Dr. Irna Sufiawati, drg., Sp.

PM
Oral Medicine Deparment
ACUTE MULTIPLE LESIONS
1.  Herpes Virus Infection
2.  Primary Herpes Simplex Virus
Infection RECURRENT ORAL ULCERS
3.  Coxsackievirus Infection 1.  Recurrent Aphtous Stomatitis
4.  Varicells-Zoster Infection 2.  Behcet s Disease
5.  Erythema Multiforme 3.  Recurrent Herpes Simplex
6.  Contact Allergic Stomatitis Infection
7.  Oral Ulcer Secondary to Cancer
Chemotherapy
SINGLE ULCERS
8.  Acute Necrotizing Ulcerative Gingivitis
1.  Histoplasmosis
CHRONIC MULTIPLE LESIONS 2.  Blastomycosis
1.  Pemphigus
2.  Subepithelial Bullous Dermatoses 3.  Mucormycosis
3.  Herpes Simplex Virus Infection in
Immunosuppressed Patients
1.  Herpes Virus Infection
2.  Primary Herpes Simplex Virus Infection
3.  Coxsackievirus Infection
4.  Varicells-Zoster Infection
5.  Erythema Multiforme
6.  Contact Allergic Stomatitis
7.  Oral Ulcer Secondary to Cancer Chemotherapy
8.  Acute Necrotizing Ulcerative Gingivitis
!  There are 80 known
herpesviruses, and eight of
them are known to cause
infection in humans ! have
been classified into three
subfamilies based on their
biologic properties. :
"  Alphaherpesviruses -
HSV-1, HSV-2, VZV
"  Betaherpesviruses - CMV,
HHV-6, HHV-7
"  Gammaherpesviruses -
EBV, HHV-8
•  HSV1, HSV2, and varicella-zoster are viruses that are
known to cause oral mucosal disease.
•  Cytomegalovirus (CMV) is an occasional cause of oral
ulceration in immunosuppressed patients, and it is
suspected as a cause of salivary gland disease in HIV-
infected patient.
•  Epstein-Barr Virus (EBV) is associated with a wide variety
of human diseases including the infectious mononucleosis
syndrome, Hodgkin's lymphoma, and nasopharyngeal
carcinoma. EBV is also an opportunistic pathogen in
immunocompromised patients, associated with
lymphoproliferative diseases and oral hairy leukoplakia.
•  Human herpes virus-8 (HHV-8) has been implicated in the
etiology of Kaposi’s sarcoma, the most common malignant
tumor associated with HIV infection.
!  HSV 1 : oral & faringeal, meningoencephalitis
HSV 2 : genital
!Gejala/Gambaran Klinis: Pemeriksaan penunjang:
•  Gejala prodromal (1-2 hr) a. Sitologi
b. Isolasi HSV
•  Vesikel kecil pada seluruh
c. Antibodi titer
mukosa oral & mudah pecah !
ulser iregular
DD/ :
•  Seluruh mukosa (palatum &
uvula), terutama mukosa - Herpangina
berkeratin - Penyakit kaki, tangan, dan mulut
•  Gingivitis marginalis akut - Varicella
generalisata dengan ulser pada - Herpes zoster
gingiva
Th/ - Antiviral agent: acyclovir
- Antipiretik: aspirin, asetaminofen)
- Anestetik topikal

(Burket, 2003)
Vesikel dan ulser yang Gingivitis marginalis akut Vesikel dan inflamasi di
dikelilingi jaringan inflamasi pada anterior mandibula sekitar molar mandibula

multinuclear giant cell pada

cytology smear dengan
pewarnaan Giemsa
(Burket, 2003)
"  Etiologi: Coxsackievirus A4 (A1-A10 dan A16-A22)
"  Sering menyerang anak-anak usia 3-10 tahun
"  Klinis :
#  Setelah periode inkubasi 2-10 hari infeksi dimulai
dengan Gemam, menggigil, anoreksia
#  Sakit tenggorokan, disfagia, sore mouth
#  Diawali dengan lesi makula ! papul ! vesikel
dalam waktu 24-48 jam ruptur ! ulser (1-2 mm) pada
posterior pharynx, tonsils, faucial pillars, dan palatum
lunak.
"  Pem. penunjang : smear dari •  Herpangina secara klinis
vesikel tidak memperlihatkan dibedakan dengan primary HSV
giant cell infection:
1)  Herpangina terjadi epidemik,
"  Th/ : self limiting (1 minggu), HSV infections tidak.
suportif, topikal anestesi 2)  Herpangina cenderung lebih
"  DD/ : ringan drpd HSV infection.
3)  Lesi herpangina terjadi pada
"  Primary HSV infection pharynx and regio posterior
"  Faringitis limfonodular akut mukosa mulut, sedangkan
"  Varicella HSV terutama menyerang
bagian anterior mulut
4)  Herpangina tidak
menyebabkan a generalized
acute gingivitis seperti pd
primary HSV infection.
5)  Lesi herpangina cenderung
lebih kecil drpd HSV.

JOE R. MONROE, Viral Infections in Children and

Adolescents, 2013.
!  Etiologi: Coxsackievirus A10
!  Klinis:
"  Distribusi lesi sama dengan
herpangina, tetapi lesi berupa
nodul kuning-putih tidak
berkembang menjadi vesikel
atau ulser Laskaris
!  Th/ : Nodul putih kekuningan pada
self-limiting palatum lunak & uvula
suportif
!  Etiologi: Coxsackie A16
!  Dari pasien berusia 8-33 tahun, 75 % anak di
bawah 4 tahun (Adler L, Epidemiologic investigation of hand-
foot-and-mouth disease. Am J Dis Child 1970;120:309)
!  Klinis :
"  Khas: demam ringan, makula non pruritus, papula dan
vesikel terutama pada permukaan ekstensor tangan dan
kaki
"  Lebih ekstensif dibanding herpangina, vesikel dan ulser
di mulut
"  Lokasi intraoral: palatum keras, lidah serta mukosa
bukal
•  Th/ : suportif
•  DD/ :
# Herpangina
# Herpes simpleks infection
# Acut lymphonodular
pharyngitis

(Laskaris, Oral Diagnosis, 2002)

•  Etiologi: chickenpox (varicella) dan shingles (herpes zoster)
!  Chickenpox: a generalized primary infection (analog dengan acute herpetic
gingivostomatitis)
!  Setelah infeksi primer, VZV laten dalam dorsal root ganglia dari spinal nerves atau
extramedullary ganglia nervus cranial.
!  VZV dapat reaktif ! lesi herpes zoster terlokalisir
!  Tanda/Gejala Klinis :
#  Chickenpox : anak-anak, lesi makulopapular yang sangat pruritus di seluruh
tubuh ! vesikel oral ! ulser
#  HZV: prodromal (2-4 hr) ! shooting pain, parestesi, rasa terbakar, sensitif
sepanjang lintasan saraf yang terkena
#  Vesikel unilateral
#  Post herpetic neuralgia (terutama pasien berusia >60 tahun)
#  Anomali dental, nekrosis pulpa, dan resorpsi internal akar
#  Pada pasien immunocompromis, lesi HZ besar kronis ! necrosis tulang dan
exfoliation of teeth
"  Pemeriksaan*penunjang:*
–  Sitologi*
–  Isolasi*virus**
–  An7body*7ter*jarang*diperlukan*kecuali*
pada*kasus*zoster'sine'erup,one'
'
"  Th/*
–  Acyclovir/valacyclovir/famciclovir**
–  Untuk*mencegah*postherpe7c*neuralgia:**
•  Systemic*cor7costeroids*untuk*pasien*
diatas*50th*masih*kontroversial*
•  Topikal*capsaicin*
•  Jika*capsaicin*7dak*efek7f*!Tricyclic*
an7depressant*or*gabapen7n*
•  Chemical*atau*surgical*neurolysis*pada*
kasus*refraktori**

(Burket, 2003)
!  Suatu penyakit inflamatori akut pada kulit dan mukosa yang
menyebabkan berbagai jenis/bentuk lesi (multiforme)
!  Deposisi kompleks imun pada mikrovaskular superfisial kulit dan
mukosa atau cell mediated immunity
!  Reaksi hipersensitivitas tipe lambat (delayed-type hypersensitivity
reaction)

!  Faktor predisposisi EM :
#  Herpes Simplex Virus ! Herpes simplex virus associated erythema
multiforme (HAEM)
#  Obat-obatan
#  Progesteron, mikoplasma, tumor ganas, radioterapi, penyakit Crohn s,
sarkoidosis, histoplasmosis, mononukleosis infeksius
Patogenesis Erythema Multiforme
"  Tanda/Gejala Klinis :
- akut, eksplosif ! demam dan malaise, asimtomatik
- dalam 24 jam ! lesi ekstensif pada kulit dan mukosa
- makula dan papula (0,5 – 2 cm), simetris
- tangan, kaki, siku, lutut ! makula, papula, vesikel

"  Lesi target ! bula sentral

"  Bentuk mayor ! Stevens-Johnson syndrome : vesikel dan

bula melibatkan kulit, mata, mulut, dan genital

"  Intra oral:

•  Bersamaan dengan lesi di kulit
•  Bula ! ulser, lesi lebih besar dari lesi virus, tidak beraturan, dalam,
mudah berdarah
•  Bibir ! krusta. Jarang : gingiva
Lesi Target Stevens - Johnson syndrome

Lesi EM intraoral
(Burket dan Laskaris)
$  DD/ :
"  Infeksi HSV
"  Pemphigus vulgaris
"  Ulser aftosa major
"  LP erosif
"  Cicatrical pemphigoid

$  Lab:
"  Pemeriksaan darah lengkap: kadar
elektrolit; determinasi BUN; laju endap
darah (LED; erythrocyte sedimentation
rate [ESR]); tes fungsi hati; Gambaran histopatologis: Inflamasi-
"  Kultur dari darah, sputum infiltrasi limfositik dan formasi vesikel
intraepithelial pada lapisan basal.
"  Citologi
Inflamasi mukosa terdiri atas makrofag
"  Isolasi virus dan limfosit (CD4+ lebih mendominasi
"  Biopsy daripada CD8+), dengan sedikit neutrofil
dan kadang-kadang eosinofil (terutama
pada kasus yang berkaitan dengan obat-
$  Th/ :
obatan).
"  Ringan : suportif (obat kumur/topikal
anestesi, diet lunak atau cair)
"  Sedang – berat : kortikosteroid sistemik
 Lima*(5)*Tipe*dan*Gambaran*Klinis*EM*

Bajaj P, Sabharwal R, PK Mohammed R, Garg D, Kapoor C. Erythema Multiforme: Classification and

Immunopathogenesis. J Adv Med Dent Scie 2013;1(2):40-47.
Perbedaan*gambaran*klinis*SJS,*SJSMTEN*overlap,*danTEN*

Bajaj P, Sabharwal R, PK Mohammed R, Garg D, Kapoor C. Erythema Multiforme: Classification and

Immunopathogenesis. J Adv Med Dent Scie 2013;1(2):40-47.
"  Reaksi hipersensitif: a delayed hypersensitivity (Type IV)

"  Etiologi :
!  Contact stomatitis akibat kontak dengan dental materials, oral
hygiene products, or foods.
!  Penyebab umum contact oral reactions: cinnamon dan peppermint,
yang sering digunakan pada makanan, permen, permen karet, produk
oral hygiene seperti pasta gigi, obat kumur, dan dental floss. Kontak
alergen dengan kulit/mukosa, karet, bahan kimia, amalgam, akrilik,
crown

Stomatitis Venenata

!  Obat-obatan ! Stomatitis Medikamentosa

"  Tanda/Gejala Klinis :
# Lesi pada daerah kontak
# Rasa terbakar, sakit disertai
eritema, vesikel dan ulser
# Plasma cell gingivitis (generalized
erythema and edema pada
attached gingiva, kadang2 disertai
Contact allergy pada mukosa labial akibat
cheilitis dan glossitis peppermint

"  Pemeriksaan penunjang: Patch test

"  Th/:
"  Ringan : menghilangkan alergen
"  Berat : aplikasi kortikosteroid
topikal

Plasma cell gingivitis

!  Efek samping dari obat antikanker ! multiple oral ulcers

!  Anticancer drugs dapat menyebab oral ulcers !

"  Directly: methotrexate, cause oral ulcers via direct effect on the
replication and growth of oral epithelial cells by interfering with nucleic
acid and protein synthesis, leading to thinning and ulceration of the
oral mucosa
"  Indirectly: Drugs that cause stomatitis indirectly depress the bone
marrow and immune response, leading to bacterial, viral, or fungal
infections of the oral mucosa.

!  Th/ :
"  Reaksi inflamasi memulai ulserasi ! obat antiinflamasi untuk
meminimalisir bone marrow–related ulceration
"  Topikal anestesi
!  Efek samping dari obat antikanker ! multiple oral ulcers

!  Empat jenis kemoterapi kanker :

1. Alkylating agents
2. Antimetabolit agents
3. Antibiotik agents
4. Alkaloid

!  Anticancer drugs may cause oral ulcers !

"  Directly: methotrexate, cause oral ulcers via direct effect on the
replication and growth of oral epithelial cells by interfering with nucleic
acid and protein synthesis, leading to thinning and ulceration of the oral
mucosa
"  Indirectly: Drugs that cause stomatitis indirectly depress the bone
marrow and immune response, leading to bacterial, viral, or fungal
infections of the oral mucosa.
"  Infeksi endogen oral yang ditandai dengan nekrosis gingiva
"  Penyebab bakteri anaerob: Treponema spp, Selemnomonas spp,
Fusobacterium spp, Bacteroides intermedius
"  ANUG klasik banyak terjadi pada pasien usia 16-30 tahun,
berhubungan dengan three major factors:
"  OH buruk

"  Merokok,

"  Stress emosional

!  Penyakit sistemik terkait: penyakit yang mengenaineutrophils

(leukemia atau aplastic anemia), malnutrisi, dan infeksi HIV.
!  ANUG progresif ! Noma
"  Tanda/Gejala Klinis :
"  Akut, sakit, hipersalivasi, rasa
logam, pendarahan spontan,
ekstrusi gigi, nyeri tekan, mobility,
interdental papil hilang
"  Tipe lesi : ulserasi nekrotik
“punched-out” pd interdental papil
"  Lesi berkembang melibatkan
tulang ! sekuester ANUG
"  Th/ :
•  Debridemen irigasi, kuret gingiva,
rootplan
•  Menghilangkan faktor lokal
•  OHI (obat kumur hidrogen peroksida
2% dan chlorhexidine 12 %)
•  Antibiotik (tetrasiklin,
metronidazole

NOMA
(Burkets dan Laskaris)
1.  RECURRENT APHTOUS STOMATITIS

2.  BEHCET S DISEASE

3.  RECURRENT HERPES SIMPLEX INFECTION

!  Etiologi':'tidak'diketahui'
dengan'pasti'
!  Faktor'predisposisi:'
multifaktorial'
"  Kelainan'autoimmune''
"  Hipersensitivitas'thp''
Streptococcus*sanguis*
"  Faktor'lainnya:''
Clinical*Charateris7cs*of*RAS*
"  Patients dengan minor aphthae or major aphthous ulcers ! periksa
kemungkinan penyakit connective-tissue, kadar serum iron, folate,
vitamin B12, dan ferritinabnormal ! rujuk ke internist
"  Identifikasi alergi makanan atau sensitivitas thp gluten
"  Major aphthous ulce ! pada pasien HIV dengan CD4 < 100/mm3

"  Pemeriksaan penunjang RAS

RAS*e.c*defisiensi*zat*besi*
DIFFERENTIAL*DIAGNOSIS*OF*RAS*
THERAPY*TO*CONSIDER*FOR*RAS*
!  Diperkenalkan oleh Turkish dermatologist Hulûsi Behçet, (1937) dengan
as a triad of symptoms (trias gejala):
"  Ulser oral rekuren,
"  Ulser genital rekuren
"  Lesi mata (uveitis)

!  Merupakan penyakit inflamasi kronis multisistem

Etiopatogenesis:
"  Disebabkan immunocomplexes yang menyebabkan vasculitis dari
pembuluh darah kecil-medium dan inflamasi epitelium yang
disebabkan oleh immunocompetent T lymphocytes dan plasma cells
"  Aktivitas neutrophil meningkat
"  Faktor genetik: berhubungan kuat dengan komponen genetik HLA-B51
*
The*Interna7onal*Study*Group*Diagnos7c*Criteria:*
*
*
*
* * * * **
* * * * **
*
+*Pathergy*tes*posi7ve* * * **
* * * **
*
*********
*
*
*
•  Behçet s syndrome pada anak sering terjadi pada usia 9-10 years,
•  Oral ulcers sangat sering tampak pada anak (95%), uveitis tampak
lebih jarang terjadi
•  A variant of Behçet’s syndrome ! MAGIC syndrome (Mouth And
Genital ulcers with Inflammed Cartilage)

Aphthous-like lesion pada pasien Behçet s syndrome

 Spectrum of organ involvement in Behçet s disease

(Verity DH et al. Br J Ophthalmol 2003;87:1175-83)

 International Study Group criteria for Behçet s disease (1990)

Criteria present Description

Reccurent oral Minor aphthous, major aphthous, or herpetiform ulceration
ulceration observed by physician or patient, which recurred at least 3 times
in any 12 month period
Plus two of :
Recurrent genital Aphthous ulceration or scarring, observed by physician or
ulceration patient
Eye lesion Anterior uveitis, posterior uveitis, or cells in vitreous on slit lamp
examination; or retinal vasculitis observed by ophthalmologist
Skin lesion Erythema nodusum observed by physician or patient,
pseudofolliculitis, or papulopustular lesions; or acneiform
nodules observed by physician in post-adolescent patients not
on corticosteroids
Positive pathergy test Read by physician at 24-48 hours
Terapi*Behcet’s*Disease**
"  Tergantung*dari*7ngkat*keparahan*dan*daerah*yang*terlibat*
"  Tujuan*utama*terapi*BD*!*untuk*meminimalisir*kerusakan*organ*jangka*
panjang*:*
–  Konstrol*symptom*
–  Menekan*inflamasi**
–  Mencegah*kerusakan*endMorgan**

"  ObatMobatan:**
"  An7inflamasi*dan*imunosupresan**(systemic*cor7costeroids*!obat*
"  Kombinasi*azathioprine*dengan*prednisone*
"  Pentoxifylline*(efek*samping*lebih*rendah)*
"  Kombinasi*cyclosporine*atau*dengan*cor7costeroids*(pada*kasus*berat)*
"  Colchicine*dan*thalidomide*(pada*BD*dengan*manifestasi*mucocutaneous*
and*gastrointes7nal)*

"  Lesi*mukosa*oral*!*steroids*topikal/intralesional*
"  Penanganan*BD*mul7disiplin**
!  Infeksi HSV rekuren oral:
"  Recurrent herpes labialis [RHL]
"  Recurrent intraoral herpes simplex infection [RIH]
!  Recurrent herpes diaktifkan oleh: trauma, fever, sinar matahari
(sunburn), immunosuppression, menstruasi, stress.
!  Beberapa mekanisme reaktivasi HSV laten: serum IgA serum
rendah
"  Penurunan cell mediated immunity
"  Penurunan salivary antiherpes activity
"  Depresi ADCC (antibody-dependent cell-mediated cytotoxicity)
dan interleukin-2 disebabkan oleh pelepasan prostaglandin pada
kulit.
•  Tanda/Gejala klinis:
•  Dimulai gejala prodromal: rasa terbakar
dan perih (tingling sensation)
•  Lesi vesikel 1-3 mm ! cluster 1-2 cm
! mudah ruptur menjadi ulser
•  Sering di gingiva, palatum, alv.ridge
(mukosa berkeratin)
•  Jarang di dasar mulut, bukal, labial
•  Pemeriksaan penunjang:
–  Cytology smears (herpetic lesions !
cells with ballooning degeneration &
multinucleated giant cells
Krusta pada RHL
–  Kultur virus
•  Diagnosis Banding:
•  RAS herpetiforme
•  Varicella-zoster infections
•  Th/
•  Eliminir faktor pemicu
•  Antivirus (acyclovir, valacyclovir,
famciclovir)
Recurrent intraoral herpes simplex infection (RIH)
 RIH RAS herpetiforme

Age mainly affected Primer : chilhood & Start in chilhood & adolescence
adolescence ! < 30 y.o (< 40 y.o)
Secunder (recurrent): adult Decreasing with age
Predilection Male = female Female > male

Etiology Viral Unclear

Etiology/precpitating Fever, sunlight, trauma, Family history, immune, stress,
factors immunosuppression trauma, def. nutrition, GIT disease,
mentruation, food alergy
Prodromal symptom fever No fever
Appearance of primary vesicle papule
lesions
Appearance of mature Shallow, punctate ulcers Ulcer with erythematous halo
lesions
Common location Keratinizing (and non- Non-keratinizing mucosa
keratizing) mucosa
mucosaNumber Few to several Few to several (10-100)
!  Penyakit major dari Chronic Multiple Lesions:
"  Pemphigus vulgaris
"  Pemphigus vegetans
"  Bullous pemphigoid,
"  Mucous membrane pemphigoid
"  Linear IgA disease
"  Erosive lichen planus
!  Herpes Simplex Virus Infection in Immunosuppressed
Patients
"  Autoimun disease
"  A potentially life-threatening disease that causes blisters and erosions
of the skin and mucous membranes ! a result of autoantibodies that
react with desmosomal glycoproteins that are present on the cell
surface of the keratinocyte. The immune reaction against these
glycoproteins causes a loss of cell-to-cell adhesion, resulting in the
formation of intraepithelial bullae.
!  The major variants of pemphigus:
"  Pemphigus vulgaris (PV)
"  Pemphigus vegetans
"  Pemphigus foliaceus
"  Pemphigus erythematosus
"  Paraneoplastic pemphigus (PNPP)
"  Drug related pemphigus'
!  The most common form of pemphigus (>80% of cases)
!  Etiopathogenesis: the binding of IgG autoantibodies to
desmoglein 3, a transmembrane glycoprotein adhesion
molecule present on desmosomes.
!  The separation of cells ! acantholysis in the lower
layers of the stratum spinosum
!  Progressive acantholysis ! suprabasilar bulla ! loss of
large areas of skin and mucosa.
!  Coexisting with other autoimmune diseases !
myasthenia gravis
"  Clinical Manifestations
"  A thin-walled bulla arising on otherwise
normal skin or mucosa
"  The Nikolsky sign
"  Oral manifestations:
"  Oral mucosa are affected in 80-90%
"  60% of cases, the oral lesions are the
first sign
"  Vesicubulous lesions ! readly rupture
"  Form erosions ! irregular (red with a
whitish suround) ! become yellowish
"  Most commonly the lesions start on the
buccal mucosa, palate and gingiva
"  Oral lesions present up to 4 months
before the skin lesions appear
"  Pemeriksaan penunjang: Biopsi
"  DD/: Bullous pemphigoid, mucous
membrane pemphigoid, erosive LP
"  Th/: Corticosteroids* Burket’s, 2013
!  PNPP is a severe variant of pemphigus that is associated
with an underlying neoplasm—most frequently non-
Hodgkin s lymphoma, chronic lymphocytic leukemia, or
thymoma
!  Severe blistering and erosions of the mucous membranes
and skin
!  Treatment is difficult
!  1 to 2% of pemphigu cases
!  Benign variant of pemphigus vulgaris
!  Two'forms'of'pemphigus'vegetans'are'
recognized:'
!  The'Neumann'type'(more'common,'large'
bullae'and'denuded'areas)'
!  The'Hallopeau'type'(less'aggressive,'pustules'
!  are'the'initial'lesions'!'followed'by'
verrucous'hyperkeratotic'vegetations.'
Oral Manifestations:
"  Oral lesions are common in both forms of pemphigus vegetans
and may be the initial sign of disease.
"  Gingival lesions may be lace-like ulcers with a purulent surface on
a red base or have a granular or cobblestone appearance
"  Oral lesions that are associated with inflammatory bowel disease
and resemble pemphigus vegetans both clinically and
histologically ! Pyostomatitis vegetans.

Chronic palatal lesions of pemphigus vegetans.

(Burket’s, 2013)
!  Characterized by a lesion in the basement membrane
zone.
!  The diseases in this group include:
"  Bullous pemphigoid (BP)
"  Mucous membrane (cicatricial) pemphigoid (MMP)
"  Linear IgA disease (LAD)
"  Chronic bullous dermatosis of childhood (CBDC)
"  Erosive and bullous lichen planus.
!  Pathologic mechanisms: the specific antigens in the
basement membrane complex involved in triggering the
autoantibody response.
!  The most common of the subepithelial blistering diseases
!  In adults over the age of 60 years
!  Self-limited and may last from a few months to 5 years
!  In conjunction with other diseases, particularly multiple sclerosis and
malignancy, or drug therapy, particularly diuretics.
!  Direct immunofluorescent: deposition of IgG bound to the basement
membrane

!  Clinical Manifestations:
Blister on an inflamed base involves
the scalp, arms, legs, axilla, and
groin.

Bullous pemphigoid lesion of the scalp.

(Burket’s, 2013)
Oral Manifestations of BP:
!  Oral involvement is common.
!  Studies:
!  Oral lesions preceded the skin lesions, most
frequently on the buccal mucosa.
!  Oral lesions in 50% (18 of 36) of BP patients
!  Oral lesions of pemphigoid are smaller, form more
slowly, and are less painful than those seen in PV,
!  The extensive labial involvement seen in pemphigus is
not present
!  The gingival lesions consist of generalized edema,
inflammation, and desquamation with localized areas
of discrete vesicle formation.
!  A chronic autoimmune subepithelial disease that primarily affects the
mucous membranes of patients > 50 years ! mucosal ulceration and
subsequent scarring
!  The primary lesion of MMP: autoantibodies directed against proteins in
the basement membrane zone, acting with complement (C3) and
neutrophils ! a subepithelial split and subsequent vesicle formation.

"  Clinical Manifestations.:

"  Most frequently involve the oral mucosa.
"  The conjunctiva is the second most
common site ! scarring and adhesions:
symblepharon
"  Corneal damage is common,
"  progressive scarring ! blindness in
close to 15% of patients. Symblepharon formation
(Burket’s, 2013)
 •  Genital mucosa lesions ! pain and sexual dysfunction.
•  Laryngeal involvement ! pain, hoarseness, and difficulty breathing
•  Esophageal involvement ! dysphagia
•  Skin lesions (usually of the head and
neck region) ! 20 to 30% of patients

Oral Manifestations:
•  Oral lesions occur in >90% of cases,
•  Desquamative gingivitis is the most
Chronic desquamative gingival lesions of MMP
common manifestation and may be the
only manifestation of the disease .
•  Lesions may present as intact vesicles
of the gingival or other mucosal
surfaces, but more frequently they
appear as nonspecific-appearing
erosions.
•  The erosions spread more slowly than
pemphigus lesions & more self-limiting.
Mucous membrane pemphigoid causing
scarring of the soft palate
(Burket’s, 2013)
!  Characterized by the deposition of IgA rather than IgG at the basement
membrane zone.
!  The cause of the drug inducedmajority of cases is unknown, but a
minority of cases have been.
!  Clinical manifestations = dermatitis herpetiformis or pemphigoid ! pruritic
papules and blisters at sites of trauma such as the knees and elbows.
!  Oral lesions are common in LAD ! up to 70% of patients.
!  Oral lesions: clinically indistinguishable from the oral lesions of MMP -!
blisters and erosions accompanied by desquamative gingivitis.
!  Th/ oral lesions of LAD :
"  Topical steroids
"  More severe ! dapsone
"  Resistant cases ! systemic corticosteroids
!  Blisteringdisorder which chiefly affects
children < 5 years.
!  Characterize: deposition of IgA antibodies
in the basement membrane zone'
!  Erosive and bullous lesions of LP ! in the severe form ! extensive
degeneration of the basal layer of epithelium causes a separation of
the epithelium from the underlying connective tissue.
!  Lesions start as vesicles or bullae ! bullous lichen planus
!  In majority of cases characterized by ulcers ! erosive lichen planus
!  Erosive LP ! drug therapy, underlying medical disorders, and
reactions to dental restorations.
!  The drugs most commonly associated with severe lichenoid reactions
include NSAIDs, hydrochlorothiazide, penicillamine, and angiotensin-
converting enzyme inhibitors.
!  Underlying disease associated with oral lichenoid reactions ! chronic
hepatitis caused by hepatitis C
!  Contact allergic reactions to flavoring agents (cinnamon & peppermint)
and to dental materials (mercury in amalgam)
 Clinical Manifestations:
•  Vesicles, bullae, or irregular shallow ulcers of the oral mucosa.
•  The lesions are usually present for weeks to months.
•  Erosive lichen planus ! present of desquamative gingivitis.
•  Desquamative gingivitis is not a disease entity but a sign of disease that
can be caused by erosive lichen planus, pemphigus vulgaris, or
cicatricial pemphigoid.
•  Desquamative gingivitis caused by lichen planus may be accompanied
by characteristic Wickham s striae.

Palatal lesions of erosive LP. Erosive LP of the labial mucosa Desquamative gingival lesions in a
patient with erosive LP.

(Burket’s, 2013)
!  Aggressive or chronic form of herpes
infection
!  Most susceptible to aggressive HSV
lesions:
"  AIDS patients
"  Transplant patients taking
Chronic herpes simplex infection in a kidney transplant
immunosuppressed drug therapy, patient receiving immunosuppressive drug therapy

patients on high doses of corticosteroids

"  Patients with leukemia, lymphoma, or
other disorders that alter the T-
lymphocyte response
!  Remain for weeks to months ! large ulcers
up to several centimeters in diameter

Chronic herpes simplex infection of the palate in a

patient taking chemotherapy for acute leukemia.
!  The most common cause of
single ulcers on the oral mucosa:
trauma ! caused by teeth, food,
dental appliances, dental
treatment, heat, chemicals, or
electricity.
!  The most important differentiation
is to distinguish trauma from
squamous cell carcinoma.
!  If ulcer healing is not evident in
this time, a
!  biopsy should be done to rule out
cancer
!  Infections cause a chronic oral
ulcer !
"  The deep mycoses
histoplasmosis, blastomycosis,
mucormycosis, aspergillosis,
cryptococcosis,
coccidioidomycosis
"  Chronic herpes simplex infection
"  Syphilis in the primary and
tertiary stage
!  Etiologi : Histoplasma capsulatum
!  Infection results from inhaling dust
contaminated with droppings,
particularly from infected birds or
!  Oral lesions ! papule, nodule, ulcer,
bats
or vegetation.
!  Primary infection is mild !
!  The most common oral lesion of
manifesting as a self-limiting
histoplasmosis in patients with HIV is
pulmonary disease that heals to
an ulcer with an indurated border on
leave fibrosis and calcification
the gingiva, palate, or tongue
similar to tuberculosis
!  Th/:
!  Oral involvement is usually
secondary to pulmonary - Ketoconazole/ Itraconazole
involvement and occurs in patients (6-12 bln)
with disseminated histoplasmosis. - Amphotericin B
!  Etiologi : Blastomycosis !  Oral manifestation:
dermatitidis ! a normal inhabitant "  Nonspecific painless
of soil verrucous ulcer with
!  Infection by inhalation ! causes indurated borders
primary pulmonary infection "  Hard nodules and
!  The skin and mucosal lesions ! radiolucent jaw lesions
subcutaneous nodules !
progress to well-circumscribed
indurated ulcers
!  Diagnosis:
"  Biopsy
"  Culturing the organism from
tissue
!  Th/ similar to Histoplasmosis
!  Etiologi : saprophytic fungus !
normally occurs in soil or as a
mold on decaying food
!  Occurs in individuals with
decreased host resistance ( poorly
controlled diabetes, hematologic
malignancies, undergoing cancer
chemotherapy or
immunosuppressive drug therapy
!  Oral manifestations:
"  Ulceration of the palate, which
results from necrosis due to
invasion of a palatal vessel
"  Lesion ! large and deep, causing
denudation of underlying bone

!  Th/
!  Surgical debridement
!  Amphotericin B (3 months)
 KNOWLEDGE'AND'SKILLS'ARE'TOOLS,''

'THE'WORKMAN'IS'CHARACTER.'

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