ANU THAPA48

1ST BATCH

ETIOLOGY AND MICROBIOLOGY OF

DENTAL CARIES

CONTENTS• Introduction• Incidence of caries • Theories of etiology of caries LEGEND OF WORMS Endogenous theories Exogenous theories new theories

• ORAL MICROORGANISM

Oral streptococci Lactobacilli Veilonella Actinomyces species

• ETIOLOGICAL FACTORS

• CONCLUSION

• REFERENCE

Introduction

• Caries = Rottenness or decay (Latin)

• Dental caries is a microbial disease of the calcified

tissues of the teeth, characterized by

dimineralization of the inorganic portion and

destruction of the organic substance of the tooth.

• According to WHO-Dental caries is a localized

post-eruptive, pathological process of external

origin involving softening of the hard tooth tissue

and proceeding to the formation of a cavity.

Incidence from prehistoric modern man

• Disease of modern civilization

Preneolithic period• No caries

Neolithic period• Caries

Modern man -• increased

caries

Theories of etiology of caries

• EARLIER THEORIES:

The legend of worms

• Endogenous theories:

– Humoral theory

– Vital theory of tooth decay

• Exogenous theories :

– Chemical theory

– Parasitic / Septic theory

• New theories

- Miller’s Chemico – Parasitic (Acidogenic) Theory

– Proteolytic Theory (Gottlieb)

– Proteolytic – Chelation Theory (Schatz & Martin)

– Sucrose Chelation Theory (Egglers and Lura )

– Autoimmune Theory (Burch & Jackson)

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The legend of worms

• Ancient Sumerian text

– “Toothache caused by a worm that drank the

blood of the teeth and fed on the roots of the

jaws”

Endogenous theoriesa. Humoral theory

Galen,Greek physician

4 elemental fluids of body – Blood,

Phlegm, Black bile, Yellow bile

Imbalance in these humors all diseases

(including caries)

Hippocrates stated that stagnation of juices

in the teeth was the cause of toothache.

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Vital theory

• Proposed at the end of 18th century

• Tooth decay originated like bone gangrene,

within the tooth itself.

Exogenous theory Chemical theory

Parmly (1820) • Unidentified ‘chymal agent’ – responsible Robertson (1895)

Food particles around teeth

Fermentation

Acids

Dental decay

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Parasitic(Septic)Theory

• Erdl (1843) – Filamentous parasites in the “surface

membrane” of teeth

• Ficinus (1847) observed filamentous micro-organisms

(denticolae) in carious cavities

• Antoni Van Leeuwenhock (1632-1723) microorganisms

were associated with carious process.

• Dubos(1954)-microorganisms can have toxic effects on

tissue.

Miller’s chemico-parasitic theory ‘Acidogenic theory’

• Blend of above theories

• Willoughby D Miller (1882)

Theory: Caries caused by acids produced by microorganisms of the mouthDental decay is a chemico-parasitic process consisting of 2 stages:1.Decalcification (preliminary step)2.Dissolution (subsequent step)Acids are produced by bacteria’s fermentation of sugar and starch

Points in favor

• Backbone of current knowledge and understanding for etiology of dental caries

• 3 factors essential for caries production:– Oral microorganism – Carbohydrate substrate– Acid

Acidogenic theory

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• Unable to explain:

– Site predilection

– Dental plaque

– Caries-free population

• Role of plaque:– localizes acid produced by bacteria – prevents anti- caries effect of saliva

The Proteolytic theory

• Gottlieb,1947• Organic matrix would be attacked before mineral

phase of enamel• The proteolytic enzymes liberated by oral bacteria

destroy the organic matrix of enamel, loosening apatite crystals, so that they are eventually lost and the tissue collapses.

2 types of carious lesions:1. Microorganism enamel lamellae attack enamel and

dentin (before clinical evidence of caries)2. No lamellae, bacteria in dental plaque acids enamel

decalcification.The early lesion chalky white

The Proteolysis- Chelation theory Chelates can be formed at neutral or alkaline

pH, the theory suggests that

demineralization of enamel could arise

without acid formation.

Schatz and Martin (1955)

Initial attack breakdown of organic matter

Breakdown products chelate with minerals of enamel dissolves it

Simultaneous attack on both organic and inorganic part of teeth

ETIOPATHOGENESIS OF CARIESNEWBRUN in 1978 proposed that dental caries to be

multifactorial disease

Microorganisms

Host (saliva

and teeth)

Substrate

Time

CARIES

No caries

No caries

No caries

No caries

• Micro flora: Acidogenic bacteria that colonize the

tooth surface.

• Host: Quantity and quality of saliva, the quality of

the tooth, etc.

• Diet: Intake of fermentable carbohydrates, especially

sucrose, but also starch.

• Time: Total exposure time to inorganic acids

produced by the bacteria of the dental plaque

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Host factors 1. TOOTHComposition of the tooth

• Fluoride content

• Surface enamel more resistant than subsurface enamel

• Surface – More fluoride, zinc, iron and lead,

Less dissolution to acids

More inorganic material and less water

• Subsurface – More carbonate, magnesium, sodium

Decreased enamel density and

permeability

Sound teeth Carious teeth

Enamel 410ppm 139ppm

Dentine 873ppm 223ppm

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Morphologic characteristics of teeth

• Deep, narrow occlusal fissures• Buccal or lingual pits• Attrition

Mand 1 molar > max 1st molar> max & mand 2nd molarsMand incisors & canines - least

• Surface susceptibilty– molars → Occlusal – lateral incisor → Lingual

Host Factors 2. SALIVA

Effect of saliva on Progression/Regression of caries

Composition Salivary buffers Antibacterial propertiesImmunoglobulins Quantity Viscosity

1. Fluoride in saliva• Formation of fluoroapatite in surface enamel

protection against caries.

• The level of fluoride in ductal saliva - 0.01-0.03ppm (lower than in plasma)

• Largely independent of salivary flow rate and are predetermined by the amount ingested.

Composition of saliva

2.Organic componentsa)Ammonia• High ammonia concentration retards plaque

formation, neutralizes acid reduction of caries

• Urea converted to Ammonium carbonate which increases the neutralizing power of saliva

Composition of saliva

b) α-Amylase

• Metabolizes starch and other polysaccharides to glucans which promotes adhesion of bacteria to tooth surface.

c)Histatins (Histidine rich proteins)• Antibacterial action and mineralization

• Inhibits spontaneous precipitation of calcium phosphate salts

from supersaturated saliva Inhibit crystal growth

• Enhances stability of hydroxyapatite present in tooth

Composition of saliva

d)Statherins

• Inhibits spontaneous precipitation of calcium phosphate salts from

supersaturated saliva Inhibit crystal growth

• Favors remineralization without formation of mineral deposits

• Lubricant – prevent tooth wear

e)Proline-rich protein

– Binds to bacteria Influence bacterial composition of enamel pellicle

(role in caries not clear)

Composition of saliva

f)Cystatins (Cysteine rich protease inhibitors)

• Prevent harmful effects of proteases on oral soft tissues

• Role in caries Bind to Hyaluronic Acid

Inhibit precipitation of calcium phosphate

(promote super saturation of saliva)

g)Mucin (Salivary mucins:MG1 & MG2)

Aggregation and oral clearance a) MG1-Contribute to enamel pellicle

Physical and chemical barrier to physical and chemical attackb) MG2 – more characteristic of mucin

Aggregation of bacteria clearance

Saliva as a Buffering fluid

Critical pH pH at which any particular saliva ceases to be saturated with calcium and

phosphate, 5.5 pH < critical pH = dissolution of inorganic component of tooth• Salivary buffers - Bicarbonate-carbonic acid and phosphate, urea

• Bicarbonate – Most important salivary buffer

– It can buffer rapidly by losing carbon dioxide

– Diffuses into dental plaque easily

– Brings pH to 9

– Higher the salivary flow rate, greater buffering capacity

Urea secreted in saliva Nitrogenous products + ammonia

Antibacterial properties of saliva

1. LACTOFERRIN

• Iron binding protein

• Prevents iron utilization by aerobic and facultative anaerobic bacteria

prevents metabolism

2. Lysozyme (N-acetylmuramide glycano-hydrolase)

• Hydrolytic enzyme with direct antimicrobial effect

• Salivary gland fluid and crevicular fluid

• Acts in many ways

1. Lysozyme - Positively charged enzyme

Binds to salivary ions like HCO3-, F-, I-, NO3

-

Complex binds to the cell wall of bacteria

Hydrolysis of glycosidic bonds between polysaccharides in the cell wall

Destabilization of cell wall

Autolysis

Antibacterial properties of salivaLysozyme

3. Salivary peroxidase system

Oxidizes sulphydryl group of oral bacteria

Inactivate enzymes of glycolytic pathway

Inhibit growth ,respiration and metabolism of most bacteria

Immunoglobulins in saliva

• IgA is predominant immunoglobin in saliva.

• Inhibits adherence and prevents colonization on mucosal

surfaces and teeth.

Quantity of saliva

• Removal of food debris and bacteria inhibition of caries

• Factors influencing effect of reduced salivary flow on caries:

– Greater food retention

– Possible alterations in bacterial flora of the mouth

Decreased Salivary flow

• Sjogrens syndrome

• Therapeutic radiation of head and neck - if glands are within

primary beam

• Surgical removal of salivary glands for neoplasms

• Sarcoidosis

• Chronic administration of anticholinergic or parasympatholytic

drugs (antisialogogue)

• Acute virus infection, Anxiety, mental stress, and depression,

dehydration

• Viscosity – largely due to mucin

• Highly viscous saliva promotes caries formation

VISCOSITY OF SALIVA

SUBSTRATE:Diet and caries Influences development of teeth , the quality and quantity of salivary secretions , improved host resistance and improved function .

Cariogenic carbohydrates

Solid and sticky CHO > liquid / solution form

Slowly clearing CHO > rapidly clearing CHO

Monosaccharides > polysaccharides

Refined, pure CHO > crude CHO

Substrate: Diet and Caries

Local effects

• Influences the metabolism of oral flora • Modifying salivary fluids and indirectly the qualitative aspects of salivary

secretion Dietary factors affecting caries • Physical form • Total dietary sugar intake• In between intake of sugars • Frequency of consumption Nutritional factors

Oral fermentable carbohydrate (concentration & retention in plaque)

Acid production

Caries

ORAL MICROORGANISM

Characteristics of cariogenic bacteria:

1. Ability to rapidly transport sugars, when in competition with

other plaques bacteria

2. Convert such sugars acid

3. Ability to maintain these activities under extreme of

conditions (low pH)

1. Acidogenic (strongly acid producing)

2. Acidouric (acid-loving)

ORAL STREPTOCOCCI

S. mutans • Catalase negative, gram positive cocci, homofermentive,

acidogenic, more aciduric • Does not colonize mouth before eruption of teeth and after

extraction• Can live on pH as less as 4.2• Homogenous group – 5 genotypes

– S mutans (a to h serotypes), S rattus, S sobrinus,

S cricetus, S ferus

• Early colonizers of the tooth surface are mainly Neisseria spp. and streptococci, including S. mutans. The growth and metabolism of these pioneer species changes local environmental conditions (e.g. pH, coaggregation, and substrate availability), thereby enabling more fastidious organisms to further colonize after them, forming dental plaque.

• Along with S. sobrinus, S. mutans plays a major role in tooth decay, metabolizing sucrose to lactic acid using the enzyme glucansucrase.[9] The acidic environment created in the mouth by this process is what causes the highly mineralized tooth enamel to be vulnerable to decay. S. mutans is one of a few specialized organisms equipped with receptors that improve adhesion to the surface of teeth.

• Sucrose is used by S. mutans to produce a sticky, extracellular, dextran-based polysaccharide that allows them to cohere, forming plaque. S. mutans produces dextran via the enzyme dextransucrase using sucrose as a substrate in the following reaction:

• n sucrose → (glucose)n + n fructose

Oral microorganism and caries

• Sucrose is the only sugar that S. mutans can use to form this sticky polysaccharide.

• However, many other sugars—glucose, fructose, lactose—can be digested by S. mutans, but they produce lactic acid as an end product. The combination of plaque and acid leads to dental decay.

• It is believed that Streptococcus mutans acquired the gene that enables it to produce biofilms through horizontal gene transfer with other lactic acid bacterial species, such as Lactobacillus.[13]

Property Comment

Sugar transport High and low affinity transport over a wide range of condition to ensure substrate uptake even under extreme

conditions e, g. low pH

Acid production Efficient glycolytic pathway - low pH level attained fast

Aciduricity Survival, metabolism and growth at low pH level

Extracellular polysaccharide (EPS)

production

Plaque formation , consolidate attachment of cells and localize acidic fermentation products

Intracellular polysaccharide (IPS)

production

Allows acid production in the absence of dietary sugars

Oral microorganism and caries

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• S. sanguis

– Occlusal fissures

– Low cariogenicity

• S. salivarius

– Not found in dental plaque; tongue, throat, saliva

– Adheres well to epithelial surface

– Produce levans

• S. mitior

– Soft, round and brown-black colonies

– Predominant in plaque

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• Lactobacilli

– Gram positive

– Non-spore forming rods

– Microaerophilic

– Homofermentive ; L.casei and L.acidophilus

– Heterofermentive – L.feremntum

– Acidogenic and aciduric

– Deeper fissures and dentinal tubules

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• Actinomyces species:

– Gram positive

– Filamentous

– Acidogenic

– Form extracellular levans; has intracellular CHO stores

– A.naeslundi and A.viscosus (facultative anaerobes)

– A.israelii and A.odontolyticus (strict anaerobes)

– Initiation of root lesions

– Most common in subgingival microflora

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• Veilonella:

– Gram negative cocci

– Lack key enzymes for energy production

– Do not utilize sugars as energy source

– Utilizes lactic acid → Propionic acid

– Increase in number after lactic acid producing

organisms have colonised

Localization of microflora in relation to caries

Oral microorganism and caries

SUMMARY   Dental Caries is a multifactorial disease, strongly associated with the dental plaque. Caries forms as a result of disturbance in the normal balance of Oral Biota. The main factors involved are susceptible tooth surfaces, time, sugar substrate and plaque bacteria.  Pits & fissure are the most susceptible areas. Frequency of sugar intake is more decisive than total consumption

Colonization by S. mutans occurs after tooth eruption, and if the fissures become colonized in their depths, then decay may be inevitable. This understanding of the ecology of S. mutans suggests that treatment strategies which interfere with the colonization of S. mutans may have a profound effect on the incidence of dental decay in human populations.

CONCLUSION

• ❑ Caries remains a major public health problem. Extensive damage from caries can lead to major problems for the individual, affecting quality of life both functionally and esthetically. Good general health also includes good oral health. Hence, preventing caries is an important element in public health efforts.

REFERENCE

• ESSENTIAL OF PUBLIC HEALTH DENTISTRY-SOBEN PETER

• TEXTBOOK OF ORAL MEDICINE,ORAL DIAGNOSIS AND ORAL RADIOLOGY 2ND EDITION-RAVIKIRAN ONGOLE

-PRAVEEN B N• Shafer'S Textbook Of Oral Pathology