Sunteți pe pagina 1din 37

MODUL 4.

KARIES GIGI

BAGIAN ILMU PENYAKIT GIGI & MULUT FK UNDIP SEMARANG


PLAK GIGI

Massa = Musin saliva + bakteri + epitel mati + KH


Plak : Sub gingiva & Supra
Subgingiva : dominan anaerob
Supra : aerob
Pembentukan plak

Plak : awal, muda, mature


Beberapa menit
Epidemiology

90% schoolchildren, 59% adult -->


experienced caries (Asian & latin
american), <<< African.
>> 70% in Indonesian.
PLAK & PENYAKIT KARIES

KH + Streptokokus Asam laktat


Asam laktat demineralisasi Ca-apatit (komponen utama email)
Kavitasi
KLINIS

Dimulai dgn destruksi lokal pada email, akibat asam hasil


fermentasi KH oleh mikroba rogga mulut.
Dimulai area putih seperti berkapur (Small chalky area)
Berkembang progresive & ireversibel
- Berkembang menjadi kavitas besar kecoklatan kehitaman di
dasar & dinding kavitas
Sering terjadi pada fissure/Pit oklusal, atau
tempat dmn sisa makanan terjebak di situ.
RISIKO KARIES

Adanya kavitas menyebabkan terjadi akumulasi sisa makanan


menjadi jejas : fisik, kimia (asam & metabolit) dan
biologi(mikroba)
Menyebabkan infeksi pada pulpa Penyakit pulpa gigi
pulp irritation, pulp inflamation and finally death of pulp.
KELUHAN :

q Tidak ada keluhan nyeri berat


q Nyeri : rangsang termal dari makanan, sampai nyeri
spontan.
q Keluhan lain : so cause : bad breath, bad sensation /foul
taste, infection & spread to surrounding soft tissue.
PENJALARAN KARIES GIGI MENJADI
PENYAKIT PULPA
PROGRESSION OF PULP
DISEASES:
1. Pulp Irritation (Iritasi pulpa)
- Lesion on enamel or cementum, but no pathologic
changes on to pulp tissue.
- Subjective : sensitive when acidic/ sweet feed/drinking
Objective :
- EO : t.a.k
- IO :
Ins : caries (+), may on multiple
surfaces.
Son : superficial, pain (-)
Per : (-), Pres : (-), Pal : (-)
Hiperemi pulpa
-Multiple injuries : acidic substance/ toxic metabolite rise on
deep cavities, when we dont treat it & cause pulp tissue
inflammation.
-1-st step is hyperemia/ vascular vasodilatation
Subj : Pain present until injuries (food/drinks) were
eliminated from cavity. No history of spontaneus pain.
Obj :
- EO : t.a.k
- IO : I : Caries +
S : Medium, severe sensitive (+++)
but decrease fastly
P/P/P : -/-/-
PARTIAL ACUTE PULPITIS

Pulp tissue inflammation on to pulp chamber


area only.
Subj : pulsation, spontaneous & long duration
pain without stimulation.
Obj : - EO : -
- IO : I : Caries +
S : medioprofunda/profunda, pain (+++)
P/P/P : +/-/-
Total acute Pulpitis

- Pulp tissue inflamation on to all


area of pulp chamber + apical canal &
spread to periapical tissue.
-Subj : Severe pain, spontaneuos,
spread in to temporal, cervical &
auricular area.
Obj :
- EO : t.a.k.
- IO : I : Caries +
S : profunda, pain (+++)
P/P/P : +/-/+
CHRONIC PULPITIS

- Chronical inflammation of pulp tissue


- Can turn to acute phase
- Subj : History exam : presenting complain, but
pain may be absence now.
- EO : t.ak.
- IO : I : caries +, calculus
might accumulated on the
same area
S : profunda, pain (++)
P/P/P : -/-/-
KEMATIAN PULPA

Pulpitis yg tidak mendapat perawatan akan


mengalami kematian. Karena kematiannya di
sertai dengan invasi MO, maka disebut
sebagai Gangren Pulpa.
Mikroba dan metabolit toksiknya menyebar
ke jaringan periodontal apikal dan
menyebabkan periodontitis apikalis.
TATA LAKSANA

Edukasi : kontrol plak gigi


Pulpitis : Simtomatik (analgetik-antiinflamasi), antiseptik
Gangren periodontitis apikalis, abses : An + Ab.
Rujuk untuk tatalaksana definitif
Definitif : Konservasi, ekstraksi.
Pulpitis
Acute Chronic

Apical Periodontitis
Acute Chronic

Periapical absces Periapical granuloma


Acute Chronic

Periapical cyst
OSTEOMYELITIS
Acute Chronic

Periostitis

Cellulitis Absces