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FUNGI

VIRUS BACTERIA

DISEASE
The oral focal infection theory

• A concept generally negleted for several


decades, is controversial yet has gained
renewed interest with progress in
clasification and identification of oral
microorganisms.

• Additionally, recent evidence associating


dental with artherosclerosis and other
chronic disease has also helped resurrect
the focal infection theory
Pathways of infection arising from oral bacteria
The three pathway that may link oral bacteria to
secondary disease distant from the oral nidus
are :
1. Metastatic infection attributable to transient bacteria in
the blood
2. Metastatic immunologic injury
3. Metastatic toxic injury

The scientific evidence weak a it is best supports of first


pathway of transient bacteriemias of oral origin
Mechanical prosthetic
valve (arrow)
Odontogenic infection

Caries dental pulpitis


Necrosis of the pulp pulp polyp

Periapical abscess
Periodontal infection

Periodontal abscess

Gingivitis ANUG
Salivary infection
Mucositis

Recurent Apthous Stomatitis


Minor

RAS Mayor
Penyakit Infeksi Bakteri Spesifik
di Rongga Mulut

Sifilis
Gonorrhea
Tuberkulosis
Lepra
SIFILIS

1.Sifilis acquired
Sifilis primer
Sifilis sekunder
Sifilis tertier
2.Sifilis kongenital
Penyebab: Treponema Pallidum
Patogenesis
Kontak seksual --- lesi primer ( chancre ) ---- hilang---
lesi sekunder -----hilang --- tertier
Transfusi darah --- lesi sekunder --- hilang --- tertier
Kongenital ----- plasenta ibu yang terinfeksi ----
tidak ada lesi primer
Sifilis Primer
- Berkembang pada tempat masuknya kuman, 3-4
minggu
- Lesi chancre -- plak keras, sedikit meninggi, ulserasi,
bulat,
indurasi dengan tepi bergulung, coklat berkrusta,
dimulai
dengan bercak atau papula --- ulser
- Diameter 5 mm - beberapa cm
- Tidak sakit
- Hilang spontan sesudah 10 hari
- Lesi dapat satu atau multiple.
- Pembesaran kelenjar limfe regional
Manifestasi di rongga mulut
- Lesi chancre
- Lokasi bibir, mukosa mulut, lidah, palatum lunak, tonsil
faring, jarang pada gusi
- Sedikit sakit karena infeksi sekunder
- Ulser ditutupi lapisan putih keabuan
- Pada ekstra oral bibir--- krusta coklat
- Dapat multiple
Diagnosa
- Riwayat kontak dengan penderita
- Smear mulut tidak terlihat
- Pemeriksaan darah negatif
- Eksudat dengan darkfield microscope positif pada akhir
stadium primer

Diagnosa Banding
-Lesi herpes pada bibir
-Squamous cell carcinoma stadium awal
-Lesi trauma kronik
-Tuberkulosis
Sifilis Sekunder
Tanda-tanda umum
- Terjadi 3-6 minggu setelah lesi primer
- Lokasi tidak berhubungan dengan lesi primer
- Erupsi difus pada kulit dan mukosa
- Makula papula pada kulit
- Pada mukosa dan kulit yang lembab terjadi : mucous patch
split papula dan condyloma latum
Mucous patch : area kecil, licin, eritematus atau erosi
superfisial, putih keabuan pada genital dan mulut, multiple dan
tidak sakit
Split papula : Lesi doble papula pada area intertrigenus
Condyloma latum : Papula besar, lembab, abu-abu, pada
mukokutan yang lembab
Manifestasi di rongga mulut
Mucous patch
- Lokasi pada lidah, mukosa bukal, tonsil, faring dan bibir
pada gusi jarang
- Lesi yang paling menular
- Plak berwarna putih keabuan, sedikit meninggi, permukaan
ulserasi, dasar eritematus
- Bentuk ovoid atau tidak teratur
- Multiple dan tidak sakit
- Pada lidah, papilla hilang diatas lesi berbatas jelas
- Trauma pada lesi dapat sakit dan berdarah
Split Papula
- Lokasi pada komisura bibir berupa fisur yang membagi dua
bibir atas dan bawah oleh papula
- Dapat terjadi pada dorsum lidah
- Tidak spesifik

Condyloma latum
- Jarang pada mulut
- Berwarna abu-abu silver, rata, seperti kutil, ulserasi
- Tidak sakit
Diagnosa Banding
Mucous patch
- Lesi herpes masa penyembuhan
- Lesi traumatik
- Eritema multiform
- Kandidiasis
- Proses alergi

Split Papula
- Angular cheilitis karena defisiensi Vitamin atau kurangnya
ruang inter maksilar

Diagnosa : Tes serologis biasanya positif


Sifilis Tertier

Tanda-tanda umum
- Asimtomatik atau simtom kompleks
- Lesi gumma pada kulit, mukosa, liver, testis, tulang
- Dapat melibatkan sistem kardiovaskular, CNS, jaringan dan
organ tertentu
- Neurosifilis ---- tabes dorsalis dan general paresis
Tabes dorsalis --- colum, spinal cord, root ganglia posterior
General paresis ---- jaringan cerebral
Manifestasi di rongga mulut

- Lesi gumma , berupa massa nodular yang padat , ulserasi,


nekrose, pada palatum --- perforasi palatum
- Lokasi : palatum, lidah, kelenjar ludah, tulang rahang
- Pada lidah --- atropi papilla, lidah keras --- luetic bald tongue
- Tabes dorsales ---- rasa sakit kepala dan leher, kehilangan
rasa pengecapan, nekrosis spontan pada
prosessus alveolaris
- General paresis ---- paresis bibir, lidah, hidung, pipi
ulserasi tidak sakit pada palatum, septum
hidung, kematian pulpa spontan
- Atropik lidah ---- epidermoid carcinoma
Diagnosa Banding
- Gumma ---- Fraktur yang tidak sembuh-sembuh
Osteomielitis yang lama bertahan
Karsinoma
Tindakan dokter gigi

- Menghindari penularan ---- sifilis primer dan sekunder


- Sebagai case finder
-Mencegah bakterial endokarditis

Perawatan
- Sifilis primer, sekunder dan laten -- Benzathine penisilin G
- Bila alergi penisilin --- tetrasiklin atau eritromisin
Sifilis kongenital ( prenatal sifilis )

Tanda-tanda umum
- Manifestasi pada 2 tahun pertama kehidupan
- Tidak ada lesi primer
- Rinitis, hidung sumbat, kehilangan berat badan, tumit
berkerut dan bersisik
- Makula, papula, bula, vesikel, deskuamasi superfisial.
- Kulit berkerut dan bersisik
- Petechie, mucous patch, condyloma latum
- Kepala bentuk empat segi, lobus frontal menonjol
- Manifestasi lanjutan sesudah 2 tahun, interstitial keratitis,
vaskularisasi kornea, ketulian, artopati
- Umur 10-12 tahun, saddle nose, deformiti tulang hidung
perforasi palatum
Umur 10-12 tahun
- Saddle nose, deformiti tulang hidung atau perforasi palatum
- Melibatkan tulang fasial dan gigi
- Dapat terjadi frontal bosse, maksila yang pendek, palatum
yang tinggi, mulberry molar.

Tanda khas
- Triad Hutchinson : Hipoplasia Incisivus dan Molar
Ketulian syaraf 8
Keratitis interstitial
Manifestasi di rongga mulut

1. Post Rhagadic scarring pada mulut


- daerah linear merah tembaga ditutupi krusta lunak pada
bibir
- Bila sembuh seperti sikatrik
2. Perobahan pada gigi
- Perobahan bentuk, warna dan ukuran gigi
- Resorbsi akar yang berkurang pada gigi desidui
- Hipoplasia gigi pada I, C dan M satu permanen
bentuk obeng, runcing pada I, bud shaphe pada M
DD dengan terapi Tetrasiklin atau Riketsia
3. Perobahan dentofasial : malokklusi dan open bite
Diagnosa
- Riwayat dilahirkan
ibu penderita sifilis
- Lesi-lesi yang khas

Perawatan
Injeksi Penisilin
Fungal infection

• Are oral fungal infections common ?


• No, most are associated with an underlying
systemic condition immunosuppression

imunodeficiency syndrome cancer therapy


anemia
diabetes
uremia
leukemia
• Patients who have conditions that modify
the normal oral environment are at
increased risk of fungal infection

Among these individuals are patients with


_ xerostomia
_ have taken broad spectrum antibiotics
Diagnosis of oral fungal infection based on :

• History
• Clinical appearance
• Culture
• Potassium hydroxide preparation
• Biopsy

• What is the most common fungal infection to affect the mouth?

• Oral candidiasis caused by Candida Albicans


What is the typical clinical presentation of
oral candidiasis ?

• Pseudomembranous candidiasis
• Hyperplastic candidiasis
• Erythematous candidiasis
• Angular cheilitis
Pseudomembranous candidiasis ( Thrush )

• Most typical clinical presentation of the


infection
• White, cottage cheesy-looking raised
lesions
• Most often of tongue or palate
• Can be scrapped off, leaving a painful, raw
bleeding base
Hyperplastic Candidiasis

• Less common
• As area leukoplakia at corners of the mouth or
the cheeks
• Unlike pseudomembranous forms, these lesions
cannot be scraped off
Erythematous Candidiasis

• Most often present on the dorsal surface


or edges tongue and palate
• The degree of mucosal erythema may be
variable
• Patients with this form of candidiasis often
complain of a burning mouth
Angular cheilitis
Viral infection

• Are viral infections of the mouth common


or rare ?

Viral infections are among the most


common causes of oral lesions
Symptoms of acute viral infections that affects the mouth

• Vesicles or rupture small ulcers


• History suggesting viremia : fever,
malaise, myalgia, upper respiratory
symptoms, anorexia
• Pain associated lesions
Group of viruses for most oral infections:

• HS type 1,2
• Varicella-zoster virus
• The epstein-barr virus
• Cytomegalovirus
• Herpes virus 6,7,8 ( infectious in
immunocompromisefd patient
HIV HAS BEEN ISOLATED FROM
BODY FLUIDS :
 HUMAN BLOOD.
 SEMEN
 VAGINAL SECRETIONS.
 BREAST MILK.
 TEARS.
 URINE.
 SALIVA.
 CEREBROSPINAL FLUID.
 AMNIOTIC FLUID.
DIAGNOSTIC TESTING FOR HIV :

1. Detection of serum antibody


ELISA.

2. Detection of viral antigen in patient’s


blood or tissue
WESTERN BLOT TEST.
PREVALENSI : 40 – 90%

HIV-related lesions have particular significance


because :

- They are often the first sign of HIV disease.


- They have prognostic value.
- They are a frequent cause a morbidity and
mortality.
- Knowledge and proper treatment can add
to the quality of life of HIV patients.
SAN FRANSISCO, AUG. 17, 1990 :

I. CANDIDIASIS.
A. Pseudomembranous candidiasis.
B. Erythematous candidiasis.
C. Angular cheilitis.

II. GINGIVITIS / PERIODONTITIS.


A. HIV – associated gingivitis.
B. HIV – associated periodontitis.
III. NECROTIZING STOMATITIS.

IV. HERPES SIMPLEX.


A. Intra oral form.
B. Perioral form.

V. CYTOMEGALOVIRUS.
VI. VARICELLA – ZOSTER VIRUS

VII. APHTHOUS ULCERATION.


A. Minor.
B. Mayor.
C. Herpetiform.

VIII. HAIRY LEUKOPLAKIA.


IX. HIV SALIVARY GLAND DISEASE.

X. ORAL KAPOSI SARCOMA.

XI. ORAL WARTS / PAPILOMA.


A. Papilloma.
B. Focal epithelial hyperplasia.
TREATMENT OF THE ORAL LESIONS
ASSOCIATED WITH HIV INFECTION.

CONDITION THERAPY

I. Candidiasis Antifungal (topical and /


or systemic).

II. HIV- associated Plaque removal, debri-


gingivitis dement, chlorhexidine,
povidone iodine.
CONDITION THERAPY

HIV- associted Plaque removal, debri-


periodontitis dement, chlorhexidine,
metronidazole.

Necrotizing sto- Debridement, chlorhe-


matitis xidine, metronidazole.

III. Herpes simplex If not self limiting, if


prolonged, if frequen-
tly recurrent  acyclo-
vir.

IV. Herpes zoster Oral Acyclovir.


CONDITION THERAPY

V. Aphthous ulcer Topically steroid

VI. Hairy leukoplakia Usually no treatment,


severe  acyclovir

VII. Kaposi sarcoma Excision, laser, radia-


tion, chemotherapy

VIII. Oral wart Excisison, laser

IX. Xerostomia Salivary stimulation,


artificial saliva.
HIV

• The main targets for the virus are cells expressing the
CD4 membrane reseptor, such as T4 helper lymphocyte,
macrophages and monocyte

• Viral replication occures within the CD4 cel, leading to its


destruction and loss of function. As a result the number
of CD4 cell declines, and the patient become at high risk
for opportunistic infections.
Many medication used to treat HIV have side
effect
• Abacavir oral ulceration
• Flycotsine myelosuppression
• Foscarnet ou &m
• Ganciclovir m
• Hydroxyurea ou
• Interferon xerostomis,metallic
taste & m
• Lopinavir u&x
• Pentamidine mt
• Rifampin salivary discoloration
• Ritonavir perioral paresthesia
• Saquinavir p, neutropenia, thrombocytopenia
• TMP/SMZP myelosup,ou, glositis
• Dideoxycytidine my & ou Zidovudine Neutropenia
VIRUS

Viral infection causing, or associated with diseases


of the oral mucosa :

VIRUS PENYAKIT
Herpes Simpleks 1 & Primary Gingivostomatitis
2 Herpetica
Herpes Labialis Recurrent
Herpes Intra Oral Recurrent
Herpetic Whitlow
Varicella - Zoster Chickenpox
Herpes Zoster
Coxsakie A Herpangina
Hand, foot and mouth disease
Viral infection causing, or associated with diseases
of the oral mucosa :

VIRUS PENYAKIT
Cytomegalovirus Salivary gland disease

Epstein Barr Hairy leukoplakia


Virus
Paramyxovirus Measles

Papilomavirus Viral warts

HIV Manifestasi oral HIV


HERPES SIMPLEX VIRUS INFECTION

Family herpesviridae

∗ Herpes simplex virus – 1


∗ Herpes simplex virus – 2
∗ Cytomegalovirus
∗ Varicella-
Varicella-zoster virus
∗ Epstein Barr virus
∗ Human herpes virus-
virus-6
∗ Human herpes virus-
virus-7
∗ Human herpes virus-
virus-8
Herpes Simplex virus – 1
⇒ perioral, eyes

Herpes Simplex virus – 2


⇒ genitals

TRANSMISSION :
1. Airbone droplets
2. Intimate contact
HERPES SIMPLEX VIRUS
INFECTION

PRIMARY RECURRENT
INFECTION INFECTION
CHARACTERISTIC PROPERTY OF HERPES
VIRUS :

after “primary infection” ⇒ latent in


cell host ⇒ reactivated by variety factors
⇒ “recurrent infection”

Trigger factors :
- Fever
- Emotional stress
- Ultraviolet radiation
- Menstruation
- Hormones
- Immunosuppression
- Ionizing radiation
PATHOGENESIS OF HSV-1 INFECTIONS :

Host (seronegative) HSV

Primary disease
or
Recurrent infection or
Subclinical infection
Shedding asymptomatic

Reactivation

Resolution
Host (seropositive)
latent virus
PRIMARY HSV-1 INFECTION :

- Seronegative for HSV


- Children, young adult
- Does not imply clinical signs & symptoms
⇒ subclinical
- Incubation periode : several days –
2 weeks
- ⇒ Primary Gingivostomatitis Herpetica
⇒ Herpetic Whitlow
PRIMARY GINGIVOSTOMATITIS
HERPETICA.
CLINICAL APPEARANCES :
- Prodromal symptoms : fever, malaise, nausea,
headache, lymphadenopathy.
- Vesicle → rupture → round/oval ulcers,
shallow, grey-
grey-white pseudomembrane, surrounded
by erythema area.
- Ulcers can coalescent → large ulcers.
- Pain, disorders of swallowing, eating,
secondarily infected.
- Location: any intra oral.
- Acute gingivitis marginalis → gingiva are
swollen with red edges that bleed easily.
- Heal : 10 – 12 days → self limiting disease,
without scar.
Treatment :

Goals :
1. To shorten the current attack.
2. To prevent recurrences.

Medications :
♥ Analgesics.
♥ Vitamin.
♥ Anaesthetic topical.
♥ Antivirus.
RECURRENT HSV INFECTION :

- Affect 20 40% 0f adult population.


- Antibody for HSV was present.
- Reactivation of latent virus by trigger
factors.
- ⇒ Recurrent Herpes Labialis
⇒ Recurent Herpes Intra Oral
⇒ Herpetic Whitlow.
RECURRENT HERPES LABIALIS.

CLINICAL APPEARANCES :
- Prodromal symptoms : mild fever, tingling,
burning or pain in which lesions will appear.
- Vesicles on the vermillion border of lip →
rupture → shallow ulcer.
- Yellow crust formation.
- Problems : pain, cosmetic disfigurement,
psychosocial effect.
- Heal : 1 – 2 weeks without scar.
- Recurrences is variable.
RECURRENT HERPES INTRAORAL.

CLINICAL APPEARANCES :
- Prodromal symptoms → mild.
- Vesicles → rupture → ulcers.
- Intraorally.

Recurrent Herpes Labialis maybe seen concurently


with the intraoral lesions or they occur alone.
HERPETIC WHITLOW :
- Primary or secondary HSV infection involving
the finger.
- Because of the physical contact with infected
individual.
- Fever, lymphadenopathy.
- Pain, redness, swelling are prominent.
- Duration : 4 – 6 weeks.
- Locations : paronychial, eponychial or
subungal portions of the distal phalanges,
finger.
other area of the finger.
VARICELLA – ZOSTER
VIRUS

⇒ DNA untai ganda


⇒ Neurotropic
⇒ Penularan : kontak langsung,
infeksi droplet.
⇒ Infeksi primer dan rekuren
⇒ bersifat laten
Varicella – zoster virus

PRIMARY INFECTION RECURRENT INFECTION

CHICKENPOX / HERPES ZOSTER /


VARISELA SHINGLES
Hospes (seronegative)

Primary infection
( Chickenpox ) Recurrent infection
( Herpes zoster )

Hospes (seropositive ) Reactivation :


Latency virus - age
Immunosupression, dll
-Immunosupression,
VARICELLA ( CHICKENPOX ) :

- seronegative individual.
- children.
- incubation periode : 2 – 3 weeks.
- prodromal symptoms : fever, chills, malaise,
headache.
- rash → vesicles → pustula / ulcerations.
- heal : 2 weeks → self limiting.
- intra oral : not consistently involved.
⇒ discrete/scattered vesicles → rupture →
shallow round ulcer surrounded by red halo.
HERPES ZOSTER :

Clinical appearancess :
- Gejala prodromal : parastesi, gatal, rasa terbakar,
nyeri di daerah dermatom yg terlibat.
- Dermatom yg terlibat : T5, C3, L1, L2, s. trigeminal
- Ruam makulopapular → vesikel → ulser dengan dasar
eritematus → krusta.
- Distribusi unilateral.
- Intra oral : vesikel → ruptur → ulkus.
∗ Cab. Maksilaris : palatum lunak, mukosa bibir atas,
uvula mukosa pipi.
∗ Cab. Mandibularis : lidah, gimngiva, mukosa bibir
bawah.
TREATMENT :

- Bed rest.
- Local applications of heat.
- Topical anesthetic.
- Antiviral.
- Analgesics.
- tranquilizers.
LOCALIZED FUNGAL INFECTIONS
∗ ORAL CANDIDIASIS

DEEP-
DEEP-SEATED FUNGAL
INFECTIONS
∗ ASPERGILOSIS
∗ CRYPTOCOCOSIS
∗ HISTOPLASMOSIS
∗ GEOTRICHOSIS
∗ BLASTOMYCOSIS
⇒ Rarely affect the oral cavity
ORAL CANDIDIASIS

A SUPERFICIAL INFECTION OF ORAL


MUCOUS
CAUSED BY THE YEASTLIKE FUNGUS
CANDIDA
ALBICANS
FACTORS PREDISPOSING TO ORAL
CANDIDIASIS :
LOCAL FACTORS SYSTEMIC FACTORS
Denture wearing Physiological
Old age, infancy, pregnancy

Saliva Endocrine disorders


Xerostomia, low pH Diabetes Melitus

Commensal flora Nutritional deficiencies


Iron, folate, vit.B 12

High-
High-carbohydrate diet Malignancies
Leukemia

Smoking tobacco Immune defects


HIV / AIDS

Drugs / medication
Broad spectrum antibiotics
Corticosteroids
Cytotoxic drugs
CLASSIFICATION OF ORAL
CANDIDIASIS :
TYPE CLINICAL

ACUTE : Creamy / white patches on the surface of


ACUTE oral mucous; forming confluent; curd-
curd-like
PSEUDOMEMBRANOUS pseudomembranes. Pseudomembranes
CANDIDIASIS can be scraped off to reveal raw,
= ORAL TRUSH erythematous base.

ACUTE ATROPHIC Small lesions, usually on the tongue, with


CANDIDIASIS reddening / inflammation of surrounding
= ANTIBIOTIC SORE TONGUE tissue
TYPE CLINICAL
CHRONIC : Chronic erythema and edema of
Chronic Atrophic Candidiasis upper palate localized to occluded /
= Denture Stomatitis traumatized tissue

Chronic hyperplastic White patch adherent to mucous on


Candidiasis an erythematous base which is not
= Candida Leukoplakia removable by digital pressure.
Usually on the anterior buccak
mucous

Angular cheilitis Erythema, fissure and encrustations


=Perleche at corners of mouth.
DIAGNOSIS :

CLINICAL APPEARANCES
+
LABORATORIUM
EXAMINATIONS :
* Culture
* Cytologic
* Serology
TREATMENT :

⇒ To correct predisposing factors


⇒ To correct sources of infection
⇒ Antifungal drugs
ANTIFUNGAL DRUGS

POLYENE AZOLES

A. AMFOTERICIN B A.IMIDIAZOLE :
- Clotrimazole
B. NYSTATIN - Ketoconazole
- Miconazole

B. TRIAZOLE :
- Fluconazole
- Itraconazole
Penyakit Infeksi Bakteri Spesifik
di Rongga Mulut

Sifilis
Gonorrhea
Tuberkulosis
Lepra
SIFILIS

1.Sifilis acquired
Sifilis primer
Sifilis sekunder
Sifilis tertier
2.Sifilis kongenital
Penyebab: Treponema Pallidum
Patogenesis
Kontak seksual --- lesi primer ( chancre ) ---- hilang---
lesi sekunder -----hilang --- tertier
Transfusi darah --- lesi sekunder --- hilang --- tertier
Kongenital ----- plasenta ibu yang terinfeksi ----
tidak ada lesi primer
•Sifilis Primer
•- Berkembang pada tempat masuknya kuman, 3-4
minggu
•- Lesi chancre -- plak keras, sedikit meninggi, ulserasi,
bulat,
• indurasi dengan tepi bergulung, coklat berkrusta,
dimulai
• dengan bercak atau papula --- ulser
•- Diameter 5 mm - beberapa cm
•- Tidak sakit
•- Hilang spontan sesudah 10 hari
•- Lesi dapat satu atau multiple.
•- Pembesaran kelenjar limfe regional
Manifestasi di rongga mulut
- Lesi chancre
- Lokasi bibir, mukosa mulut, lidah, palatum lunak, tonsil
faring, jarang pada gusi
- Sedikit sakit karena infeksi sekunder
- Ulser ditutupi lapisan putih keabuan
- Pada ekstra oral bibir--- krusta coklat
- Dapat multiple
Diagnosa
- Riwayat kontak dengan penderita
- Smear mulut tidak terlihat
- Pemeriksaan darah negatif
- Eksudat dengan darkfield microscope positif pada akhir
stadium primer

Diagnosa Banding
-Lesi herpes pada bibir
-Squamous cell carcinoma stadium awal
-Lesi trauma kronik
-Tuberkulosis
Sifilis Sekunder
Tanda-tanda umum
- Terjadi 3-6 minggu setelah lesi primer
- Lokasi tidak berhubungan dengan lesi primer
- Erupsi difus pada kulit dan mukosa
- Makula papula pada kulit
- Pada mukosa dan kulit yang lembab terjadi : mucous patch
split papula dan condyloma latum
Mucous patch : area kecil, licin, eritematus atau erosi
superfisial, putih keabuan pada genital dan mulut, multiple dan
tidak sakit
Split papula : Lesi doble papula pada area intertrigenus
Condyloma latum : Papula besar, lembab, abu-abu, pada
mukokutan yang lembab
Manifestasi di rongga mulut
Mucous patch
- Lokasi pada lidah, mukosa bukal, tonsil, faring dan bibir
pada gusi jarang
- Lesi yang paling menular
- Plak berwarna putih keabuan, sedikit meninggi, permukaan
ulserasi, dasar eritematus
- Bentuk ovoid atau tidak teratur
- Multiple dan tidak sakit
- Pada lidah, papilla hilang diatas lesi berbatas jelas
- Trauma pada lesi dapat sakit dan berdarah
Split Papula
- Lokasi pada komisura bibir berupa fisur yang membagi dua
bibir atas dan bawah oleh papula
- Dapat terjadi pada dorsum lidah
- Tidak spesifik

Condyloma latum
- Jarang pada mulut
- Berwarna abu-abu silver, rata, seperti kutil, ulserasi
- Tidak sakit
Diagnosa Banding
Mucous patch
- Lesi herpes masa penyembuhan
- Lesi traumatik
- Eritema multiform
- Kandidiasis
- Proses alergi

Split Papula
- Angular cheilitis karena defisiensi Vitamin atau kurangnya
ruang inter maksilar

Diagnosa : Tes serologis biasanya positif


Sifilis Tertier

Tanda-tanda umum
- Asimtomatik atau simtom kompleks
- Lesi gumma pada kulit, mukosa, liver, testis, tulang
- Dapat melibatkan sistem kardiovaskular, CNS, jaringan dan
organ tertentu
- Neurosifilis ---- tabes dorsalis dan general paresis
Tabes dorsalis --- colum, spinal cord, root ganglia posterior
General paresis ---- jaringan cerebral
Manifestasi di rongga mulut

- Lesi gumma , berupa massa nodular yang padat , ulserasi,


nekrose, pada palatum --- perforasi palatum
- Lokasi : palatum, lidah, kelenjar ludah, tulang rahang
- Pada lidah --- atropi papilla, lidah keras --- luetic bald tongue
- Tabes dorsales ---- rasa sakit kepala dan leher, kehilangan
rasa pengecapan, nekrosis spontan pada
prosessus alveolaris
- General paresis ---- paresis bibir, lidah, hidung, pipi
ulserasi tidak sakit pada palatum, septum
hidung, kematian pulpa spontan
- Atropik lidah ---- epidermoid carcinoma
Diagnosa Banding
- Gumma ---- Fraktur yang tidak sembuh-sembuh
Osteomielitis yang lama bertahan
Karsinoma
Tindakan dokter gigi

- Menghindari penularan ---- sifilis primer dan sekunder


- Sebagai case finder
-Mencegah bakterial endokarditis

Perawatan
- Sifilis primer, sekunder dan laten -- Benzathine penisilin G
- Bila alergi penisilin --- tetrasiklin atau eritromisin
Sifilis kongenital ( prenatal sifilis )

Tanda-tanda umum
- Manifestasi pada 2 tahun pertama kehidupan
- Tidak ada lesi primer
- Rinitis, hidung sumbat, kehilangan berat badan, tumit
berkerut dan bersisik
- Makula, papula, bula, vesikel, deskuamasi superfisial.
- Kulit berkerut dan bersisik
- Petechie, mucous patch, condyloma latum
- Kepala bentuk empat segi, lobus frontal menonjol
- Manifestasi lanjutan sesudah 2 tahun, interstitial keratitis,
vaskularisasi kornea, ketulian, artopati
- Umur 10-12 tahun, saddle nose, deformiti tulang hidung
perforasi palatum
Umur 10-12 tahun
- Saddle nose, deformiti tulang hidung atau perforasi palatum
- Melibatkan tulang fasial dan gigi
- Dapat terjadi frontal bosse, maksila yang pendek, palatum
yang tinggi, mulberry molar.

Tanda khas
- Triad Hutchinson : Hipoplasia Incisivus dan Molar
Ketulian syaraf 8
Keratitis interstitial
Manifestasi di rongga mulut

1. Post Rhagadic scarring pada mulut


- daerah linear merah tembaga ditutupi krusta lunak pada
bibir
- Bila sembuh seperti sikatrik
2. Perobahan pada gigi
- Perobahan bentuk, warna dan ukuran gigi
- Resorbsi akar yang berkurang pada gigi desidui
- Hipoplasia gigi pada I, C dan M satu permanen
bentuk obeng, runcing pada I, bud shaphe pada M
DD dengan terapi Tetrasiklin atau Riketsia
3. Perobahan dentofasial : malokklusi dan open bite
Diagnosa
- Riwayat dilahirkan
ibu penderita sifilis
- Lesi-lesi yang khas

Perawatan
Injeksi Penisilin

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