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Oral Path Exam 5 > STOMATITIS > Flashcards

STOMATITIS Flashcards

1
Q

6 types of Bacterial infections

A
  1. Impetigo
  2. Tonsillitis and pharyngitis
  3. Syphilis
  4. Tuberculosis
  5. Actinomycosis- Bacterial infection
  6. Necrotizing Ulcerative Gingivitis
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2
Q

2 types of Fungal Infections

A
  1. Candida albicans

2. Deep fungal infections

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3
Q

6 types of Candida albicans

A
  1. seudomembranous candidosis (candidiasis)
  2. Erythematous “acute atrophic” candidosis
  3. Chronic atrophic candidosis
  4. Chronic hyperplastic candidosis
  5. Angular cheilitis
  6. Median rhomboid glossitis “chronic atrophic candidosis”
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4
Q

types of Viral infection

A
  1. Human papilloma viruses (HPVs): DNA viruses
  2. Human herpes viruses (HHVs): DNA viruses
  3. Coxsackie A viruses
  4. Paramyxoviruses
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5
Q

bacteria cause infection in impetigo

A

Streptococcus pyogenes and Staphylococcus aureus

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6
Q

where does impetigo infect and who? what causes it?
it spread how?
can it be treated?

A

face and extermitiesFacial lesions usually develop around the nose and mouth
—
Poor hygiene, crowded living conditions, hot & humid climate Previous trauma: abrasions, insect bites, dematitis
—-
Spread by skin contact
Vesicles that rupture, leaving light brown (amber) colored crusts (“Cornflakes glued to the surface”)
—
Unlike HSV, lesions persist until treated

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7
Q

antibiotic to treat impetigo

A

Mupirocin topical Cephalexin, dicloxacillin

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8
Q

what organism causes Tonsillitis and pharyngitis?

age it affects?

other name?

A

Children aged 5 - 15 years
——–
“Strep throat”: sore throat, headache, fever, tonsillar

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9
Q

sign and symptoms of Tonsillitis and pharyngitis?

how does it spread?

A

Culture and treat with antibiotics: penicillin, amoxicillin, cephalosporin

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10
Q

Complications of Strep throat

A

Scarlet fever
Rheumatic fever
Glomerulonephpritis

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11
Q 
organism causes  Scarlet fever
----
age?
----
sign and symptoms 
----
how does it affect body?
A

Children aged 3-12 years
—-
Skin rash, fever, palatal petechiae, “strawberry tongue”
—-
Organisms elaborate an erythrogenic toxin that attacks blood vessels

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12
Q

how does Rheumatic fever affect body?

A

Rheumatic fever

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13
Q 
organism causes syphilis 
---------
how does it spread
-----
what is the incident( in what population)
A

Direct contact with mucosal surfaces (e.g. sexual contact, mother to fetus)
————-
Increased incidence in African Americans, prostitutes, and drug abusers
50-100x higher prevalence in the United States compared with other industrialized countries

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14
Q

what is chancre? syphilis

when does primary infection occur?

is it infectious

A 
painless ulcer at site of inoculation External genitalia, anus, lip
-------
3-90 days after initial exposure
Regional lymphadenopathy
TPHA + FTA-ABS
-------
 Highly infectious
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15
Q

when does secondary infection occur?

what type of ulcer occur? what are signs and symptoms?

is it infectious?

A 
4-10 weeks after initial infection
-------
Mucous patches
“Snail track” ulcers
Condylomata lata (papillomas), maculopapular cutaneous rash
Lymphadenopathy, sore throat, fever
-------
Highly infectious
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16
Q

when does latent syphilis show symptoms

A

1-30 years

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17
Q

what percentage of infected population with syphilis will have 3 syphilis?

what type of necrosis occur?

what type of lesion will occur?where they occur? disease associated with it?

A

Gumma – unique type of necrosis
———
Indurated, nodular or ulcerated lesion Intraorally, usually affects palate (perforation) or
tongue
——
Glossitis, atrophy and loss of dorsal tongue papillae (Luetic glossitis)
Syphilitic leukoplakia
Cardiovascular system and CNS involvement

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18
Q

signs and symptoms of congenital syphilis

A

Frontal bossing, underdeveloped Mx, high arched palate, saddle nose deformity

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19
Q

Hutchinson’s triad

A

Interstitial keratitis of cornea
VIIIth nerve deafness
Dental abnormalities:
Screwdriver-shaped “Hutchinson’s incisors” “Mulberry molars” bumps on occlusal surface

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20
Q

how to treat it?

A

Antibiotics: penicillin

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21
Q

what are dental abnormalities associated with congenital syphilis

A
  1. Screwdriver-shaped “Hutchinson’s incisors”

2. “Mulberry molars” bumps on occlusal surface

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22
Q

organism associated with Tuberculosis?
where it occurs?
how does TB becomes an active disease

A

Primary infection of lungs
—–
Immunodeficiency (old age, poverty, HIV/AIDS) contributes to progression from infection to active dis

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23
Q

clinical features of TB

A

Clinical Features: Fever, night sweats, fatigue, weight loss, productive cough, hemoptysis
Lymph node involvement (“scrofula”)
Skin: “Lupus vulgaris”
Oral: chronic painless ulceration usually involving tongue or palate, atypical periodontal disease

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24
Q

Histology and biopsy of tissues culture

A

Biopsy shows granulomas with central areas of necrosis AFB- Acid fast bacillus stain shows typical red bacilli
PCR (polymerase chain reaction)
PPD skin test and chest radiograph
Isoniazid (INH) and rifampin

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25
Q

how does Actinomycosis- Bacterial infection occur?
—-
where does most of the cases occur by this infection orally?

A

History of surgery or trauma
—–
55% of cases occur in cervicofacial areas
Injury, periodontal pocket, nonvital tooth, extraction
socket, infected tonsi

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26
Q

what are the clinical features of Actinomycosis- Bacterial infection

A

Abscesses and draining sinus tracts

Colonies of organisms are yellow “sulphur granules”

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27
Q

how to treat actinomycosis?

A

Long-term high doses of antibiotics
Can range from 6 weeks to 12 months, depending on
extent of infection.
Localized acute infections (e.g. periapical or pericoronal actinomycosis) may be treated more conservatively
Removal of infected tissue usually produces sufficient aeration that antibiotics aren’t needed (follow-up)

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28
Q 
other name for Necrotizing Ulcerative Gingivitis?
----
what organism causes it?
---
what causes it?
-----
what age?
A

Bacillus fusiformis and Borrelia vincetii
—–
Frequently occurs in situations of stress, immunodeficiency or malnourishment
——–
Young and middle-aged adults

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29
Q

dental association with NUG, ANUG

A

Interdental papillae are highly inflamed and hemorrhagic Papillae are blunted with areas of “punched-out” necrosis that are covered with a gray pseudomembrane

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30
Q

Is NUG associated with odor?

A

Fetid odor and intense pain

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31
Q

how to treat NUG

A

ebridement by scaling or curettage
Chlorhexidine rinses
Systemic antibiotics if fever or lymphadenopathy is present

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32
Q

what is the most common oral infection

A

Candida albicans

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33
Q

what organism causes Candida albicans

A

Dimorphism: yeast form and pathogenic hyphal form

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34
Q

Organism of low virulence in healthy, need “opportunity” for growth
Predisposing conditions like?

A

Antibiotic therapy
Cancer chemotherapy Corticosteroid therapy Dentures
Diabetes mellitus Pregnancy
Iron deficiency Newborns
Advanced malignancy Xerostomia
Other immunocompromised states (HIV/AIDS)

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35
Q

Overgrowth of Candida albicans, ————

can culture it in up to —–% of patients but with——-, probably present in all patients

A 
part of the normal oral flora
----
50%
--------
PCR
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36
Q

sign and symptoms associated with a. Pseudomembranous candidosis (candidiasis)

A

White material that can be wiped off: tangled hyphae, yeasts, dead epithelial cells, & debris
Normal or erythematous mucosa underneath Symptomatic, burning sensation to pain
Metallic taste

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37
Q

what candida albican organism causes metallic taste

A

Pseudomembranous candidosis (candidiasis)

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38
Q

symtpms and signs of b. Erythematous “acute atrophic” candidosis

A 
ainful, burning sensation
Often associated with antibiotics: “antibiotic sore
mouth”
Usually affects gingiva
Loss of filiform papillae on tongu
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39
Q

what organism is associated with antibiotic sore mouth

A

Erythematous “acute atrophic” candidosis

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40
Q

this organism of candida causes Loss of filiform papillae on tongue

A

Erythematous “acute atrophic” candidosis

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41
Q

what organism causes Denture stomatitis” “denture sore mouth

A

chronic atrophic candidosis

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42
Q

sign and symptoms of Chronic atrophic candidosis

A

Denture stomatitis” “denture sore mouth” Erythematous change limited to mucosa covered by denture and confined to denture bearing tissues
Only Mx and in patients who wear dentures 24 hrs/day Asymptomatic to symptom

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43
Q

characteristics of Chronic hyperplastic candidosis

A

“Candidal leukoplakia” Indistinguishable from leukoplakia
White lesion that does not wipe off
Which came first - the candida or the leukoplakia? Biopsy if no resolution with anti fungal therapy

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44
Q

what causes angular chelties?

A

Candida about 90%, rest caused by Strep or Staph-

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45
Q

sign and symptoms of Angular cheilitis

A

Erythema or fissuring at labial commissures
Unilat or bilat
Predisposing factors: reduced vertical dimension and accentuated folds at the corners of the mouth

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46
Q

sign and symptoms of f. Median rhomboid glossitis “chronic atrophic candidosis”

A

ho“Central papillary atrophy”

Well-defined, erythematous, rhomboid (diamond- shaped) area at midline of posterior dorsal tongue Often asymptomatic

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47
Q

how does Median rhomboid glossitis “chronic atrophic candidosis diagnose

A

Diagnosis by clinical features, mucosal smear and tissue culture
Exfoliative cytology: PAS stain

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48
Q

how to treat Median rhomboid glossitis “chronic atrophic candidosis?

A

Oral or systemic antifungal therapy
Nystatin (Mycostatin®)
Oral suspension: 1 tsp. 5x daily for 2 wks.
Clotrimazole (Mycelex®)
Troches: 10 mg 5x daily for 7-10 days
The “azoles”: ketoconazole and fluconazole are absorbed systemically
Fluconazole (Diflucan®): 2 tabs. (200mg) Day 1 and then 1 tab. (100mg) daily for 2 wks.

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49
Q

what puts are susceptible to it?

A

ncreased susceptibility to infection and recurrence in
immunocompromised (HIV+)

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50
Q

examples

A

Chronic, nonhealing intraoral ulcers which can mimic
squamous cell carcinoma
—–
Histoplasmosis
Coccidiomycosis
Blastomycosis Cryptococcosis Aspergillosis

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51
Q

how to diagnose and treat deep fungal infection

A

Biopsy with tissue staining and culture Systemic antifungal medications

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52
Q

organisms associated with Subcutaneous fungal &Opportunistic fungal infectionsinfections

A

ubcutaneous fungal infections Sporotrichosis
Opportunistic fungal infections
Zygomycosis (mucormycosis)
Often in immunosuppressed/ diabetics

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53
Q

types of Human papilloma viruses (HPVs): DNA viruses

A
  1. Papilloma (usually HPV subtypes 6 and 11)
  2. Verruca vulgaris (HPV subtypes 2, 4, 6, 40)
  3. Condyloma acuminatum (HPV subtypes 2, 6, 11, 53, 54, 16, 18)
  4. Focal epithelial hyperplasia (HPV subtypes 13 and 32)
  5. HPV and cancer. Only some types, esp 16, 18, 6, 11, 30s, 50s
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54
Q

Human herpes viruses (HHVs): DNA viruses

A
  1. Herpes simplex viruses (HHV-1 and HHV-2 / HSV-1 and HSV-2)
  2. Varicella-zoster virus (VZV / HHV-3)
  3. Epstein-Barr virus (EBV / HHV-4)
  4. Cytomegalovirus (HHV-5)
  5. HHV-8
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55
Q

how many types?
most adults have at least?
is it hard to distinguish between different kinds of HPV?

A

Over 100 types
Most adults have buccal epithelial cells containing at least one type, tends to “clear” in health patients
Yes, Can be difficult to distinguish between the various lesions of HPV

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56
Q 
Papilloma (usually HPV subtypes 6 and 11)
what age?
where does it occur?
what are clinical presentation
what cancer does this
A

Age 30 to 50 years
Tongue, lips,↑ soft palate
17
White/red/normal color “cauliflower” shaped exophytic nodule, sessile or pedunculated
Usuallysmall, but can be as large as 3 cm

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57
Q

“common wart” is caused by what virus?

A

Verruca vulgaris (HPV subtypes 2, 4, 6, 40)

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58
Q 
Verruca vulgaris (HPV subtypes 2, 4, 6, 40) affects what age group?
where does it occur?
clinical presentation ?
A

Children
Usually on skin of hands
Oral mucosa: vermillion border, labial mucosa, anterior tongue
Pink/white nodule with rough, pebbly surface
Usually less than 5 mm

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59
Q

histological feature of Verruca vulgaris (HPV subtypes 2, 4, 6, 40)

A

Koilocytes (enlarged cells with cytoplasmic clearing)
Large keratohyaline granules
Contagious, can spread to other parts of skin or mucosa by auto inoculation

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60
Q

treatment of Verruca vulgaris (HPV subtypes 2, 4, 6, 40)

A

liquid nitrogen, cryotherapy/surgical excision/salicylic acid

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61
Q 
Condyloma acuminatum (HPV subtypes 2, 6, 11, 53, 54, 16, 18) affects what age group?
where does it affect?
where does it affect on oral mucosa
A

Teenagers and young adults
Affects oral mucosa, larynx, genitalia
Oral mucosa: labial mucosa, soft palate, lingual frenum

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62
Q

how does Condyloma acuminatum (HPV subtypes 2, 6, 11, 53, 54, 16, 18) transmitt?

A

Transmitted through sexual transmission or self- inoculation

incubation of 1 to 3 months from time of sexual contact

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63
Q

when does the risk of malignancy increases?

A

Pink to white exophytic mass with short, blunted surface projections
1 to 1.5 cm, can be as large as 3 cm
Often occur in clusters and not quite as exophytic and papillary as papillomas or vurruca
——
Anogenital condylomata infected with HPV-16 and HPV- 18 have been associated with increased risk of malignant transformation

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64
Q

what virus causes the “Heck’s Disease”

A

Focal epithelial hyperplasia (HPV subtypes 13 and 32)

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65
Q

what age group and what population is affected by this virus

A

Most common in children often malnourished and
In poor living conditions
1st described in Native Americans and Eskimos

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66
Q

where does this virus occur in the mouth as what cells?

A

Labial, buccal, and lingual mucosa

Koilocytes and mitosoid cells

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67
Q

Histology of Focal epithelial hyperplasia (HPV subtypes 13 and 32)

A

HPV identified by DNA in situ hybridization, immunohistochemical analysis, and PCR

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68
Q

what types of HPV viruses cause cervical and oropharyngeal cancer

A

16, 18, 6, 11, 30s, 50s

25 yrs ago, 20-25% of throat cancer was HPV, today 75%

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69
Q

How does HHV virus survive in human body

A

Humans are natural reservoirs for the virus
All HHVs can reside throughout the life of an infected host and are characterized by dormancy or latency where they reside within the host with the potential to be reactivated and produce recurrent patterns of disease

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70
Q

what type of HSV cause oral infection

A

HSV-1 usually causes oral infections

71
Q

what type of HSV cause genital infection about 20% crossover

A

HSV-2 usually causes genital infections, about 20% crossover

72
Q

More than 90% of primary infections are ———

A

asymptomatic

73
Q

what age group ?
——

A

Oral disease caused by initial infection of herpes simplex virus, very acute in onset
Usually in children 6 months to 5 years old, but can occur in adults
Fever, lymphadenopathy, nausea, irritability

Painful, erythematous gingiva and tiny (1–3 mm) coalescing vesicles progress to widespread, multiple sharply marinated ulcers
of oral mucosae and skin around mouth & lips In adults, may presents as pharyngotonsillitis Lesions heal spontaneously in 1 to 2 weeks

74
Q

what % of population have
recurrent herpes simplex infection ?

where does it stay dormant?

A

irus is neurotrophic and persists in a latent state in the trigeminal ganglion

75
Q

what causes recurrent clinical lesions?

A

Old age, ultraviolet light, emotional stress, pregnancy, allergy, trauma, illness, dental therapy

76
Q

Where does recurrent herpes simplex occur?
—-
clinical presentation of herpes simplex?

A

At jct of vermillion and skin, not on mucosa (aphthae)
Intraoral: limited to keratinized mucosa that is bound to bone → hard palate and gingiva
——
Tiny vesicles or ulcers that coalesce
Heal within 7 to 10 days
Herpetic whitlow (fingers)
Histologic examination shows multinucleated, infected epithelial cells (viral cytopathic effect)

77
Q

how does herpes simplex diagnosed?

A

iagnosis usually based on clinical findings Cytologic smear and/or tissue biopsy
Serologic tests for HSV antibodies are positive 4 - 8 days after initial exposure

78
Q

percentage of pt having HSV DNA virus in their saliva

A

At any time, 5-30% of your patients will asymptomatically excrete and will have HSV DNA in their saliva

79
Q

how to treat simplex herpes

A

opical and systemic antiviral medications Effective when administered early prodrome period in primary or recurrent infection
20
Acyclovir (Zovirax®):
800 mg tablet every 4 hours orally for 7 to
10 days
5% ointment applied to affected areas topically with a finger cot q4h
Or pencicylovir topical
Famciclovir (Famvir®):
single 1500 mg dose or single-day (750 mg 2x for one day) dose
Valacyclovir (Valtrex®):
2g (four 500mg tablets) q12h for one day

80
Q

at what age does Varicella-zoster virus (VZV / HHV-3) occur?
is it contagious?
what is the incubation period?
what are the signs and symptoms?
where does it occur orally?
what is the recovery time and is there a vaccine?

A 
Usually in children 5 - 9 years of age
----
Highly contagious
-----
10 – 21 day incubation
------
Headache, fever
erythemavesiclepustulehardened crust on skin and mucous membranes
Skin: extremities, face, trunk
----
Perioral and oral lesions: vermillion border of lips, palate and buccal mucosa
----------
Tx: symptomatic
Recovery in 2 to 3 weeks
-------
VZV vaccine
81
Q 
what is Herpes zoster (“shingles”)
---
adult or children?
----
what are some predisposing factor
A

reactivation of VZV
VZV may lie dormant in sensory neural ganglia after initial chickenpox infection
Herpes zoster occurs if the virus becomes reactivated
—-
Immunosuppression, treatment with cytotoxic drugs, radiation, malignancy, old age, alcohol abuse, dental treatment

82
Q

what are the Prodromal symptoms of shingle

A

ntense pain, fever malaise, headache

83
Q

oral implication of shingles

A

oral lesions occur if trigeminal nerve is involved and lesions may be present on the movable or bound mucosa

84
Q

clinical presentation of shingle

A 
Unilateral painful eruption of vesicles along the distribution of a sensory nerve classically stops at the midline
Postherpetic Neuralgia (chronic infection) may
take months to resolve
85
Q

what is Ramsay Hunt syndrome

A

Infection of external auditory canal with involvement of the ipsilateral facial and auditory nerves producing facial paralysis, hearing deficits and vertigo

86
Q

what virus causes the kissing disease?

A

Epstein-Barr virus (EBV / HHV-4)

87
Q

population affected by it?
—————————-
what are the sign and symptoms of Infectious mononucleosis( kissing disease)?
——————–
How to diagnose kissing disease?

A

adolescents/ young adults in developed countries
————————————
Sore throat, fever, lymphadenopathy, tonsillitis, fatigue, enlarged spleen
Petechiae on hard/soft palate as prodrome
————————–
Serum analysis shows presence of heterophil antibody and elevated white blood cell count Self-limiting in 4 to 6 weeks, treatment is symptomatic

88
Q

What are the sign and symtoms of hairy leukoplakia

A

Corrugated white lesion, usually on lateral border of tongue

Cannot be wiped off

89
Q

What infection is hairy leukoplakia associated with?

A

Often associated with candidal infection

90
Q

How can Hairy leukoplakia be diagnosed?

A

EBV can be identified by in situ hybridization, PCR, immunohistochemistry and is the cause

91
Q

Most commonly occurs in——— patients, but can occur in other

A

Most commonly occurs in HIV+ patients, but can occur in

others

92
Q

cancers associated with hairy leukoplakia

A

Burkitt’s lymphoma other lymphomas (B cells have

receptors for EBV) Nasopharyngeal carcinoma

93
Q 
What population is affected by 
Cytomegalovirus (HHV-5)?
-----
Common in what population?
------
How does transmitt?
------
A

Common in AIDS patients
———–
Transmitted through exchange of bodily fluids
—–

94
Q

90% of infections are ——– but can produce a mono like illness
——- complications leading to ——,——-, and severe ——and ——– retardation

A

90% of infections are asymptomatic but can produce a mono like illness
Canserious complications leading to organ failure, blindness, and severe mental and motor retardation

95
Q

oral lesions associated with Cytomegalovirus (HHV-5)

A

Chronic ulceration, affects endothelial cells and blood flow
Can reside latently in salivary gland cells
Infected cells show “owl eye” appearance

96
Q

“Owl eye” cell appliance associated with what virus ?

A

Cytomegalovirus (HHV-5)

97
Q

Treatment of Cytomegalovirus (HHV-5)

A

Systemic antiviral treatment is necessary in immunosuppressed individuals

98
Q 
What causes Kapok's sarcoma?
---
What do lesions look like?
---
where does it affect in oral cavity?
A 
HHV-8
-----
Reddish-purple flat or raised lesions
------
Orally, most commonly on palate, gingiva, and tongue
99
Q

what virus causes herpangia ?

A

Coxsackie A viruses

100
Q

what is herpangia?

A

Hand-foot-and-mouth disease

101
Q

How does it transmit?

A

Transmitted by fecal-oral route

102
Q

what other body parts are affected by Coxaackie A virus?
——
How can infection associated with this virus be treated?

A

ainful vesicles and ulcers intraorally
Vesicles on soft palate with erythematous pharyngitis in herpangina
Hyperplastic lymphoid tissue on soft palate and tonsils in acute lymphonodular pharyngitis
——-
Papules occurring on skin of feet, toes, hands, and fingers in hand-
foot-and-mouth disease
—–
Infection usually resolves in 7 to 10 days

103
Q

Two diseases associated with Paramyxoviruses

A

Mumps

Measles (Rubeola)

104
Q 
What age group is affected by measles?
---
oral clinical features of measles ?
----
treatment?
A

“Koplik’s spots” may be an early intraoral manifestation
Small, red patches with white, necrotic centers
—-
MMR vaccine

105
Q

Mumps is associated with??

A

Salivary gland pathology

106
Q

What are “canker sore”

A

recurrent aphthous ulcerations

107
Q

Aphtha means?

A

“to inflame”

108
Q

What are the causes of Recurrent Aphthous Stomatitis (RAS)

A

trauma (e.g. dental procedures) or emotional
stress
Evidence of immunologic cause: T cell mediated
Specific histocompatibility (HLA) antigens have been associated, indicating a possible genetic predisposition

109
Q

What are the three types of RAS?

A 
Minor aphthae (80%)
Major aphthae (10%)
Herpetiform aphthae (10%)
110
Q 
What age group affected by minor aphthae?
-------
is male more affected than female
-----
signs?
----
location
-----
How does it heal?
A

No, Affect females more than males
——
Prodromal symptoms of burning, itching
Less than 1.5 cm
Painful tan ulcers with erythematous borders
———
Almost exclusively on moveable mucosa (not covering bone) Most often occur on buccal and labial mucosa
—-
Heal spontaneously in 7 to 14 days without scarring Recurrence rate is variable

111
Q 
Major Aphthae is what disease?
----
age group?
-----
where does it affect orally?
----
Healing?
A 
“Sutton’s disease”
Onset in adolescence
--------
1.5 – 3+ cm, deeper than minor aphthae
-----
Most commonly affect soft palate, tonsillar fauces or pharyngeal mucosa
----
Can take 2 – 6 weeks to heal, may cause scarring Recurrent episodes
112
Q

What is “Sutton’s disease” caused by?

A

Major aphthae

113
Q 
clinical features of Herpetiform aphthae 
---
onset?
--- 
female is more affected T or F?
----
what do the ulcers resemble?
A 
1 to 3 mm ulcers occurring in clusters
----
Onset in adulthood
----
Female predominance
---
herpes simplex virus ulcers
114
Q

Healing?

A

Heal in 7 to 10 days

115
Q

Treatment of RAS

A

Topical steroids:
Dexamethasone elixir 0.01% (shouldn’t swallow) Fluocinonide (Lidex®) gel 0.05%
Chlorhexidine
Amlexanox 5% oral paste (Aphthasol®)

116
Q

what are the diseases associated with “Pseudo” aphthae?

A

1.Associated with systemic diseases
2.GI malabsorption diseases 3.(Crohn’s disease)
4. Vitamin deficiencies: iron, folate, B1, 2, 6, 12
5.Chronic, recurrent disease resulting from a systemic vasculitis
6. Immunogenetic basis: strong association with specific HLA types (B51)
7.Correlation with environmental antigens
Oral (99%), ocular (70 – 85%), genital (75%), and systemic involvement

117
Q

syndrome associated with Pseudo” aphthae?

A

Behcet’s syndrome

118
Q

clinical features and location of “Pseudo” aphthae
——
what other body parts affected by it?

A

6 or more, commonly involving soft palate and oropharynx Ragged borders and variation in size
Surrounded by diffuse erythema
—-
Pustules on skin of trunk and limbs with genital and corneal ulceration
10 – 25% show CNS involvement, canparalysis and and dementia Vasculitis may affect cardiovascular, GI, hematologic, pulmonary, muscular, renal systems

119
Q

Treatment of “Pseudo” aphthae

A

Systemic and topical steroids

Other immunosuppressives like amlexanox Chlorhexidine

120
Q

Reason behind naming of Lichen Planus

A

Named for its similar appearance to the plant lichen (moss) Lichen = moss, planus = Latin for “flat
”

121
Q 
what causes Lichen Planus
----
age group?
----
More female or male affected?
-----
A 
Cause unknown but pathogenesis is immune mediated through T cells, slight association with hepatitis C
---------
Most patients are middle-aged adults
26
Women represent about 2/3 of patients
122
Q

what is Koebner phenomenon

A

Lichen Planus Tends to affects tissues that are irritated or traumatized

123
Q

clinical presentation of Lichen Planus in skin and mouth?

A

Skin: purple, pruritic, polygonal papules
Orally: reticular/erosive/bullous/plaque-like clinical appearance

124
Q

What is the most common type of Lichen Planus

A

Most common type is reticular characterized by Wickham’s striae

125
Q

Most common causes of desquamative gingivitis

A

LP, pemphigus vulgaris, pemphigoid, allergy)

126
Q

Histologic features of lichen planus

A

Saw-toothed rete ridges with destruction of the basal cell layer (liquefactive degeneration), with band like infiltrate of small lymphocytes (T cells) just under the epithelium

127
Q

what are lichenoid reactions?

A

Lesions that look like LP but aren’t: Assoc with Systemic drugs, hypersensitivity reactions, esp cinnamon and
amalgam and epithelial dysplasia

128
Q

what is Vesiculo-bullous (blistering) diseases associated with?

A

Lichen planus

129
Q

How to treat Lichen planus?

A

Fluocinonide (Lidex®) gel 0.05% applied topically 3-4xs daily Clobetasol (Temovate®) gel 0.05% applied topically twice a day

130
Q

age group affected by it?

A

Most often in adults age 40’s and 50’s

131
Q

Foliaceus defintion

A

Severe progressive autoimmune disease that affects the

skin and mucous membranes: oral lesions are usually the first to appear

132
Q

clinical features of Pemphigus ?

A

Epithelial desquamation produces painful superficial erosions and ulcerations. Affects most mucosal surfaces but often affects gingiva producing chronic desquamative gingivitis. You can induce epithelial separation by manipulating tissue or producing lateral pressure (+ Nikolski sign). Rarely see blisters since they break early

133
Q

Histological features of Pemphigus?

A

The individual cells lose their cohesion and round up (acantholysis) producing a suprabasilar separation within the epithelium

134
Q

How to diagnose Pemphigus ?

A

Biopsy shows characteristic suprabasilar epithelial separation with acantholysis. Direct immunofluorescence demonstrates autoantibodies (usually IgG and C3) around the individual keratinocytes (chicken coop wire)

135
Q

How to treat Pamphigus

A

Systemic steroids ± steroid sparing drug

136
Q

What is Paraneoplastic pemphigus?

A

Affects patients who have a neoplasm, usually lymphoma or leukemia
Very serious: high morbidity and mortality

137
Q

age? more male or female?
—–
Is it more common than pemphigus vulgaris?

A

Average age 50 – 60, 3x more common in females
—-
Considerably more common than pemphigus vulgaris

138
Q

where does Benign mucous membrane pemphigoid (cicatricial pemphigoid) affect in the body?

A

Affects oral, ocular, and genital mucosa ± larynx and esophagus and ± skin

139
Q

clinical features of Benign mucous membrane pemphigoid (cicatricial pemphigoid)

A

ery similar to pemphigus but not as severe. Tissue desquamation produces erosions and ulcers. + Nikolski sign. Most commonly affected site is gingiva where it produces desquamative gingivitis
-Bullae form at separation of epithelium from connective tissue, producing a subepithelial split from the connective tissue Blisters rupture, leaving large areas of ulceration

140
Q

Ocular scarring in Benign mucous membrane pemphigoid (cicatricial pemphigoid) can progress to ——–if untreated

A

blindness

141
Q

Diagnosis of Benign mucous membrane pemphigoid (cicatricial pemphigoid)

A

Biopsy shows characteristic subepithelial separation. Direct IF shows autoantibodies at junction of epithelium and connective tissue

142
Q

How to treat Benign mucous membrane pemphigoid (cicatricial pemphigoid)

A

Ophthalmologic consultation Topical or systemic steroids

143
Q

Desquamative Gingivitis can be a clinical manifestation of?

A

Lichen Planus
Pemphigus vulgaris
Mucous membrane pemphigoid Allergic reaction

144
Q

Allergic reaction causes Desquamative Gingivitis

A

Toothpaste – most commonly tartar control toothpastes Cinnamon-flavored products (containing a flavoring agent called cinnamic aldehyde)
Preservatives (e.g. sodium benzoate)

145
Q

what is the flavored agent in toothpaste causes allergic reaction

A

cinnamic aldehyde

146
Q

What causes Erythema multiforme?

A

Most often following systemic medications or often as a post infectious process, esp post viral. Sometimes a cause cannot be

147
Q

clinical feartures of Erythema multiforme?

A

Acute onset, immune mediated blistering mucocutaneous condition

148
Q

Clinical features of Erythema multiforme?

A

It often follows a bacterial or viral (herpes simplex) infection or drug exposure (antibiotics, analgesics)
Prodromal symptoms: fever, malaise, headache, cough, sore throat

Skin

  • Skin lesions highly variable “multiforme”
  • Characteristic target or “bull’s eye” lesions
  • Can occur without oral lesions
  • Classically affects palms and soles

Mucosa

  • Oral ulcers with erythema and irregular borders
  • Lips, labial mucosa, tongue, floor of mouth, soft palate
  • Crusting and bleeding at vermillion zone of lips

Steven-Johnson syndrome

  • More severe form of erythema multiforme
  • Extensive mucosal ulceration
  • Also affects genital and ocular mucosa
  • Usually triggered by medications
  • Can affect internal organs and can be life threatening

Toxic epidermal necrolysis

  • Most severe form of erythema multiforme
  • Triggered by drug exposure
  • Female predilection
  • Diffuse sloughing of skin and mucosal surfaces
149
Q

Male or female is more affected ?

A

Young adults 20s and 30s, men affected more

150
Q

What body parts affected by Erythema multiforme?

A

Affects skin and mucous membranes, rarely only the mouth

151
Q

Prodromal symptoms of Erythema multiforme

A

fever, malaise, headache, cough, sore throat

152
Q

What is the recurrence rate of Erythema multiforme

A

20% recurrence rate

153
Q

Multiforme and Bull’s eyes features associated with what disease?

A

Erythema multiforme

154
Q

Steven-Johnson syndrome

A

More severe form of erythema multiforme

  • Extensive mucosal ulceration
  • Also affects genital and ocular mucosa
  • Usually triggered by medications
  • Can affect internal organs and can be life threatening
155
Q

what is the most severe for erythema multiforme

A

Steven-Johnson syndrome

Toxic epidermal necrolysis

156
Q

How to treat erythema multiforme

A

Topical and high dose systemic steroids

157
Q 
what is geographic tongue?
---
other names?
---
is it a common disease and is is it more common in female or male?
----
A

“Erythema migrans”, “benign migratory glossitis”
—–
Relatively common (1 – 3% of population)
2x more common in females

158
Q

clinical features of Geographic tongue

A

Primarily affects dorsal and lateral borders of tongue
Depapillated areas that are erythematous or normal colored with characteristic yellow-white borders that marginate the lesions. heal spontaneously and recur at different sites Usually asymptomatic but occasional burning
Increased incidence in psoriatic patients

159
Q

Is treatment necessary for geographic tongue

A

No treatment necessary, topical steroids if symptomatic

160
Q

Is Reiters Syndrome associated with geographic tongue

A

it is very rare

161
Q

Disease associated with

geographic tongue

A

Urethritis, arthritis, conjunctivitis

162
Q

It is common in what age group?

A

8x more common in women, average age is 31

163
Q

What disease is butterfly rash associated with?

A

Lupus erythematosus

50 – 80% have skin lesions

164
Q

What is Discoid LE

A

lesions confined to skin
Erythematous rash on sun-exposed skin
25% have oral lesions: erythematous plaques or erosions with white striations

165
Q

what is Systemic LE

A

chronic and progressive, can be life-threatening and affect multiple organs: CNS, heart, kidney
Periods of remission and disease inactivity

166
Q

What are the lab tes used to diagnose LE

A

NA (antinuclear antibodies) & antibodies to the patient’s own DNA

167
Q

How to treat LE?

A

Corticosteroids, anti-malarial drugs (hydroxychloroquine), and other immunosuppressive medications are used in systemic LE Aspirin and NSAIDS are given for symptomatic treatment Antimalarial drugs for more severe conditions

168
Q

Is it common in male or female more?

A

Usually adults, 3:1 women.

169
Q

What is Raynaud’s phenomenon associated with Systemic Sclerosis “ Scleroderma”

A

vasoconstrictive event in extremities triggered by stress, cold.

170
Q

Body parts affected by Systemic Sclerosis “ Scleroderma”

A

Skin: Diffuse, hard, taut “hide bound disease”
Oral: Microstomia in 70%, dysphagia, ± xerostomia, diffuse
widening of PDL, resorption of ramus or condyle or coronoid Affects other organs and can lead to organ failure

171
Q

How to diagnose Systemic Sclerosis “ Scleroderma”

A

Clinical features and Anti-Scl 70 antibodies

Topoisomerase 1

172
Q

How to treat Systemic Sclerosis “ Scleroderma”

A

D- penicillamine and Ca channel blockers

173
Q

prognosis of Systemic Sclerosis “ Scleroderma”

A

Dependent on organ involvement

174
Q 
Graft vs Host Disease?
---
Does it have oral implication 
---
treatment?
----
cancer associated with it ?
A

Most have oral lesions that can appear lichenoid and painful
—-
Treated with immunosuppressive meds and corticosteroids
—–
Pts at increased risk for dysplasia and oral cancer

Oral Path Exam 5 (3 decks)

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