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MIKROBIOLOGIMIKROBIOLOGI

PEMBENTUKAN PLAKPEMBENTUKAN PLAK

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DENTAL PLAK

Substansi terstruktur berupa depositlunak, berwarna kuning keabu-abuan

yang melekat erat pada permukaankeras rongga mulut,

terutama terdiri dari kompleks bakteridalam suatu matriks ekstraseluler

berupa lipid, glikoprotein saliva danpolisakarida

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Material AlbaAkumulasi lunak dari sel bakteri dan sel

 jaringan yang membentuk struktur dental pltetapi bersifat lebih mudah dihilangkan dengSemprotan air

CalculusCalculus

Deposit keras yang berupa mineralisasi dariplak dan dilapisi plak yang belum bermineralisasi

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STRUKTUR DAN KOMPOSISI

PLAK Komposisi utama : bacterial mikroorganism

! g plak : !"!! bakteri

#ebih dari $"" spesies

%on bacterial mo : mycoplasma, jamur,proto&oa dan virus

'atriks interseluler : sel host ( epitel,

makrofag, leukosit Komponen inorganik dari saliva : fosfor,

kalsium

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Muhlemann & Schroeder, 1964“the differentiation between dental plaque

and materia alba is determined by the

strenght of adherence of the deposit”

If it is removed by the mechanichalaction of strong water spray, thematerial is termed MATERIA ALA

If it withstands the water spray, itcalled !E"TAL #LA$%E

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PLAK

)erdasarkan posisinya thd margin gingiva :

*lak supragingiva

*lak marginal, jk berkontak langsung dg '+

  +ingivitis

 

*lak subgingiva

Diantara gigi dan epitel sulkus gingiva

Di bawah margin gingiva

  destruksi jaringanlunakperiodontitis

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*lak supragingiva )ag pmkaan gigi : +ram kokus dan

rods

)ag luar : +ram . rods, /lamen

*lak subgingiva

 0ergantung kedalaman poket )ag apikal : spirochetes, kokus, rods

)ag koronal : /lamen

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*lak subgingiva Komposisi beda ok lingk anaerob

*roduk dari darah

%utrisi dari +12

Sel dan mediator in3

)erdasarkan perlekatan dengan gigi,dibedakan :

 0ooth-associated 4attached5 : +ram kokus, rods

 0issue-associated 4unattached5 : +ram . kokus,rods, /lamen, spirochetes

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PM!NTUKAN PLIKL

*elikel menutupi seluruh permukaan 6' Dalam nanoseconds stl polishing, gigi

ditutupi oleh lapisan yang sangat tipis dari

saliva 4 Acquired Pellicle5 *elikel t7d : glikoprotein 4musin5, protein

yang kaya prolin dan histidin, lysosim,fosfoprotein 4statherin5 dan en&im 48-

amylase5 Komponen spesi/k pelikel tgt materi /sio-

kimia permukaan dibawahnya

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PRLKATAN !AKTRI A"AL

9 0ahap

2ase ! : transport to the surface

2ase : initial adhesion 4reversible52ase ; : attachment 4irreversible5

2ase 9 : coloni&ation of the surface and

bio/lm formation

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2ase ; : Attachment Spesi/c interaction : kovalen, ionic, hydrogen

*ada pmkaan yang kasar : perlekatan lebihbesar shg perub mjd irreversible lebih mudah

dan lebih sering <katan dari adhesion 4protein ekstrasel mo5

dan receptor 4protein, glikoprotein,polisakarida pelikel5

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KOLONI A I DAN

PMATAN#AN PLAK

 0erjadi intrabacterial connections4coaggregation5

=arly 1oloni&er : Streptococcus,Actinomyces

Secondary : Actinobacillus a,fusobacterium, prevotela, p7 gingivalis,

treponema denticola

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Initial coloni&ation ' #rimary

coloni&ersStreptococci dan Actinomyces :

/mbrae - proline rich protein

pelikel 4>lock n key? mechanism5

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Secondar$ colon%er'

 After the initial colonization of the tooth

surface, plaque increases by two distinct

mechanisms: 1 ) the multiplication of bacteria

already attached to the tooth surface, and 2)

the subsequent attachment and multiplication

of new bacterial species to cells of bacteria

already present in the plaque mass.

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Ter(%ar$ colon%er'

 After one wee# of plaque accumulation, other

Gramne!ati"e species may also be present

in plaque. These species represent what is

considered to be the &tertiary colonizers&, and

include Porphyromonas gingivalis,

Campylobacter rectus, Eikenella corrodens,

 Actinobacillus actinomycetemcomitans, andthe oral spirochetes 'Treponema species).

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The structural characteristics of dental

plaque in this time period re"eal comple$

patterns of bacterial cells of cocci, rods,

fusiform, filaments, and spirochetes. (n

particular, specific associations of different

bacterial forms ha"e been obser"ed. or

e$ample, the adherence of cocci to filamentsresults in a typical form referred to as &test

tube brushes& or &corncob& arrays.

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The structural interactions of the bacteria probably are

a reflection of the comple$ metabolic interactions that

are #nown to occur between different plaque

microor!anisms. *ne e$ample of this is the production

of succinic acid from Campylobacter   species that is

#nown to be used as a !rowth factor by

Porphyromonas gingivalis. Streptococcus  and

 Actinomyces species produce formate, which may then

be used by Campylobacter   species. Fusobacterium species produce both thiamine and isobutyrate that

may be used by spirochetes to support their !rowth.

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PM!NTUKAN PLAK

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)U!UN#AN MO PLAK DAN PN*AKIT

PRIODONTAL

*+ipotesa Pla, Nonspesifi,*+ipotesa Pla, Nonspesifi,    -%alter "oesche./0123-%alter "oesche./0123   Peny4 perio disebab,an oleh perluasan produ,Peny4 perio disebab,an oleh perluasan produ,

  berbahaya dr seluruh flora pla,berbahaya dr seluruh flora pla,

*+ipotesa Pla, 'pesifi,*+ipotesa Pla, 'pesifi,   +anya pla, ttt yg patogeni, dmn patogenisanya+anya pla, ttt yg patogeni, dmn patogenisanya

  tgt ada 5 mening,atnya M4& spesifi,.tgt ada 5 mening,atnya M4& spesifi,.   mis : A.actynomycetemcomitans sbg penyebabmis : A.actynomycetemcomitans sbg penyebab   Local. Aggressive Period.Local. Aggressive Period.

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KRITRIA PRIODONTAL PATO#N

RITRIA PRIODONTAL PATO#N

'enurut 6obert Koch :

Dapat diisolasi pada individu yang sakit

Dapat tumbuh jika dikultur di lab Dapat menyebabkan penyakit yang

sama jk dicobakan pada hewan coba

Dapat direcoveri dari lesi hewan coba

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KRITRIA PRIODONTAL PATO#N

RITRIA PRIODONTAL PATO#N

Menurut 'igmund 'ocrans,yMenurut 'igmund 'ocrans,y 66 Pening,atan 7ml organismePening,atan 7ml organisme

Ber,urang 5 hilang stlh perawatanBer,urang 5 hilang stlh perawatan Menun7u,,an respon host dg ,erusa,anMenun7u,,an respon host dg ,erusa,an

respon imun selular 5 humoralrespon imun selular 5 humoral Mampu menyebab,an peny4 pd hewanMampu menyebab,an peny4 pd hewan

percobaanpercobaan Menun7u,,an fa,tor 8irulensi ygMenun7u,,an fa,tor 8irulensi yg

menyebab,an ,erusa,an 7ar4periomenyebab,an ,erusa,an 7ar4perio

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PRU!A)AN MO DALAM PN*AKIT

PRIODONTAL

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PRU!A)AN MO DALAM PN*AKIT

PRIODONTAL

+ram menjadi +ram .

%onmotile menjadi motile

4bkembang biak dgn cepat5 2acultative anaerob menjadi

obligate anaerob

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KMAMPUAN !AKTRI DALAM

MRUSAK +ARIN#AN

Scr langsung mendegradasi jar yangmenyebabkan pengeluaran bahan-bahanaktif dari sel jar7tubuh

*roduk bakteri menghambatpertumbuhan selmengganggu aktivitassel,e@: fatty acid, indole,peptide

=n&ym yang mampu merusak seluruh

 jaringan matriks interselular *roduk bakteri merusak sistem imun

kerus7 Baringan

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M%roor-an%'me .ada Pen$a%(

Per%odon(al /Samarana$ae,002

Kondisi Proporsi bakteri Mikroorganisme Dominan

Sehat Sebagian besar bakteri kokus Gram positif dengan sedikitspirochaeta atau motile rods

Streptococcus sanguisStreptococcus oralis

 Actinomyces naeslundii Actinomyces viscosusVeillonella spp

Gingivitis marginalis kronis Bakteri Gram positif sebanyak55% dengan sesekali terdapatspirochaeta atau motile rods

Streptococcus sanguisStreptococcus milleri

 Actinomyces naeslundii Actinomyces israelii Prevotella intermediaCapnocytophaga spp

 Fusobacterium nucleatumVeillonella spp

Periodontitis kronis 5% Bakteri Gram positif dengan!"% anaerob# Spirochaetaatau motile rods prominen

 Porphyromonas gingivalis Prevotella intermedia Fusobacterium nucleatum Bacteroides forsythus Actinobacillus actinomycetemcomitansCapnocytophaga sppSpirochaeta

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Re3erence'

Neman e( al, 5arran&a6' 5l%n%cal

Per%odon(olo-$ , 1(h, 06

L%ndhe e( al, 5l%n%cal Per%odon(olo-$and Im.lan( Den(%'(r$ , 4(h, 07

Samarana$ae, ''en(%al

M%cro8%olo-$ 3or Den(%'(r$ , 0nd, 00

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 0C= =%D