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

Cariogenic
S mutans, A
viscosus, L baccilus

Caries

Periodontopathy
Actinobacilus, Spricaetes,
Bacteriodes, Vaillonella

Periodontal
Diseases

Immunosupressif
agent :
LPS, LTA
Dextran - levan

Sistemic
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

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 :

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

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 :
: t.a.k
- EO
: I : Caries +
- IO
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.
gangren pulpa dan metabolit
Mikroba
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.

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
Acute

Periapical granuloma

Chronic

OSTEOMYELITIS
Acute

Periapical
cyst

Chronic

Periostitis

Cellulitis

Absces

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.

focus
:
infeksi
apikal
Close
(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 :
: Sinusitis max, faringitis
THT
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