Ch. 16 Flashcards
if a pt presents w. targets/raised edematous papules distributed acrally w/ involvement of one or more mucus membrane.. what kind of reaction is this
=erythema multiforme = type IV hypersensitivity
what are aphthous ulcers associated with?
celiac dz
IBD
behcet dz
when does dental plaque biofilm form?
when microorganisms adhere to the surface of some object in a moist environment and begin to reproduce
-microorganisms form an attachment to surface of the object by secreting slimy, glue like substance
what do the oral lesions for melanotic pigmentation present
(see in addison dz)
hemochromatosis
fibrous dysplasia of bone (albirght syndrome)
& Peutz-jegher syndome (pic) - genetic disorder; develop polys & dark spots that appear on various parts of body - greater risk for CA
what is the most common fungal infxn of the oral cavity?
what influences the infxn?
Candidiasis. (also most most freq of human fungal infxns)
influenced by :
- strain of C. albicans
- compostition of normal flora
-
immune status of pt -
- neutrophils, macrophages & Th17 = imp protection against Candida
what is gingivitis
what population is the most prevalent and severe
inflamof the oral mucosa surrounding the teeth caused by accumulation of dental plaque and calculus
plaque => sticky, colorless, biofil that collects btn & on the surface of teeth (AKA dental plaque) –> if not removed - becomes calculus
plaque beneath gumline –> gingivitis (can contribute to development of caries)
*adolescence*
What population is are these typically found in?
=pyogenic granuloma
gingiva of children, young adults & pregnant women (“pregnancy tumor”)
What population presents with torus palatinus the most?
what are characteristics of torus palatinus
F>M
= asymp bony outgrowth (exostoses) bc genetics or environment
=localized, benign benign protrusions
no cartilage involement
periodontits may be apart of systemic and/or immunodeficiency syndromes
which ones??
AIDS
Leukemia
Crohns
Diabetes
Down syndrome
Sacoidosis
syndromes w/ defects in neutrophils
infective endocarditis
pul or brain abscess
what is the etiology of SCC
1. HPV
2. tobacco/alc
3. betel quid/paan (india/asia) = combo of betel leaf, areca nut and slacked lime (aka gutka)
- a__ctinic radiation (sunlight) & esp in pipe smokers (lower lip)
- seen a rise in oral SCC (esp tongue) in < 40 y/o who doesnt smoke or have HPV - No known risk factors
How do you differentiate aspergillus fumigatis from mucor
aspergillus - septated 45 degree uniform branches
mucor- nonseptated 90 degree branches
What is the etiology of sialadenitis
etiology = inflam (-itis) of salivary gland
- trauma - mucocele (MC) & ranula
- autoimmune dx - sjogrens
- viral- mumps = MCC
- bacterial- staph aureus/strep viridins
what is the range of differentiation for SCC
range from well-differentiated keratinizing neoplasms
to
anaplastic, maybe sarcomatoid tumors
& also range in growth - slow to rapidly growing lesions
*degree of histological differentiation (determined by degree of keratinization) IS NOT correlated w/ behavior
what do the oral lesions look like in myeloid neoplasms ( tumors w/ monocytic differentiation)
=AML w/ monocytic maturation - nonspecific esterase (+); see monoblasts/mature monocytes in blood
infiltrate the skin (luekemia cutis) & gingiva
present before pancytopenia presents
a pt w/ DM presents complaining of facial pain and numbness w/ progressive conjunctival suffusion and blurry vision. after looking at the noncontrast CT which shows complete opacification of the lumen of the right maxillary sinus w/ bony erosion, what is on your DDx
what are you worried about?
Rhinocerebral mucormycosis
worried that infxn will spread to the orbits, cause cavernous sinus thrombosis and possibly invade basilar brain
what are characteristics of salivary gland neoplasms
relatively uncommon (<2 % of tumors in humans)
adults - F slightly more than male
5% in children < 16 yo
benign tumors - 50s-70s & malignant = later
(ex: pleomorphic adenoma, warthin tumor, mucoepideral carcinoma, adenoid cystic carcinoma)
compare the 5-yr survival rate of :
smoke/alc related SCC (early stage)
smoke/alc related SCC (late stage)
HPV
smoke/alc related SCC (early stage): 80%
smoke/alc related SCC (late stage): 20%
HPV-SCC: Better than non-HPV associated
*2nd primary tumor of oral cavity = 3-7% –> higher risk of malignancy
what is the clinical presentation of HNSCC
non-specific symptoms - sore throat, ear ache, pain on swallowing, wt loss.
possible metastasis to LN (submandibular & cervical)
If a pt presents w/ gray-white exudative membrane caused by acute pharyngitis/tonsilittis and the underlying cause is a result of EBV.. what does this pt have?
infxous mono
-also see cervical LAD and palatal petechiae
Pt w/ positve pregnancy test comes to your office with oral changes. what are these changes?
pregnancy tumor=
friable, red, pyogenic granuloma protruding from gingiva
how does HSV orofacial infxn present in adults
most = latent HSV-1 in
reactivation = recurrent herpetic stomatitis = at the site of primary inoculation or in adjacent mucosa w/ same ganglion
herpes labialis (pic) = latent in trigeminal ganglion = 1-3 mm vesicles to large bullae - 1st filled w/ clear serous fluid but rapidly rupture to yield painful, red-rimmed shallow ulcerations - clear w/i 3-4 weeks spontaneously
–> intracell and intercell edema (acantholysis)
what are 3 sources of brain abscesses?
- spread of infxn from pericranial contiguous focus (sinuses, middle ear, dental infxns)
- dental infxns, ethmoid/frontal sinusitis
- subacute/chronic otitis media/mastoidosis
which bacteria is most associated with periodontitis in adults
- Aggregatibacter (actinobacillus) actinomycetemcomitans
- Porphyromonas ginginvalis
- Prevotella intermedia
what is the MCC salivary gland lesion
Mucocele
MC in toddlers, young adults and elderly (who are more prone to falling)
= fluid filled on lower lip due to trauma - fluctuant fluid filled lesion (filled w/ mucinous material & lined by organizing granulation tissue)
Tx: complete excision
*NOT A CYST- bc no epithelial lining
The development of SCC is driven by…
accumultion of mutations & epigenetics changes –> alter expression & fxn of oncogenes & tumor suppressor genes –> cancer hallmarks
–> cell death, increased prolif, induce angiogenesis and ability to invade/metastasize
genetic alterations have molecular consistency of tobacco carcinogen induced cancers (DNA adducts)
-freq involve p53 path & proteins responsible for squamous differntiation p63 & NOTCH1
explain the genetic alterations identified for cancer development
what is the role of p63?
TP63 –> instructions for making a p63
=TF - attaches to certain region of DNA and controls the activity of particular genes
present in leukoplakia & SCC
what are histological features of candida albicans
pseudohyphae - chain of budding yeast cells joined end to end at constrictions
What is one of the most common dz’s worldwide and main cause of tooth loss before age 35?
how does it occur
dental caries!
-focal demineralization of enamel & dentin by acidic metabolities of fermented sugar produced by bacteria
oral lesions can be the first sign of….
underlying systemic conditions
which one is reversible, gingivitis or periodontitis?
BOTH!
what is the relationship of salivary gland tumor size and malignancy
malignancy = inversely proportional to size of gland
NO RELIABLE clinical criteria to diff btn benign and malignant - have to Bx
describe the gross and histological findings for pyogenic granulomas
surface = ulcerate, red-purple; growth may be rapid (worry about malignancy)
histologically - highly vascular proliferation of organizing granulation tissue
what is the fxn of salivary glands
produce saliva
- digestion (ptyalin/salivary amylase)
- lubrication for swallowing
protection (IgA, lactoferrin, lysozome)
explain the process of formation of dental caries
health-associated streptococci –> [poor oral hygiene, high sugar diet, salivary/immunologic/microbial factors] –>
- S. mutans- glucan production, biofilm formation, acid tolerant/producing
- late colonizers - acid tolerate & producing
–> dental caries
(picture also lists how to prevent!)
What are some conditions assocaited w/ compromise immune state that may predispose the pt to Candida infxns
AIDs
HIV (*if pt present w/ candida and no obv cause -test for HIV!)
DM
newborns
kids on oral steriods for asthma
organ/BM transplant
pregnant
broad spectrum ABx
what population are peripheral ossifying fibromas most common?
presentation?
treatment?
young/teenage females
= red, ulcerated & nodular lesions of gingiva
complete surgical excision down to the periosteum
what provides the simplest and rapid diagnostic test for Candida species?
wet mount - vaginal discharge
Candida vaginitis - DM women, or on OC
=intense itching, thick, curdlike discharge
what do you see on histology slides of pts w/ hairy leukoplakia
hyperkeratosis & acanthosis w/ “balloon cells” in upper spinous layer
what are characteristics of erythoplakia
red, velvety, eroded areas w/i oral cavity that usually remains level w/ or may be slightly depressed in relation to surrounding mucosa
less common but more ominous bc almost always associated w/ dysplasia/carcinoma in situ (CIS = has not broken basal membrane yet)
what oral changes are seen in pts w/ HIV
predisposition to opportunistic oral infxn, particulary
herpes virus
candida
kaposi sarcoma
hairy leukoplakia
compare the oral changes in pemphigus vs bullous pemphigoid
pemphigus - vesicles & bullae prone to rupture, leaving hyperemic erosions covered w/ exudates
bullous pemphigoid - orally look like pemphigus lesions- need to differentiate via histology
what strep infxn can cause dental infxn/periodontitis/caries?
Viridans group strep
-microaerophilic
also cause endocardititis –> so life threatening!
what is the MC cancerous lesion of the head/neck
SCC = 95%
= 6th MC neoplasm in the world
(have high rate of multiple primary tumors)
What oral manifestations may a pt w/ measles present w/
spotty exanthema before skin rash
koplik spots = made by ulcerations on buccal mucosa about stensen duct
(cough, coryza, conjunctivitis)
what are histological features for pleomorphic adenomas
great heterongenity
epithelial elements in ductal formations, acini, irregular tubules, strands or sheets
mesenchymal foci of cartilage, bone, fat in myxoid stroma
what is the role of cyclin D1
= protein required for progression thru G1 phase of cell cycle; in G1-phase -made rapidly and accumulated in nucleus and is degraded as the cell enters S-phase
= regulatory subunit of CDK4 & CDK6
expressed in both leukoplakia and SCC
how can infxns occur in the resp, GI, GU tract in healthy ppl
virulent microorganisms with ability to damage or penetrate the epidermis/mucosal epithelium
transfer via contact (direct/indirect), resp route, fecal-oral, sex, vertical transmission, insect/arthropod vectors
infxn if virulence factros overcome host defense or if host is compromised
what are complications of dental caries
pain - affects daily living
wt. loss/nutritional probs
loss of self confidence/esteem
potential life-threatening
what are characteristics of pleomorphic adenoma/mixed tumors
pleomorphic adenoma =well demarcated mass (vary in size) benign tumor that consists of mixture of ductal (epithelial) & myoepithelal cells (histologically = mixed tumor)
parotid > submandibular >>> minor
RF = ionizing radiation
reoccur is not completely excised
invasive to acini - malignancy arise as long as they are untreated
PLAG1 gene rearrangement- overexpression
What are characteristics of Ranula
due to trauma
=cyst of sublingual gland - usually intra-oral but can bulge out
Tx: excise completely - if not may reoccur
what do all these have in common:
focal fibrous hyperplasia (traumatic fibroma)
pyogenic granuloma (pregnancy tumor)
peripheral ossifying fibroma
peripheral giant cell granuloma
ALL BENIGN!
if a pt presents w/ a fiery red tongue w/ prominent papillae, what could be the underlying cause?
what are other ways it could present
= raspberry tongue –> scarlet fever
could present w/ white coated tongue through which hyperemic papillae project (strawberry tongue)
(group A beta hemolytic - strep pyogenes)
which deep fungal infxns have a predilection for the oral cavity & head/neck?
What is the predisposing factor
predisposing factor: immunosuppression
histoplasma, blastomycosis, coccidiodomycosis
aspergillosis
cryptococcosis
zygomycetes - mucor, absidia, rhizopus
Label this
What does HPV demonstrate tropism for? explain the process
HPV - tropism for lymphod assocaited structures of the oropharynx (including palatine & lingual tonsils)
in oropharynx- HPV gains access to basal kertinocyte progenitors via fenestrations in retuculated epithelium of tonsil crypts
infxn of tonsillar epithelium –> aberrant basal cell differntiation, dysplasia, carcinoma in situ & invasive carcinoma
what is the MC orofacial herpetic infxn & what population does it present in most
HSV-1 (but HSV-2 possible)
primary infxn MC in kids 2-4 (often asymptomatic)
what oral manifestations will a pt w/ diptheria present w/
dirty white, fibrinosuppurative, tough, inflam membrane over the tonsils & retropharynx
What are characterisitics of Warthin tumors (papillary cystadenoma lymphomatosum)
almost always parotid
M > F
10% multifocal & 10% bilateral
=smokers 8x greater risk
distinctive double layer of neoplastic epithelial cells resting on a dense lymphoid stroma, sometimes bearing germinal centers
Describe this lesion
What is it and what is the presentation
single ulceration w/ an erythematous halo around a yellowish fibropurulent membrane
=aphthous ulcer (canker sore)- single/multiple shallow, hyperemic ulceration covered by thin exudate & rimmed w/ narrow zone of erythema
painful, superficial oral mucosal ulceration of UNKNOWN ETIOLGY; resolves spontaneously in 7-10 days
what are traumatic/irritation fibromas
aka focal fibrous hyperplasia
=submucosal nodular mass of fibrous CT stroma on bucal mucosa along bite line or gingiva (could be sessile or pedunculated)
=reactive prolif bc of trauma
remove w/ complete surgical excision
what is the association of HPV and oropharyngeal SCC (OPSCC)
70% OPSCC (esp of base of tongue, tonsils, and pharynx) = associated w/ HPV-16 (oncogenic varient)
highest risk: 35-55 yo, non-smoking, white male
greater survival rate than HPV-neg tumors
How do you treat pyogenic granulomas
they can regress, mature into dense fibrous masses and form peripheral ossifying fibromas
-complete surgical excision is the definitive Tx
What are oral changes are seen in the following hematologic disorders:
- pancytopenia
- leukemia
- monocytic leukemia
- (agranulocytosis, aplastic anemia) –> severe infxn - gingivitis, pharyngitis or tonsillitis ; may spread to neck = cellulitis (ludwig angina)
- (see above) -similar bc neutropenia
- leukemic infiltration & enlargement of gingivae w/ periodontitis
what viral infxns can involve the oral cavity &/or head/neck region
HSV 1 & 2
herpes zoster
EBV (mono, nasopharyngeal carcinoma, lymphoma)
CMV
Enterovirus (herpangina, HFM dz, acute lymphodocular pharyngitis
rubeola
what is the prevalence, etiology and complication of xerostoma
increase risk w/ age - 20% pt >70 yo
etiology
- due to meds (anticholingerics, antidepressant/antipsychotics, diuretic, antiHTN, sedative, M relaxant, analgesics, antihistamines)
- sjogrens syndrome
- radiation therapy
complication - burning mouth syndrome - may also suggest HYPOfxn of PNS
Which genes are mutated in HPV associtated - OPSCC
HPV:
E6 –l p53 –> p53 degrades
E7 –l RB
HPV is integrated into host genome
what will make erythema multiforme an emergency
SJS/TEN
= widespread blisters predom on the trunk & face
= erythematous or pruritic macules
epidermal detachment
what are characteristics of oral candidiasis (thrush)
= superficial, gray-white inflam membrane made of matted organisms enmeshed in fibrinosuppurative exudate-
can be scraped off to reveal underlying erythematous inflam base
(remain superficial EXCEPT in compromised pt - organ/bone marrow transplant, neutropenia, chemo pt, AIDs, DM)
what define and explain dysplastic cells
=disordered growth
-loss of uniformity & loss of architectural orientation
may exhibit considerable pleomorphism - often have hyperchromatic nuclei w/ high nuclear-to-cytoplasm ratio
more abundant mitotic figures & seen in all layers
Overexpression of which tumor suppressor contributes to HPV-induced SCC
p16 = tumor supressor protein encoded by CDKN2A
surrogate marker bc p16 overexpressed in HR-HPV-(+) OPSCC
what does hairy leukoplakia look like?
what population and how does it occur
distictive oral lesions on the lateral border of the tongue
seen in immunocompromised pts
caused by EBV
what are characterisitics of leukoplakia
=white patches/plaques- canNOT be scraped off & canNOT be characterized clinically or pathologically w/ any other dz
3% world pop
25% of lesions = premalignant- until proven otherwise, think of ALL leukoplakia as precancerous
describe multilocular keratocytic odontogenic tumors
=epithelial lined cyst in mandible & maxilla
need to differentiate from other cysts becuase of its aggressive behavior
seen at any age; but MC 10-40 yo
Males
w/i posterior mandible
how do you differentiate hairy leukoplakia from candida infxn
hairy leukoplakia - white confluent pathches of “hairy”, hyperkarototic thickening - usually on lateral tongue (canNOT be wiped off-like in Candida)
*but can have a superimposed candida infxn - contributes to “hairiness”
what is the oral side effect of phenytoin (Dilantin) ingestion
fibrous enlargement of gingiva (gingival hyperplasia)
often due to poor hygiene or side effect of medications (Dilantin- anti-seizure med)
how will HNSCC present histologically
numerous nests & islands of malignant keratinocytes invading the underlying CT stroma and sk. M
if HPV related - nonkeratinizing SCC formed by basophillic cells w/ indistinct borders & scanty cytoplasm, w/ strong expression of p16
what auto. dom. disorder presents w/ multiple congenital aneurysmal telangtasia beneath mucosal surfaces of the oral cavity and lips
osler-weber-rendu dz (aka hereditary hemorrhagic telangiectasia- HHT)
-affect blood vessels throughout the body - cause vascular dysplasia –> increase tendency to bleed
MC presentation = recurrent/severe epistaxis –> severe anemia - need transfusions
what locations will oral cavity SCC present
what is important to find for long-term survival
tumor on ventral tongue, floor of mouth, lower lip, soft palate or gingiva *look under dentures*
premalignant lesions can be heterogenous in presentation & present before classic malignancy (EXCEPT HPV-SCC - no premalignant lesion) ==> early detection of all premalignant lesions critical for long term survival
= firm, pearly plaques that may ulcerate/protrude w/ irregular borders
what are characterisitcs of mucoepidermoid carcinoma
15% of all salivary gland tumors (MC primary malignancy)
60-70% occur in parotid
balanced chromosomal translocation (11:19)(q21;p13) produces a fusion gene product (MECT1-MAML2)
prognosis dep on grade
= low grade - look normal and tend to grow/spread slowly compared to high-grade
3 diff types of cells - solid epithelial squamous, intermediate celll and mucus producing cells (see on histology w/ mucus stains & cyst like spaces w/ mucus)
what is periodontitis?
poor oral hygiene w/ resultant change in oral flora (anaerobic/gram (-)) –> inflam process that affects the supporting structures of the teeth (periodontal ligaments) alveolar bone and cementum
–> can lead to complete destruction of ligament –> loosen and lose teeth
What are characteristics of adenoid cystic carcinoma
relatively uncommon
10% in MINOR salivary glands (palatine gland)= poorer prognosis
slow growing BUT unpredictable
50% disseminate (bone, liver, brain) decades after primary tumor removal
cells = clear cytoplasm but cells someitme solid and other times vacuolated
pain bc grow along nerve (perineural)
how does primary infxn of HSV in orofacial region present
10-20% acute herpetic gingivostomatitis = abrupt onset of diffuse oral vesicles w/ ulcerations (esp in gingiva) [also have LAD, fever, anorexia and irritability]
explain the lympathic drainage of the oral cavity and pharynx
- upper lip, teeth & submental LN –> submandibular LN –> SDC nodes –>IDC nodes
- hard palate & lateral tongue –> submandibular LN –> SDC nodes –> IDC nodes
- soft palate –> retropharyngeal nodes –> SDC nodes –> IDC nodes
- pharyngeal arches –> SDC nodes –> IDC nodes
- tonsils –> jugular diagastric nodes
- lateral lip cross over and tip of tongue cross over –> submental LN –> submandibular LN or IDC nodes
- middle of tongue cross over –> IDC nodes
what is the Tzanck test for HSV
= fluid from vessicle on micro slide and stained w/ Wright or Giemsa stain
(+) = acantholytic keratinocytes or multinucleated giant acantholytic keratinocytes (multinucleated polykaryons), or eospinophilc intranuclear viral inclusions
(+) in 75% of early cases (primary or recurrent)
what oral changes are associated w/ lichen planus
reticulate, lacelike, white keratotic lesions
sometimes ulcerate and rarely form bullae
are peripheral ossifying fibromas neoplastic?
how do they form
no, most likely = reactive
from pyogenic granuloma or de nova from periodontal ligament cells
