DENTAL CARIES

CONTENTS INTRODUCTION EPIDEMIOLOGY DEFINITION CLASSIFICATION THEORIES OF CARIES CURRENT CONCEPTS IN CARIES

ETIOLOGY HISTOPATHOLOGY CONCLUSION

INTRODUCTION

EPIDEMIOLOGY

Pre-historic man have decreased caries prevalence

Decreased caries prevalence in African and Asian communities

Factors affecting caries prevalence:1. Race2. Age3. Sex 4. Familial

Current trends in caries incidence:

DEFINITION1. “Dental caries is a microbial disease of the

calcified tissues of the teeth, characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth” [Shaffer]

2. “Localized post eruptive pathologic process of external origin involving softening of the hard tissue and proceeding to the formation of a cavity” [WHO]

3. “An infectious microbiological disease of the teeth that results in localized dissolution and destruction of calcified tissues” [Sturdevant]

CLASSIFICATION

I. STURDEVANT

Based on - Location - Extent - Rate of progression

According to location: a. Primary caries b. Caries of pit and fissure origin c. Caries of enamel smooth surface origin d. Backward caries e. Forward caries f. Residual caries g. Root surface caries h. Secondary (recurrent) caries

• According to extent: a. Incipient (reversible) caries b. Cavitated (irreversible) caries

• According to rate of progression: a. Acute (rampant) caries b. Chronic (slow or arrested) caries

G.V.Black’s Classification • Class-I: - caries on the occlusal surfaces of molars

and premolars - occlusal 2/3 of the buccal and lingual

surfaces of molars - lingual surfaces of the anterior teeth• Class-II: - lesions found on the proximal surfaces

of molars and premolars• Class-III: - lesions found on the proximal surfaces

of anterior teeth, but do not involve the incisal angle

• Class-IV: - lesions found on the proximal surfaces of anterior teeth and involving incisal angle

• Class-V: - lesions found on the gingival third of the facial and lingual surfaces of anterior and posterior teeth.

• Class-VI: - were not included in Black’s classification

- proposed by Siomon - lesions on the incisal edge and

cusp tips of the teeth

GRAHAM MOUNT’S CLASSIFICATION

Based on • Location of caries• Size of the carious lesion

Cavity site

Size 1(minimal)

Size 2(moderate)

Size 3(enlarged)

Size 4(extensive)

Size 1Pit and fissure

1.1 1.2 1.3 1.4

Size 2Contact area

2.1 2.2 2.3 2.4

Size 3Cervical region

3.1 3.2 3.3 3.4

PIT AND FISSURE CARIES Limited to the – occlusal surfaces of molars and premolars - buccal pits of molars - lingual surfaces of maxillary anterior teeth Poor self cleansing features Usually occurs before smooth surface caries Clinically - black or brown in color - slightly soft consistency - “catch” the tip of a fine explorer Adjacent enamel appears bluish white “Internal Caries”

Smooth Surface Caries Develops on - proximal surfaces of the teeth - gingival third of the buccal and lingual surfaces (cervical caries)

Preceded by the formation of dental plaque.

Usually initiate just below the contact point.

Clinically- initially as faint white opacity or yellow brown pigmented area.

Adjacent enamel appears bluish white.

Cervical CariesAppears as crescent shaped lesion.May extend proximally.Almost always an open cavity.Lack of oral hygiene on the part of

patient.

Backward CariesLateral spread of the lesion along the

DEJ exceeds the caries in the contiguous enamel, caries extends into this enamel from the junction.

Forward CariesCaries cone in enamel is larger or at

least the same size as that in dentin

Residual CariesCaries that remains in a completed

cavity preparationNot acceptable if - present at DEJ - prepared enamel

wall

Root Surface CariesIn old age patients

Initiates at the surface of a mineralized dentin and cementum which have greater organic content

Usually have rapid clinical course

Recurrent (secondary) caries:Occurs at the junction of the

restoration and the cavosurface of the enamel

May extend beneath the restoration

Indicates unusual susceptibility to caries attack, poor cavity preparation, defective restoration.

Also indicates presence of microleakage.

Incipient (reversible) caries:First evidence of caries

activity in enamelClinically as white opaque

region Subsurface demineralization

has occurred but no cavitationMay take up extrinsic stains May undergo

remineralization- called as “caries reversibility” or “consolidation” of early enamel carious lesion

Cavitated (irreversible) caries:

Lesion that has advanced into dentin with broken surface

Remineralization is not possible

Treatment include cavity preparation and restoring with suitable material.

Linear enamel caries (odontoclasia):

Atypical form of dental caries in primary dentition

Lesion predominates on the labial surface of the maxillary anterior teeth in the region of neonatal zone

Lesion is crescent shape Increase caries susceptibility

of posterior teeth.

Odontoclasia: - variant of linear enamel caries - results in gross destruction of the labial surfaces of incisor teeth - cause may be an inherent structural defect

Acute dental caries:Rapid clinical course resulting in early

pulp involvementFrequently in children and young adultsEntry of lesion remains small while rapid

spread along the DEJClinically appears light yellow in colourPain is often present

Chronic dental cariesSlowly progressive lesion that

involves pulp much later Common in adultsLarge entrance of the lesionDentin is stained deep brown Moderate lateral spread of caries at

DEJPain is not a common clinical finding.

Rampant caries:Sudden and rapid onset

and almost uncontrollable destruction of teeth

Involves teeth that are ordinarily caries free (mandibular incisors)

Ten or more new increments of carious lesion in one year

Nursing Bottle (Infancy or Soother) Caries

Rapidly progressing caries affecting primary dentition usually during first 2 years of life

4 maxillary anterior are affected first

If unchecked, maxillary and mandibular molars may also get involved

Lower anterior are spared (characteristic feature)

Adolescent caries:Acute caries attack at 11-18

years of ageLesion in teeth and surfaces

that are relatively immune to caries

Small opening in enamel with extensive undermining

Rapid clinical courseLittle or no secondary dentin

formation

Arrested caries:Caries which becomes static or

stationary and does not show any tendency for progression

Almost exclusively occurs on occlusal surfaces

Both dentitions are affectedLesion appears as large open

cavity with lack of food retention

Superficially softened and decalcified dentin gets burnished and has brown stained polished appearance

“Eburnation of dentin”

Xerostomia induced caries (radiation caries)

Complication of radiation therapy of oral cancer lesion

Radiation induced xerostomia produces caries conducive environment

Carious lesion develops as early as 3 months after onset of xerostomia

May be caused by other factors like salivary gland tumors, autoimmune diseases, prolong illness

Senile CariesCaries activity that spurts up during

the old age.They are located exclusively on the

root surfaces of the teeth.Also seen in association with partial

denture clasps.Causes: gingival recession, decreased

salivary secretion, poor oral hygiene.

Occult Caries / Hidden Caries

• Not clinically diagnosed, but detected only on radiograph.

• Seen in persons with low caries index suggestive of increased fluoride exposure.

• Also called as fluoride bombs or fluoride syndrome

1. Simple caries: one surface is involved

2. Compound caries: two surfaces are involved

3. Complex caries: three or more surfaces are involved

ETIOLOGICAL THEORIES

Early theories

Endogenous theories

Exogenous theories

EARLY THEORIES1. The Legend of the Worm:• According to an ancient Sumerian text, tooth

ache was caused by a worm that drank the blood of the teeth and fed on the roots of the jaws

• Antony Van Leeuwenhock (1700) the father of modern microscopy wrote a letter to the Royal Society of London describing little worms taken out of a corrupt tooth and said that they caused the pain in tooth ache.

ENDOGENOUS THEORY• Humoral Theory “dental caries is produced by internal

action of acid and corroding humors”.• Four elemental fluids of the body-blood, phlegm, black bile and yellow bile

• Vital Theory “tooth decay originated, like bone

gangrene, from within the tooth itself”

EXOGENOUS THEORY

• Chemical (Acid) theory: “ teeth are destroyed by acids formed in the

oral cavity ”

• Parasitic (Septic) theory: “ microorganisms are associated with

carious process ”

Acidogenic Theory Proposed by W.B.Miller 1890, most accepted “Acids formed due to the fermentation of dietary

carbohydrates by oral bacteria leads to progressive decalcification of tooth structure with subsequent disintegration of organic matrix.”

He isolated micro-organisms from his experiments & stated that many were involved in the carious process.

3 important factors which can influence process of tooth destruction in process of dental caries:

Dietary carbohydrates, micro-organisms and acid

• Limitations– Did not explain sub-surface

demineralization

– Failed to justify rampant caries

– Did not explain caries in impacted

tooth

– Phenomenon of arrested caries is

not explained

– Smooth surface caries is not

accounted in this theory

Proteolytic Theory Proposed by Gottlieb in 1941. “formation of dental caries is essentially

proteolytic process. Bacteria present produce hydrolytic enzymes and cause proteolysis leading to the dissolution of organic substance.”

Microorganisms invade the organic substance first.

He did admit that, acid formation accompanied the proteolysis.

Yellow pigmentation of dental caries is because of pigment production by proteolytic organism.

Caries is initiated at slightly alkaline pH.

Limitations:In vitro studies didn’t prove the

proteolytic process of caries.Proteolytic bacteria are uncommon in oral

cavity.Didn’t explain about the role of sucrose,

pH and fluoride in dental caries.Protein content of enamel is 0.6%. So,

initiation of caries by proteolytic process is questionable.

Proteolytic-chelation Theory Proposed by Schwatz in 1955. Stated that two processes are involved in caries –

proteolysis & chelation. Chelation is a process involving complexing of

ions into a complexing substance by covalent bond which results in a highly stable, poorly dissociated and weekly ionized compound called chelate.

Bacterial attack on enamel is initiated by keratolytic microorganisms.

Eg: citrates, lactates Chelates are always –ve.

Limitations: Fails to make a mention of sugar and acid

production. Scientists proved that chelates are weak

and can not cause de calcification. Schwatz said, carbohydrates does not cause

acid production but it stimulates proteolysis, which is not true.

Lactobacillus in dental caries is because of chelation and said that microorganisms are not involved in caries.

Sucrose Chelation Theory• If there is a very high concentration of

sucrose in mouth of a caries active individual, there can be formation of complexes like calcium saccharates, calcium complexing intermediaries, etc by action of phosphorylating enzymes

• These complexes cause release of Ca, P ions from enamel and result in DC

•Limitations Sucrose readily gets metabolized to

form acids, hardly any scope for

formation of calcium saccharates, etc.

Very high levels of pH required for

formation of Calcium saccharates,

which is no achievable in the oral cavity

Autoimmune Theory

Few odontoblast cells at specific sites within pulp of specific teeth are damaged by autoimmune mechanism

Due to this the defense capacity & integrity of of enamel and dentin in those specific areas are compromised and act as potential sites for caries development in future

Sulfatase Theory Proposed by Pincus in 1951. Bacterial sulfatases hydrolyses the

mucoitin sulfate of enamel and chondroitin sulfate of dentin producing sulfuric acid that in turn causes decalcification.

Limitation: Sulfated polysacharide in enamel is

very small and not readily accessible as a substrate for enzymatic degradation. So, this is highly unlikely hypothisis for the degragation of tooth enamel.

Levine’s theory Proposed by Levine in 1977. Established chemical relationship between

enamel, plaque and factors which favors the movement of minerals between them.

Also called as “SEW – SAW” mechanism. Said enamel demineralization and

remineralization is a continuous process. Movement of ions between enamel and plaque

occurs in both direction which depend upon - plaque ph - calcium and phosphate ions at the interface - fluoride ion concentration

CURRENT CONCEPTS IN CARIES ETIOLOGY

KEYE’S DIAGRAM VENN DIAGRAM

Secondary Factors:

• Saliva• Other dietary

factors• Vitamins &

minerals• Hereditary

factors

Primary Factors: Teeth Diet Microorganisms

Etiological Factors:

1. Morphology:• Accentuated pits and fissures• Enamel hypoplasia• Mottled enamel• Bucco-lingual width of carious teeth2. Position:• Malpositioned teeth• Rotated teeth

TEETH

3. Composition: • Surface vs subsurface enamel

DIET• Carbohydrate is a cariogenic diet• Cariogenicity is based on1. Physical nature2. Chemical nature3. Mode of intake4. Clearance rate5. Frequency of intake 6. Other dietary factors

PLAQUE AND MICROORGANISMS

PLAQUE:• The concept about dental plaque was first

proposed by Williams in 1897• Consist of - salivary component- mucin - desquamated epithelial cells - microorganisms - calcium and phosphate

To produce caries, micro organisms should have following properties:

1. Should be acedogenic.2. Should be aceduric.3. Should posses attachment

mechanism.4. Should have the capacity to store

sucrose.5. Should be able to synthesize

extracellular glucans.

1. Pioneer / primary bacteria – initiate caries

• S.mutans (smooth surface caries)• Lactobacillus acidophilus (pit &

fissure caries)• Actinomyces (root surface caries)

1. Invaders / secondary bacteria• Staphylococcus, Veillonellae

Streptococci mutans:• Chief etiological agent in dental caries disease 1. it can produce low pH (acidogenic) 2. it can survive in low pH (acidouric) 3. utilize sucrose at a faster rate than other bacteria 4. can metabolize sucrose to synthesize glucan and fructan ( attachment mechanism ) 5. it can store intracellular glycogen amylopectin

type polysaccharides that act as a reservoir of substrate and prolongs its metabolic activity

Other Bacteria• Lactobacillus acidophilus

– Found in carious dentin & saliva of persons with high caries activity

– Release lactic acid• Actinomyces

– Found esp. in root caries– Acidogenic – Attachment to tooth by glycoprotein called

Lectin

Acids produced area) Lactic acid b) Acetic acidc) Butyric acid d) Propionic acide) Traces of formic acid• Lactic acid is the strongest acid

Plaque pH: Critical pH- 5.5 Caries active, pH- 5 to 5.5 Caries immune, pH- 6.8

STEPHEN’S CURVE

MINOR FACTORSI. SALIVA:

1. Flow rate2. Viscosity3. Buffering capacity4. Amount of saliva

Components of saliva:• Bicarbonates• Anti-bacterial agents• Ig-A• Salivary urea and bicarbonates

II. Dietary factor– Diet containing Phosphates decreases caries– Proteins & fat also prevents or decreases caries, as

they prevent attachment of carbohydrates to tooth– Trace elements of Vanadium & Molybdenum

decreases caries – Selenium increases risk of caries– Vitamin A & B are important in formation of hard

tissues. Thus if they are deficient, hypoplasia of teeth is seen, teeth more prone to caries

– Fibrous food help in cleansing of teeth, removal of lodged food

III. Hereditary factors:

HISTOPATHOLOGYImportant for:1. Research purpose2. To know the changes taking place in

dental caries Not important for diagnosis.Studied under: Light microscope Electron microscope Polarized microscope microradiographs

– Loss of inter-rod substance

– prominent enamel-rods

– Appearance of transverse striations of

enamel rods due to segmental

demineralization

– Accentuation of incremental striae of

Retzius

H/F of early enamel caries

H/F of Advanced enamel caries

Classified on the basis of pore volume and

mounting media used Zone 1 – Translucent zone

Zone 2 – Dark zone

Zone 3 – Body of lesion

Zone 4 – Surface zone

• These zones are from the dentin towards the outer

enamel surface

Translucent Zone• Is deepest & forms advancing front of

lesion• Not seen always, seen in 50% of cases.

When seen, appear clear due to mounting media which enters these big pores making them look clear/bright

• Pore volume is 1%, which is more than normal (0.1%)

• Zone cant be easily identified clinically / radiographically

Dark zone / positive zone• Dark zone as mounting media cant penetrate

this zone. Positive zone as it is always present• Pore volume – 2-4%. 2 types of pores seen here large & small

• Initially only large pores, later change to micro-pores. This change mainly due to demineralization occurring in deeper areas which release ions & there is remineralization of superficial areas

• This zone is narrower in rapidly advancing caries & wider in slowly advancing caries

Body of the lesion• Largest zone, between dark & surface zone• Greater amount of demineralization taking

place. Pore size – 5-25%• 5% variation is near periphery, 25% at

center• Prominent striae of Retzius due to

demineralization of inorganic minerals• Contains apatite crystals larger than that

found in normal enamel

Surface Zone

• Quite intact, appears radio-opaque

• Unaffected despite subsurface

demineralization; may be due to:

– surface remineralization by salivary ions

– More amount of fluoride

Dentinal Caries

• Once lesion spreads to DEJ, there is lateral

spread of caries

• Surface enamel gets unsupported enamel rods

enamel # greater cavitation

• Zones of dentinal caries

– Zones start from pulpal side towards dentinal side

1. Zone of Fatty Degeneration of Tomes’ process

2. Zone of Sclerosis

3. Zone of Decalcification without Bacterial

Invasion

4. Zone of Decalcification with Bacterial Invasion

5. Zone of Decomposed Dentin / Infected dentin

Fatty Degeneration of Tomes’ Process

• Innermost layer of dentinal caries towards pulp

• Due to deposition of fatty tissue in odontoblastic processes

• Seen usually in rapidly progressing caries• No crystals or bacteria in lumen of tubules• Intertubular dentin normal

Zone of Sclerosis/Sub-Transparent Dentin

As the microorganisms cause destruction to dentin, initially there is an attempt to stop the advancement of caries by depositing the minerals.

There is a deposition of mineral in intertubular dentin.

Zone is called “transparent zone” Odontoblasts are also start depositing dentin. At the periphery of sclerotic dentin, dead tracts

are present.

Zone of Decalcification without Bacterial Invasion /

Transparent Dentin• Decalcification is by bacterial acid diffusion

• Very narrow zone, softer than normal dentin

• Further loss of minerals from inter tubular

dentin

• Large crystals within lumen of dentinal

tubules

Zone of Decalcification with Bacterial Invasion / Turbid

Dentin• Initially only few tubules are involved & micro-

orgs also less

• These are acidogenic, pioneer bacteria

(initiators), present long before lesion is

clinically detected

• Bacteria multiply within tubules & are seen in

advancing front of lesion

• Walls of tubules are thin & when micro-orgs penetrate, they cause irregularities/distensions of walls ROSARY BEAD appearance

• Later, bacteria have proteolytic activity, areas of proteolysis appear as spaces containing necrotic material & bacteria

• These areas “Liquefaction Foci of Miller”.

• These areas vary in number & are parallel to dentinal tubules

Zone of Decomposed Dentin / Infected Dentin

• Outermost zone, large scale destruction of

dentin

• Foci of Miller join together

• Areas of dentin decomposition, occur

perpendicular to dentinal tubules

“Transverse Clefts”

• Mechanism of formation of Clefts - not known

– May follow course of incremental lines or

– May result from coalescence of liquefaction of

adjacent tubules

– Also may rise by extensive proteolytic activity

along interconnecting lateral branches of

odontoblastic processes

• Bacteria shift from dentinal tubules to the peri &

inter tubular dentin

Secondary / Reactionary dentin

• Protective mechanism to protect pulp

• Develops as a result of localized, non-specific

irritation to odontoblasts

• Hyper mineralized,less number of dentinal

tubules having irregular & torturous course

Root Caries / Cemental CariesHistopathology:• Outer surface of cementum – hyper mineralized,

thus more caries resistant• Resistance due to

– Reprecipitation of minerals from within– Precipitation of minerals from Plaque

• Clefts formed, through which bacteria penetrate & cause tooth structure destruction

• Penetration occurs along course of Sharpey's fibers

• Once cementum completely exposed & destroyed, underlying dentin is involved