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

Periodontopathy
Actinobacilus, Spricaetes, Bacteriodes, Vaillonella

Immunosupressif agent : LPS, LTA Dextran - levan

Caries

Periodontal Diseases

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 - IO

: t.a.k. : 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 Chronic

Periapical granuloma

Periapical cyst

OSTEOMYELITIS
Acute 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