PLAK GIGI Peran Plak Gigi pada Patogenesis Penyakit Periodontal & Karies Gigi

PLAK GIGIMassa = Musin saliva + bakteri + epitel mati + KHPlak : Sub gingiva & SupraSubgingiva : dominan anaerobSupra : aerob

Pembentukan plakPlak : awal, muda, matureBeberapa menit

Dental Plaque Cariogenic

S mutans, A viscosus, L baccilus Periodontopathy

Actinobacilus, Spricaetes, Bacteriodes, Vaillonella

Immunosupressif agent :LPS, LTADextran - levanCariesPeriodontal DiseasesSistemic Diseases

Plak Gigi & Penyakit PeriodontalInflamasi pada jaringan penyangga gigiJaringan periodontal : gingiva, membran periodontal, tulang alveolus, sementumPenyebab : Plak, infeksi bakterial, viral, hormonal dll (lihat kuliah DR. Oedijani)

Keluhan Gusi bengkakSakitBerdarah (ringan sd spontan)Bau mulutGigi goyang

Kelanjutan penyakit periodontalGingivitis jika tidak dirawat berlanjut menjadi periodontitis marginalis terus :

Pocket periodontalAbses periodontalAbses intra oralAbses ekstra oral

PenatalaksanaanCausatif : Kontrol plak (initial)Tergantung keparahan.MedikamenOperatif : Curretage, Gingivectomy, gingival graft, bone graft, fiksasi, systemic controlScalling Polisihing edukasi : habit

Plak & Penyakit KariesKH + Streptokokus Asam laktatAsam laktat demineralisasi Ca-apatit (komponen utama email)Kavitasi

History of caries Archeological evidence : caries is ancient diseaseSkulls 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), 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 :qLocation : m, d, o, b, l, or combinedqEtiology : baby botle, early, childhood, rampant caries, etc.q Rate of Progression : Acute, chronic, recurent.qAffected 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 : 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: qNo pain to severe pain q Pain : by heat, cold, sweet foods /drinks, spontaneous. qAlso 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.kIO : 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: qPreventif : 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.

PulpitisAcute ChronicApical PeriodontitisAcute ChronicPeriapical abscesAcute ChronicPeriapical granulomaPeriapical cystOSTEOMYELITISAcute ChronicPeriostitisCellulitisAbsces

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 q Pulpa : Gangren Pulpa/ absesStrept Viridans, Staph. Aureus, Fusobacterium, ActinimycesqSulcus gingiva/ periodontium : Periodontal diseaseActinomyces, Spirochaetes, Bacteriodes

q Caries : Strep. mutans, sanguis.Lip: Recurent herpes (HSV), syphilis primary ( Trep. Palidum), Cheilitis angularis ( candida alb) q Gingiva : ANUG/ vincents infection (B melaninogenicus, Fusobact., Borr. Vincentii)q Palatum : Denture stomatitis ( c albicans, Strp. B-hemoliticus)

q Tongue : Oral trush (c albicans), actinomycosis (Act israeli), TBC (Myc tbc)Mucosa & soft tissue : (sda)

qToksin mikroorganisme yang menyebabkan kerusakan jaringan. Eksotoksin : stimulasi sel T-h, resorbsi tulang. Endotoksin : lipopolisakarida resorbsi tulang dan respon sistemik dengan melepas epinefrin.qReaksi 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: q Posisi anatomis sumber infeksiq Motilitas bakteri q Daya tahan tubuh atau jaringan qEnzim bakteri berpengaruh pada penyebaran : kolagenase, hialuronidase, DNA-ase, koagulase

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