PLAK GIGI

Peran Plak Gigi pada

Patogenesis Penyakit
Periodontal & Karies Gigi
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
Plak Gigi & Penyakit
Periodontal
• Inflamasi pada jaringan
penyangga gigi
• Jaringan periodontal : gingiva,
membran periodontal, tulang
alveolus, sementum
• Penyebab : Plak, infeksi
bakterial, viral, hormonal dll
(lihat kuliah DR. Oedijani)
Keluhan

• Gusi bengkak
• Sakit
• Berdarah (ringan sd spontan)
• Bau mulut
• Gigi goyang
Kelanjutan penyakit
periodontal
• Gingivitis jika tidak dirawat
berlanjut menjadi periodontitis
marginalis  terus :
Pocket periodontal, resesi
gingiva, resorbsi tulang, migrasi
gigi
• Abses periodontal, IO & EO
Penatalaksanaan

• Causatif : Kontrol plak (initial)

• Tergantung keparahan.
• Medikamen
• Operatif : Curretage,
Gingivectomy, gingival graft,
bone graft, fiksasi, systemic
control
• Scalling – Polisihing – edukasi :
habit
Plak & Penyakit Karies

• KH + Streptokokus  Asam
laktat
• Asam laktat  demineralisasi
Ca-apatit (komponen utama
email)
• Kavitasi
History of caries

• Archeological evidence : caries is

ancient disease
•Skulls from neolithic period : show sign
of caries, coherent to the increase of
plant food containing carbohydrates.
•Sumerian text (5000 BC) describes a
“tooth worm” as the cause of caries.
• North Americans Indians : Increase
caries incidence after contact with
Europeans colonizing -> go to
farming/agriculture era.
Epidemiology

• 90% schoolchildren, 59% adult -->

experienced caries (Asian & latin
american), <<< African.
• >> 70% in Indonesian.
Clinical finding:

• Is the localized destruction of the

hard tissues of the tooth by acid,
produced from the bacterial
degradation of fermentable
sugars/carbohydrates as sucrose,
fructose & glucose.
• - Initially, it may appear as a small chalky
area (as indicating an area of
demineralization) but eventually develop
into a large and brown/ blueblack
cavitation.
• Commonlly started in fissure, pit occlusal,
and interdental surface, because food
remain to be happen in these areas.
• Could be determined from non carious
lession (Abrassion, atrition, erosion
and fracture)
Classification:
Numerous ways to classify caries
is by :
q Location : m, d, o, b, l, or combined
q Etiology : baby botle, early,
childhood, rampant caries, etc.
q Rate of Progression : Acute,
chronic, recurent.
q Affected hard tissue : enamel,
dentinal, root caries
Diagnosis & examination

• Primary diagnosis involves :

• Inspect to all visible tooth surface,
using : good light source, mirror,
sonde and explorer.
• Explore cavity, eliminate food debris,
dried with cotton or airflow  to
know cavity expantion & pulpal
response.
• Routine examination : Sondation,
percussion, pressure & palpation.

• X-rays, transillumination
fibreoptic : when the naked eye
couldn’t detect the lesion, at
interproximal, cervical, or apical.
Caries Risk :

qFood debris impact/accumulate on

the cavity raise multiple injuries
(physical, chemical (acid, toxic
metabolite & biological; microbe)
• Cause diseases of pulp tissue : pulp
irritation, pulp inflamation and finally
death of pulp.
Symtoms:

q No pain to severe pain

q Pain : by heat, cold, sweet foods
/drinks, spontaneous.
q Also 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 don’t 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 : -/-/-
Pulp death

• Pulpitis yg tidak mendapat perawatan akan

mengalami kematian (nekrosis). Karena
kematiannya di sertai dengan invasi MO,
maka disebut sebagai Gangren Pulpa.

• Mikroba gangren pulpa dan metabolit

toksiknya menyebar ke jar. periodontal
apikal menyebabkan periodontitis apikalis.
• Nekrosis pulpa juga dapat
menyebabkan periodontitis apikalis,
akibat dari jaringan nekrotik pulpa
yang lisis bersifat toksik.
• - Subj : Pada kondisi akut, muncul
keluhan sakit. Pada kondisi kronis
tidak ada keluhan.
• Obj : EO : t.a.k.
• IO :
• Inspection : profunda, pulp
perforate, colour change.
• S : profunda, pain (-)
• Percussion : +/-, Pressure : +/-
• Palpation : luxation (+)
Management:

q Preventif : 1) Personal oral hygiene --

> brushing & flossing daily, to
minimize etiologic agent, remove &
prevent formation of plaque. 2).
Dietary modification 3). Others
q Curatif :
• Basic treatment : conservative to
maximize the function of
masticatory, phonetic and aesthetic.
Extract when : excesive caries,
posterior.
PENJALARAN

• Penyakit karies yang tidak mendapat

perawatan, menyebabkan kematian
pulpa. Penjalaran infeksi odontogen
dapat menjalar secara lokal (IO dan
EO) menjadi periapical diseases. Gigi
gangren dan periapical diseases juga
dapat menjadi sumber infeksi (focal
of infection) yg menyebar ke organ
lain melalui foramen apikal.
 Pulpitis
Acute Chronic

Apical Periodontitis
Acute Chronic

Periapical absces Periapical granuloma

Acute Chronic

Periapical cyst
OSTEOMYELITIS
Acute Chronic

Periostitis

Cellulitis Absces
 Dental Plaque

Periodontopathy Immunosupressif
Cariogenic agent :
S mutans, A Actinobacilus, Spricaetes, LPS, LTA
viscosus, L baccilus Bacteriodes, Vaillonella Dextran - levan

Caries Periodontal Sistemic

Diseases Diseases