DENTAL CARIES

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. Race 2. Age 3. Sex

4. Familial

 Current trends in caries incidence:

DEFINITION

1. “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 1 Pit and fissure

1.1 1.2 1.3 1.4

Size 2 Contact area

2.1 2.2 2.3 2.4

Size 3 Cervical 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 Caries

 Appears as crescent shaped lesion.

 May extend proximally.

 Almost always an open cavity.

 Lack of oral hygiene on the part of

patient.

Backward Caries

 Lateral spread of the lesion along the DEJ exceeds the caries in the

contiguous enamel, caries extends into this enamel from the junction.

Forward Caries

 Caries cone in enamel is larger or at

least the same size as that in dentin

Residual Caries

 Caries that remains in a completed cavity preparation

 Not acceptable if - present at DEJ

- prepared enamel

wall

Root Surface Caries

 In 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 enamel

 Clinically as white opaque region

 Subsurface demineralization has occurred but no cavitation

 May 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 involvement

 Frequently in children and young adults

 Entry of lesion remains small while rapid spread along the DEJ

 Clinically appears light yellow in colour

 Pain is often present

Chronic dental caries

 Slowly progressive lesion that involves pulp much later

 Common in adults

 Large entrance of the lesion

 Dentin is stained deep brown

 Moderate lateral spread of caries at DEJ

 Pain 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 age

 Lesion in teeth and surfaces that are relatively immune to caries

 Small opening in enamel

with extensive undermining

 Rapid clinical course

 Little 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 affected

 Lesion 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 Caries

 Caries 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 THEORIES

1. 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 teeth 2. Position:

• Malpositioned teeth

• Rotated teeth

TEETH

3. Composition:

• Surface vs subsurface enamel

DIET

• Carbohydrate is a cariogenic diet

• Cariogenicity is based on 1. Physical nature

2. Chemical nature 3. Mode of intake 4. Clearance rate

5. 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 are a) Lactic acid

b) Acetic acid c) Butyric acid d) Propionic acid

e) 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 FACTORS

I. SALIVA:

1. Flow rate 2. Viscosity

3. Buffering capacity 4. 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:

HISTOPATHOLOGY

Important for:

1. Research purpose

2. 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 Caries

Histopathology:

• 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