STOMATITIS Flashcards

(174 cards)

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
what organism causes Actinomycosis- Bacterial infection --- how does Actinomycosis- Bacterial infection occur? ---- where does most of the cases occur by this infection orally?
↑Actinomyces israelii: normal saprophytic anaerobic inhabitant of oral cavity, ------ History of surgery or trauma ----- 55% of cases occur in cervicofacial areas Injury, periodontal pocket, nonvital tooth, extraction socket, infected tonsi
26
what are the clinical features of Actinomycosis- Bacterial infection
Abscesses and draining sinus tracts | Colonies of organisms are yellow “sulphur granules”
27
how to treat actinomycosis?
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)
28
``` other name for Necrotizing Ulcerative Gingivitis? ---- what organism causes it? --- what causes it? ----- what age? ```
NUG, ANUG, “trench mouth” ------ Bacillus fusiformis and Borrelia vincetii ----- Frequently occurs in situations of stress, immunodeficiency or malnourishment -------- Young and middle-aged adults
29
dental association with NUG, ANUG
Interdental papillae are highly inflamed and hemorrhagic Papillae are blunted with areas of “punched-out” necrosis that are covered with a gray pseudomembrane
30
Is NUG associated with odor?
Fetid odor and intense pain
31
how to treat NUG
ebridement by scaling or curettage Chlorhexidine rinses Systemic antibiotics if fever or lymphadenopathy is present
32
what is the most common oral infection
Candida albicans
33
what organism causes Candida albicans
Dimorphism: yeast form and pathogenic hyphal form
34
Organism of low virulence in healthy, need “opportunity” for growth Predisposing conditions like?
Antibiotic therapy Cancer chemotherapy Corticosteroid therapy Dentures Diabetes mellitus Pregnancy Iron deficiency Newborns Advanced malignancy Xerostomia Other immunocompromised states (HIV/AIDS)
35
Overgrowth of Candida albicans, ------------ | can culture it in up to -----% of patients but with-------, probably present in all patients
``` part of the normal oral flora ---- 50% -------- PCR ```
36
sign and symptoms associated with a. Pseudomembranous candidosis (candidiasis)
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
37
what candida albican organism causes metallic taste
Pseudomembranous candidosis (candidiasis)
38
symtpms and signs of b. Erythematous “acute atrophic” candidosis
``` ainful, burning sensation Often associated with antibiotics: “antibiotic sore mouth” Usually affects gingiva Loss of filiform papillae on tongu ```
39
what organism is associated with antibiotic sore mouth
Erythematous “acute atrophic” candidosis
40
this organism of candida causes Loss of filiform papillae on tongue
Erythematous “acute atrophic” candidosis
41
what organism causes Denture stomatitis” “denture sore mouth
chronic atrophic candidosis
42
sign and symptoms of Chronic atrophic candidosis
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
43
characteristics of Chronic hyperplastic candidosis
“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
44
what causes angular chelties?
Candida about 90%, rest caused by Strep or Staph-
45
sign and symptoms of Angular cheilitis
Erythema or fissuring at labial commissures Unilat or bilat Predisposing factors: reduced vertical dimension and accentuated folds at the corners of the mouth
46
sign and symptoms of f. Median rhomboid glossitis “chronic atrophic candidosis”
ho“Central papillary atrophy” | Well-defined, erythematous, rhomboid (diamond- shaped) area at midline of posterior dorsal tongue Often asymptomatic
47
how does Median rhomboid glossitis “chronic atrophic candidosis diagnose
Diagnosis by clinical features, mucosal smear and tissue culture Exfoliative cytology: PAS stain
48
how to treat Median rhomboid glossitis “chronic atrophic candidosis?
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.
49
what deep fungal infection causes ---- what puts are susceptible to it?
Most cause primary lung involvement ---- ncreased susceptibility to infection and recurrence in immunocompromised (HIV+)
50
how does deep fungal infection mimic squamous cell carcinoma? -- examples
Chronic, nonhealing intraoral ulcers which can mimic squamous cell carcinoma ----- Histoplasmosis Coccidiomycosis Blastomycosis Cryptococcosis Aspergillosis
51
how to diagnose and treat deep fungal infection
Biopsy with tissue staining and culture Systemic antifungal medications
52
organisms associated with Subcutaneous fungal &Opportunistic fungal infectionsinfections
ubcutaneous fungal infections Sporotrichosis Opportunistic fungal infections Zygomycosis (mucormycosis) Often in immunosuppressed/ diabetics
53
types of Human papilloma viruses (HPVs): DNA viruses
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
54
Human herpes viruses (HHVs): DNA viruses
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
55
how many types? most adults have at least? is it hard to distinguish between different kinds of HPV?
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
56
``` Papilloma (usually HPV subtypes 6 and 11) what age? where does it occur? what are clinical presentation what cancer does this ```
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
57
“common wart” is caused by what virus?
Verruca vulgaris (HPV subtypes 2, 4, 6, 40)
58
``` Verruca vulgaris (HPV subtypes 2, 4, 6, 40) affects what age group? where does it occur? clinical presentation ? ```
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
59
histological feature of Verruca vulgaris (HPV subtypes 2, 4, 6, 40)
Koilocytes (enlarged cells with cytoplasmic clearing) Large keratohyaline granules Contagious, can spread to other parts of skin or mucosa by auto inoculation
60
treatment of Verruca vulgaris (HPV subtypes 2, 4, 6, 40)
liquid nitrogen, cryotherapy/surgical excision/salicylic acid
61
``` 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 ```
Teenagers and young adults Affects oral mucosa, larynx, genitalia Oral mucosa: labial mucosa, soft palate, lingual frenum
62
how does Condyloma acuminatum (HPV subtypes 2, 6, 11, 53, 54, 16, 18) transmitt?
Transmitted through sexual transmission or self- inoculation | incubation of 1 to 3 months from time of sexual contact
63
clinical feature of Condyloma acuminatum (HPV subtypes 2, 6, 11, 53, 54, 16, 18) ----- when does the risk of malignancy increases?
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
64
what virus causes the “Heck’s Disease”
Focal epithelial hyperplasia (HPV subtypes 13 and 32)
65
clinical feature of Focal epithelial hyperplasia (HPV subtypes 13 and 32) ------ what age group and what population is affected by this virus
Multiple soft, flattened papules clustered together --------- Most common in children often malnourished and In poor living conditions 1st described in Native Americans and Eskimos
66
where does this virus occur in the mouth as what cells?
Labial, buccal, and lingual mucosa | Koilocytes and mitosoid cells
67
Histology of Focal epithelial hyperplasia (HPV subtypes 13 and 32)
HPV identified by DNA in situ hybridization, immunohistochemical analysis, and PCR
68
what types of HPV viruses cause cervical and oropharyngeal cancer
16, 18, 6, 11, 30s, 50s | 25 yrs ago, 20-25% of throat cancer was HPV, today 75%
69
How does HHV virus survive in human body
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
70
what type of HSV cause oral infection
HSV-1 usually causes oral infections
71
what type of HSV cause genital infection about 20% crossover
HSV-2 usually causes genital infections, about 20% crossover
72
More than 90% of primary infections are ---------
asymptomatic
73
what are symptoms of acute herpetic gingivostomatitis ----- what age group ? ------
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
what % of population have recurrent herpes simplex infection ? where does it stay dormant?
Occurs in 15-45% of the U.S. population --- irus is neurotrophic and persists in a latent state in the trigeminal ganglion
75
what causes recurrent clinical lesions?
Old age, ultraviolet light, emotional stress, pregnancy, allergy, trauma, illness, dental therapy
76
what is herpes labials(“cold sore” or “fever blister”)? --- Where does recurrent herpes simplex occur? ---- clinical presentation of herpes simplex?
Prodromal symptoms of pain, burning, or tingling- ---- 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
how does herpes simplex diagnosed?
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
percentage of pt having HSV DNA virus in their saliva
At any time, 5-30% of your patients will asymptomatically excrete and will have HSV DNA in their saliva
79
how to treat simplex herpes
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
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?
``` 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
``` what is Herpes zoster (“shingles”) --- adult or children? ---- what are some predisposing factor ```
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
what are the Prodromal symptoms of shingle
ntense pain, fever malaise, headache
83
oral implication of shingles
oral lesions occur if trigeminal nerve is involved and lesions may be present on the movable or bound mucosa
84
clinical presentation of shingle
``` 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
what is Ramsay Hunt syndrome
Infection of external auditory canal with involvement of the ipsilateral facial and auditory nerves producing facial paralysis, hearing deficits and vertigo
86
what virus causes the kissing disease?
Epstein-Barr virus (EBV / HHV-4)
87
How does Epstein-Barr virus (EBV / HHV-4) transmit? ------------------------------ population affected by it? ---------------------------- what are the sign and symptoms of Infectious mononucleosis( kissing disease)? -------------------- How to diagnose kissing disease?
Transmitted through close contact or saliva Late ------------------------------- 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
What are the sign and symtoms of hairy leukoplakia
Corrugated white lesion, usually on lateral border of tongue | Cannot be wiped off
89
What infection is hairy leukoplakia associated with?
Often associated with candidal infection
90
How can Hairy leukoplakia be diagnosed?
EBV can be identified by in situ hybridization, PCR, immunohistochemistry and is the cause
91
Most commonly occurs in--------- patients, but can occur in other
Most commonly occurs in HIV+ patients, but can occur in | others
92
cancers associated with hairy leukoplakia
Burkitt’s lymphoma other lymphomas (B cells have | receptors for EBV) Nasopharyngeal carcinoma
93
``` What population is affected by Cytomegalovirus (HHV-5)? ----- Common in what population? ------ How does transmitt? ------ ```
Usually affects newborns and immunosuppressed adults ----------- Common in AIDS patients ----------- Transmitted through exchange of bodily fluids -----
94
90% of infections are -------- but can produce a mono like illness ------- complications leading to ------,-------, and severe ------and -------- retardation
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
oral lesions associated with Cytomegalovirus (HHV-5)
Chronic ulceration, affects endothelial cells and blood flow Can reside latently in salivary gland cells Infected cells show “owl eye” appearance
96
"Owl eye" cell appliance associated with what virus ?
Cytomegalovirus (HHV-5)
97
Treatment of Cytomegalovirus (HHV-5)
Systemic antiviral treatment is necessary in immunosuppressed individuals
98
``` What causes Kapok's sarcoma? --- What do lesions look like? --- where does it affect in oral cavity? ```
``` HHV-8 ----- Reddish-purple flat or raised lesions ------ Orally, most commonly on palate, gingiva, and tongue ```
99
what virus causes herpangia ?
Coxsackie A viruses
100
what is herpangia?
Hand-foot-and-mouth disease
101
what age group is affected by Coxsackie A viruses? --- How does it transmit?
Usually affect children under age 5, often in epidemics --------- Transmitted by fecal-oral route
102
oral clinical features associated with Coxsackie A viruses ----- what other body parts are affected by Coxaackie A virus? ------ How can infection associated with this virus be treated?
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
Two diseases associated with Paramyxoviruses
Mumps | Measles (Rubeola)
104
``` What age group is affected by measles? --- oral clinical features of measles ? ---- treatment? ```
Childhood, highly contagious( with skin rash) ----- “Koplik’s spots” may be an early intraoral manifestation Small, red patches with white, necrotic centers ---- MMR vaccine
105
Mumps is associated with??
Salivary gland pathology
106
What are "canker sore"
recurrent aphthous ulcerations
107
Aphtha means?
“to inflame”
108
What are the causes of Recurrent Aphthous Stomatitis (RAS)
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
What are the three types of RAS?
``` Minor aphthae (80%) Major aphthae (10%) Herpetiform aphthae (10%) ```
110
``` What age group affected by minor aphthae? ------- is male more affected than female ----- signs? ---- location ----- How does it heal? ```
Begin to develop in childhood or adolescence -------- 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
``` Major Aphthae is what disease? ---- age group? ----- where does it affect orally? ---- Healing? ```
``` “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
What is “Sutton’s disease” caused by?
Major aphthae
113
``` clinical features of Herpetiform aphthae --- onset? --- female is more affected T or F? ---- what do the ulcers resemble? ```
``` 1 to 3 mm ulcers occurring in clusters ---- Onset in adulthood ---- Female predominance --- herpes simplex virus ulcers ```
114
where do Herpetiform aphthae occur orally? ---- Healing?
Occur anywhere in the oral cavity (vs. herpes simplex ulcerations, which are usually on mucosa covering bone) No systemic signs or symptoms, as in primary herpetic gingivostomatitis ---- Heal in 7 to 10 days
115
Treatment of RAS
Topical steroids: Dexamethasone elixir 0.01% (shouldn’t swallow) Fluocinonide (Lidex®) gel 0.05% Chlorhexidine Amlexanox 5% oral paste (Aphthasol®)
116
what are the diseases associated with “Pseudo” aphthae?
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
syndrome associated with Pseudo” aphthae?
Behcet’s syndrome
118
clinical features of “Pseudo” aphthae ulcers is similar to? ---- clinical features and location of “Pseudo” aphthae ------ what other body parts affected by it?
Oral lesions are similar to aphthous ulcers ---- 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
Treatment of “Pseudo” aphthae
Systemic and topical steroids | Other immunosuppressives like amlexanox Chlorhexidine
120
Reason behind naming of Lichen Planus
Named for its similar appearance to the plant lichen (moss) Lichen = moss, planus = Latin for “flat ”
121
``` what causes Lichen Planus ---- age group? ---- More female or male affected? ----- ```
``` 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
what is Koebner phenomenon
Lichen Planus Tends to affects tissues that are irritated or traumatized
123
clinical presentation of Lichen Planus in skin and mouth?
Skin: purple, pruritic, polygonal papules Orally: reticular/erosive/bullous/plaque-like clinical appearance
124
What is the most common type of Lichen Planus
Most common type is reticular characterized by Wickham’s striae
125
Most common causes of desquamative gingivitis
LP, pemphigus vulgaris, pemphigoid, allergy)
126
Histologic features of lichen planus
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
what are lichenoid reactions?
Lesions that look like LP but aren’t: Assoc with Systemic drugs, hypersensitivity reactions, esp cinnamon and amalgam and epithelial dysplasia
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what is Vesiculo-bullous (blistering) diseases associated with?
Lichen planus
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How to treat Lichen planus?
Fluocinonide (Lidex®) gel 0.05% applied topically 3-4xs daily Clobetasol (Temovate®) gel 0.05% applied topically twice a day
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Meaning of Pemphigus ---- age group affected by it?
“Pemphigus” = Greek for blister ---- Most often in adults age 40’s and 50’s
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Foliaceus defintion
Severe progressive autoimmune disease that affects the | skin and mucous membranes: oral lesions are usually the first to appear
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clinical features of Pemphigus ?
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
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Histological features of Pemphigus?
The individual cells lose their cohesion and round up (acantholysis) producing a suprabasilar separation within the epithelium
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How to diagnose Pemphigus ?
Biopsy shows characteristic suprabasilar epithelial separation with acantholysis. Direct immunofluorescence demonstrates autoantibodies (usually IgG and C3) around the individual keratinocytes (chicken coop wire)
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How to treat Pamphigus
Systemic steroids ± steroid sparing drug
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What is Paraneoplastic pemphigus?
Affects patients who have a neoplasm, usually lymphoma or leukemia Very serious: high morbidity and mortality
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What is Benign mucous membrane pemphigoid (cicatricial pemphigoid)? ---- age? more male or female? ----- Is it more common than pemphigus vulgaris?
Chronic, autoimmune disease where patients produce antibodies against the structural proteins in their hemidesmosomes which anchor the basal keratinocytes to the underlying connective tissue, is a family of related disorders where antibodies are not directed against a single antigen, but many different antigens that comprise the hemidesmosomes ----- Average age 50 – 60, 3x more common in females ---- Considerably more common than pemphigus vulgaris
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where does Benign mucous membrane pemphigoid (cicatricial pemphigoid) affect in the body?
Affects oral, ocular, and genital mucosa ± larynx and esophagus and ± skin
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clinical features of Benign mucous membrane pemphigoid (cicatricial pemphigoid)
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
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Ocular scarring in Benign mucous membrane pemphigoid (cicatricial pemphigoid) can progress to --------if untreated
blindness
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Diagnosis of Benign mucous membrane pemphigoid (cicatricial pemphigoid)
Biopsy shows characteristic subepithelial separation. Direct IF shows autoantibodies at junction of epithelium and connective tissue
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How to treat Benign mucous membrane pemphigoid (cicatricial pemphigoid)
Ophthalmologic consultation Topical or systemic steroids
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Desquamative Gingivitis can be a clinical manifestation of?
Lichen Planus Pemphigus vulgaris Mucous membrane pemphigoid Allergic reaction
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Allergic reaction causes Desquamative Gingivitis
Toothpaste – most commonly tartar control toothpastes Cinnamon-flavored products (containing a flavoring agent called cinnamic aldehyde) Preservatives (e.g. sodium benzoate)
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what is the flavored agent in toothpaste causes allergic reaction
cinnamic aldehyde
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What causes Erythema multiforme?
Most often following systemic medications or often as a post infectious process, esp post viral. Sometimes a cause cannot be
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clinical feartures of Erythema multiforme?
Acute onset, immune mediated blistering mucocutaneous condition
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Clinical features of Erythema multiforme?
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
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what population is affected by Erythema multiforme? ------- Male or female is more affected ?
Young adults 20s and 30s, men affected more
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What body parts affected by Erythema multiforme?
Affects skin and mucous membranes, rarely only the mouth
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Prodromal symptoms of Erythema multiforme
fever, malaise, headache, cough, sore throat
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What is the recurrence rate of Erythema multiforme
20% recurrence rate
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Multiforme and Bull's eyes features associated with what disease?
Erythema multiforme
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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
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what is the most severe for erythema multiforme
Steven-Johnson syndrome | Toxic epidermal necrolysis
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How to treat erythema multiforme
Topical and high dose systemic steroids
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``` what is geographic tongue? --- other names? --- is it a common disease and is is it more common in female or male? ---- ```
Inflammatory tongue condition of unknown etiology --- “Erythema migrans”, “benign migratory glossitis” ----- Relatively common (1 – 3% of population) 2x more common in females
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clinical features of Geographic tongue
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
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Is treatment necessary for geographic tongue
No treatment necessary, topical steroids if symptomatic
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Is Reiters Syndrome associated with geographic tongue
it is very rare
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Disease associated with | geographic tongue
Urethritis, arthritis, conjunctivitis
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Lupus erythematosus is what kind of disease? ---- It is common in what age group?
Autoimmune disease --- 8x more common in women, average age is 31
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What disease is butterfly rash associated with?
Lupus erythematosus | 50 – 80% have skin lesions
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What is Discoid LE
lesions confined to skin Erythematous rash on sun-exposed skin 25% have oral lesions: erythematous plaques or erosions with white striations
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what is Systemic LE
chronic and progressive, can be life-threatening and affect multiple organs: CNS, heart, kidney Periods of remission and disease inactivity
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What are the lab tes used to diagnose LE
NA (antinuclear antibodies) & antibodies to the patient’s own DNA
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How to treat LE?
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
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clinical features of Systemic Sclerosis “ Scleroderma” -------- Is it common in male or female more?
Rare immune mediated deposition of collagen in skin and other tissues ---- Usually adults, 3:1 women.
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What is Raynaud’s phenomenon associated with Systemic Sclerosis “ Scleroderma”
vasoconstrictive event in extremities triggered by stress, cold.
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Body parts affected by Systemic Sclerosis “ Scleroderma”
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
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How to diagnose Systemic Sclerosis “ Scleroderma”
Clinical features and Anti-Scl 70 antibodies | Topoisomerase 1
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How to treat Systemic Sclerosis “ Scleroderma”
D- penicillamine and Ca channel blockers
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prognosis of Systemic Sclerosis “ Scleroderma”
Dependent on organ involvement
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``` Graft vs Host Disease? --- Does it have oral implication --- treatment? ---- cancer associated with it ? ```
Immune reaction following allogenic bone marrow transplantation. Divided into acute (first 100 days) and chronic (over 100 days) ----- 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