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
 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
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
Abses periodontal
Abses intra oral
Abses ekstra oral
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
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 :
Location : m, d, o, b, l, or combined
Etiology : baby botle, early,
childhood, rampant caries, etc.
Rate of Progression : Acute,
chronic, recurent.
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
couldnt detect the lesion, at
interproximal, cervical, or apical.
Caries Risk :

Food 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:

No pain to severe pain

Pain : by heat, cold, sweet foods
/drinks, spontaneous.
Also cause : bad breath, bad
sensation /foul taste, infection &
spread to surrounding soft tissue.
Penjalaran karies Gigi
kePenyakit 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 : -/-/-
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:

Preventif : 1) Personal oral hygiene

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

Kompetensi GP : Simtomatik
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
OSTEOMYELITIS cyst
Acute Chronic

Periostitis

Cellulitis Absces
 Maping

Gambarkan maping
Biar gak lupa
ORAL FOCAL OF
INFECTION
Suatu penyakit di suatu tempat di tubuh,
sering bersumber / berhubungan dengan
infeksi di rongga mulut. Pengamatan ini
berkembang mulai awal abad 20-an, hingga
muncul oral focal of infection .
Infeksi fokal (focal infection) diartikan
sebagai infeksi di suatu tempat sebagai
hasil metastasis dari fokal (focal of
infection) berupa mikroba dan atau
toksinnya
 FOKUS INFEKSI ORAL (oral focal
of infection) : diartikan sebagai
suatu infeksi di rongga mulut yang
dapat menjalar ke organ lain untuk
menimbulkan/ memperberat infeksi di
tempat tersebut, meliputi :
Open focus : lesi karies dalam,
kalkulus, gingivitis, periodontitis
marginalis, luka bekas pencabutan,
tumpatan gigi/ protesa yang rusak.
 Close focus : infeksi apikal
(periodontitis apikalis), gigi tidak
erupsi tapi terinfeksi (perikoronitis),
pulpa terinfeksi (pulpitis/ Gangren).
PENYEBARAN :

- Perkontinuitas/ jaringan fascia

- Langsung via tractus digestivus/
respiratorius
- Limfogen
- Hematogen
- Serabut syaraf
- Kelenjar saliva
- Reaksi imunologis
Mikroba dan Sumber infeksi

Pulpa : Gangren Pulpa/ abses

Strept Viridans, Staph. Aureus,
Fusobacterium, Actinimyces
Sulcus gingiva/ periodontium :
Periodontal disease
Actinomyces, Spirochaetes,
Bacteriodes
 Caries : Strep. mutans, sanguis.
Lip: Recurent herpes (HSV), syphilis
primary ( Trep. Palidum), Cheilitis
angularis ( candida alb)
Gingiva : ANUG/ vincents
infection (B melaninogenicus,
Fusobact., Borr. Vincentii)
Palatum : Denture stomatitis ( c
albicans, Strp. B-hemoliticus)
 Tongue : Oral trush (c albicans),
actinomycosis (Act israeli), TBC (Myc
tbc)
Mucosa & soft tissue : (sda)
Toksin mikroorganisme yang
menyebabkan kerusakan jaringan.
Eksotoksin : stimulasi sel T-h,
resorbsi tulang. Endotoksin :
lipopolisakarida resorbsi tulang dan
respon sistemik dengan melepas
epinefrin.
Reaksi imunologis : mediator
peradangan (IL, TNF, IFN)
 Penyakit yang muncul karena atau
diperberat oleh infeksi oral :
THT : Sinusitis max, faringitis
MATA : Uveitis
Kulit : dermatitis, pruritis,
urtikaria
Interna : tetanus, rematoid
artritis, glomerulonefritis, DM
 FAKTOR YANG BERPERAN dalam
penyebaran:
Posisi anatomis sumber infeksi
Motilitas bakteri
Daya tahan tubuh atau jaringan
Enzim bakteri berpengaruh pada
penyebaran : kolagenase,
hialuronidase, DNA-ase, koagulase