Ujwal Gautam431, BDS 2009

College of Dental Surgery, BPKIHS

Pathogenesis of Dental Caries

SUGAR + TEETH + MICRO-ORGANISMS

ORGANIC ACID

Caries

Caries Tetralogy, Newbrun, 1982

Dental Caries

Dental Caries is an irreversible microbial disease of the calcified tissues of the teeth, characterized by de-mineralisation of inorganic portion and destruction of organic substance of the tooth, which often leads to cavitation.

Shafer’s Textbook of Oral Pathology, 6th edition

Can remineralisation explain the reversibility?

Caries initiation is due to demineralisation of inorganic component and destruction of organic component. Which occurs first?

Does cavitation necessarily involve in the carious process?

Role of Carbohydrates

• Carbohydrate caries content in diet incidence

suggested by;HopeWood House Study, Sullivan and Harris- 1958, Harris-1963

Vipeholm Study, Gustaffson et al, 1954Patient with Hereditary Fructose Intolerance have less chance of developing caries, Newbrun- 1969

Fermentable Carbohydrates

CARIOGENIC BACTERIA

acid

Role of Carbohydrates

Sucrose is more cariogenic than fructose

While Xylitol, sorbitol and Sachharin are found to be non- cariogenic.

Role of Carbohydrates

Cariogenicity of Carbohydrates determined by:

Sticky, solid Carbohydrate more cariogenic than liquidMono or di- saccharides more cariogenic than poly saccharideIncreased frequency of diet has more chance of cariogenicityIn-between diets increase the chance of caries

Cariogenicity of Starch???

• Starch are very slowly diffused into the diet and they also require extra cellular amylase to become hydrolysed before they can be assimilated and metabolised by plaque bacteria.

Role of Carbohydrates

• Role of Salivary Carbohydrates???»NO EFFECT

as they are bound to proteins and are not available for microbial degradation

Role of Carbohydrates

Role of microorganismsAntoni Van Leeuwenhock (1632-1723)

indicated the presence of microorganisms in the scrappings obtained from the carious lesion of tooth surface

Erdl, in 1843, first associated filamentous

microorganisms to caries on a causative basis

___ Parasitic Theory

Evidence for role of microorganisms:

– Oral organisms can demineralise tooth enamel in vitro and produce lesions similar to the naturally occurring dental caries; Miller, 1889

– Streptococcus mutans is invariably isolated from carious lesions in the teeth of British patients; Clark, 1924

– certain bacteria with acidogenic potential can be isolated and identified from the carious lesions; Florestano, 1942

• S. mutans : development of early carious lesions in enamel

• Lactobacilli : associated with dentinal caries

• Actinomyces : associated with root surface caries

• Vellionella: possibly anti-cariogenic

Role of S. mutans:a) Lactic acid productionb) Formation of adhesive plaquesc) Production of fermentable sugars

Streptoc

occus

mutans • Catalase -ve, gram +ve, facultative

anaerobic cocci• Grow as convex colonies in mitis salivarius bacitracin agar

Cariogenicity due to:• Aciduric, can survive at pH as low as 4.2• Present in large number in saliva• Can adhere to acquired pellicle thus facilitating plaque formation

• Can adhere and grow even in hard and smooth tooth surfaces

• Homofermentive; lactic acid being the major product

Sucrose glucose + fructose

glucans fructans

invertase

Glucosyltransferase

Fructosyltransferase

Promoteaccumulationof plaque

reservoirfor

fermentablesugars for

oral bacteria

enzymes produced byS. mutans

acidogenic + aciduric

Possibility as Secondary invaders due to their acidophilic nature

Predominant site of attack are deep fissures and deep dentinal lesions

• gram +ve, non spore forming rods• grow best in microaerophilic

condition• grows in rogosa agar (low pH

suppresses others)

Lactob

acillu

s

acidop

hilus

Role of acid

“..dental caries is caused by acid formed by fermentation of food particles around the teeth”

Robertson, 1835___Chemical (acid) theory

most accepted & backbone of current knowledge and understanding of etiology of Dental caries

“.. dental caries is caused by acid produced by microorganisms from the fermentation of dietary

carbohydrates”

W. D. Miller, 1889 _____ Miller’s Chemicoparasitic Theory

Chemical TheoryParasitic Theory

Role of acid

ACID CAUSE DISSOLUTION OF THE HYDROXYAPATITE CRYSTALS OF THE ENAMEL

FOLLOWED BY DENTINE(Demineralisation)

• Major degradation product of carbohydrates;Lactic acidButyric acidResulting from anaerobic catabolism

Role of acid

mere presence of acid is of less significance

‘acidic saliva causes tooth decay’

Localisation of acid upon tooth surface

holding mechanism = Dental Plaque

Role of acid

Role of Dental Plaque Miller ruled out role

of Plaque in Carious process and regarded it as a protective layer over the enamel

G. V. Black, 1889, associated Dental Plaque with caries and described it as a separate identity

Bibby described the nature of plaque, its role in caries and adherence on tooth surface

• Plaque is the soft, non mineralised, thin transparent film

predominently consisting of micro organisms suspended in

salivary mucins and extracellular bacterial

polysaccharides.• Initiation of Plaque is with

formation of acquired pellicle from salivary

glycoproteins which later harbors organisms such as S.

sanguis, A. viscous, A. naeslundii, Veillonellae aka

pioneering organisms• S. mutans appears in due

course

Plaque Hypotheses Theories

Non-Specific Plaque Hypothesis purports the caries disease is an outcome of the overall activity of the total plaque microflora and not a specific organism.

Specific Plaque Hypothesis proposes that among the diverse collection of bacteria encompassing the plaque microflora, only a few species of bacteria are involved in the disease. The plaque per se is not pathogenic, but the presence of pathogenic species within the plaque causes dental caries.

Harbors the cariogenic bacteria on tooth surface

Acid production on plaque-tooth interface through fermentation of carbohydrates

Localisation of acid thus produced

Prevents the diffusion of acid

Restrict the buffering action of saliva

Buffering capacity of Saliva

» Bicarbonate» Urea» Arginine-rich proteins

** Sellman, 1949 found that total amount of acid required to reduce the salivary pH is always greater for saliva

from caries resistant persons

• Initiation of caries occurs at pH 5.2 - 5.5;At 5.5 pH, saliva ceases to be saturated with

calcium and phosphate leading to the dissolution of inorganic components of tooth CRITICAL pH

describes the changes in pH ocurring within dental plaque when it is subjected to a carbohydrate diet

Homeostasis at normal pH

Saliva is supersaturated with respect to enamel

Saliva

Enamel

Ca10(PO4)6OH2

[Ca] [PO4][Ca] [PO4]Ca+statherin Ca+aPRP

Demineralization

Saliva

Enamel

Ca10(PO4)6OH2

[Ca] [PO4][Ca] [PO4]Ca+statherin Ca+aPRP

Dietary CHO + biofilm = lactic acid; diffusion into enamel = local pH drop

Enamelsolubilityincreases

[Ca][PO4]exit tosaliva

CHO CHO CHO

[H+]

[H+]

[H+][H+]

[H+]

pH at‘plaque-tooth interface’

less than 5.5

loss of calcium and phosphates from the surface and subsurface enamel, creating a

white spot lesion.

enamel demineralization process begins

1st detectable evidence ofEnamel demineralisation

frank cavitation if the bacterial plaque is not

regularly removed from the tooth surface.

Remineralization

Saliva

Enamel

Ca10(PO4)6OH2

[Ca] [PO4][Ca] [PO4]statherin Ca+aPRP

Saliva flow clears CHO; salivary HCO3 returns pH to normal

Enamel becomeslesssoluble

[Ca][PO4]move intoenamel

CHO

CHO

[HCO3]

[HCO3][HCO3]

demineralization process is reversible provided that the

acidogenic properties of the biofilm are neutralized.

Buffering capacity of saliva

If dietary carbohydrates are removed / pH = 7 REMINERALISATION occurs

Once the pH returns to higher than the critical point, demineralization is

arrested and minerals can be added back to the partially dissolved enamel

crystallites.

Alternating cycles ofDemineralisation & Remineralisation

• Net loss– Subsurface demineralization– New caries– Progression of old lesions

• Net gain - remineralization of existing lesions

Remineralization, a conservative alternative to conventional caries removal

and dental restoration

• natural process for repairing subsurface non-cavitated carious lesions caused by organic acids created by bacterial metabolism of fermentable carbohydrates.

• Fluoride ions in the presence of calcium and phosphate promote remineralization by building a new surface on existing crystal remnants in subsurface demineralized lesions thus favoring the formation of the more favored fluorapatite crystal in the enamel.

Dental caries

Robert H Selwitz, DDS, Amid I Ismail, DrPH and Nigel B

Pitts, BDS

The LancetVolume 369, Issue 9555, Pages 51-59

(January 2007)DOI: 10.1016/S0140-6736(07)60031-2

Copyright © 2007 Elsevier Ltd Terms and Conditions

Diagram of the caries process as regular flux of demineralisation (destruction) and remineralisation (repair); Adapted from Kidd and Joyston-Bechal, 199749

Caries, a Proteolytic process

Proteolytic enzymes liberated by cariogenic bacteria

destruction of the organic matrix

detachment of inorganic crystals from one another

collapse of whole structure

CAVITATION.

Gottlieb (1994) and Gottlieb, Diamond and Applebaum (1946)_______ Proteolytic theory

however,

• Proteolytic bacteria are rare in oral cavity

• No explanation for role of carbohydrates, acid, etc in dental caries

• Carious lesions cannot be reproduced in vitro by the proteolytic mechanisms

• Gnotobiotic studies: caries can occur in absence of proteolytic organisms.

• Enamel is largely inorganic. So, the caries

initiation from proteolytic activity is less likely

THOUGH ITS ROLE IN CARIES PROGRESSION CANNOT BE RULED OUT

CARIES = acidogenic + proteolytic,a possibility?

______ Manley and Hardwick (1951)

Both type of organisms can be present, each functioning independently.

Possible mechanisms;

microorganisms invade enamel lamellae, attack enamel and involve dentine before clinical evidence of caries.

Alteration in enamel prior to invasion by micro organisms through decalcification

Proteolytic Chelation theoryProteolytic breakdown of organic portion

of enamel

Proteolytic breakdown products + acquired pellicle + food debris =

chelating agent

CHELATION -vely charged chelating agent releases +vely charged Calcium

ions from enamel/dentine

Dissolution of inorganic component of tooth

_______ Schatz et al, 1955

Factors that influence Dental Caries(Workshop on Dental Caries mechanisms & Control Techniques,

University of Michigan, 1947)

Host factors ComponentsA. Tooth 1. Composition

2. Morphologic characteristics

3. PositionB. Saliva 1. Composition

a. Inorganicb. Organic2. pH3. Quantity4. Viscosity5. Antibacterial factors

C. Diet 1. Physical factorsa. Quality of Diet2. Local factorsb. Carbohydrate contentc. Vitamin contentd. Fluorine content

D. Systemic conditions

Histological Changes

Pit and Fissure caries

Early lesions appear black/ brown; feel soft and ‘catch’

Region bordering the lesion appear opaque bluish white

Undermining occurs through lateral spread at DEJ

May penetrate into dentine through dentinal tubules

Due to Poor self-cleansing/ developmental faults of tooth

Smooth surface caries

Earliest change is the appearance of white chalky spot which is due to the loss of interprismatic substance of enamel

Earliest microscopic change involves accentuation of striae of Retzius and Perikymata

Appears as well demarcated faint opacity or yellow/brown pigmentation with adsorption of exogenous materials by porous region

With progression, forms a cone shaped lesion with base towards the tooth surface

Eventual loss of enamel leads to roughening and superficial decalcification

Longitudinal ground sections reveal 4 zonesTranslucent zoneadvancing front of enamel lesionappears structureless after imbibition with quinolone in

transmitted lightpore volume 1% compared to 0.1% of sound enamelno evidence of protein lossDark zoneusually present as a dark brown zone in the transmitted light due

to excessive demineralisationshows birefringence with sound enamel after imbibition

with quinolone in polarised light, so called positive zonecontains 2-4% pore volumeBody of Lesionarea of greatest demineralisationpolarised light shows pore volume of 5% near periphery

and 25% in the centre regionappears translucent when examined in quinolone under transmitted

lightshows birefringence with sound enamel after imbibition

with waterSurface zonepartial dimeneralisation of 1- 10%pore volume less than 5% of the spacesnegative birefringence of surface region with water imbibitionpositive birefringence of porous subsurfaceregion

Dentinal Caries

• Defense reaction ofpulpo-dentinal complex– Sclerotic dentine– Reactionary dentine formation– Sealing of dead tracts

• Carious destruction– Demineralisation– Proteolysis

Early dentinal changes: Deposition of fat globules Sclerosis of dentinal tubules Decalcification of wall of dentinal tubules

Pioneer bacteria Microbial invasion: Proteolytic, Acidogenic

Advanced Dentinal Changes: Decalcification and confluence of dentinal

tubules Thickening of sheath of Neuman Increase in diameter of Dentinal tubules with

lodging of microorganisms Formation of Liquifaction foci Acidogenic and proteolytic activity Formation of transverse clefts Caries progression with apex pulpally and base

towards enamel

Zones in advancing lesion of dentinal caries:

i. Zone of fatty degeneration of Tomes’ fibres

ii.Zone of dentinal sclerosisiii.Zone of decalcification of Dentineiv.Zone of bacterial invasionv. Zone of decomposed dentine

Root Caries

• Initiates on mineralised cementum and dentin surfaces which have greater organic component than enamel tissue

• On buccal or lingual surface of tooth• Dental plaque and microbial invasion important aspect

• Decalcification of cementum follows destruction of remaining matrix

Arrested caries

• No tendency for further progression

• Exclusively in occlusal surface• Large open cavity in which the superficially softened and decalcified dentine is burnished to a brown, polished hard surface.

ORAL HEALTH CONSEQUENCES

• apical periodontitis• periapical abscess• osteomyelitis of

the jaw

Pathogenesis of Dental Caries

Fermentation of dietary sugars by Oral micro-organisms

De-mineralisation Re-mineralisation Further demineralisation and

Cavitation Initiation / Formation of

Caries

Dental Caries is a multifactorial disease

Histopathologist stages of lesion viewed microscopically.

Chemist interrelationship beetween pH, mineral flux and solubility at tooth-saliva interface

Microbiologist interaction involving oral bacteria and dental tissue

Current concept of caries etiology implies interplay of host, microbial floras, substrate

and time as the principle factors

References• Shafer, Hine, Levy; Shafer’s Textbook of Oral Pathology;

6th Ed.; Elsevier; 2009• Shobha Tandon; Textbook of Pedodontics; 2nd Ed.; Paras

Medical Publisher• M. W. Roberts, J. T. Wright; The Dyanamic Process of

Demineralisation and Remineralisation; Dimensions of Dental Hygiene. July 2009; 7(7): 16, 18, 20-21

• J.D.B. Featherstone; The Continuum of Dental Caries—Evidence for a Dynamic Disease Process; Journal of Dental Research; July 2004 Vol.83 no. suppl 1

• M. Hurlbutt, B. Novy, D. Young; Dental Caries: A pH-mediated disease; CDHA Journal – Winter 2010

• Alexander V. Zavgorodniy, Ramin Rohanizadeh, Michael V. Swain, Ultrastructure of dentine carious lesions, Archives of Oral Biology, Volume 53, Issue 2, February 2008, Pages 124-132, ISSN 0003-9969, 10.1016/j.archoralbio.2007.08.007. (http://www.sciencedirect.com/science/article/pii/S0003996907001999)