Flashcards in STOMATITIS Deck (174):
6 types of Bacterial infections
2. Tonsillitis and pharyngitis
5. Actinomycosis- Bacterial infection
6. Necrotizing Ulcerative Gingivitis
2 types of Fungal Infections
1. Candida albicans
2. Deep fungal infections
6 types of Candida albicans
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”
types of Viral infection
1. Human papilloma viruses (HPVs): DNA viruses
2. Human herpes viruses (HHVs): DNA viruses
3. Coxsackie A viruses
bacteria cause infection in impetigo
Streptococcus pyogenes and Staphylococcus aureus
where does impetigo infect and who? what causes it?
it spread how?
can it be treated?
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
antibiotic to treat impetigo
Mupirocin topical Cephalexin, dicloxacillin
what organism causes Tonsillitis and pharyngitis?
age it affects?
Bacterial or viral in origin: group A, beta-hemolytic streptococc
Children aged 5 - 15 years
“Strep throat”: sore throat, headache, fever, tonsillar
sign and symptoms of Tonsillitis and pharyngitis?
how does it spread?
hyperplasia, yellowish tonsillar exudate, erythema, palatal petechiae, lymphadenopathy
Culture and treat with antibiotics: penicillin, amoxicillin, cephalosporin
Complications of Strep throat
organism causes Scarlet fever
sign and symptoms
how does it affect body?
Group A, beta-hemolytic streptococci
Children aged 3-12 years
Skin rash, fever, palatal petechiae, “strawberry tongue”
Organisms elaborate an erythrogenic toxin that attacks blood vessels
how does Rheumatic fever affect body?
organism causes syphilis
how does it spread
what is the incident( in what population)
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
what is chancre? syphilis
when does primary infection occur?
is it infectious
painless ulcer at site of inoculation External genitalia, anus, lip
3-90 days after initial exposure
TPHA + FTA-ABS
when does secondary infection occur?
what type of ulcer occur? what are signs and symptoms?
is it infectious?
4-10 weeks after initial infection
“Snail track” ulcers
Condylomata lata (papillomas), maculopapular cutaneous rash
Lymphadenopathy, sore throat, fever
when does latent syphilis show symptoms
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?
evelops in 30% of patients
Gumma – unique type of necrosis
Indurated, nodular or ulcerated lesion Intraorally, usually affects palate (perforation) or
Glossitis, atrophy and loss of dorsal tongue papillae (Luetic glossitis)
Cardiovascular system and CNS involvement
signs and symptoms of congenital syphilis
Frontal bossing, underdeveloped Mx, high arched palate, saddle nose deformity
Interstitial keratitis of cornea
VIIIth nerve deafness
Screwdriver-shaped “Hutchinson’s incisors” “Mulberry molars” bumps on occlusal surface
Blood tests associated with congenital syphilis
how to treat it?
VDRL and RPR- sensitive but not specific TPHA and FTA-ABS
what are dental abnormalities associated with congenital syphilis
1.Screwdriver-shaped “Hutchinson’s incisors”
2. “Mulberry molars” bumps on occlusal surface
organism associated with Tuberculosis?
where it occurs?
how does TB becomes an active disease
Mycobacterium tuberculosis: acid-fast bacillus
Primary infection of lungs
Immunodeficiency (old age, poverty, HIV/AIDS) contributes to progression from infection to active dis
how does TB spread?
clinical features of TB
Spread through airborne droplets from patients with active disease
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
Histology and biopsy of tissues culture
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
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
what are the clinical features of Actinomycosis- Bacterial infection
Abscesses and draining sinus tracts
Colonies of organisms are yellow “sulphur granules”
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)
other name for Necrotizing Ulcerative Gingivitis?
what organism causes it?
what causes it?
NUG, ANUG, “trench mouth”
Bacillus fusiformis and Borrelia vincetii
Frequently occurs in situations of stress, immunodeficiency or malnourishment
Young and middle-aged adults
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
Is NUG associated with odor?
Fetid odor and intense pain
how to treat NUG
ebridement by scaling or curettage
Systemic antibiotics if fever or lymphadenopathy is present
what is the most common oral infection
what organism causes Candida albicans
Dimorphism: yeast form and pathogenic hyphal form
Organism of low virulence in healthy, need “opportunity” for growth
Predisposing conditions like?
Cancer chemotherapy Corticosteroid therapy Dentures
Diabetes mellitus Pregnancy
Iron deficiency Newborns
Advanced malignancy Xerostomia
Other immunocompromised states (HIV/AIDS)
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
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
what candida albican organism causes metallic taste
Pseudomembranous candidosis (candidiasis)
symtpms and signs of b. Erythematous “acute atrophic” candidosis
ainful, burning sensation
Often associated with antibiotics: “antibiotic sore
Usually affects gingiva
Loss of filiform papillae on tongu
what organism is associated with antibiotic sore mouth
Erythematous “acute atrophic” candidosis
this organism of candida causes Loss of filiform papillae on tongue
Erythematous “acute atrophic” candidosis
what organism causes Denture stomatitis” “denture sore mouth
chronic atrophic candidosis
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
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
what causes angular chelties?
Candida about 90%, rest caused by Strep or Staph-
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
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
how does Median rhomboid glossitis “chronic atrophic candidosis diagnose
Diagnosis by clinical features, mucosal smear and tissue culture
Exfoliative cytology: PAS stain
how to treat Median rhomboid glossitis “chronic atrophic candidosis?
Oral or systemic antifungal therapy
Oral suspension: 1 tsp. 5x daily for 2 wks.
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.
what deep fungal infection causes
what puts are susceptible to it?
Most cause primary lung involvement
ncreased susceptibility to infection and recurrence in
how does deep fungal infection mimic squamous cell carcinoma?
Chronic, nonhealing intraoral ulcers which can mimic
squamous cell carcinoma
Blastomycosis Cryptococcosis Aspergillosis
how to diagnose and treat deep fungal infection
Biopsy with tissue staining and culture Systemic antifungal medications
organisms associated with Subcutaneous fungal &Opportunistic fungal infectionsinfections
ubcutaneous fungal infections Sporotrichosis
Opportunistic fungal infections
Often in immunosuppressed/ diabetics
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
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)
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
Papilloma (usually HPV subtypes 6 and 11)
where does it occur?
what are clinical presentation
what cancer does this
Age 30 to 50 years
Tongue, lips,↑ soft palate
White/red/normal color “cauliflower” shaped exophytic nodule, sessile or pedunculated
Usuallysmall, but can be as large as 3 cm
“common wart” is caused by what virus?
Verruca vulgaris (HPV subtypes 2, 4, 6, 40)
Verruca vulgaris (HPV subtypes 2, 4, 6, 40) affects what age group?
where does it occur?
clinical presentation ?
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
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
treatment of Verruca vulgaris (HPV subtypes 2, 4, 6, 40)
liquid nitrogen, cryotherapy/surgical excision/salicylic acid
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
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
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
what virus causes the “Heck’s Disease”
Focal epithelial hyperplasia (HPV subtypes 13 and 32)
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
where does this virus occur in the mouth as what cells?
Labial, buccal, and lingual mucosa
Koilocytes and mitosoid cells
Histology of Focal epithelial hyperplasia (HPV subtypes 13 and 32)
HPV identified by DNA in situ hybridization, immunohistochemical analysis, and PCR
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%
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
what type of HSV cause oral infection
HSV-1 usually causes oral infections
what type of HSV cause genital infection about 20% crossover
HSV-2 usually causes genital infections, about 20% crossover
More than 90% of primary infections are ---------
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
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
what causes recurrent clinical lesions?
Old age, ultraviolet light, emotional stress, pregnancy, allergy, trauma, illness, dental therapy
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)
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
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
how to treat simplex herpes
opical and systemic antiviral medications Effective when administered early prodrome period in primary or recurrent infection
800 mg tablet every 4 hours orally for 7 to
5% ointment applied to affected areas topically with a finger cot q4h
Or pencicylovir topical
single 1500 mg dose or single-day (750 mg 2x for one day) dose
2g (four 500mg tablets) q12h for one day
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
10 – 21 day incubation
erythemavesiclepustulehardened crust on skin and mucous membranes
Skin: extremities, face, trunk
Perioral and oral lesions: vermillion border of lips, palate and buccal mucosa
Recovery in 2 to 3 weeks
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
what are the Prodromal symptoms of shingle
ntense pain, fever malaise, headache
oral implication of shingles
oral lesions occur if trigeminal nerve is involved and lesions may be present on the movable or bound mucosa
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
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
what virus causes the kissing disease?
Epstein-Barr virus (EBV / HHV-4)
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
What are the sign and symtoms of hairy leukoplakia
Corrugated white lesion, usually on lateral border of tongue
Cannot be wiped off
What infection is hairy leukoplakia associated with?
Often associated with candidal infection
How can Hairy leukoplakia be diagnosed?
EBV can be identified by in situ hybridization, PCR, immunohistochemistry and is the cause
Most commonly occurs in--------- patients, but can occur in other
Most commonly occurs in HIV+ patients, but can occur in
cancers associated with hairy leukoplakia
Burkitt’s lymphoma other lymphomas (B cells have
receptors for EBV) Nasopharyngeal carcinoma
What population is affected by
Common in what population?
How does transmitt?
Usually affects newborns and immunosuppressed adults
Common in AIDS patients
Transmitted through exchange of bodily fluids
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
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
"Owl eye" cell appliance associated with what virus ?
Treatment of Cytomegalovirus (HHV-5)
Systemic antiviral treatment is necessary in immunosuppressed individuals
What causes Kapok's sarcoma?
What do lesions look like?
where does it affect in oral cavity?
Reddish-purple flat or raised lesions
Orally, most commonly on palate, gingiva, and tongue
what virus causes herpangia ?
Coxsackie A viruses
what is herpangia?
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
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-
Infection usually resolves in 7 to 10 days
Two diseases associated with Paramyxoviruses
What age group is affected by measles?
oral clinical features of measles ?
Childhood, highly contagious( with skin rash)
“Koplik’s spots” may be an early intraoral manifestation
Small, red patches with white, necrotic centers
Mumps is associated with??
Salivary gland pathology
What are "canker sore"
recurrent aphthous ulcerations
What are the causes of Recurrent Aphthous Stomatitis (RAS)
trauma (e.g. dental procedures) or emotional
Evidence of immunologic cause: T cell mediated
Specific histocompatibility (HLA) antigens have been associated, indicating a possible genetic predisposition
What are the three types of RAS?
Minor aphthae (80%)
Major aphthae (10%)
Herpetiform aphthae (10%)
What age group affected by minor aphthae?
is male more affected than female
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
Major Aphthae is what disease?
where does it affect orally?
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
What is “Sutton’s disease” caused by?
clinical features of Herpetiform aphthae
female is more affected T or F?
what do the ulcers resemble?
1 to 3 mm ulcers occurring in clusters
Onset in adulthood
herpes simplex virus ulcers
where do Herpetiform aphthae occur orally?
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
Treatment of RAS
Dexamethasone elixir 0.01% (shouldn’t swallow) Fluocinonide (Lidex®) gel 0.05%
Amlexanox 5% oral paste (Aphthasol®)
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
syndrome associated with Pseudo” aphthae?
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
Treatment of “Pseudo” aphthae
Systemic and topical steroids
Other immunosuppressives like amlexanox Chlorhexidine
Reason behind naming of Lichen Planus
Named for its similar appearance to the plant lichen (moss) Lichen = moss, planus = Latin for “flat
what causes Lichen Planus
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
Women represent about 2/3 of patients
what is Koebner phenomenon
Lichen Planus Tends to affects tissues that are irritated or traumatized
clinical presentation of Lichen Planus in skin and mouth?
Skin: purple, pruritic, polygonal papules
Orally: reticular/erosive/bullous/plaque-like clinical appearance
What is the most common type of Lichen Planus
Most common type is reticular characterized by Wickham’s striae
Most common causes of desquamative gingivitis
LP, pemphigus vulgaris, pemphigoid, allergy)
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
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
what is Vesiculo-bullous (blistering) diseases associated with?
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
Meaning of Pemphigus
age group affected by it?
“Pemphigus” = Greek for blister
Most often in adults age 40’s and 50’s
Severe progressive autoimmune disease that affects the
skin and mucous membranes: oral lesions are usually the first to appear
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
Histological features of Pemphigus?
The individual cells lose their cohesion and round up (acantholysis) producing a suprabasilar separation within the epithelium
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)
How to treat Pamphigus
Systemic steroids ± steroid sparing drug
What is Paraneoplastic pemphigus?
Affects patients who have a neoplasm, usually lymphoma or leukemia
Very serious: high morbidity and mortality
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
where does Benign mucous membrane pemphigoid (cicatricial pemphigoid) affect in the body?
Affects oral, ocular, and genital mucosa ± larynx and esophagus and ± skin
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
Ocular scarring in Benign mucous membrane pemphigoid (cicatricial pemphigoid) can progress to --------if untreated
Diagnosis of Benign mucous membrane pemphigoid (cicatricial pemphigoid)
Biopsy shows characteristic subepithelial separation. Direct IF shows autoantibodies at junction of epithelium and connective tissue
How to treat Benign mucous membrane pemphigoid (cicatricial pemphigoid)
Ophthalmologic consultation Topical or systemic steroids
Desquamative Gingivitis can be a clinical manifestation of?
Mucous membrane pemphigoid Allergic reaction
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)
what is the flavored agent in toothpaste causes allergic reaction
What causes Erythema multiforme?
Most often following systemic medications or often as a post infectious process, esp post viral. Sometimes a cause cannot be
clinical feartures of Erythema multiforme?
Acute onset, immune mediated blistering mucocutaneous condition
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 lesions highly variable “multiforme”
- Characteristic target or “bull’s eye” lesions
- Can occur without oral lesions
- Classically affects palms and soles
- Oral ulcers with erythema and irregular borders
- Lips, labial mucosa, tongue, floor of mouth, soft palate
- Crusting and bleeding at vermillion zone of lips
- 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
what population is affected by Erythema multiforme?
Male or female is more affected ?
Young adults 20s and 30s, men affected more
What body parts affected by Erythema multiforme?
Affects skin and mucous membranes, rarely only the mouth
Prodromal symptoms of Erythema multiforme
fever, malaise, headache, cough, sore throat
What is the recurrence rate of Erythema multiforme
20% recurrence rate
Multiforme and Bull's eyes features associated with what disease?
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
what is the most severe for erythema multiforme
Toxic epidermal necrolysis
How to treat erythema multiforme
Topical and high dose systemic steroids
what is geographic tongue?
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
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
Is treatment necessary for geographic tongue
No treatment necessary, topical steroids if symptomatic
Is Reiters Syndrome associated with geographic tongue
it is very rare
Disease associated with
Urethritis, arthritis, conjunctivitis
Lupus erythematosus is what kind of disease?
It is common in what age group?
8x more common in women, average age is 31
What disease is butterfly rash associated with?
50 – 80% have skin lesions
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
what is Systemic LE
chronic and progressive, can be life-threatening and affect multiple organs: CNS, heart, kidney
Periods of remission and disease inactivity
What are the lab tes used to diagnose LE
NA (antinuclear antibodies) & antibodies to the patient’s own DNA
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
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.
What is Raynaud’s phenomenon associated with Systemic Sclerosis “ Scleroderma”
vasoconstrictive event in extremities triggered by stress, cold.
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
How to diagnose Systemic Sclerosis “ Scleroderma”
Clinical features and Anti-Scl 70 antibodies
How to treat Systemic Sclerosis “ Scleroderma”
D- penicillamine and Ca channel blockers
prognosis of Systemic Sclerosis “ Scleroderma”
Dependent on organ involvement