Finals - Fall 2018 Flashcards
Primer does what?
Increases surface tension of dentin to allow for bonding agent to reach collapsed collagen.
Vitrebond is a
RMGI
No need to use GLUMA if you are using —- or if you are using ——
VitreBond liner
ScotchBond Universal adhesive
- Typically refers to Commercial plans
- Estimate - No guarantee of payment
- Allows verification of benefits letting the patient know how much they need to pay, and the College know how much to collect.
Pre-Determination: (Could take 4-6 weeks)
- For ALL Medicaid/Agency related plans. (Month to month eligibility)
- Payer requires approval in advance of starting a procedure to ensure they will pay for the procedure.
- College receives a preauthorization approval number for the specific CDT Code and we have to include that on the bill for payer.
Preauthorization: (Could take 4-6 weeks)
Dx occlusal adjustment of the mounted casts to:
Provide —– at the recorded —- (grinding list to record the reductions in order)
Determine the correct and desirable —-.
maximum intercuspation
CR
OVD
mounted in CR:
- restoring all posterior teeth in one or both arches
- restoring all teeth in one arch
- complete dentures
- occlusal equilibration
Post height = crown length
Guarded
3/4 of root length > crown length
Good prognosis
May be best for extremely tapered, funnel
shaped canals.
Cast post
For post, endo will tell you
….
1. The color which will indicate the size
(red, blue, black or red)
2. The length to which they removed gutta
percha. (Should be a reference-i.e.
buccal cusp, remaining lingual portion of
tooth etc.
Paracore etch:
No need for this.
Five-minute exposure to 21.3% AlCl3 - hemodent
. Complete smear layer removal and noticeable dentin etching, some tubules remain partly occluded
Gluma is made of —- in water and helps to reduce hypersensitivity of dentin and reduce the incidence of post-operative sensitivity in restorative dentistry procedures.
5% glutaraldehyde and 35% HEMA (hydroxyethyl methacrylate)
The —– in Gluma works by blocking the dentinal tubules, thereby preventing the flow of fluid and decreasing sensitivity. —– forms deep resin tags and then occludes the dentinal tubules.
glutaraldehyde
HEMA
If the tooth is vital and asymptomatic, stop excavating after you are —% through dentin to avoid pulp exposure.
75
SDF: • Diamine ~
Ammonia (8%) o Stabilizer
o Vaporizes at body temperature
SDF: • Silver (25%)
o Antimicrobial: denatures proteins, breaks cell walls and membranes, inhibits DNA replication
curing light inhibitis
deep penetration of SDF into dentin
Gingiva effects to SDF
o Short-term: transient inflammation (24 h)
o Long-term: reduces plaque and gingival inflammation where it is applied (antimicrobial)
• Composite and Glass Ionomer bond strength —- by SDF
unaffected
SMART –
silver modified atraumatic restorative technique
Fluoride toxicity
5mg/kg is PTD
Colophony aka
rosin is a resin obtained from pine trees and other coniferous plants
dental materials contain colophony
Root canal sealers, cements
Colophony has been known to cause —– in affected individuals
—–
ALLERGIC CONTACT DERMATITIS
Type IV Hypersensitivity
Colophony tx
Oral antihistamine
Diphenhydramine
5mg/kg/day, four divided doses
Max dose 300mg/day
Type I:
Anaphylactic/Atopy Ex: Food allergies, eczema
Type II:
Cytotoxic/Antibody dependent
Ex: Autoimmune hemolytic anemia, myasthenia gravis
Type III:
Immune Complex
Ex: Systemic lupus erythematosus, rheumatoid arthritis
Type IV:
Delayed type/Cell-Mediated Ex: TB Mantoux test, contact dermatitis
Make sure that balls given to children younger than three are at least —” in diameter
1.75
• differs from chronic inflammatory enlargement • fibrous, firm and pale pink, w/ little tendency to bleed • occurs slowly • occurs 1st in papilla • spreads to gingival margin • may cover & interfere w/ eruption or occlusion • may improve or resolve when medication discontinued • genetic component to susceptibility • severity affected by adequacy of oral hygiene • severity affected by gingival concentration of the medication
Drug-induced gingival overgrowth
Prominent max frenum - tx
Treatment usually delayed until permanent incisors & cuspids erupted to allow natural closure of diastema
• If orthodontic treatment planned, postpone surgical treatment until diastema has been closed
Aggressive perio - localized affects ——, gernalized affects —-
young pts, young adults
Localized aggressive (formerly “juvenile”) periodontitis (LAP / LJP)
- characterized by loss of attachment & bone around permanent incisors & 1st permanent molars
- attachment loss is rapid, occurring at 3X rate of adult onset disease
LAP
• At least some cases appear to be inherited as an autosomal dominant trait
Treatment of LPP
• Antibiotic therapy combined with debridement
• Tetracyclines, commonly used to treat LJP,
contraindicated for LPP because of potential
for staining of developing permanent teeth
• Metronidazole&amoxicillinor
• Azithromycin
Hypophosphatasia
• geneticdisorderin which the enzyme, —— is deficient or defective
bone alkaline phosphatase
Leukocyte adhesion deficiency (LAD) • group of rare, recessive genetic syndromes • severity variable • affects how --------- • susceptibility to -------`
- absence of pus at infection sites
- recurrent ———–
- periodontal disease symptoms manifested in —— dentition
- inflammation & bone loss
- scrupulous oral hygiene measures needed
- adequate compliance may be difficult to achieve
- —— can be curative
white blood cells (leukocytes) respond & travel to site of
wound or infection
bacterial infections
otitis media, & other bacterial infections of soft tissues
primary
bone marrow transplant
Papillon-LeFèvre syndrome
• rare genetic disorder
• onset of —— in primary or transitional dentition
• severe inflammation & rapid bone loss characteristic
• easily identified ——- of the palms of the hands and soles of the feet
severe
periodontitis
hyperkeratosis
Langerhans Cell histiocytosis
• Diagnosed by —–
biopsy
—-, but not usually —-, may present w/ gingival enlargement caused by infiltrates of leukemic cells
AML
ALL
Max Dose Lidocaine =
4.4mg/kg
• Max Dose Articaine =
7mg/kg
Odontogenic facial cellulitis
- bacteria from tooth
* alpha-streptococci
- skin or mucous membrane trauma
- sinus bacteria
- Hemophilis influenzae
- Hib vaccine lowered incidence
Nonodontogenic facial cellulitis
- bactericidal
- narrow but appropriate spectrum for milder infections
- resistance possible
- amoxicillin has less frequent dosage schedule and better taste
• Penicillin or amoxicillin
- oral Augmentin (amoxicillin and clavulanate) • IV Unasyn (Ampicillin and Sulbactam)
- resistance unlikely
- bactericidal
penicillins w/ b-lactamase inhibitor
Addition of —— to penicillin or amoxicillin • covers anaerobes, so broader spectrum
metronidazole
less resistance
• bacteriostatic
clindamycin oral or IV •
- erythema
- induration
- tenderness of periorbital tissues
- rarely progresses to orbital cellulitis
• “Pre-septal cellulitis”
- more common in children • bulging eye (proptosis)
- loss of vision
- pain in eye
- brain abscess
• Orbital cellulitis
• blood pressure maintained by increased cardiac work
• rapid pulse
• not indefinitely
sustainable
compensated shock
- blood pressure can no longer be maintained
* emergency
uncompensated shock
Veau lip Class I :
Unilateral notching of the vermillion
border, not extending into lip (microform)
Veau lip Class II:
– Class II : UL cleft extending into the lip (incomplete)
Veau lip Class III:
– Class III : UL cleft involving the floor of the nose (complete)
Veau lip Class IV:
– Class IV: Any bilateral cleft of the lip
Veau Cleft PALATE
– Class I :
Isolated soft palate cleft only
Veau Cleft PALATE
– Class II :
UL soft and hard palate cleft
Veau Cleft PALATE
– Class III :
UL cleft involving soft/hard palate through the alveolus (usually involves lip too)
Veau Cleft PALATE
– Class IV:
Same as class II but BILATERAL
CleftLip:
Causedbypartialorcompletelackof fusion of the maxillary prominence with the medial nasal prominence
Etiology of CLP • Environmental -------- exposure to ionizing radiation (suspected) • Genetic ---------
– Maternal smoking
– Teratogens (e.g. alcohol, anticonvulsants)
– Maternal obesity, nutrition, infection, hyperthermia,
– IRF6, 8q24 locus, VAX1 (confirmed)
Etiology of CLP • Environmental -------- exposure to ionizing radiation (suspected) • Genetic ---------
– Maternal smoking
– Teratogens (e.g. alcohol, anticonvulsants)
– Maternal obesity, nutrition, infection, hyperthermia,
– IRF6, 8q24 locus, VAX1 (confirmed)
The ones that really, really, really need tx NOW are:
Permanent tooth avulsions (!!!)
– All permanent tooth luxations
– Permanent tooth Class II and Class III fractures
Class II Fractures
Emergency Treatment
Permanent teeth
- Do nothing?
- Bond fragment if available
- Composite/GI “Band-Aid” – then monitor for symptoms
- Restore with composite/GI
Class II Fractures Follow-Up Care Permanent teeth • 6-8 weeks: • 1 year:
clinical and radiographic exam – If emergency tx was provisional restoration,
consider definitive restoration
clinical and radiographic exam
• No matter how minor the injury, we’re always concerned about loss of vitality
• Continue to monitor for signs and symptoms
Class III Fractures
Emergency Treatment
Permanent teeth
• Young tooth with open apex or closed apex
– Direct pulp cap
– Partial pulpotomy (Cvek technique)
Class III Fractures
Emergency Treatment
Permanent teeth
Mature tooth with closed apex
– Pulpectomy
– (Direct pulp cap and partial pulpotomy are also options)
Cvek Partial Pulpotomy Technique
Using a diamond or 330 bur, access the pulp chamber to a depth of 1- 2mm
• Extend the preparation to allow for sufficient access, but keep it in dentin
Obtain hemostasis
• Use a moist cotton pellet to apply firm pressure to the pulp
– Moisten with chlorhexidine or sterile water
– Apply pressure for 5 minutes
After 5 minutes, reassess the tooth
– There should be no more oozing of blood from the pulp chamber
• If bleeding continues:
– Apply further pressure
– Reassess and consider deeper preparation to amputate pulp further
Placemedicament
• Condenseasufficient thickness of dry calcium hydroxide powder or Biodentine to densely fill the preparation
– At least 1mm in depth, avoiding cavosurface margin
– Biodentine preferred over MTA for faster setting time and lack of staining
• Apply vitrebond directly over the medicament
– Apply up to the cavosurface margin
– Avoid placing vitrebond over enamel
• Compositeband-aid placed over fractured tooth
– Etch, Bond, Flowable
• Buildupcompletedat later date after healing confirmed
– Prefer to keep tooth out of occlusion to prevent further trauma
Cvek Partial Pulpotomy Technique - barium
Barium added for radiopacity; Do not add any liquid
1:3 Ratio of Barium:Calcium Hydroxide
Cvek partial pulpotomy criteria for success:
– No clinical signs or symptoms—no pain, no
mobility, no fistula
– No radiographic pathology
– Continued development of immature roots
– Formation of calcific barriers
– Sensitivity to electrical stimulation
– The tooth is vital!
Restoration can occur after success of Cvek has been ascertained
– Typically after — weeks
– Strip crown or composite buildup
6-8
Mostcriticalfactor for permanent tooth avulsion
– Maintaining an intact and viable PDL on the root surface
Avulsion
Emergency Treatment
Permanent Teeth
• Reimplantassoonaspossible.Everyminute counts! The person who is holding the tooth is the person to put it back in.
• Flexiblesplintfor2weeks
• Medications
– Systemic antibiotics-–best choice depends on age
– Chlorhexidine mouth rinse
– Ibuprofen: pain + inhibits bone resorption
Avulsion
Follow-Up
Permanent Teeth
• Closed apex:
remove pulp and fill with CaOH within 7-10 days
• Splint removal after 2 weeks (4 weeks if dry time >60 minutes)
• Complete gutta percha fill in 2-12 months
– No need to complete endo if it becomes ankylosed
Avulsion Follow-Up Permanent Teeth • What if the tooth is immature? – First, ---- – Our goal is to revascularize the severed pulp
WAIT for signs of necrosis
Avulsion
Follow-Up
Immature Permanent Teeth
• Bestprognosisif replanted within — minutes
20
Avulsion
Follow-Up
Immature Permanent Teeth
Recallevery—- weeks
3-4
Avulsion
Follow-Up
Immature Permanent Teeth
• Ifsignsofnecrosis, —-
extirpate pulp and do revascularization procedure
Revascularization
these are not the specifics
- Stimulate bleeding through apex
- Place MTA on top of clot
- Allows continued root development and root wall thickening
What do you do when the tooth becomes ankylosed?
• Maintain it as long as possible
– This will depend on the patient’s age
• When it starts to submerge and become an esthetic issue, decoronate + flipper
Extrusion Emergency Treatment Permanent teeth • Reposition with digital pressure • Flexible splint for ---- weeks • Rx -----
2
chlorhexidine mouth rinse
Extrusion
Follow-Up
Permanent teeth
• Closed apex:
likely pulp necrosis. Remove pulp and fill with CaOH when indicated.
Extrusion
Permanent teeth
• Complete gutta percha fill in —– if no inflammatory resorption
2 months
Intrusion Emergency Treatment Permanent teeth • Openapex,----- :spontaneouseruption • Openapex,-------:orthodonticor surgical repositioning • Closedapex,-------:spontaneouseruption • Closedapex,-------:orthodonticorsurgical repositioning • Closedapex,-------:surgical repositioning
upto7mm
morethan7mm
upto3mm
3-7mm
morethan7mm
Intrusion
Follow-Up Care
Permanent teeth
• Closed apex: —–
remove pulp and fill with CaOH within 2-3 weeks
• Complete gutta percha fill in 2 months if no inflammatory resorption
Intrusion Emergency Treatment Primary teeth • Which way did the tooth go? • If tooth was displaced -----, then allow spontaneous re-eruption • If tooth displaced -----, then extract
labially
into developing tooth bud
– Developmental mucocutaneous conditions
Ectodermal dysplasia • Hypohidrotic ectodermal dysplasia • (polygenetic oligodontia) – White sponge nevus – Peutz-Jeghers syndrome – Hereditary hemorrhagic telangiectasia
• Immune-mediated
– Pemphigus vulgaris – Mucous membrane pemphigoid – Bullous pemphigoid – Erythema multiforme – Erythema migrans (geographic tongue) – Lichen planus • Cutaneous lichen planus • Oral lichen planus – Lichenoid mucositis – Lupus erythematosus • Chronic cutaneous (CCLE) • Systemic (SLE) – Systemic sclerosis – CREST syndrome
– Ectodermal dysplasia
• Group of inherited disorders in which — or more —— structures do not develop normally or fail to develop (hypoplasia or aplasia)
two
ectodermally derived
• Clinical features: –Hypoplasia or aplasia of: • Skin • Hair • Nails •Teeth • Sweat glands
– Ectodermal dysplasia
– Ectodermal dysplasia • Clinical features: Hypohidrotic ectodermal dysplasia –One of the best known types –------ – lack of ------ –Features often more pronounced in -----
–Fine, ——–
Teeth: –——
–------- hyperpigmentation –Protuberant -------- –Prominent ------ –Varying degrees of ----- –Dystrophic or brittle -----
Heat intolerance
sweat
glands
males than females
sparse blond or light color hair, eyebrows, eyelashes
Hypodontia –Oligodontia (lack of development of 6 or more teeth) –Conical roots –Abnormally-shaped crowns (conical, tapered, pointed, smaller)
Periocular
lips (midface hypoplasia)
forehead
xerostomia
nails
• Polygenetic oligodontia – This is not an —-
–Dental findings can mimic ——
ectodermal dysplasia
White sponge nevus
• occurs Due to a defect in the —-
normal keratinization of the oral mucosa
• Genodermatosis – genetically determined skin disorder
White sponge nevus
• ——- – genetically determined skin disorder
Genodermatosis
– White sponge nevus
• Clinical features:
–Relatively rare
–Autosomal —- with variable expressivity
–Appears at ——, sometimes adolescence
–Asymptomatic
–Thick, —– appearance of buccal mucosa bilaterally
–Other oral sites may be affected
–——– mucosa may be involved
dominant
birth or early childhood
white
Nasal, esophageal, laryngeal, anogenital
– White sponge nevus • Histopathologic features: –------- sometimes more diagnostic than scalpel biopsy –-------- (thickening of spinous layer) –------- of cytoplasm is pathognomonic
Exfoliative cytology
Parakeratosis with acanthosis
Perinuclear eosinophilic condensation
– White sponge nevus • Treatment: –------ but cosmetic concern –------- reported to help –Reassure the patient that this is a harmless condition –------ prognosis
None necessary
Tetracycline rinses
Good
Peutz-Jeghers syndrome
• Clinical features:
–Rare, but well-recognized, usually noted
in childhood
–Usually inherited, autosomal —— (~ 35% new mutations)
–—— gene mutation allowing uncontrolled cell growth
–—— polyps of gastrointestinal tract, esp. jejunum and ileum
–Can cause ——
–Bowel problems become evident in the
—— (i.e. 20’s)
–High risk of developing cancer — times greater than control population (GI tract, pancreas, male and female genital tract, ovary, breast)
–—— of lips and oral mucosa (also can occur around eyes, nostrils, anus, hands, feet), may fade with age
–~ 1 in 100,000-200,000 births, although more frequent by some reports
dominant
STK11
Benign hamartomatous
bowel obstruction due to intussusception (“telescoping” of proximal segment into distal segment)
3rd decade
18
Hyperpigmented macules
– Peutz-Jeghers syndrome
• Histopathologic features: –—— are not
precancerous
• Benign growths of —–
Gastrointestinal polyps
intestinal glandular epithelium
– Peutz-Jeghers syndrome • Treatment: –Genetic counseling, parents and patient –Monitor for -----
intussusception and for tumor development
Peutz-Jeghers syndrome
• Prognosis:
–—— may self-correct or may require surgery to prevent ischemic necrosis
–If cancer develops, treat appropriately
Intussusception
– Hereditary hemorrhagic telangiectasia (HHT)
• Clinical features:
–Telangiectasia – small collection of
dilated capillaries
–Uncommon autosomal —— –~ 1 in 10,000
–Mutation of one of two genes which are responsible for ————
–Frequent spontaneous —— – may be
initial clue to diagnosis
–Numerous ——- red papules blanch with diascopy
–Telangiectasias may be seen on —–
Oral, oropharyngeal, nasal, genitourinary,
conjunctival mucosa and GI mucosa
–Arteriovenous fistulas may affect the —-
–Oral lesions often most dramatic and
most easily identified • Vermilion zones
• Tongue
• Buccal mucosa
dominant
blood vessel wall integrity
epistaxis
1 mm – 2 mm
mucosa and skin, including hands and feet
lungs (30% of patients), liver (30%) or brain (10-20%)
– Hereditary hemorrhagic telangiectasia (HHT)
• Diagnosis HHT requires 3 of 4 features:
–Recurrent spontaneous ——-
–Telangiectasias of mucosa and skin
–——- involving the lung, liver or brain
–Family history of HHT
epistaxis
AV malformation
– Hereditary hemorrhagic telangiectasia (HHT)
• Histopathologic features:
–Collection of thin-walled blood vessels in the —–
superficial connective tissue
– Hereditary hemorrhagic telangiectasia (HHT) • Treatment: –Genetic counseling, parent and patient –Mild HHT – ---- –Moderate HHT – -------- –Severe – -------
no treatment
selective cryotherapy or electrocautery bothersome lesions
septal dermoplasty to prevent epistaxis
– Hereditary hemorrhagic telangiectasia (HHT)
• Prognosis:
–Generally good, 1-2% mortality sometimes noted due to complications related to blood loss
–If —– develops, 10% mortality can be anticipated, despite early diagnosis and appropriate treatment
brain abscess
– Pemphigus vulgaris (PV)
• —– etiology
• Inappropriate production of —– by the host directed against host tissue (autoantibodies)
–Damage to host by host’s own immune response
Autoimmune
antibodies
– Pemphigus vulgaris (PV)
• In PV —– destroy —–
autoantibodies
desmosomes
– Pemphigus vulgaris (PV)
• Clinical features:
–Relatively rare, ~ — cases per million diagnosed each year in general population
–Average age — y.o. –No gender predilection
5
50
– Pemphigus vulgaris (PV)
• Clinical features (con’t):
– Oral lesions
“first to show, last to go”
• In other words – the oral lesions often are the initial manifestation of the disease and the most difficult to resolve with treatment
– Pemphigus vulgaris (PV) • Clinical features (con’t): • Flaccid -----, ---- on skin; rarely seen intact intraorally • + Nikolsky sign - inducing a ---- by applying firm, lateral pressure to normal appearing skin
vesicles
bullae
bulla
– Pemphigus vulgaris (PV)
• Biopsy
–Normal tissue adjacent to ulceration or erosion should be sampled for direct —— (in Michel’s solution) and for light microscopic evaluation
• Sample at periphery – not the ulcerated center
immunofluorescent
– Pemphigus vulgaris (PV)
• Histopathologic features:
–Microscopically, —— above the basal layer (i.e. within the epithelium)
–—— (breakdown of spinous layer; cells appear to fall apart) – is also usually evident
intraepithelial clefting
Acantholysis
• Direct immunofluorescence (DIF) used to detect
autoantibodies bound to the patient’s tissues
• Indirect immunofluorescence (IIF) used to detect antibodies
circulating in the blood
– Pemphigus vulgaris (PV)
• Immunopathologic features:
–—–) immunofluorescence studies will be positive in pemphigus vulgaris
–Autoantibodies bind —— components (desmoglein 1 & 3)
Both direct (DIF) and indirect (IIF
desmosomal
– Pemphigus vulgaris (PV)
• Treatment:
–——, often with azathioprine or other steroid-sparing agents
–Topical —– have little effect (PV is a systemic disease)
–~ —% resolve on their own after 10 yrs
Systemic corticosteroids
corticosteroids
30
– Pemphigus vulgaris (PV) • Prognosis: –Usually ---- if not treated • *Severe infection • Loss of fluids/electrolytes • Malnutrition due to mouth pain –Prior to corticosteroid therapy, 60-90% mortality
fatal
– Pemphigus vulgaris (PV) • Prognosis (con’t): –Complications of long-term steroid may lead to mortality –Today, ---% mortality, usually due to complications of therapy (side effect of steroids, immune- suppression; azathioprine suppresses bone marrow and is a carcinogen)
5-10
– Mucous membrane pemphigoid (MMP)
Also known as —– • Clinical features:
–Resembles PV due to blister formation (i.e. pemphig”oid”)
–Twice as common as PV
–Older age than PV, average 50 – 60 y.o. –2:1 female predilection
cicatricial (scarring) pemphigoid
– Mucous membrane pemphigoid (MMP)
• Clinical features (con’t):
–Any mucosal surface, occasionally affects
skin –Scarring
• Skin
• —– (conjunctiva) • Scarring on oral mucosa rare
Symblepheron
MMP: –May see intact —- because
the split is —-
intraoral blisters
subepithelial
– Mucous membrane pemphigoid (MMP)
• Clinical features (con’t):
–—– gingivitis – descriptive term: erythema, desquamation, ulceration
• May be seen in several disorders
Desquamative
– Mucous membrane pemphigoid (MMP)
• Most significant aspect of this condition is ocular involvement of symblepheron
–Scarring obstructs the —–
–Dryness leads to —— of the corneal epithelium, leading to blindness
orifices of glands that produce tears, resulting in a dry eye
keratinization
– Mucous membrane pemphigoid (MMP)
• For biopsy:
–Must include generous sample of normal mucosa, —– away from areas of ulceration/erythema, as epithelium easily strips off
–Tissue should be submitted in ——
0.5-1.0 cm
both formalin and Michel’s solution
– Mucous membrane pemphigoid (MMP)
• Histopathologic features:
–—— formation – separation of the epithelium from the connective tissue at the basement membrane zone (BMZ)
Subepithelial cleft
– Mucous membrane pemphigoid (MMP) • Immunopathologic features: –----- deposition of immunoreactants at the BMZ –Positive DIF; negative IIF (only 5-25% of patients will have circulating autoantibodies)
Linear
– Mucous membrane pemphigoid (MMP) • Treatment: –Depends on extent of involvement • Oral lesions alone - --------, tetracycline/niacinamide or dapsone may be sufficient • Frequent dental prophylaxis,----mos. Refer patient to ophthalmologist for exam and follow-up • If ocular involvement, systemic immunosuppressive therapy indicated
topical steroids
q 3-4
– Mucous membrane pemphigoid (MMP) • Prognosis: –Rarely fatal –Condition can usually be controlled –Blindness results in patients with untreated ocular disease –Rarely undergoes -----
spontaneous resolution
Bullous pemphigoid (BP)
• Clinical features:
–Most common of autoimmune blistering
conditions ~ 10 cases per million per year
–Usually older population affected, average age 75 – 80 y.o.
–Primarily on skin but mucous membrane involvement occurs
No gender predilection
–—– early symptom, followed by the development of multiple, tense bullae, blisters on normal or erythematous skin
–Rupture, crust, heal without scarring
Pruritus
– Bullous pemphigoid (BP)
• Clinical features (con’t):
–Oral involvement uncommon
• —– rupture sooner than on skin (constant trauma?) leaving —–
Bullae
large shallow ulcerations with smooth, distinct margins
– Bullous pemphigoid (BP)
• Histopathologic features: –—– cleft similar to MMP
• Immunopathologic features:
–—- DIF and IIF with immunoreactants deposited at the —-
Subepithelial
Positive
BMZ
Bullous pemphigoid (BP) • Treatment: –Management similar to ----, but most BP cases resolve spontaneously in ---- years
cicatricial pemphigoid
1-2
– Bullous pemphigoid (BP)
• Prognosis:
–Many patients —–
–Problems may develop with use of —- therapy in older population
• Mortality — times higher than age and sex matched population
experience remission
immunosuppressive
3
– Erythema multiforme (EM)
• Etiology:
–Probably —–
• —— stimulated by trigger that produces the disease
immune-mediated
Immunologic derangement
– Erythema multiforme (EM)
• Etiology (con’t):
–50% cases- —- –25% - —–
–25% - ——
unknown
preceding infection;
• *Viral (herpes), • Bacterial (Mycoplasma pneumoniae)
medication-related (antibiotics and analgesics)
– Erythema multiforme (EM)
• Clinical features:
–Acute onset —- disorder skin and
mucous membranes –Young adult , age ——-
ulcerative
20’s – 30’s
– Erythema multiforme (EM)
• Clinical features (con’t):
–—— symptoms ~ 1 week before onset (fever, malaise, headache, cough, sore throat)
–Previous studies showed —– predilection, more recent studies show —- predilection
Prodromal
male
female
– Erythema multiforme (EM) • Clinical features EM minor: –Skin (extremities) –Mucosa (oral, conjunctival, genitourinary, respiratory) »---- crusting of vermilion zones –Skin • Variety of appearances “multiforme” • ------ on skin of extremities • ----- with ------ centers
–Mucosa
• Erythematous patches oral mucosa that undergo —– and result in large, shallow erosions and ulcers with irregular borders
• ——- usually spared
HemorrhagicRound, dusky-red patches - “target lesions”
Bullae
necrotic
necrosis
Gingiva and hard palate
– Erythema multiforme (EM) • Clinical features EM major: –------ mucosal sites in conjunction with skin lesions • Mucosal, lip and skin lesions as seen in EM minor –Ocular involvement can produce ------
2 or more
symblepheron
• Stevens-Johnson syndrome (SJS) –
at least two mucosal sites plus skin involvement
• Toxic epidermal necrolysis (TEN) - (Lyell’s disease) –
diffuse bullous involvement of skin and mucosa
- Difference between SJS and TEN: –Degree of —– involvement and age
- SJS <10% and usually ——
- TEN >30% and usually over
skin
younger patient
60 y.o.
• SJS and TEN almost always triggered by a —–, rather than —-
• SJS and TEN skin lesions begin as ——-
–Within 2 weeks ——- develop
–Patients may appear ——- - usually treated in —–
–Almost all patients have —— involvement, esp. oral
drug
infection
red macules on trunk rather than extremities
skin sloughing and flaccid
bullae
badly scalded
burn unit
mucosal
– EM, SJS and TEN
• Diagnosis:
–Usually based on —–
–DIF and IIF —–, not helpful except to rule-out other immune- mediated condition
clinical
presentation
non-specific
– EM, SJS and TEN • Histopathologic features: –------ vesicles –Necrotic ------ –Mixed inflammatory cell infiltrate –May see ------ inflammation
Subepithelial or intraepithelial
basal keratinocytes
perivascular
– Erythema multiforme (EM)
• Treatment (supportive therapy):
–Discontinue causative drug!
–Systemic or topical steroids early on (benefits controversial)
–—– re-hydration
–Topical anesthetic or analgesic for pain
IV
• Treatment SJS and TEN (con’t):
–—– are avoided in the management of TEN – associated with increased mortality
–IV administration of —— seems helpful in resolution of TEN by blocking apoptosis of epithelial cells
Steroids
pooled human immunoglobulins
– Erythema multiforme (EM)
• Prognosis:
–EM minor and major - —–
–—% of patients get recurrences (esp. spring and autumn)
• If HSV is trigger maintenance antiviral –Not life-threatening except severe cases
self-limiting (2 – 6
weeks)
20
- Prognosis SJS and TEN: –Mortality rate
* SJS —– •TEN —–
1% - 5%
25%-30%
- Prognosis SJS and TEN (con’t): –If patient survives
- Skin heals in —- weeks
- Oral lesions take longer
- Ocular damage in —-% of patients
3 – 5
50
– Erythema migrans (geographic tongue, benign
migratory glossitis)
• Etiopathogenesis unknown
• Probably —–
• One of the more common oral conditions, occurring in —- of the population considered a “common oral lesion”
immune-mediated
1-3%
Erythema migrans
• Erythema is due to ——– and shearing off of the —- - remaining epithelium thins, results in red appearance
atrophy of filiform papillae
parakeratin
– Erythema migrans (geographic tongue, benign migratory glossitis) • Clinical features: –Occurs in --- of patients who have fissured tongue –Wax and wane –Heal then develop in different area –Characteristically ------ of the tongue –On other ----- surfaces - “ectopic geographic tongue” can be referred to as erythema migrans
Multiple, well-demarcated zones of erythema surrounded at ———-–Can be singular - “persistens
1/3
dorsal and lateral
anterior 2/3
non-keratinized mucosal
least partially by a slightly elevated yellow-white serpentine or scalloped border
– Erythema migrans (geographic tongue, benign
migratory glossitis)
• Histopathologic features:
–Similar to psoriasis “——” description on Bx report
–—– with extensive —— formation in the superfical —– layer
psoriasiform
mucositis
Parakeratosis
microabscess (neutrophils)
spinous
– Erythema migrans (geographic tongue, benign
migratory glossitis)
• Treatment:
–
None generally necessary
–Occasionally sensitive or painful to hot, spicy foods
• Potent topical steroid
Erythema migrans (geographic tongue, benign
migratory glossitis)
• Prognosis: –—–
• Reassure patient this is a benign condition
Good
– Lichen planus (LP)
• Chronic —– disorder
• Cutaneous – may resolve in —– yrs
• —— – typically managed as chronic condition
immune-mediated
7 – 10
Mucosal
– Cutaneous lichen planus • Clinical features: –Adults ~---- years of age –---- predilection –Purple polygonal pruritic papules with ------ (lacy white lines) –Flexor surface of -------
30-60
Female
Wickham’s striae
wrists, lumbar region, shins, but other locations
– Oral lichen planus (OLP)
• 2 forms:
–—– (lacy white lines)
–—– (ELP)- erythematous, may ulcerate
Reticular
Erosive
– Oral lichen planus (OLP/ELP)
• Clinical features:
–May occur alone or with skin lesions –Adults, with —- predilection (3:2) –—– form is most common
–Erosive form is most —–, especially with acidic, salty or spicy foods
female
Reticular
symptomatic
–Reticular LP:
interlacing white lines
–Erosive LP:
shallow ulcers, peripheral erythema and radiating white lines
Oral lichen planus –Dorsal tongue involvement may appear as ------ –------ may be superimposed on either • ------ conditions worsen with a superimposed ------ infection
patchy keratosis and atrophy
Candida albicans
Oral ulcerative
candidal
– Oral lichen planus (OLP/ELP)
• Histopathologic features: (characteristic, but not specific)
–Varying degrees of —–, atrophy or ulceration
–Absent or pointed —- ridges (“saw- toothed”)
–Degeneration of the —- layer
• Degenerating —– –Band-like infiltrate of lymphocytes –Varying thickness of —– layer
hyperkeratosis
rete
basal cell
keratinocytes
spinous
OLP histo
–—- non-specific except to r/o other
immune-mediated condition –Controversy ——• Inflammatory response to —– (especially mild) can have same histology as ——
DIF
malignant transformation
epithelial dysplasia
lichen planus
– Oral lichen planus (OLP/ELP)
• Treatment:
–Rule-out candidiasis; treat if + culture
–Reticular LP ——
• Patient may feel “rough” areas of hyperkeratosis, but no pain
usually no Tx needed
– Oral lichen planus (OLP/ELP)
• Treatment (con’t):
–ELP treat with
potent topical steroid
• “off label”
• Systemic steroids not needed
– Oral lichen planus (OLP/ELP)
• Prognosis: varies
–Some patients are well-controlled, others
can be difficult to control –Recurring —– a challenge
• Dry mouth, dentures, ATB, inhaler
• Topical steroid predisposes to —–
candidiasis
candida
– Lichenoid mucositis
• A number of conditions can mimic
• —— reaction; lichenoid amalgam reaction; oral mucosal cinnamon reaction; lichenoid foreign body gingivitis; oral lesions of graft-vs.- host disease (GVHD); oral lesions of LE; some epithelial dysplasias
oral lichen planus, both clinically and histopathologically
Lichenoid drug
– Lupus erythematosus (LE)
• Most common ——– tissue diseases in U.S., > 1.5 million people
• 3 forms:
collagen vascular/connective
• Chronic cutaneous lupus
erythematosus (CCLE)
• Systemic lupus erythematosus (SLE)
• Subacute cutaneous lupus erythematosis (SCLE) intermediate between CCLE and SLE will not be discussed in this lecture
– Chronic cutaneous lupus erythematosus
(CCLE)
• Clinical features:
–May have no signs or symptoms –Primarily affects ——- –Also known as “——” –Exacerbated by —– –Waxing/waning nature
–Skin – —— patches in
sun-exposed areas, esp. H&N
• Heal then reappear in different area; may result in —-
–Mucosa– —–, essentially identical to ELP, but seldom occur without skin lesions
–Painful, esp. with acidic, salty or spicy foods
skin and mucosa
discoid lupus
sun exposure
scaly, erythematous
atrophy and scarring with hypo- or hyperpigmentation
lichenoid mucositis
– Systemic lupus erythematosus
• Clinical features:
–Waxing/waning nature
–Females affected —- times more than males
–—– more than Caucasians –Average age at diagnosis —-
–—– manifestations initially
• Fever, weight loss, arthritis, fatigue, general malaise
–—— spares nasolabial folds
–Skin lesions flare with —–
–———– of patients
is most significant aspect of disease –—– involvement common
• Pericarditis
• Libman-Sacks endocarditis
8 – 10
Women of color
31 y.o.
Protean
Malar “butterfly rash”
UV exposure
Renal involvement 40% - 50%
Cardiac
Systemic lupus erythematosus
–Oral involvement—– of patients
• May appear —— • Palate, buccal mucosa, gingiva
• Vermilion zones “lupus cheilitis”
5% - 25%
non-specific or lichenoid
– CCLE and SLE
• Histopathologic features:
–—– features with —–
–May show subtle differences (e.g. subepithelial edema) which may help lead to the Dx
Lichenoid
vasculitis
– Lupus erythematosus
• Diagnosis: Can be difficult, especially early stages
–Clinical appearance skin lesions in CCLE characteristic
–SLE - criteria by —-
–Serum studies show —–) present in 95% of SLE patients, negative in CCLE
–ANA - measures the amount and pattern of —– in your blood that work against your own body; a non-specific finding but can be used as a screening tool.
–Positive lupus band test – deposition of a band of —— at the basement membrane zone of normal skin; not specific to SLE; is also positive in other immune-mediated conditions
–Also, some patients with systemic LE are —– for the lupus band test
American Rheumatism Association for clinical and lab findings
anti-nuclear antibodies (ANAs
antibodies
immunoreactants
negative
– Lupus erythematosus
• Treatment:
–Sunscreens, avoid excessive UV exposure
–NSAIDS
–Antimalarial drug therapy, low dose thalidomide if resistant to topical Tx
–Topical steroids for skin and/or mucosa
–Systemic steroids or immunomodulating agents for more severe cases
• Complications from long-term steroids
–Kidney transplant may be needed
– Chronic cutaneous lupus erythematosus
• Prognosis:
Good
–~ 50% resolve after several years
–~ 5% - 10% of patients with CCLE transform to SLE
– Systemic lupus erythematosus
• Prognosis: —-
–Depends on —–
–Most common cause of death is —-
failure
• 5-year survival rate 95% • 15-year survival rate 75%
Variable
which organs affected and
how frequently SLE is reactivated –Worse for men than women –Worse for blacks than whites
renal
Screening test:
Test used on people apparently free of disease in order to detect the disease in early stages
Case-finding
Test
used to analyze abnormal clinical finding or symptomatic patient in order to establish or suggest diagnosis
Brushtest results
Negative -
no precancerous cells
Brushtest results
n Atypical -
abnormal cells
Brushtest results
n Positive -
dysplastic cells
Brushtest results
n Incomplete Specimen –
insufficient cells
Chemiluminescence -
as the result of a chemical reaction.
-
n
long
standing diagnostic adjunct in detection of premalignant lesions of cervical mucosa
Abnormal epithelial cells will have altered reflective properties.
–
form of fluorescence when excited by light
molecules that emit energy in the collagen,
Fluorophores
– Systemic sclerosis • Relatively rare condition characterized by ------- –Replaces and destroys normal tissue • Probably immunologically mediated • Has also been termed “-----
inappropriate deposition of dense collagen
Scleroderma” sclero = hard; derma = skin
– Systemic sclerosis
• Clinical features:
–——- texture of skin
————-
Diffuse, hard, smooth
–Raynaud phenomenon
–Sclerodactyly (claw-like deformity)
–Acro-osteolysis (resorption terminal phalanges) ± ulceration
–“mask-like” face
–Atrophy of alae
–Mouse facies – pinched appearance of nose
–Microstomia –Dysphagia
– Systemic sclerosis
• Clinical features:
–— cases/million annually
–Women affected —- times more frequently than men; adult age group
20
3
–Raynaud’s phenomenon
- Discoloration of the fingers and/or toes after exposure to changes in temperature or emotional events causing spasm of blood vessels.
- Not specific for systemic sclerosis
– Systemic sclerosis
• Clinical features (con’t):
–Claw-like deformity of fingers due to collagen deposition, ulceration of the fingertips - ——
–——–
• Destruction of the digit tips, including bone
sclerodactyly
Acro-osteolysis
– Systemic sclerosis • Clinical features (con’t): –Microstomia “purse-string” appearance –Dysphagia with ----- involvement –Pulmonary, renal, cardiac and GI fibrosis may be seen, with pulmonary hypertension
esophageal
– Systemic sclerosis • Diagnosis: –Generally stiffened skin with development of Raynaud’s phenomenon suggestive of Dx –Skin biopsy –Lab studies –Serologic studies • Autoantibodies directed against ----- • ----- antibodies • Limited cutaneous systemic sclerosis
Scl-70
Anticentromere
– Systemic sclerosis • Treatment: –Difficult, mainly symptomatic –Several drugs have been used to inhibit ------, increase ------ to decrease symptoms of Raynaud’s –------ do not seem to help
collagen production
peripheral blood flow
Steroids
– Systemic sclerosis
• Treatment:
–ACE inhibitors for HTN, esp. due to — –Esophageal dilatation
–Oral hygiene instruction
–Fabricate prostheses with design to accommodate microstomia
renal
– Systemic sclerosis • Prognosis: –Death due to ------ • ------ involvement has worse prognosis • Most deaths due to ------
internal organ deposition
of collagen
Cardiac
pulmonary involvement
– Systemic sclerosis • Prognosis (con’t): –Limited cutaneous involvement ---------- –Diffuse cutaneous involvement 10-year survival rate =------
10-year survival rate 75% - 80%
55% - 60%
– CREST syndrome • Clinical features: –Calcinosis cutis, Raynaud’s phenomenon, Esophageal dysfunction, Sclerodactyly, and Telangiectasia –Milder variant of ------ –Women, 6th to 7th decade of life
systemic sclerosis
– CREST syndrome
• Treatment:
–—- - similar to systemic
sclerosis
• Prognosis: —— than systemic sclerosis
–6-year survival rate 80% –12-year survival rate 50%
Symptomatic
better
• Effects of nicotine exposure: – Absorbed into blood stream
• Stimulation of ——– to produce ——-
–CNS stimulated, increases ——–
–Stimulates release of dopamine (pleasure reward)
adrenal gland
epinephrine
blood pressure, heart rate and respirations
• Some HPV types are not sexually transmitted
– HPV 6, 11: ——-
– HPV 2: ——–
squamous papillomas
non-genital warts
Some HPV types are sexually transmitted
– HPV 6, 11: Venereal warts (condyloma acuminatum)
–HPV 16, HPV 18
Squamous papilloma • Clinical features (con’t): – Usually ------, but can be ----- – ----- with fingerlike projections giving a “cauliflower” or “wart-like” appearance – Projections can be ------
pedunculated
sessile
Exophytic
pointed or blunted
Sessile –
base is the widest
Pedunculated –
base is narrower
Squamous papilloma • Clinical features (con’t): – Low --, low ---- – Soft – Painless – Color depends on amount of -----
infectivity
virulence
keratin
Squamous papilloma • Treatment: – ----- • Prognosis: – Recurrence ----- – ------ possible
Conservative excision
unlikely
Spontaneous remission
Verruca vulgaris
• Dermatologic term for common wart • Contagious
– Self-inoculation
Verruca vulgaris • Treatment: – Skin lesions - ---- – Oral lesions – ------ • Prognosis: – May recur – Spontaneous remission possible
topical therapies, surgery
surgery, laser, cryotherapy, electrosurgery
HPV’s and Sexually Transmitted Infections (STI)
• Low risk: —–
– May have —– with high risk type
• High risk: especially —— implicated in cancers
condyloma acuminatum
co-infection
HPV 16 and HPV 18
Venereal warts (Condyloma acuminatum)
• Treatment:
–
Excision, cryotherapy, laser (concern for airborne virus)
– Topical agents for anogenital lesions
Venereal warts (Condyloma acuminatum)
• Prognosis:
– —— infected with HPV 16, 18 have higher risk for malignant transformation to —–
– Oral condylomata have not shown this
Anogenital condylomata
SCC
HPV infects
basal cells
HPV infection
Terminal differentiation infected —-
– Viral shedding
– Mutations leading to —–
keratinocytes
pre-cancerous then cancerous
transformation
– Over — percent of HPV infections are cleared by the body within ——– years
90
2 - 3
• High-risk HPV types make proteins E6, E7 and L1, L2
– E6, E7 allow cell to ——
– L1, L2 comprise the ——
grow in uncontrolled manner and avoid cell death
virus capsid (shell) required for virus transmission, spread and survival
– Oropharyngeal:
base of tongue, soft palate, palatine tonsils, and pharyngeal wall.
• OPSCC can be —–
• Not all patients who have high-risk HPV in saliva will develop OPSCC
• Since 1988 the incidence of —– oropharyngeal cancers increasing, while —- oropharyngeal cancers decreased (smoking)
– Increase in oral sexual behavior – Decrease in tobacco use
HPV + or HPV –
HPV+
HPV-
Oropharyngeal Cancer
• Diagnosis HPV+ OPSCC:
HPV-16 infection is not characterized by the presence of HPV- 16 alone:
E6, E7 within the tumor cells must be expressed AND
Serum presence of E6 or E7 antibodies must be present
Oropharyngeal Cancer
• Treatment HPV + OPSCC – Early disease:
– Late disease:
- Platinum-based chemoradiotherapy
- Surgery
- Surgery
- Chemotherapy • Radiation
• Prognosis HPV + OPSCC
– Good
– Comorbidities (smoking, immunodeficiency) have negative effect on prognosis
From best to worst - OPSCC prognosis
• Prognosis:
– HPV +, non-smoker – HPV +, smoker
– HPV -, non-smoker – HPV -, smoker
HPV testing is important in oropharyngeal squamous cell carcinoma to identify patients that should have ——
treatment de-escalated
What does HPV + mean in relation to oropharyngeal cancer? • Improved 3-year survival (80% for HPV+ vs. 40% for HPV -) – Fewer ----- – Better response to ------
genetic alterations
therapy (surgery and/or radiotherapy)
- Nevus –
“mole” (junctional – compound – intradermal/intramucosal)-benign melanocytic lesion. Often notice a decrease in pigmentation as nevi progress from junctional to compound to intradermal
- Ephelides –
“freckles” brown pigmentation that develops following sun exposure. More common in children and fair skinned individuals
- Lentigo-
benign melanocytic lesion. Macular (flat), increase in number in Caucasians with age, no change in color intensity with exposure to UV light
- Seborrheic keratosis-
benign skin lesion with a “stuck on” appearance. Looks like “dropped on candlewax”
- Dermatosis papulosa nigra-
variant of seborrheic keratosIs that occurs in ~ 30% of black population
- Actinic keratosis-
precursor lesion for cutaneous squamous cell carcinoma. “Sandpaper” texture. Tx either surgical excision or topical, immune-activating agents such as Aldara. Use of sun blocking agents, limit sun exposure
- Telangectatic capillaries-
prominent vessels, often an indication of sun damage
- Sebaceous hyperplasia-
usually over 40 y.o. often seen on forehead, once achieve 1 to 2 mm size, minimal to no further growth. Central umbilication (sebaceous duct)
- Basal cell carcinoma-
most common cancer in humans. “Mask” area, rolled borders, umbilicated center, and telangiectasia. Also associated with nevoid basal cell carcinoma syndrome.
- Fordyce granules-
ectopic sebaceous glands. Can be seen anywhere in the mouth, buccal mucosa most common location also may be seen on lips
- Angular cheilitis-
associated with loss of vertical dimension. Candida, some may have co-infection with Candida and Staph. If external only, can use topical application of combination antifungal/corticosteroid cream.
- Herpes labialis-
most common site for recurrent HSV-1 is vermilion border and/or adjacent skin of lips
- Melanotic macule-
focal increase in melanin; also can occur as reactive melanosis in response to local trauma.
- Mucocele-
focal deposition of mucous. Cause is damage to associated minor salivary gland duct. Treatment is conservative-remove extravasated mucous and associated minor salivary glands.
- Leukoedema-
intracellular edema
- Linea alba-
found along occlusal plane.
- Morsicatio buccarum, linguarum, labiorum -
cheek, tongue, lip nibbling/chewing-shredded keratin, at a site(s) accessible to teeth.
- Fibroma-
benign collection of dense fibrous connective tissue. Conservative removal.
- Lichen planus-
immunologically mediated process. Often has “striae” or lacy clinical presentation. Does not wipe off. “Lichenoid mucositis” is a descriptive term which could apply to several conditions.
- Maxillary torus-
comprised of dense, vital lamellar bone.
- Inflammatory papillary hyperplasia-
found under sub-optimally fitting RPD or full denture, may also reflect nearly constant wear. Also has been noted with high palatal vault. Conservative excision, new denture.
- Nicotine stomatitis-
inflamed minor salivary glands of the palate with hyperkeratosis around the orifices. Most commonly seen in pipe smokers; can also be seen with long-term use of hot beverages.
- Black hairy tongue-
overgrowth of chromogenic bacteria and filiform papillae.
- Fissured tongue –
multiple grooves in tongue, fissured tongue-
patients often also have geographic tongue.
- Geographic tongue-
patients may be symptomatic e.g. tongue sensitive to spicy or acidic food, when lesions are present. Ectopic geographic tongue occurs in locations other than dorsal or lateral tongue.
- Foliate papilla-
part of Waldeyer’s ring. Vertical lines at posterior lateral tongue often see lymphoid tissue in that area as well.
- Mandibular tori-
vital lamellar bone. Often bilateral, commonly seen on lingual.
- Amalgam tattoo-
silver in amalgam stains reticulin fibers in associated connective tissue. If unusual presentation, may need to excise to rule out melanoma.
- Parulis (intraoral opening of sinus track)-
rule out an odontogenic source of infection.
- Pericoronitis-
most common in mandibular third molars-food, etc. gets caught between the overlying soft tissue (operculum) and crown of partially impacted tooth. Ideally, remove offending tooth and opposing third molar. May need to initially decrease local inflammation e.g. with rinses, then surgery.
- Necrotizing ulcerative gingivitis (NUG)-
punched out interdental papillae that do not regenerate. Seen in persons with poor oral hygiene and/or poor diet and stress.
- Inflammatory fibrous hyperplasia-
associated most often with poorly fitting dentures. Conservative excision, construct well-fitting dentures.
- Varix-
most often older patients, lower lip frequent site. If thrombosed, will NOT blanch with diascopy.
- Ulcer-
loss of continuity of an epithelial or epidermal covered surface.
- Aphthous ulcer-
immune mediated. Found on freely movable oral mucosa. “Canker sore” laypersons term. Ulcer on an erythematous base
- Squamous papilloma-
associated with NON-oncogenic human papillomaviruses. Color depends on amount of keratin on the surface
- leukoplakia-
rule-out dysplasia. White patch with crisply defined margins that does not rub off and cannot be diagnosed clinically or microscopically as anything else. Perform a biopsy to identify exact nature of the lesion.
- Periapical cyst-
need to do biopsy to confirm. Assess vitality of adjacent teeth.
- Dentigerous cyst-
develops due to fluid entrapment between crown of impacted tooth and reduced enamel epithelium.
- Antral pseudocyst-
collection of fluid below maxillary sinus. Maxillary sinus lining will be superior to the fluid collection. May get referred pain to maxillary teeth with altitudes e.g. during flying.
- Condensing osteitis-
look for tooth or teeth with deep caries in associated area.
- Exostoses-
bony protuberances arise from cortical plate. Tori are exostoses.
- Idiopathic osteosclerosis –
seen on radiograph; dense vital bone, no identifiable etiology, blends with surrounding trabeculae. Also called enostosis or dense bone island.
The risk of developing malignant melanoma:
Answer
: Is increasing, as are the incidence and mortality of malignant melanoma
What is the prognosis for central ossifying fibroma?
Answer: Excellent
Which are features of nevoid basal cell carcinoma syndrome?
Answer: Multiple OKCs, especially when occurring younger than 15 years old, and multiple BCCs most less aggressive than typical BCC
The most common soft tissue location for metastatic disease to present in the oral cavity is:
Answer: Gingiva
Which cyst feels firm because it is filled with keratin?
Answer: Gingival cyst of the newborn
- Definition of leukoplakia
i) White patch that cannot be wiped off AND cannot be diagnosed clinically or microscopically as any other condition
- Leukoplakia clinical appearance
i) White patch with —–
ii) Male > — y.o.
iii) Smooth,—–
iv) ——mostcommonoverallsite
v) Flat to slightly elevated
vi) Thinorthick
crisply defined borders
50
verrucousormicronodularsurface
Buccalmucosa
Leukoplakia
High-risk sites:
a. Floor of mouth
b. Ventral tongue
c. Soft palate
- Leukoplakia risk factors
i) Male > —- y.o.
ii) Tobacco use, especially cigarettes (products of combustion). More than 80% of patients with
leukoplakia are ——.
iii) Alcohol–—– effect
iv) Reverse-smoking
v) Use of —– products
vi) UVradiation
vii) Microorganisms
viii)Use of betel quid and similar products
ix) Biopsy-provenoralepithelialdysplasiaorsquamouscellcarcinoma
x) Immunocompromised state (HIV+, chemotherapy, systemic steroids)
50
smokers
synergistic
sanguinaria
80% leukoplakias microscopically show what? i) ——- without ——
Hyperkeratosis
epithelial dysplasia
- Definition of erythroplakia
i) —— that cannot be ——-
Red patch
wiped off AND cannot be diagnosed clinically or microscopically as any
other condition
- Erythroplakia clinical appearance
i) —–
a. Due to the lack of —– production on the surface of the lesion
b. Mucosa is —–; underlying —— shows through
ii) Well——
iv) Usually —–
Velvety red
keratin
atrophic
vasculature
demarcated
asymptomatic
Erythroplakia
iii) Mostcommonsites:
a. Floor of mouth
b. Ventral tongue
c. Soft palate/tonsillar pillars
- Erythroplakia risk factors
i) Same as —- but no ——
ii) More serious/severe than —–
leukoplakia
gender predilection
leukoplakia
- 90% erythroplakias microscopically show what?
i) Severe epithelial dysplasia or worse
- Actinic cheilitis ≠
exfoliative cheilitis
- Basal cell carcinoma (BCC) risk factors
i) Age (esp. over 40 y.o.)
ii) Fair complexion
iii) Chronic and intermittent sun (UV) exposure
iv) Frequentsunburns
v) Outdoor occupation or hobby
vi) Tendency for freckling in childhood
vii) Other: PUVA for psoriasis, tanning beds, immunosuppression
viii) Basal cell carcinoma syndrome ix) Male>female
- BCC types
i) Nodulo-ulcerative BCC - most common
ii) Pigmented BCC
iii) Sclerosing (morpheaform) BCC - least common
iv) Others:superficialBCC,BCCassociatedwithsyndromes,fibroepithelioma
Most common BCC
nodulo-ulcerative BCC
Least common BCC
Sclerosing BCC
- BCC clinical features of nodulo-ulcerative
i) —– papule
ii) —– enlargement
iii) Central —— which often ulcerates
iv) Rolledborders
v) —— when pressed
vi) No—-
vii) Telangiectasia – collection of small blood vessels near surface
viii) History of —– (patient may think they scratched it or shaved it)
Firm, painless
Slow
umbilication (depression)
Pearly, opalescent
hair
intermittent bleeding then healing
Telangiectasia –
collection of small blood vessels near surface
- BCC Tx
i) Scalpel excision
ii) Electrodesiccation and curettage
iii) Cryotherapy
iv) Radiationtherapy
v) Mohs micrographically controlled surgery; uses pathology and surgery
vi) UV protection with SPF products, hats
- Cutaneous squamous cell carcinoma (SCC) risk factors
i) Chronic sun (UV) light exposure
ii) Medical ionizing radiation
iii) Pre-existing —–
actinic keratosis
- Cutaneous SCC clinical features
i) Any sun-exposed site (dorsum of hands, arms)
ii) —- head and neck (i.e., face, helix of ear, scalp esp. with thinning hair)
iii) Non-healing—–
iv) Slowgrowth
v) Plaque, papule or nodule
vi) Variabledegreesofscale,ulcerorcrust
vii) Often —- base
~ 70%
ulcer
erythematous
- Cutaneous SCC prognosis
i) —– if identified and treated early
Good
- SCC lip risk factors
i) —– exposure
ii) Arises in setting of —–
Chronic (UV) sun
actinic cheilitis
- SCC lip clinical features
i) Especially lower lip
ii) Rare on upper lip (protected by forehead, nose and mustache)
iii) Rough,scaly
iv) Oftenulcerated
v) Slow growing, non-healing
- SCC lip prognosis
i) Relatively —- for lower lip, upper lip has ——-
ii) Good overall if identified early
good
high risk for lymph node metastasis
- Oral SCC risk factors
i) ~ —% of cases occur in patients under — years-old with no risk factors, typically on the
- —–
25
40
ventrolateral tongue
b. —-% patients Dx’d with OSCC have Hx TOB
80
OSCC
iii) Intrinsicfactors:
a. Biopsy proven —- or SCC
b. Presence of ——
c. Leukoplakia in high-risk site
d. Immunosuppression, i.e. taking systemic steroids, HIV or transplant patients
e. Heredity not major role; few heritable conditions
f. Older male >—-
g. —– male predilection
h. ± pain (pain usually a late feature)
oral epithelial dysplasia
erythroplakia or PVL
50
2:1
i) Most common sites OSCC:
a. Tongue – most common (especially posterior/lateral/ventral)
b. Floor of mouth (often near midline) almost as common as tongue
(i) Other site:
1. Gingiva – women 2:1, often non-smoker
2. Soft palate (esp. posterior/lateral) R/O sinus primary
3. Labial and buccal mucosa (not common, but occurs)
4. Hard palate (reverse-smoking)
iii) Exophytic
(mass-forming;fungating,papillary,andverruciform)
iv) Endophytic(
invasive,burrowing,andulcerated)
OSCC
ix) Can resemble a
non-specific ulcer,infection(TB,syphilis,deepfungal)orulceratedimmune-
mediated condition
- Oral SCC radiographic features
i) —– usually a late feature
ii) “—–” radiolucency, ——- margins
iii) —— fracture possible
Bone invasion
moth-eaten
ill-defined
Pathologic
- Oral SCC prognosis
i) Depends on stage
ii) Generally —–; most OSCC present in Stage —-
iii) Metastasis to lymphnodes
iv) —– 5-yearsurvival
v) Periodic follow-up after Tx completed
vi) 10-25% of these patients will develop new —
poor
III or IV
60%
upper aerodigestive tract malignancies, particularly if
carcinogenic habits are continued
- Melanotic macule etiology
i) —– etiology (post-traumatic melanosis?)
ii) Similar lesions associated with —–
Unknown
systemic conditions, medications and genetic disorders
- Melanotic macule clinical features
i) Common, harmless
ii) Maximum dimension achieved rapidly then remains constant
iii) Roundtooval7mmorless
iv) Not dependent on sun exposure
v) Female predilection
vi) Averageage43,butbroadagerange
vii) Lip or oral mucosa (lower lip vermilion zone most common location)
viii) Uniformly tan to dark brown
ix) Demarcatedmargins
- Melanotic macule Tx
i) None indicated unless for —–
ii) ——- Bx if recent onset, large size, irregular pigmentation, unknown duration, recent
enlargement (early —– can have similar appearance)
esthetics
Excisional
melanoma
- Melanotic macule prognosis
i) Considered —–
ii) One report of ——
benign
malignant transformation
- Melanoma risk factors
i) Whites, esp. fair-skinned
ii) Light hair/eyes
iii) Family history of melanoma
a. Genetic predisposition
iv) Personalhistoryofmelanoma
v) Tendency to sunburn/freckle easily
vi) History of blistering sunburn early in life
a. Acute sun exposure > chronic
vii) Indoor occupation; outdoor recreation viii)History dysplastic or congenital nevus
ix) >100commonnevi
x) Immunocompromised – organ transplant
xi) 40-70 years of age
a. Female predilection under age 40 xii) Male predilection in older pts.
xiii) Overall, slight male predilection
Melanoma ABCDE
a. Asymmetry
b. Border irregularity
c. Color variegation
d. Diameter greater than 6 mm (size of a pencil eraser)
e. Evolving – enlarging or changing color
- Melanoma types
i) Lentigo maligna melanoma
ii) Superficial spreading melanoma – most common type
iii) Nodularmelanoma
iv) Acrallentiginousmelanoma
a. Most common type of melanoma seen in the oral cavity is —— with the following:
acral lentiginous
clinical features:
(a) Dark, may see color variegation
(b) Can be amelanotic
(c) Irregular margin
(d) Macule which develops into nodule
(e) Male predilection
(f) 5th – 7th decade
(g) Hard palate/maxillary alveolar mucosa (70% - 80%)
(h) + ulceration
(i) + pain, usually if ulcerated
(j) Soft to palpation
(k) Cervical lymph node metastasis
- Melanoma Tx
i) Surgical excision
ii) Lymph node dissection
iii) Genotype-directed immunotherapy
iv) Chemotherapy
v) Close clinical follow-up
vi) SPFproducts,hats
- Melanoma prognosis
i) Depends on —-
ii) Better prognosis:
a. Younger than —-
b. Female
c. Worse for ——
d. Worse for ——
iii) Oral melanoma - —-
a. 5-year survival rate ~——
b. Difficulty achieving ——-
c. Early metastasis
depth of invasion
50
cutaneous on trunk, head and neck (esp. scalp and neck)
mucosal than cutaneous
poor
10% - 25%
wide surgical margins
- Mucocele/ranula etiology
i) Rupture of salivary gland duct → spillage of mucin
a. Ranula
(a) Arises from —-
(b) FOM, right or left of midline
(c) Similar clinical features as ——–
sublingual gland
mucocele
Mucocele/ranula Tx
i) Microscopic exam to rule-out neoplasm
ii) Some resolve with no
iii) Excision of mucous deposit including ——-
iv) Txranulamayincludemarsupialization–unroofing
treatment (especially superficial)
involved gland
- Sialolithiasis clinical features
i) Hard submucosal mass in soft tissue
ii) Submandibular gland (—-%), but can also affect parotid or minor glands
iii) ± symptoms
iv) May have swelling prior to or during meals
80
i) Sialadenitis
a. Bacterial, often penicillinase-producing staph
b. Viral, most often mumps
c. Ductal obstruction, retrograde infection - associated with xerostomia, may follow general
anesthesia
Sialadenosis
a. Non-infectious etiology
b. Associated with underlying systemic condition
(a) Diabetes
(b) Malnutrition (c) Alcoholism (d) Bulimia
i) Sialadenitis features
a. Diffuse
b. Unilateral swelling
c. Painful/tender, especially around meal times
d. May feel warm
e. Overlying skin may be erythematous
f. May have low-grade fever
g. May have trismus
h. Acute usually parotid
i. Purulent exudate expressed from the parotid papilla
j. Chronic - usually submandibular gland
ii) Sialadenosis
a. Slowly evolving enlargement of —–
b. Usually —–
c. ± pain
parotid or submandibular gland
bilateral
Sialadenitis tx
a. —– to rule-out sialolith
b. Antibiotic therapy – —- spectrum
c. ——- if purulence
d. Massage (with caution)
e. Warm compress
f. Sialogogues with hydration
g. Sugarless lemon drops
h. Ductal —–
i. ——- with saline irrigation
j. Surgical drainage
k. Surgical removal of affected gland may be needed
Screening radiograph
broad
Culture and sensitivity
stenting
Sialoendoscopy
ii) Sialadenosis tx
a. Often —– – control of underlying disease
b. Partial —— cosmetic reasons
c. —— reported to be beneficial
unsatisfactory
parotidectomy
Pilocarpine
- Most common major salivary gland to have a neoplasm
i) Parotid
- Most likely major salivary gland to have a malignancy
i) Sublingual
- Most common minor salivary glands to have a malignancy
i) Tongue, retromolar region
- Pleomorphic adenoma clinical features
i) 80% occur in the —-
ii) 4th – 6th decade (mean age 45 y.o.)
iii) Slightfemalepredilection
iv) ——growing
v) Painless
vi) —–able
vii) —— on palpation
viii) Usually —–, but —— may be present secondary to trauma
ix) Lesions of the hard palate are not moveable due to normal anatomy of the palate
x) Palatal lesions are usually —– to the midline
xi) Usually round when small, —– as it grows
parotid
Slow
Move
Rubbery-firm
non-ulcerated
ulceration
lateral
bosselated
- Pleomorphic adenoma Tx
i) Parotid –
remove lesion with the involved lobe
- Pleomorphic adenoma Tx
ii) Submandibular –
remove lesion and the involved gland
- Pleomorphic adenoma Tx
iii) Hard palate–
remove lesion, including overlying mucosa down to periosteum
- Pleomorphic adenoma Tx
iv) Softpalate,labialandbuccalmucosa-
enucleation
- Mucoepidermoid carcinoma clinical features
i) —— salivary gland malignancy
ii) Wide age range, 2nd to 7th decade
iii) May also be found —- within maxilla or mandible
iv) Well——
v) Non-tender
vi) Usually ——, but can be
vii) Ulceration and pain may develop as lesion progresses
viii) —— on palpation
ix) May have —– due to entrapped ——
a. ——— should be considered mucoepidermoid carcinoma until proven otherwise!!
Most common
centrally
demarcatedorinfiltrative
non-ulcerated
Fluctuant to hard
bluish tinge
mucin
Mucocele-appearing lesion of retromolar area
- Mucoepidermoid carcinoma Tx i) Depends on the grade
a. Low-grade – —-
b. High-grade – ——
wide surgical excision
wide surgical excision plus radiation
- Inflammatory fibrous hyperplasia (IFH, “denture epulis”) clinical features
i) Flange of ill-fitting denture
ii) May have central fissure/ulcer
- Name “3 P’s”
i) Pyogenic granuloma
ii) Peripheral ossifying fibroma
iii) Peripheralgiantcellgranuloma
- Langerhans cell histiocytosis radiographic features
i) Any bone affected but skull, mandible, ribs, vertebrae most frequent
ii) Solitary or multiple
iii) May break out of bone
iv) Radiolucent
v) Well-defined (usually) but not corticated
vi) Occasionally ill-defined
vii) Severe bone loss can resemble periodontal disease
viii) “scooped-out” appearance of superficial bone, esp. posterior mandible
ix) Extensivealveolarinvolvementcausesteethtoappearasiftheyare“floatinginair”
- Myelophthisic anemia associated with leukemia
i) Normal bone marrow cells replaced by —–
a. Fatigue, shortness of breath (SOB), pallor (decreased RBC’s)
b. Easy —– (decreased platelets)
c. —— (decreased WBC’s)
leukemic cells
bruising
Infection
- B signs associated with lymphoma
i) Fever
ii) Weight loss
iii) Drenchingnightsweats
iv) Generalizedpruritus(itching)
- Multiple myeloma radiographic features
i) Widespread —- lesions of bone
ii) Any bone can be affected
iii) —— radiolucencies,especiallyskull
iv) May appear as ——
v) Mandible involved ~ —-% of cases
lytic
“punched-out”non-corticated
osteomyelitis
30
- Multiple myeloma Tx - to control disease and keep pt. comfortable
i) Chemotherapy
ii) Bone marrow transplant
iii) Radiationonlyaspalliativetreatment
iv) Bisphosphonateshelppreventfracture
- Cleidocranial dysplasia clinical/radiographic dental features
i) —– retained because permanent teeth don’t erupt
ii) Numerous ——–
iii) Plenty of teeth; not erupting in the correct space, or, not erupting at all
Primary dentition
impacted and supernumerary teeth
- Osteitis deformans (Paget disease) radiographic features
i) “—–” appearance of bone
ii) May have extensive —-
Cotton wool
hypercementosis
- Osteitis deformans (Paget disease) Tx
i) If asymptomatic, —-
ii) —-
no Tx
Bisphosphonates
- Cemento-osseous dysplasia, types
i) Periapical COD
ii) Focal COD
iii) Floridosseousdysplasia
- Cemento-osseous dysplasia clinical features
i) Most commonly seen in ——, followed by ——, then ——–
a. ======= type reported to be more common in ======
b. However, COD can affect both genders and any ethnic group
ii) Usually found incidentally on x-ray
iii) Tooth-bearing areas of jaws
iv) Asymptomatic,
v) Swelling, discomfort unusual
vi) **——
black females
east Asian females
white females
Focal
white females
Teethtestvital
- Cemento-osseous dysplasia radiographic features
i) Ranges from —— to —— with a thin radiolucent rim (—–
remains intact)
completely radiolucent
densely radiopaque
PDL
ii) Florid osseous dysplasia shows multiple “——- in at least 2 quadrants of
the jaws
iii) May be associated with ——
cotton wool” type radiopacities
simple bone cyst
- Cemento-osseous dysplasia Tx
i) None indicated for —–
ii) Bx may be indicated for —- to r/o other disease processes
iii) Bx generally not necessary for ——
iv) Regular visits for dental prophylaxis and OHI to prevent periodontal disease and need for
extractions
v) Encourage pts to retain their teeth
vi) Ideally avoid ——–onset of symptoms associated with ———
periapical COD
focal
florid osseous dysplasia
surgical procedures
exposure of sclerotic bone to
oral cavity
vii) Management of symptomatic pt with secondary osteomyelitis difficult
a. Debridement
b. Antibiotics (often not effective)
c. Chlorhexidine rinse
i) Central ossifying fibroma - conditions
a. Hyperparathyroidism-jaw tumor syndrome
ii) Osteoma - condition
a. Gardner syndrome
iii) Centralgiantcellgranuloma - conditions
a. Hyperparathyroidism
b. Renal osteodystrophy
Chondrosarcoma clinical features
i) Mostly —–, 4th – 6th decade
ii) Mainly ——
iii) May present with ——
iv) 10%headandneck
v) May mimic ——
a. ± pain, swelling, loose teeth
adult males
femur, pelvis or ribs
pain, swelling
dental infection
- Chondrosarcoma radiographic features
i) Poorly defined —— with variable amounts of ——
ii) Larger lesions may appear ——-
iii) May see widened —- in area of tumor
radiolucency
radiopacity
multilocular
PDL
- Chondrosarcoma Tx
i) Radical surgery “one chance for cure”
- Osteosarcoma clinical features
i) —– – usually around knee, mean age 18 y.o.
ii) Jaws – mean age ~ — y.o.
iii) Painofteninitialcomplaintlongbonesandjaws
iv) Jaws
a. Swelling
b. Loose teeth
c. Paresthesia
Long bones
28
- Osteosarcoma radiographic features
i) “=====” pattern uncommon in jaws
ii) Mixed ===== with ill-defined borders
iii) SymmetricallywidenedPDLofteethinthearea
sun-burst
radiolucent/radiopaque
- Metastatic disease to the oral cavity clinical features
i) Paresthesia, tooth mobility, swelling, hemorrhage, pathologic fracture, trismus
ii) Lack of a healing tooth socket consider:
a. Granulation tissue
b. Lymphoma
c. Metastatic disease
- Metastatic disease radiographic features
i) Poorly defined —-
ii) Less commonly, ——
iii) “motheaten”
radiolucency
radiopacity
- Metastatic disease prognosis
i) Very poor, most patients die within —– of the diagnosis
ii) —-% of jaw metastases are initial manifestation
one year
22
- Odontogenic keratocyst clinical features
i) Usually —–
ii) Peak incidence —- decade
iii) Slightlydecliningincidenceinsubsequentdecades
iv) Anterior maxilla favored after —- y.o.
v) No cases under —- y.o. unless pt. has syndrome
vi) Mandible—-
asymptomatic
3rd
70
10
2:1
- Odontogenic keratocyst radiographic features
i) Majority (up to 80%) —- radiolucencies with —– margins and a thin —–
border
ii) Can ——, however can be expansile and symptomatic
iii) Only20%—–
unilocular
well-demarcated
sclerotic
hollow-out the mandible without expansion
exhibitmultilocularappearance
- Nevoid basal cell carcinoma syndrome (Gorlin syndrome) clinical features, significance to dentistry
i) Enlarged —– circumference (60 cm or more in adults)
ii) —– ridges – frontal bossing
iii) Broad —–
iv) Mildocularhypertelorism(wide-set)
v) Basal cell carcinomas that:
are —–
occur in —— skin
develop at an ——
often show —– pigmentation
are usually —–, with a few being aggressive
occipitofrontal
Heavy brow
nasal root
multiple
unexposed, as well as exposed,
earlier age (puberty-35 years)
melanin
quiescent
Gorlin syndrome:
vi) OKCs of the jaws develop in at least —% of affected patients
a. May begin in 1st decade, after age 7 years
b. May be —– - more likely to have syndrome if —–
75
single or multiple
multiple
- List the tissue of origin for each odontogenic neoplasm discussed in class
i) Odontogenic epithelium
a. Ameloblastoma
b. Adenoid odontogenic tumor
c. Calcifying epithelial odontogenic tumor
- List the tissue of origin for each odontogenic neoplasm discussed in class
ii) Mixed odontogenic epithelium and odontogenic ectomesenchyme
a. Ameloblastic fibroma
b. Ameloblastic fibro-odontoma
c. Odontoma
- List the tissue of origin for each odontogenic neoplasm discussed in class
iii) Odontogenicectomesenchyme
a. Odontogenic myxoma
b. Cementoblastoma
i) Compound odontoma a. Usually —- jaw
ii) Complex odontoma
a. Usually —– jaw
anterior
posterior
i) Compound odontoma
a. Collection of —– surrounded by narrow —– rim
b. Often overlies —–
small malformed teeth
radiolucent
impacted tooth
ii) Complex odontoma
a. —- mass, if fully formed has density of tooth structure
b. Surrounded by narrow —- rim
c. Typically overlies —-
Calcified
radiolucent
impacted tooth
- Ameloblastoma clinical features
i) —, but locally aggressive
ii) Painless
iii) Frequency equals combined frequency of all other odontogenic tumors
iv) Nogenderpredilection
v) Average age of diagnosis – —- y.o.
vi) ——growing
a. Usually ——- bone
Benign
33
Slow
expands, rather than perforates
- Ameloblastoma radiographic features
i) Most in —– region of mandible, but can occur anywhere
ii) ~ —-% associated with impacted tooth
iii) Unilocular/multilocularwithwell-definedbutnotscleroticborders,especiallysmalllesions
iv) —— “soap bubble” or “honeycomb”
v) May —– teeth/resorb roots
molar/ramus
20
Multilocular expansile radiolucency
displace
- Ameloblastoma prognosis
i) Guarded
a. Recurrence rates reported up to —-%
ii) Can be —-, especially lesions of maxilla
iii) Rare——transformation
iv) Annual radiographic follow-up for —– years
15
fatal
malignant
8 – 10
- List 4 developmental mucocutaneous conditions discussed in class
i) Ectodermal dysplasia
ii) White sponge nevus
iii) Peutz-Jegherssyndrome
iv) Hereditary hemorrhagic telangiectasia
- Peutz-Jeghers syndrome clinical features lips and oral mucosa
i) —- macules of lips and oral mucosa (also can occur around eyes, nostrils, anus, hands, feet), may fade with age
Hyperpigmented
- Hereditary hemorrhagic telangiectasia (HHT) clinical features
i) Frequent spontaneous —– – may be initial clue to diagnosis
ii) Numerous —– red papules blanch with diascopy
iii) Telangiectasiasmaybeseenonmucosaandskin,includinghandsandfeet
iv) Oral,oropharyngeal,nasal,genitourinary,conjunctivalmucosaandGImucosa
v) —– may affect the lungs (30% of patients), liver (30%) or brain (10-20%)
vi) Orallesionsoftenmostdramaticandmosteasilyidentified
a. Vermilion zones b. Tongue
c. Buccal mucosa
epistaxis
1 mm – 2 mm
Arteriovenous fistulas
- Hereditary hemorrhagic telangiectasia (HHT) prognosis
i) Generally good, —- mortality sometimes noted due to complications related to —–
ii) If brain abscess develops, —% mortality can be anticipated, despite early diagnosis and appropriate
treatment
1-2%
blood loss
10
