous stomatitis
what has more lesions, simple or complex aphthous stomatitis?
complex - has numerous lesions vs simple has one to several
what takes longer to resolve, simple or complex aphthous stomatitis?
complex - 4-6 weeks
simple - lasts up to 14 days
what is most common form of aphthous stomatitis, complex or simple?
simple
morphology of aphthous stomatitis
- Minor ulcers <1 cm
- Major ulcers >1cm
- Herpetiform are 1-2 cm typically in clusters
pathogenesis of aphthous stomatitis
- immune dysregulation
- exaggerated pro-inflammatory process
- weak anti-inflammatory response
- instigated by antimetabolites like methotrexate
- vit B12, folic acid, iron deficiency
- neutropenia of any cause
what can exacerbate aphthous stomatitis?
certain foods
what is aphthous stomatitis seen in, in terms of disease?
bowel disease (celiac, IBD, chron's) -conditions that decrease mucosal thickening
risk factors of aphthous stomatitis
- Smoking cessation
- Familial tendency
- Trauma
- Dental cleaning (from trauma)
- Hormonal factors (Progestin level fall in luteal phase of menstrual cycle)
- Emotional stress
- Food or drug hypersensitivity
- Immunodeficiency (HIV)
clinical presentation of aphthous stomatitis
- one to five lesions
- round to oval
- clearly defined ulcers
- yellowish center
- small (1-3 cm)
- erythematous rim
- painful
dx of aphthous stomatitis
- Patient history and PE
- History of recurrent self-limited oral ulcers
- Biopsy not needed
oral hygiene for management of aphthous stomatitis
non-alcohol mouthwash and soft toothbrush
pain control for management of aphthous stomatitis
- Viscous lidocaine (swish & spit)
- Diphenhydramine liquid (swish & spit)
- Dyclonine lozenges
second-line/refractory txts for aphthous stomatitis
Topical steroids:
- dexamethasone elixir (swish & spit)
- clobetasol gel
- traimcinolone paste
Management for complex aphthous stomatitis
- Intralesional or oral steroids for recalcitrant lesions or severe disease
- Colchicine
- Dapsone (aczone)
- Pentoxifylline (bronchodilator and immunomodulator)
- Thalidomide in HIV patients
thalidomide med for complex aphthous stomatitis
for HIV patients with aphthous stomatitis
- recurrent after cessation of therapy
- cat X
- can only be rx thru special program
oral leukoplakia
- benign reactive process (can develop oral cancer)
- early step in transformation of premalignant lesions from hyperplasia -> dysplasia -> carcinoma in situ -> invasive malignant lesions
what does oral leukoplakia’s clinical significants depend on?
degree and presence of dysplasia
oral leukoplakia epidemiology
- men>women
- association w/HPV
- similar to SCC
- common in smokeless tobacco users (chew)
- seen in pure inflammatory conditions not associated with malignancy
oral leukoplakia clinical manifestations
- leukoplakia lesions that show up in trauma prone regions where mucosa is thicker (cheek and dorm of tongue)
- NOT painful (vs thrush is)
- white/grey lesions
- flat & no well defined
- can’t scrape off (vs thrush can)
thin areas of mucosa show more what in oral leukoplakia?
more dysplasia
-ventral tongue, retromolar triangle
oral leukoplakia dx
- hx & PE
- whitish res that can’t scrape off
- all indurated areas should be biopsied
oral leukoplakia management
- most don’t need txt (watch & see)
- surgical removal
- cryoprobe
- chemoprevention
- oral retinoids
oral hairy leukoplakia
- different than oral leukoplakia
- NOT premalignant
- EBV associated
- occurs almost ENTIRELY in HIV infected pts
Herpes (HSV-1) aka?
aka herpes labialis
HSV-1 effects what sites?
multiple sites in the body especially perioral and oral cavity (80%) and 20% genital lesions
what has HSV-1 been associated with?
increasing cases of genital herpes
HSV-1 more common in?
women
By who are a majority of infections transmitted?
people who don’t know they have it
HSV-1 pathophysiology
enters -> latency -> survives in neural ganglia
-prevents elimination by immune response
- recurrent infection is common
- usually localized symptoms only
types of HSV-1 infections
primary
-highly variable and usually severe & systemic
recurrent
-common & typically less severe and local
clinical manifestations of HSV-1
- systemic symptoms = primary
- affects gingiva (primary = gums, recurrent = buccal mucosa & lips)
- HERPETIC GINGIVASTOMATITIS
- multiple oral vesicular lesions and erosions surrounded by erythematous base
- painful
- prodome (burning, tingly, pain)
what is the most common clinical manifestation of HSV-1?
herpetic gingivastomatitis
where does primary HSV-1 occur?
gums
where does recurrent HSV-1 occur?
buccal mucosa and lips
children <5 w/ HSV-1 may have?
-fever, LAD, drooling, decreased oral intake
prodrome of HSV-1?
burning, tingling, pain
-25 hours prior to outbreak
where are recurrent outbreaks of HSV-1 usually?
lip borders
what may be first indication of infection in HSV-1?
recurrence
HSV-1 risk factors
sunlight, stress, trauma
HSV-1 diagnosis
- Tzanck smear, immunofluorescence smear or viral cx
- unroof vesicle
- serology for HSV by PCR
HSV-1 management
-systemic acyclovir, valacyclovir, famciclovir w/in 48-72 hours
- swish and spit miracle mouthwash (internal lesions)
- supportive
- popsicles (ice pack)
oral candida involves?
mucous membranes
- oropharyngeal
- esophageal
oral candida epidemiology
- Young infants
- Older adults who wear dentures
- Antibiotics
- Radiation of head and neck
- Immunodef
- Inhaled corticosteroids
- Xerostomia
oral candida pathophysiology
-Candida albicans
also c. galbrata, c. krusei, c. tropicalis
oral candida classification
pseudomembranous & atopic (denture stomatitis)
pseudomembranous oral candida
most common form
-white plaques on buccal mucosa, palate, tongue, oropharynx
atrophic (denture stomatitis) oral candidy
- most common form in older adults
- found under upper dentures
- erythema w/out plaques
asymptomatic manifestations of oral candida
- dry mouth
- loss of taste
- pain with swallowing or eating (esophageal thrush)
- also have angular chelitis
- painful fissuring
pseudomembranous oral candida clinical manifestations
- White plaques on buccal mucosa, palate, or tongue
- PAINFUL
atrophic (denture stomatitis) oral candida clinical manifestations
- erythema w/out plaques
- NOT painful
- beeft, red tongue (worst case)
oral candida dx
- Usually based on risk factors
- White plaques usually removable
- Fungal culture
- KOH prep
- Refractory thrush should warrant HIV testing
oral candida management for HIV negative patients
- Local therapy
- Nystatin suspension swish and swallow
- Clotrimazole troches (suckers)
- Miconazole buccal tabs
- Diflucan PO (More extensive disease can warrant this)
