DENTAL CARIES AND
PREVENTION
KRITHIKA G
FINAL YEAR
CONTENTS
INTRODUCTION
DEFINITION
THEORIES OF DENTAL CARIES
ETIOLOGY
STUDIES
CARIES RISK ASSESSMENT
CARIOGRAM
PREVENTION
VACCINE
CONCLUSION
INTRODUCTION
DEFINITION
Dental caries is an infectious microbial disease of the
teeth.It is characterized by the equation + Fermentable
Carbohydrate = Acid
Acid + Enamel = Dental carries.
Global Burden of Disease during 2017- 3.5 Billion
people wordwide.
Out of which 530 million children affected by primary
teeth.
WHO recorded -1.61 - 2012
in the year of - 1.74-2002.
AFRO -1.15
AMRO -2.76
EMRO -1.58
EURO -2.57
SEARO - 1.12
WPRO - 1.48
GLOBAL AVAERAGE- 1.61
THEORIES OF DENTAL CARIES
Chemical Parasitic The The Proteolysi
(acid) (septic) Acidogeni Proteolyti s chelation
theory theory c theory c theory theory
CHEMICAL (ACID) THEORY
In 17th and 18th century,there emerged a
concept that teeth are destroyed by acids
formed in the oral
cavity by fermentation of food particles
around the teeth
PARASITIC (SEPTIC) THEORY
Microorganisms were associated with the carious processcess
ACIDOGENIC THEORY
W.D Miller was the first well known scientist and
investigator of dental caries and published his results in
1882
According to him dental decay is a chemoparasitic
process
It is a two stage process there is decalcification of
the enamel which also results in the destruction of
the dentin. in the second stage there is dissolution
of the softened residue of the enamel and dentin
In the first stage there is
destruction is done by the
acid attack where as the
dissolution of the residue is
carried by the proteolytic
action of the bacteria
This whole process is supported by the presence of
carbohydrates microorganisms and dental plaque
PROTEOLYTIC THEORY
There has been evidence that the organic portion of the tooth plays an
important role in the development of dental caries
The are some enamel structure which are made of the organic material
such enamel lamelle and enamel rods
These structure prove to be the path ways for the advancing
microorganisms. It has been established that enamel contains 0.56 % of
organic matter of which 0.18% is keratin and 0.17 % is a soluble protein
Microorganisms produce proteolytic enzymes,which destroy the organic
matrix of enamel,loosening the apatite crystals….so they are eventually
lost and tissue collapses…
PROTEOLYSIS CHELATION THEORY
It IIis a process in which there is complexion of the metal ions
to form complex substance through coordinate covalent
bond which results in poorly dissociated /or
weakly ionized compound
Example of chelation reaction:
Hemoglobin in which 4 pyrrole nuclei are linked to iron by a
similar bondChelation is independent of the PH of the medium
•The bacterial attack on the surface of the enamel results in the
breakdown of the protein ,chiefly keratin and results in the
formation of soluble chelates with calcium which decalcify enamel
even at neutral PH..
ETIOLOGY OF DENTAL CARIES
ROLE OF BACTERIA
Micro organisms are a perquisite for caries initiation
A single type of micro organism is capable of inducing caries
The ability to produce acid is a prerequisite for caries
induction, but not all acidogenic organisms are cariogenic
Organisms vary greatly in their capacity to induce caries
Role of plaque
•Plaque is an adhesive layer which deposits on
the surface of the tooth and has colonies of
bacteria
•Plaque tends to stick to the surface of the teeth
and in this way the bacteria can have cariogenic
effect on the tooth
ROLE OF SALIVA
• SALIVA ALSP POSSESS BUFFERING CAPACITY
• BUFFERING CAPACITY OF SALIVA DEPENDS ON:
• CONCENTRATION OF BICARBONATE IONS
• VOLUME OF SALIVA
• Salivary proteins contribute to pellicle to protect the
outer surface.
HOPEWOOD HOUSE STUDY
• Hopewood House (NSW, Australia) for 10 years. •
SULLIVAN –in 1958;
HARRIS –in 1963 •
Diet sugar & refined carbohydrates were excluded.
• Dental surveys ages 3 & 14 years.
Carbohydrates given :
• • Whole wheat bread
Soya beans
Wheat germ
Oats
Rice
Potatoes
Molasses etc
Dairy products
Raw vegetables
Fruits Nuts
Vegetarian diet with adequate protein,
fats,
minerals
& vitamins •
Fluoride content of water was insignificant •
No tea was consumed
RESULT AND CONCLUSION
At the end of 10 years •
13 yr old children had mean DMF = 1. 6 with 53 % being
caries free
• General child population 10. 7 only 0. 35% being caries
free.
• Children’s oral hygiene was poor with prevalent gingivitis
in 75% cases
Conclusion : • Dental caries can be reduced to by Spartan
diet & without beneficial influence of fluoride & in
presence of unfavorable oral hygiene
VIPEHOLM STUDY
• GUSTAFSSON et al – in 1954 • In 1939 Swedish
Government requested the Royal Medical Board to
investigate the measures that should be followed to
reduce dental disease in Sweden.
• Study Vipeholm study at Vipeholm hospital, Lund an
institution for mentally disabled individuals diet & dental
caries
• 436 patients 6 experimental groups & one control group.
• Control group low carbohydrate, high fat diet free from
refined sugar.
Experiment Groups In Study
• SUCROSE GROUP 300 gm sucrose at mealtime
• BREAD GROUP 345 gm of sweet bread containing 50 gm
sugar.
• CHOCOLATE GROUP 300 gm sugar with meals 100 gm
supplemented by 65 gm of milk chocolate between meals
during 2 nd year
• CARAMEL GROUP 22 caramels daily in 2 portions
• 8 TOFFEE GROUP 8 toffees in 2 portions
• 24 TOFFEE GROUP 24 toffees between meals
Conclusion : VIPEHOLM STUDY
1. Risk of sugar increasing caries activity is great if sugar
is consumed in a form with a strong tendency to be
retained.
2. Risk is greatest sugar is consumed between meals
3. Increase in caries activity due to intake of sugar rich
foodstuff consumed in a manner favoring caries lesion
disappears on withdrawal of such foodstuff from diet
4. Carious lesion may continue to appear despite the
avoidance of refined sugar, maximum restriction of natural
sugars & total dietary carbohydrates.
5. Risk of increase in caries activity is intensified with an
increase in duration of sugar clearance from saliva.
TURKU STUDY
• Turku, Finland • By Scheinin & Makinen et al in 1975 A. D.
• 2 year study.
Aim : To Compare cariogenicity of Sucrose, Fructose &
Xylitol.
125 Young Adults 3 Groups
1 -- Sucrose Group (35 people)
2 – Xylitol Group (52 people)
3 – Fructose Group (38 people)
RESULT : TURUKU STUDY
1 st year :
• Sucrose Group = Fructose Group (Caries Prevalence) •
Xylitol Group almost no caries
2 nd year
• Caries continued to increase in sucrose group
• Unchanged in fructose group
• Xylitol some white spots had been remineralized
HEREDITARY INTOLERANCE TEST
• In 1959– Froesch • Inborn error of fructose metabolism
transmitted by autosomal recessive gene.
• Metabolic error deficiency of hepatic fructose-1
phosphate which inhibits fructose phosphorylation.
• C/F pallor, nausea, vomiting, coma & convulsion
following ingestion of fructose containing products
• Reduced caries experience seen in such patients as
compared to control group of same age
PREVENTION
PRIMARY SECONDARY TERTIARY
PRIMARY PREVENTION
AIMED AT REDUCING THE OCCURRENCE OF NEW CASES OF CARIES IN
A POPULATION
SECONDARY PREVENTION
AIMS AT REDUCING THE PREVALENCE OF
CARIES .THE USE OF RADIOGRAPH TO DIRECT
INITIAL CARIOUS LESION LEADS TO
PREVENTION AT THE SECONDARY LEVEL
TERTIARY PREVENTION
INVOLVES TREATMENT PHASE AIMED AT MAXIMUM LIMITATION
OF DISABILITY AND MAXIMUM REHABILITATION
CARIES VACCINE
Vaccine strategies have been invoked often to diminish or
prevent the impact of infectious disease, especially among
the young. Given a general appreciation for the infectious
component of dental caries, injected vaccines containing
lactobacilli were administered with limited success in the
1940s. However, at that time, the molecular pathogenesis
of S. mutans was unknown, nor there was an
understanding of the immune mechanisms in the oral
cavity. Most virulence characteristics were unclear, with
the exception of the ability of cariogenic bacteria to
produce enamel-dissolving acid. Vaccines are an
immunobiological substance designed to produce specific
protection against a given disease. It stimulates the production
of a protective antibody and other immune mechanisms.
dhesins, for example, the family of adhesions from S.
mutans and Streptococcus sobrinus have been shown to be effective
antigens, both as intact proteins and as subunit vaccines. These single
polypeptide chains are approximately 1600 residues in length and in S.
mutans, contain salivary binding domains associated with an alanine-rich
tandem repeating region in the N terminal third and a proline-rich repeat
region in the centre of the molecule. Abundant in vitro and in vivo evidence
using a variety of active and passive immunization approaches indicates that
antibody with specificity for mutans streptococcal adhesins can interfere with
bacterial adherence and subsequent dental caries caused by S. mutans.
Effective subunit vaccines have been designed using synthetic peptides or
recombinant proteins to direct the immune response to domains of salivary
binding function. Immunization with these constructs is also protective in
experimental systems. Protection in these experiments could conceivably
occur by antibody blockade of initial colonization events in the dental biofilm
or by antibody-mediated aggregation and clearing of adhesion bearing
streptococci from the “bulk fluid” salivary phase.
•Oral
•Systemic (subcutaneous)
•Active gingivo-salivary
•Passive dental immunization.
CONCLUSION
Since dental caries is a highly prevalent disease , control of dental
caries is a concern of all the people.for developing country like
india the focus should be on assessing the caries risk and
identifying those individuals at high risk to develop
caries.preventive measures can be targeted at this group thereby
not only reducing economin burden of restorative care but also
eliminating the overall quality of life.
REFERENCE
Arora B, Setia V, Kaur A, Mahajan M, Sekhon HK, Singh H. Dental caries vaccine: An
overview. Indian J Dent Sci [serial online] 2018 [cited 2022 Sep 20];10:121-5. Available
from: http://www.ijds.in/text.asp?2018/10/2/121/233976
SOBEN PETER:Essentials of Preventive and Community Dentistry(3rd & 4th edition)
