Kuliah Gigi Dan Mulut

8/11/2019 Kuliah Gigi Dan Mulut

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DENTAL ANATOMY &

PHYSIOLOGY

Represented and Modified by

HELMIN ELYANI

Reviewed by:


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Part A: Oral Embryology

Study of developmental

stages of the individual

Prenatal

Natal

Postnatal

Zygote: First 2 wks

Embryo: 2 wks-8wks

Fetus: 9 wks-birth


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Fertilization

Cell division and

specialization

Proliferation

Cytodifferentiation

Histodifferetiation

Morphodifferentiation


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Embryonic Stage

Three primary

embryonic cell layers

Oral cavity and teeth

derived from ectoderm


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Factors Influencing Prenatal

Development

Genetic

Environment


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Palatal Development

Formed during week 5 or 6

Cleft palate

Cleft lip

Unilateral or bilateral

Opening in hard or soft palate

Missing or malaligned teeth


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Life Cycle of a Tooth

Intitiation

Bud stage

Proliferation

Cap stage

HistodifferentiationBell stage

Morphodifferentiation


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Developmental Problems

Ameloblastomas

Anodontia

Supernumerary

Osteodentin

Dentinogenesis

imperfecta

Amelogenesisimperfecta

Macrodontia

Microdontia

Twinning

Hutchinsons incisors

Enamel hypoplasia

Hypocalcification

Mottled enamel

Tetracycline staining


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Eruption Period

Problems

Impaction

Malpositioned teeth AnkylosisFunctional

Prefunctional


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Factors Contributing to Tooth Eruption

Pressure asroots form

Formation andresorption

of bone

Pressure ofmuscles

Growth ofroots

Formation

of crown

Tooth

eruption


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Maturation Stage

Attrition

Bruxism Erosion

Abrasion


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Dental Anatomy and Physiology

After viewing this lecture, attendees should be able to:

Identify the major structures of the dental anatomy

Discuss the primary characteristics of enamel, dentin, cementum, anddental pulp

Describe the biologic functions that take place within the oral cavity


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Primary (deciduous)Secondary (permanent)

Definition (teeth): There are two definitions


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A tooth is made up of three elements:

Water

Organic materials

Inorganic materials

Elements


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Primary (deciduous)

Consist of 20 teeth

Begin to form during the firsttrimester of pregnancy

Typically begin erupting around 6months

Most children have a completeprimary dentition by 3 yearsof age


Dentition (teeth): There are two dentitions

1. Oral Health for Children: Patient Education Insert. Compend Cont Educ Dent.


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Secondary (permanent)

Consist of 32 teeth in most cases

Begin to erupt around 6 yearsof age

Most permanent teeth have eruptedby age 12

Third molars (wisdom teeth) are theexception; often do not appear untillate teens or

early 20s

Dentition (teeth): There are two dentitions

Mandible

Maxilla Incisors

Canine (Cuspid)

Premolars

Molars


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Classification of Teeth:

Incisors (central and lateral)

Canines (cuspids)

Premolars (bicuspids)

Molars


Identifying Teeth

Incisor Canine Premolar Molar


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Identifying Teeth2

Incisor Canine Premolar Molar

Incisorsfunction as cutting or shearing instruments for

food.

Caninespossess the longest roots of all teeth and arelocated at the corners of the dental arch.

Premolarsact like the canines in the tearing of food

and are similar to molars in the grinding of food.

Molarsare located nearest the temporomandibular joint

(TMJ), which serves as the fulcrum during function.


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Dental Anatomy

and Physiology

Apical Labial

Lingual

Distal

Mesial

Incisal

Teeth: Identification

Tooth Surfaces

Labial

Apical

Lingual

Distal

Apical

Mesial

Incisal Incisal


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Dental Anatomy

and Physiology

Apical: Pertaining to the apex or

root of the tooth

Labial: Pertaining to the lip;

describes the front surface ofanterior teeth

Lingual: Pertaining to the tongue;

describes the back (interior)

surface of all teeth

Distal: The surface of the tooth

that is away from the median line Mesial: The surface of the tooth

that is toward the median line

Labial

Apical

Lingual

Distal

Apical

Mesial


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Enamel

Alveolar Bone

Pulp

Chamber


Enamel (hard tissue)

Dentin (hard tissue)

Odontoblast Layer Pulp Chamber (soft tissue)

Gingiva (soft tissue)

Periodontal Ligament (soft tissue)

Cementum (hard tissue)

Alveolar Bone (hard tissue)

Pulp Canals Apical Foramen

The Dental Tissues: Dentin

Odontoblast Layer Gingiva

Periodontal Ligament

Cementum

Pulp Canals

Apical Foramen


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Anatomic Crown

Anatomic Root

Pulp Chamber

The 3 parts of a tooth:

Anatomic Crown

Anatomic Root

Pulp

Chamber



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Anatomic Crown

Anatomic Root

Pulp

Chamber


The anatomiccrownis the portion

of the tooth covered by enamel.

The anatomic rootis the lower two

thirds of a tooth.

The pulp chamberhouses the

dental pulp, an organ of myelinated

and unmyelinated nerves, arteries,

veins, lymph channels, connective

tissue cells, and various other cells.


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Enamel Dentin

Cementum

Dental Pulp

The 4 main dental tissues:


Enamel

Dentin

Cementum

Dental Pulp


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Structure

Highly calcified and hardest tissue inthe body

Crystalline in nature

Enamel rods

Insensitiveno nerves

Acid-solublewill demineralize at a pHof 5.5 and lower

Cannot be renewed

Darkens with age as enamel is lost

Fluoride and saliva can help withremineralization


Dental TissuesEnamel2


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Dental TissuesEnamel2


Enamel can be lost by:3,4

Physical mechanism

Abrasion (mechanical wear)

Attrition (tooth-to-tooth contact) Abfraction (lesions)

Chemical dissolution

Erosion by extrinsic acids (from diet)

Erosion by intrinsic acids (from the oralcavity/digestive tract)

Multifactorial etiology

Combination of physical and chemicalfactors


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Softer than enamel

Susceptible to tooth wear (physicalor chemical)

Does not have a nerve supply but canbe sensitive

Is produced throughout life

Three classifications Primary

Secondary

Tertiary

Will demineralize at a pH of 6.5 andlower

Dental TissuesDentin2



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Three classifications:

Primary dentinforms the initial shape of the tooth.

Secondary dentinis deposited after the formation of the primary dentin on all internal aspects of

the pulp cavity.

Tertiary dentin, or reparative dentin is formed by replacement odontoblasts in response to

moderate-level irritants such as attrition, abrasion, erosion, trauma, moderate-rate dental caries,

and some operative procedures.

Dental TissuesDentin2



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Dentin

Pulp

Tubule

Fluid Nerve Fibers

Odontoblast

Cell

Dental Anatomy

and Physiology

Dental TissuesDentin (Tubules)2

Dentinal tubulesconnect the dentinand the pulp

(innermost part of the tooth, circumscribed by the

dentin and lined with a layer of odontoblast cells)

The tubules run parallel to each other in an S-

shape course

Tubules contain fluid and nerve fibers

External stimuli cause movement of the dentinal

fluid, a hydrodynamic movement, which can result

in short, sharp pain episodes


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Dental Anatomy

and Physiology

Presence of tubules renders dentin

permeable to fluorideNumber of tubules per unit area varies

depending on the location because of the

decreasing area of the dentin surfaces in

the pulpal direction



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Association between erosion anddentin hypersensitivity3

Open/patent tubules

Greater in number

Larger in diameter

Removal of smear layer

Erosion/tooth wear

Enamel

Exposed

Dentin

Receding

Gingiva

Tubules

Odontoblast

Dental Anatomy

and Physiology



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Thin layer of mineralized tissuecovering the dentin

Softer than enamel and dentin

Anchors the tooth to the alveolarbone along with the periodontalligament

Not sensitive

Dental TissueCementum2


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Innermost part of the tooth

A soft tissue rich with blood vessels andnerves

Responsible for nourishing the tooth The pulp in the crown of the tooth is

known as the coronal pulp

Pulp canals traverse the root of the tooth

Typically sensitive to extreme thermalstimulation (hot or cold)

Dental TissueDental Pulp2



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Pulpitisis inflammation or infection of the dental pulp, causing extreme sensitivity and/or pain.

Pain is derived as a result of the hydrodynamic stimuli activating mechanoreceptors in the nervefibers of the superficial pulp (A-beta, A-delta, C-fibers).

Hydrodynamic stimuli include: thermal (hot and cold); tactile; evaporative; and osmotic

These stimuli generate inward or outward movement of the fluid in the tubules and activate thenerve fibers.

A-beta and A-delta fibers are responsible for sharp pain of short duration

C-fibers are responsible for dull, throbbing pain of long duration

Pulpitis may be reversible (treated with restorative procedures) or irreversible (necessitating rootcanal).

Untreated pulpitis can lead to pulpal necrosis necessitating root canal or extraction.

Dental TissueDental Pulp2,5



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Gingiva

Alveolar Bone Periodontal Ligament

Cementum

Periodontal Tissues6


Gingiva

Alveolar bone

Cementum



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Gingiva:The part of the oral mucosa overlying

the crowns of unerupted teeth

and encircling the necks of erupted teeth,

serving as support structure forsubadjacent tissues.

Dental TissueDental Tissue6


Gingiva


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Alveolar Bone:Also called the alveolar

process; the thickened ridge of bone

containing the tooth sockets in the mandible

and maxilla.



Alveolar bone


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Periodontal Ligament:Connects the

cementum of the tooth root to the alveolar

bone of the socket.





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Cementum:Bonelike, rigid connective tissue

covering the root of a tooth from the

cementoenamel junction to the apex and lining

the apex of the root canal. It also serves as an

attachment structure for the periodontal

ligament, thus assisting in tooth support.



Cementum


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Plaque

Saliva

pH Values

Demineralization

Remineralization

Oral Cavity/Environment



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Dental Anatomy

and Physiology

Plaque:7,8

is a biofilm

contains more than 600 differentidentified species of bacteria

there is harmless and harmful plaque

salivary pellicle allows the bacteria toadhere to the tooth surface, which beginsthe formation of plaque

Oral Cavity


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Dental Anatomy

and Physiology

Saliva:7,8

complex mixture of fluidsperforms protective functions:

lubricationaids swallowing

mastication

key role in remineralization of

enamel and dentin

buffering

Oral Cavity


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Dental Anatomy

and Physiology

pH values:7,8

measure of acidity or alkalinity of asolution

measured on a scale of 1-14

pH of 7 indicated that the solution isneutral

pH of the mouth is close to neutral untilother factors are introduced

pH is a factor in demineralization andremineralization

Oral Cavity

3. Strassler HE, Drisko CL, Alexander DC.


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Dental Anatomy

and Physiology

Demineralization:7,8

mineral salts dissolve into the

surrounding salivary fluid:

enamel at approximate pH of 5.5 or

lower

dentin at approximate pH of 6.5 or

lower

erosion or caries can occur

Oral Cavity


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Dental Anatomy

and Physiology

Remineralization:7,8

pH comes back to neutral (7)

saliva-rich calcium and phosphates

minerals penetrate the damaged enamelsurface and repair it:

enamel pH is above 5.5

dentin pH is above 6.5

Oral Cavity


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ORAL IMMUNOLOGY


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Sistem ImunitasPendahuluan

Rongga Mulut merupakan pintu utamamasuk mikroorganisme

Adanya bakteri oportunis yang dapatmenjadi pathogen

faktor yang terlibat dalam pertahananSECARA anatomis maupun fisiologis,seperti :

Epitel, aliran air liur, anatomi gigi

Imunitas humoral dan seluler


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Sistem ImunitasKomponen Jaringan

Membran Mukosa

..

Makrofag, Antibody

Keratin

Lapisan Granula

Membran Dasar

Air Liur

Pembuluh Darah

..


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Sistem imunitasKomponen Jaringan

Mukosa

merupakan barier protektif yangterdiri atas lapisan-lapisan sel

Nodus LimfatikusAgregasi limfoid intraoral, seperti

tonsil

Kelenjar Air Liur

yang memproduksi IgA

Jaringanterdapat sel-sel imunokompeten dan

molekul-molekul imunitas


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Sistem ImunitasAir Liur

Air Liur disekresikan oleh Kelenjar Besar dan Kecil yang sangat berperandalam membersihkan sisa makanan dan mikroorganisme

Diproduksi 19 ml perjam yang meningkat saat makan. Bila ada penurunandihubungkan dengan penyakit karies gigi dan parotitis

Senyawa yang berperan

Lisosim dan muramidase

Peroksidase (penghambatan pemakaian lisin oleh Lactobacillus)

Laktoferin (bakteriostatik)

Komponen C3.

Leukosit dapat hidup dalam air liur.

Antibodi merupakan unsur penting pada air liur berupa sIgA.


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Sistem ImunitasGusi Celah

Struktur Celah Gusi

1

2

3

4

5

1. Kapiler

2. Jaringan Subepitel

3. Epitel Junctional

4. Cairan Gusi

5. Air Liur

Si I i


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Sistem ImunitasKomponen Seluler dan Humoral

Darah Cairan Celah Gusi

IgG, IgM, IgA

Protein

Komplemen

Enzim-enzimElektrolit

Neutrofil

Sel T, Sel B

Makrofag

Cairan Celah Gusi

Cairan Mulut

sIgA, IgG, IgM

Protein,

Enzim

ElektrolitNeutrofil

sIgA

ProteinEnzim

Elektrolit

Domain air liur

Air LiurAir LiurKelenjar

Air liur


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Respon Imun thd Plak dan BakteriPendahuluan

Mikroorganisme yang pertama ada setelah kelahiranadalah Streptococcus salivarius. Diikuti Veillonellaalcalescens, Lactobacilli dan Candida albicans

Actinomyces dan kuman anaerob lainnya ada setelah1 bulan kemudian

Sedang Streptococcuc sanguinus dan Streptococcusmutans baru tumbuh mengikuti erupsi gigi-gigi.

Plak merupakan agregat sejumlah besar danberbagai macam mikroorganisme pada permukaangigi.

Awal plak gigi dimulai dengan melekatnya bakteriaerob (kuman yang pertama kali melekat adalah S.sanguis)

Begitu gigi erupsi akan dilindungi oleh glikoproteinyang disebut acquired pellicle.

i


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Respon Imun thd Plak dan BakteriPlak dan Respon Imun

Komponen Plak Gigi

Bahan Imunopotensiasi

dan Imunosupresi

Mikroorganisme

Kariogenik

Mikroorganisme

Periodontopati

Streptococcus mutans

Actinomyces viscous

Lipopolisacharida

Dekstran

Levan

Asam Lipotekoat

Actinomyces

Actinobacillus

Vaillonella

Bacteriodes

CapnocytophagaEikenella

Spirochaeta

Respon imun

AntibodiIgG, IgM,IgA, sIgA,

IgE

AktivasiKomplemenJalur klasik

Jalur alternatif

KemotaksisPMN, Makrofag FagositosisPMN dan MakrofagMembunuh,

Penglepasan,

Enzim2 Lisosomal.

Limfosit T dan BMembantu,Menekan,

Proliferasi,

Limfokin,

Memori.

Karies GigiGingivitis

Periodontitis


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PERIO ONTITIS


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Respon Imun thd Plak dan BakteriPlak dan Respon Imun

Bakteri pada plak gigi bervariasi dankomplek.

Produk bakteri, seperti : LPS, LTA, Dekstrandan Levan dapat merangsang respon imun,

a.l. : Komplemen

Proloferasi Limfosit dan pelepasanlimfokin

Pergerakan Makrofag


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Imunologi Kelainan Periodontal

Pendahuluan

Kelainan gusi dan periodontal diinduksioleh plak bakterial.

Respon imun kelainan ini dapatdikelompokkan kedalam 4 stadium

Komponen sistem imun yang ikut berperan

adalah : Sistem imun sekretori

Neutrofil

Antibodi

Komplemen

Limfosit Makrofag

Sitokin (limfokin dan monokin)

I l i K l i P i d l


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Imunologi Kelainan PeriodontalStadium Respon

Stadium Parameter

Stadium I Merupakan respon inf lamasi awal, ter li hat adanya : neutrofil , kompplek imun,akti vasi komplemen dan kemotaksis

Stadium II Terl ihat infi ltr asi lokal Sel L imfosit T dan B. Dalam sir kulasi limfosittersensiti sasi, terl ihat dengan kemampuannya melepas limfokin

Stadium III Lesi menetap, ter l ihat adanya : i nf i l trasi sel plasma lokal , l imfosit padasir kul asi berplori ferasi

Stadium IV Respon imun destrukti f, dii ku ti u lserasi pada epitel celah gusi dan destruksikolagen ser ta destruksi tulang.

Destruksi yang progresif mengakibatkan kehi langan gigi

l G


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Imunologi Karies Gigi

Pendahuluan

Agregat kuman asidogenik(utamanya : S mutans) di

dalam plak gigi akan

memfermentasi dietary

menjadi asam. Glukose

menjadi sakarose.

Ca10(PO4)6(OH)2+ 8H+

10Ca2+ + 6HPO62-+ 2H2O

Karies Gigi, yang berperanadalah sIgA dan yang melaluicelah gusi adalah IgA, IgG danIgM

Bila telah mengenai pulpa, makadiawali dengan inflamasi yangmerupakan respon awal

Imunisasi adalah solusi yangpaling mungkin untukmencegah kerusakan gigi.


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oral bacteria


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dental caries

I l i K i Gi i


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Imunologi Karies GigiSkematik

S. mutans

Sukrosa

sIgA

Plak Gigi

Karbohidrat Diet

Asam

Dekalsifikasi email

dan dentin

Karies Gigi

Peningkatan koloni

kuman asidurik

dan asidogenik

Penurunan pH

plak dan air liur

Sisa makanan

karbohidrat

Faktor lain


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FOCAL INFECTION

OF SISTEMIC DISEASE


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PERIODONTITIS AND SISTEMIC DISEASE


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. VASULAR DISEASE


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VASCULAR DISEASE


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ATEROSKLEROSIS


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diabetes melitus


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diabetes melitus


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low birth infant


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Dental Anatomy & PhysiologyReferences

References

1. Oral Health for Children: Patient Education Insert. Compend Contin Educ Dent. 2005;26(5 Suppl 1):Insert.

2. Sturdevant JR, Lundeen TF, Sluder TB Jr. Clinical significance of dental anatomy, histology, physiology, and occlusion. In: Robertson TM,

Heymann HO, Swift EJ Jr, eds. Sturdevants Art and Science of Operative Dentistry . 4th ed. Mosby: St. Louis, MO; 2002:13-61.

3. Strassler HE, Drisko CL, Alexander DC. Dentin hypersensitivity: its inter-relationship to gingival recession and acid erosion.Inside

Dentistry. 2008;29(5 Special Issue):3-4.

4. Imfeld T. Dental erosion. Definition, classification and links.Eur J Oral Sci. 1996;104(2 (Pt 2)):151-155.

5. Dentin hypersensitivity: current state of the art and science. In: Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity:Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity.Inside Dentistry. 2008;4(9 Special

Issue):8-18.

6. Dorlands Medical Dictionary. 29thEd. Philadelphia, PA: W. B. Saunders Company; 2000.

7. Robertson TM, Lundeen TF. Cariology: the lesion, etiology, prevention, and control. In: Robertson TM, Heymann HO, Swift EJ Jr, eds.

Sturdevants Art and Science of Operative Dentistry . 4th ed. Mosby: St. Louis, MO; 2002:63-132.

8. Tooth Erosion in ChildrenUS Perspective.Inside Dentistry. 2009;5(3 Suppl):8.


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visit the IFDEA at www.ifdea.org


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Dental Anatomy & Physiology

This I FDEA Educational Teaching Resource was

underwritten by an unrestr icted educational grant from:

Kuliah Gigi Dan Mulut

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