COMMUNITY DENTISTRY

BY

DR J. O. TAIWO
DEPARTMENT OF PERIODONTOLOGY AND
PREVENTIVE DENTISTRY
UNIVERSITY COLLEGE HOSPITAL
IBADAN
INTRODUCTION
 What is prevention?
 Present approach to health (dental health)
 Current debates on the limitations of medicine and
dentistry.
 What is health and what is disease and what is illness?
 Health behaviour, Dental health behaviour, illness
behaviour and sick role behaviour. At risk behaviour.
 Factors influencing oral health
 Common problems with health care
 Prevention of dental disease
 Prevention strategies
 Methods of prevention
 Aim of prevention
 Principles of prevention
PREVENTION OF ORAL DISEASES
Definition: Prevention in its narrow scope means the
act of keeping from happening or of rendering
impossible, an anticipated event. In modern medicine
its meaning has been expanded to include arresting
an already existing process of a disease which is
reversible or reducing disabilities from an irreversible
disease. Disease prevention is normally used to
represent strategies designed either to reduce risk
factors for specific disease or to enhance host factors
that reduce susceptibility to disease e.g. Fluoridation.
Disease prevention can also include activities or
strategies designed to reduce consequences of
disease once established.
Prevention is divided into:-
 Primary prevention
 Secondary prevention
 Tertiary prevention
1. In primary prevention we prevent the
occurrence of a disease. e.g
Immunization
Clean sir
Housing projects
Brushing with Fluoride toothpaste
2. Secondary prevention involves early
detection of a condition which if treated
would be cured. It involves identification
of high risk groups e.g. screening for pre
cancerous lesions in the mouth (Class
exercise name them).
3. Tertiary prevention involves minimizing
disability arising out of existing disease
e.g. rehabilitation of the mouth of an
edentulous patients, diabetes, epilepsy
etc.
It is futile to take of free choice when
considering these behaviors. Abdicate the
responsibility for the health of their nation.
It might have been nor apt to ask if the
condition of organised dentistry mighty not
have been achieved at a lower cost much
ill-health in Britain today arises from over
indulgence and unwise behaviour. The
greatest potential and the greatest
problems for preventive medicine now lie
in changing behaviour and attitudes to
health
PRESENT APPROACH TO DENTAL HEALTH
 The present approach to health is hospital centered and
based on mechanical or engineering approach to
disease. It has the following characteristics.
 A curative rather than a preventive orientation
 An individualistic rather than a population approach
 An emphasis on high technology
 A focus on acute rather than chronic illness.
 Specialized fragmented treatment rather than holistic
care.
This emphasis on acute hospital service and the
relative neglect of community services is the outcome
of an approach which stresses cure rather than
prevention
By the middle of the 20th century health care
systems had become major institutions with the
advanced industrialized nations. Due to
scientific discoveries and therapeutic
successes. This led to the investment in health
care facilities e.g founding of NHS in Britain and
medicaid and medicare in the US & Health
insurance in Canada with an aim of improving
the physical and mental health of people through
prevention, diagnosis treatment of illness. This
was not achieved instead this lead to dramatic
increase in health care cost as a part of the
GNP and in absolute terms. This naïve believe
was tempered by a growing skepticism.
CURRENT DEBATES ON THE LIMITATIONS OF
MEDICINE AND DENTISTRY
Many authors have written on the limitations of
medicine and dentistry to mention a few:
Mackeown, John Powells, Illich, Cochrance,
Kennedy etc (Cochrances argument of
randomizing controlled trials).
It is said that the present approach to health is
called the medical model which must be
identified and treated. The body is analogues to
a machine. (interventionist approach and
mechanistic approach). The overwhelming
emphasis on cure in modern health care system
has led to a relative neglect of the ecological
approach to health.
Current debate question the validity of this medical model-
(i.e mechanistic approach to the human body) i.e the
concept that human health depends on the mechanistic
approach to the human body. Mackeon and Dubois
suggested that curative medicine is too limited in scope
to bring about further improvement in the health of the
population. He stated that and an awareness that
increased spending on health care has had a limited
impact on the population. The gap between inputes in
terms of resources and outputs in the form of health has
been the focus of critical appraisal of health care system.
Mckeon’s work has been influential in spawning the health
promotion movement.
Those diseases responsible for the majority of deaths can
be prevented by environmental change or changes in
personal behaviour.
Dubois believes that many diseases are due to
the influence (or change) in the environment e.g.
the bacteria which lives in a high concentration
of sulphur may be affected when this high level
sulphur environment is changed.
These critical appraisal of medicine coupled with
the rising cost of health care and continued high
mortality rates from cancer and heart diseases
(failure of medicine) brought about a shift in
health care policies from curative in the late
1970s with the subsequent emergence of
prevention as key government strategy towards
health.
To facilitate a broader preventive approach one
has to:
1. View the social and physical environment as
determinants of health and social well-being.
2. Encourage prevention to be a shared
responsibility that is assumed by various
levels within the society.
3. Encourage a stronger consideration of health
protection measures across all age groups
(adopt a health behaviour)
4. Implement appropriate comprehensive long
term planning approaches in addition to the
usual immediate crisis oriented strategies.
What is health disease and illness
We have referring to health throughout in the text. It will be
good for us to know what health disease and illness are.
1. Health is a state of complete mental, physical and social
well-being not merely an absence of disease. It
encompasses physical health, mental health, spiritual
health and societal health.
2. Disease are the named pathological entities diagnosed
by means of clinical signs and symptoms e.g. cancer or
caries.
3. Illness refers to the subjective response of the individual
to being unwell. It refers to how the person feels and
what effect this has on her normal everyday life. Health
and illness are subjective states and more difficult to
define and recognise than disease.
It is possible to experience different combination of these 3.
a. It is possible to have a disease and to feel
healthy and well and not to consider onself ill
e.g. someone with diabetes whose disease is
adequately controlled.
b. It is possible not to have a disease and to
consider oneself as healthy by nevertheless to
feel ill e.g a pregnant woman with morning
sickness.
c. Not to have a disease but to feel unhealthy e.g
someone who feels lethargic generally under
the weather or unfit.
d. Have a disease, to feel unwell but
nevertheless to consider oneself as healthy e.g
someone who gets migraine may feel unwell,
need medication and have to stay off work but
nevertheless consider herself as healthy.
 HEALTH BEHAVIOUR, SICK ROLE BEHAVIOUR AND ILLNESS
BEHAVIOUR

1. Illness Behaviour: is any activity undertaken by an

individual who perceive himself as having a health problem
for the purpose of defining his state of health and
discovering and undertaking an appropriate remedy
2. Health behaviour: is any activity undertaken by an
individual who sees himself as healthy for the purpose of
preventing disease or detecting it at an asymotomatic
state.
3. Sick Role behaviour: Activities undertaken by an individual
who considers himself ill for the purpose of getting well.
4. At risk role behaviour: Activities undertaken by an
individual who knows that one or more risk factors exist
5. Dental Health Behaviour: Maintaining oral hygiene e.g
brushing with F- dendrites 2. Conscious reduction or sugar
consumption 3. Dental service use.
 ICEBERG PHENOMENON

Institutions Hospital
Health Caries etc
Private Medical Practice
Quaks and other unqualified
persons
Home Traditional remedies or modern
patient medicines
Sub clinical disorders it unaware of
disease

Note: Institutional hospitals etc often see only the tip of the iceberg.
The extent of the larger mass benefits the surface can be discovered
by well-designed epidemiological studies.
FACTORS INFLUENCING ORAL HEALTH

Health care
organisations Environment

Lifestyle
Bioengineering
factors
FACTORS THAT INFLUENCE ILLNESS BEHAVIOUR

1. The visibility, recognizability and perceptual silence of

the symptoms.
2. The perceived seriousness of the symptoms
3. The extent to which symptoms disrupt work, family and
other social activities
4. The frequency of the appearance a symptoms and
their persistence or frequency of occurrence.
5. The tolerance threshold other exposed to the
symptoms.
6. The knowledge, cultural assumptions and
understanding of the person and relevant others.
7. Other needs and practical matters competing with the
illness
LALONDE’S DIAGRAM
 Factors influencing oral health can be grouped
under:
1. Environmental factors: These are all factors related
to health which are external to the human body and
over which the individual has little control
2. Life style factors: Consists of aggregation of
decisions by individuals which affect their health and
over which they have control. Standard reactions
and behaviour patterns that are developed through
the process of socialisation. These are learnt
through social interactions with parents, peer groups
and friends and siblings or through the influence of
schools, the mass media etc.
3. Bioengineering factors: are factors which involve
the human Biology and general health and
involve factors such as genetic inheritance,
process of maturation, aging and many
complex internal systems.
4. Health care organisation: dental services. It
involves the quality and resources in the
provision, nature and relationships of people
and resources in the provision of health care.
Health care organisations can also have a
negative affect on the oral health of an
individual is iatrogenesis.
Factors in the dental services which affect
health Public Health as:
1. Availability
2. Accessibility
3. Affordability
4. Acceptability
Also effectiveness and appropriateness.
All the factors of dental services affect
access to health and utilization of
services.
However the main causes of sickness and deaths
are rooted in human biology, environment and
lifestyle.
External forces and personal behaviour are
predominant determinants of health e.g caries
and sugar, personal oral health hygiene
behaviour and periodontal disease.
Therefore community based preventive measures
should have priority over dentist based
prevention. i.e dentist based prevention deals
with the individuals and has little effect on the
population as a whole
PREVENTION OF DENTAL DISEASES

Prevention is directed at
1. Environmental influences
2. Behavioural change
3. Specific preventive therapeutic
measures.
PREVENTION STRATEGIES
It will be helpful to distinguish 2 kinds of
aetiological questions
1. The causes of cases e.g why do some
individuals have caries
2. The causes of incidence e.g why do some
populations have much caries whilst in others
it is rare.
There are two strategies in the prevention of
diseases:
a. The high –risk approach or strategy
b. The population approach or strategy.
The High Risk Strategy
This strategy seeks to identify high-risk
susceptible individuals and offer them
some individual protection. It is the
traditional medical approach to prevention
and it aims at truncation i.e cutting off the
risk distribution. This is illustrated in the
diagram below. (a graph of % of
population is plotted against the risk of
having caries)
 % POP 100%
% POP 100%

Relatives Risk of having caries Relatives of having caries

In the high risk strategy we target X
individuals who are at risk of having the
disease or condition and concentrate our
prevention efforts on them i.e concentrate
on those who are highly susceptible to the
disease.
The population approach or strategy
This strategy in an attempt to control the
determinants of incidence i.e to shift the whole
population to a better health i.e shift x to y. e.g
fluoride toothpaste and its effect on the
reduction of caries. Water fluoridation, small-pox
vaccine.
Realistically many diseases will long continue to
call for both approaches as is the case of HIV
infection and AIDS. Nevertheless the priority of
concern should always be the population
strategy.
% population

y x

Relatives Risk of having caries

Aim of Prevention

 Prevention aims to conserve health.

 Population strategies to reduce the
incidence of disease are the classical
public health approach.
Principles of Prevention
 Early pre-symptomatic diagnosis of disease
 Detection and prevention of disability after the
disease stopped
 To give preventive therapy
 To reach a majority of the population i.e
emphasis on the population rather than the
individuals
 To reach a majority of the population
 To reduce geographical and gender disparities
reduce inequality in health care delivery
 To provide adequate information to the patient.
METHODS OF PREVENTION
 What is the difference between prevention and
treatment. Don’t forget to write on
1. Dental fluorosis and its prevention
2. Secondary prevention in caries early caries treatment
using already mentioned methods in the lecture
notes ,
3. diagnosis & treatment.
4. Methods of diagnosis preventing recurrent Caries –
Controlling cariogenic flora,
removing plaque, diet control,
periodic recall
Extension for preventions
Preparing enatrovey walls
Fluoride application topical .
Prevention of Dental Caries
Aim: To equip the students with the knowledge of
the different methods of preventing dental
caries.
Objectives: Students
 Should be able to define dental caries
 Should be aware of the different factors that
contribute to the initiation and progress of caries
 Should have a knowledge of how the various
factors can be used as a tools in prevention.
 Should be equipped with new concept of
demineralisation and remineralisation, its
implications in preventing dental caries.
Prevention of Dental Caries Contd..
 Should have a knowledge of the
mechanism of action of fluoride
 Should be aware of the toxic effect of
fluoride
 Should be able to evaluate the
effectiveness, disadvantages and
advantages of the different methods of
fluoridation.
 Should be acquainted with other methods
of preventing caries, their effectiveness
and feasibility and cost benefits.
PREVENTION OF DENTAL DISEASES
1. Definition of dental caries
2. What is a multi-factorial disease?
3. Factors that are involved in the initiation and
progress of caries
4. How each factor affect the progress of caries
5. The various factors as tools in preventive
dentistry. Host factors as a tool in preventive
dentistry
6. Fluoridation
7. Forms of fluoridation
8. Short history of fluoridation
9. What is PPM?
PREVENTION OF DENTAL DISEASES contd..
10. Mechanism of action of fluoride in reducing dental
caries
a. Pre-eruptive effect
b. Post-eruptive effect
11. Systemic fluoridation
12. Topical application of fluoride
13. Caries vaccine
14. Supragingival plague micro-organisms as a tool in
preventive dentistry.
a. Mechanical control
b. Substances that inhibit bacteria growth
c. Introduction of competitors? Predators? Or
Commensals
15. Substrate (free sugars) as a tool in preventive dentistry
16. Time as a tool in preventive dentistry
PREVENTION OF DENTAL DISEASES
The two major oral health problems in the
world and in Africa are periodontal disease
and dental caries. Other oral health
problems are oral tumours, malocclusionm
in Africa traumatised anterior teeth and
enamel fluorosis are common.
It is assumed that you already know the
epidemiology of the above mentioned
dental diseases.
We shall concentrate on the prevention of
the two commonest dental diseases.
PREVENTION OF DENTAL CARIES
What do you understand by dental caries?
Definition of dental caries:- Dental caries is a
pathological process involving the demineralization
of enamel, dentin and cementum of the tooth under
the action of acid producing bacteria mainly
streptoccocus mutans lactobacillus spp. And
actinomyces viscosus. Lets take a brief look at the
aetiology of dental caries . Dental caries is a
multifactorial disease. What so we understand by
the above statement?. It means different factors are
involved in the initiation and progress of caries. Four
main factors are involved. Name them
a. Host (teeth) b. Supragingival plague c. Diet
d. Time
FACTORS INFLUENCING ORAL HEALTH

Supragingival
plague
microorganism Substrate (diet)

Time
Host
Host Factors
1. Structure of the enamel
a. Morphology b. Fissure patterns
c. Fluoride distribution in the enamel
d. Ability of the enamel to remineralize
e. Age f. saliva g. teeth arrangement
Susceptibility of different areas of the enamel on the same
tooth to a standard acid attack in vitro vary markedly.
Different areas of the same tooth are more susceptible
than others
Shape and size of fissures play an important part in the
process of caries.
Shallow fissures are easy to clean and are less prone to
caries process than deep narrow and difficult to clean
fissures.
 Shallow fissures Deep fissures

Composition and Flow of Salva

a. Buffering capacity to saliva
b. Quantity of saliva
c. Thickness of saliva
d. Antibacterial factors in Saliva – Lysozyme, lactoferin.
Lactoperoxidase
e. Immunological aspects salivary immunoglolin
SALIVA 99% WATER 1%
We think of saliva when we don’t have it in the
mouth. This is equivalent to a desert without
water.
Saliva is a liquid secreted by salivary glands.
Secretion is between 0.5-1.0L daily
Salivary secretion stimulation
1. Psycological this is well developed in animals
e.g dog
2. Chemical – Salt, sweat, sour taste
3. Biological – Wound in oral cavity increases
salivary flow – Connected to healthy progress
4. Mechanic- Mastication
SALIVA FUNCTION
1. Lubrication
2. Ion reservoir
3. Buffering
4. Cleansing e.g food debris
5. Antimicrobial
6. Pellicle formation
7. Digestion
8. Taste
9. Water balance
10. Agglutination
Saliva has almost the same composition as
blood plasma
Salivary proteins considered as agglutinies.
They agglutinate strep mutans etc.
Hydrogen is important in the inorganic
component.
Calcium is another important ion.
It is ionized and non-ionised.
2 types of saliva composition low flow rate –
Magnesium & Phosphate.
High floor rate – Protein, Sodium & Bicarbonate.
Fluoride is present in the two .This depends
mostly on external introduction.
Low flow rate – Is not good it has poor buffering
capacity. Increases accidity
Fast flow rate – is better. Better Buffering
capacity.
Unstimulated saliva
Stimulated saliva
OTHER FACTORS AFFECTING SALIVARY
SECRETION

 Fear
 Sleep
PROTECTIVE FACTORS OF SALIVA
1. Salivary flow rate
2. Buffering Capacity
MEASURE OF FLOW RATE OF SALIVA
1. Stimulated – give chewing gum to stimulate
use stop a stop and collect saliva in a cup.
2. Unstimulated
LOW FLOW RATE
 Increase sucrose clearance time
SALIVARY GLAND HYPOFUNCTION
1. Xerostomia – dry mouth
2. Hyposecreation
Xerostomia is related to dehydration even in
the presence of sufficient saliva they still
feel dryness of the mouth.
CAUSES
There is a relationship between drugs & dry
mouth
 SIGNS
 ORAL  NON ORAL
Mucosal dryness and Dry nose
soreness Depression
Burning sensation of Mental stress
mucosa & tongue Side effect of drugs
Difficulty in speech Systemic disorder
Difficulty in
swallowing
Difficulty in wearing
dentures
EVALUATION PROCEDURE
 Measurement of stimulated saliva
 Ananestic data
There is enough evidence that saliva flow
rate is related to caries experience.
There is an inverse relationship between
saliva flow rate and caries.
TREATMENT OF PATIENT
 General health
 Oral hygiene
 Dietary counseling (change diet oral hygiene
often sugar consumption.
 Antimicrobials e.g chlorhexidire
 Remineralisation F. treatment
 Minimally invasive treatment animation
technique with GIC and finish with raisin
 Dental chewing gum to increase salivary flow
 Patients suffering from improved salivary
secretions should received and individually
tailored prophylactic dental program including
intensive caries preventive care.
The mechanical washing action of salva is
important in removing food debris and
unattached microorganisms from the mouth e.g
in diseases like sjogrens syndrome where
salivary flow is compromised rampant caries
develops.
The buffering capacity of saliva helps in
neutralizing acids produced by plague bacterial
What is the normal pH of saliva?
During the action of plague micro-organism’s
associated with caries the pH can fall as low as
4.5-5
Substrate (diet)
 Several studies to name them:
Human observation studies
Human interventional studies
Animal experiments
Plague pH studies
Labouratory experiments
Have shown beyond doubt that free sugars
contribute a great deal to the initiation and
progress of caries.
Dietary factors important are:-
a. The concentration of the free sugar. The dose
response curve for sugar and caries is (S shaped) and
at levels of sugar consumption below 10kg/person/year
the incidence of caries is acceptably low. Whilst at
levels beyond 15kg the incidence increases more
rapidly.
b. Consistency:- Sticky thick sugary foods encourage the
progress of caries.
c. Frequency: The rate at which the sugary food is taken
is proportional to the incidence of caries.
d. Other additives can influences the process of caries.
Some foods and elements and vitamins are known to
have a deterrent effect on the process of caries e.g.
Inorganic phosphates, organic phosphate and phytate.
Supragingival plague micro-organisms
There is a wealth of evidence showing that
micro-organisms in the supragingival
plague are responsible for dental caries
The most cariogenic among them are
a. Streptococcus mutans group
1. S. Mutans, S. Subrinus, S. Cricetus
b. Actinomyces viscosus
c. Lactobacillus group
a. Casei b. Acidophillus
FACTORS RELATED TO CARIOGENICITY OF
STREPTOCOCCUS MUTANS

1. They produce acids to lower the pH to

4.2 – 4.6 in glucose broth.
2. The ability to make extra cellular
polysacharides and both solube and
insoluble glucans from sucrose
3. Ability to make intra cellular
polysaccharides
4. The ability to colonise hard tissue
surfaces. e.g human teeth and even
artificial teeth.
TIME

Studies have shown that it takes 3 years to

4 years for a smooth surface lesion to
progress to the stage where the dentine is
invaded and therefore there is adequate
time to intercept the carious process.
How do the above mentioned factors act
as tools in Preventive Dentistry
Host factors
Prevention can be directed to enhance the
resistance of the host to dental caries by
1. Strengthening the structure of the
enamel
1. Fluoridation
2. Remove factors that will disturb the flow of
saliva
2. Immunization of the host (caries vaccine)
FLUORIDATION
Fluoride studies can be divided into two
groups.
(1). The effect of fluoride taken systemically
a. in water b. in the form of tablets c. drop
d. in enriched milk e. Salt f. Fruit juice
(2). Tropical application of fluoride in the form of
a. Solutions b. Gels c. Mouth rinses
d. Tooth paste
These are in a much higher concentration than
found in water supplies.
A SHORT HISTORY OF FLUORIDE
 The effect of fluoride was 1st discovered in 1901 by
Mckay (a dentist) in Colorado Springs and was
known as Colorado stains. He named it mottled
enamel.
 The relationship between the concentration of F with
mottled teeth and caries was 1st shown by Dr. H.
Trendley Dean. He proofed an inverse relationship
between endemic flurosis and caries.
He proofed that at 1ppm F_ in drinking water gives
maximal reduction in caries experience and does
not cause mottlening or could cause only sporadic
instances of the mildest forms of dental fluorosis of
no practical or aesthetic significance (1942).
 WHAT DO YOU UNDERSTAND BY 1PPM?

Means 1 part of fluoride to every

No of Caries Experience million part of water (equivalent to
1mg/litre quarter) (Source health
education Authority

MECHANISM OF ACTION OF
FLUORIDE IN REDUCING DENTAL
CARIES

1. Pre- eruptive effect

F- content of water
2. Post-eruptive effect
PRE-ERUPTIVE EFFECT
1. It affects the morphology of the tooth. It has been
observed that children from the water fluoride areas do
not have the deep V shaped fissures but instead they
have the U shaped shallow fissure and shallow pits
(Refer to former diagrams)
2. Enamel mineral consists of closely packed rod shaped
crystals that contain mainly calcium, phosphate and
hydroxyl ions. Each ion occupies a definite, position I
relation to the others. The spatial arrangements is such
that the repeating unit contain Ca 2+, P04 3- and 2 0H is
replaced by F_ to form fluorapatite which is more
resistant to the acid effect i.e Ca 10 (P04)6 (0H)2 + 2F –
Ca10 (P04) 6F2. It should be noted that enamel crystal do
not contain pure fluorapetite but a mixture of fluohydroxyl
apatite.
POST ERUPTIVE EFFECT OF CONCENTRATION
OF FLUORIDE

(1). F_ in dilute acid reduce enamel dissolution

(2). F_ accelerates the remineralization of early carious lesions.

(enamel block covered in mouth Micro hardness Softening

with ceflon gauze) testing

(enamel block in mouth Micro hardness hardness

with ceflon removed) testing

(enamel block in mouth Micro hardness Hardness

with ceflon removed) testing
accelerates
Invivo Experiment by Koulouride
3. Fluoride becomes concentrates in plague but
exist mostly in bound form. Concentration of
fluoride in plague is 6ppm.
4. Acid solube F_ may exert inhibitory effects on
further acid production by certain micro-
organisms in plague.
5. F_ might alter the ease of colonisation of the
tooth surface.
6. F_ interferes with the uptakes of glucose across
the cell membrane.
SYSTEMIC FLUORIDATION
As it has already been described it could take
place in the form of water fluoridation and
fluoride supplementation.
WATER FLUORIDATION
Water fluoridation is the upward adjustment of
F_concentration of the community’s central
water supply to optimum level of 1pm for the
purpose of preventing caries.
The use of fluoride is recognized as the most
effective means available for the prevention of
dental caries in community based programmes
(WHO)
 Fluoridation is needed where caries prevalence
is moderate or high, where there is efficient
water supply, where there is low natural fluoride
of the water supply and where manpower
resources are low.
When the community’s water supply is fluoridated,
caries experience is reduced by 40-50% in high
caries prevalence's areas.
The softy range of water fluoridation is 1ppm-
1.2ppm 0.8-1.2ppm.
To carry out water fluoridation the community
would need the following-
1. Equipment 2. Constant flow of water supply 3.
Materials 4. Personnel 5. Will
require the consent of local authorities
ADVANTAGES
 Safe
 Require no effort on the part of the recipient and
therefore compliance is good i.e links into
existing behaviour
 The overall cost is low
 It enables equitable distribution of F_ in the
community
 High cost benefit 40-50% reduction in caries
experience
 It is radical. It attacks the problem from the root.
DISADVANTAGES
 Requires the installation of equipment
which could be expensive
 To carry out water fluoridation a
community will need a constant supply of
water
 It will require the consent of the local
authorities as well as the public and such
formalities could be cumbersome
 Infringes on the freedom of the recipient in
making a choice.
The efficacy of communal water fluoridation
in reducing dental caries is greatest for
the deciduous (30-60%). For adults
efficacy is 15-35%.
Water fluoridation has a significant post-
eruptive caries reducing effect on tooth
surface. The greatest effect was on free
smooth surface then a proximal surfaces.
The least effect was on pits and fissures
School Based Water Fluoridation
Here the equipment is installed only for the
school where only the school water is
fluoridated.
Unliked the communal water supply the
fluoridated water is taken only during school
time and because of that the concentration of
fluoride in the school water fluoridation.
The effectiveness of the school water
fluoridation in reducing caries experience is
30-35%
The disadvantages is as stated for communal
water fluoridation but in addition the school
water fluoridation has the disadvantages of not
being administered throughout the year and
immediately after the school year it is stopped.
Also the children do not start on the programm
until they enter school and that is at 6 years.
This means that the children do not experience
the benefits of the fluoride treatment before the
age of 6 years. Also they are not exposed to
the effect of F_ throughout the day since
schools close by afternoon.
 Why is the level of fluoride in school
water fluoridation 4.5 to 5 times higher
than that of community water supply?

1. Children consume only part of their daily intake

at school and only attend school a maximum of
about 200 days per year
2. Children do not enter school before 6 years of
age when incisor teeth can be considered no
longer at risk of developing fluorosis (Mottled
enamel)
FLUORIDE SUPPLEMENTS

These fall into a groups

a. Those where the fluoride supplements are
given daily at home and are started before
schoolage (Home based) and effectiveness in
reducing caries experience is 40-80%
b. Those where fluoride supplements are
distributed in school and only on school days
and without additional supplementation during
holidays or before school
HOME BASED FLUORIDE SUPPLEMENTATION

This requires:
a. High level of parental motivation
b. Supervision
c. Supervision and education of over-zealous parents
to prevent fluorosis
The home based fluoride supplements i.e the tablets and
the drops have an effectiveness of 30% to 80%.
It is best administered as follows: 0.25mg/24 hours the
1st 2 years then 0.5mg/24 hours the third year and
1mg/24 hours there-after. This form of administration
is appropriate and safe however additional studies
are needed to determine optimal dosage for infants.
FLUORIDIZED SALTS
 In populations that lack central water supply salt
fluoridation is more practical so far as regions with
optimal or greater concentration of F_ in drinking
water are known not to exist. Before salt
fluoridation is implemented in a country or region
valid sampling of all drinking water source should
be undertaken to ensure that there are no large
variation in water fluoride concentration. If there
are then establishing a suitable fluoride
concentration in salt for the area presents serious
problems. Recommended concentration of F_ in
salt in 250mg F/kg salt. The effectiveness is 39%
reduction in caries experiences
DISADVANTAGES
1. Technically involved will require equipment
and this can make it expensive initially
2. It is difficult to make large portions with equally
distributed concentration of fluoride
3. Difficult to measure or regulate people use
since people use different amount of salt.
4. Implementation would require administrative
and political support.
5. People are not given real choice
6. Can give people a false sense of security.
ADVANTAGES
 Require no motivation because it links into
existing behaviour
 Uses only 3% of the quantity of fluoride used in
water fluoridation
 Safe – no known adverse effect has been
reported for the stated concentration
 Has a life long effect
 Acceptable to the individual
 Reduced Inequality
 No dental personnel required
FLUORIDATED MILK AND FRUIT
JUICES
Natural fluoride level in milk is low 0.3ppm. It has
been shown (Ericsson 1958) that F_ is readily
absorbed from the gut just as readily from milk
as water.
Fluoridized fruit juice may be an alternative in hot
climates. Effectiveness is 28% reduction in
caries experience.
The present recommendations to discontinue
dietary fluoride supplementation, sometime
during the teen-age years are congruent with the
current knowledge that fluoride continues to
benefit the dentate throughout their lifes.
TOPICAL APPLICATION OF FLUORIDE
The effectiveness of topical application of fluoride in
reducing caries experience is 20-40%. It is divided into
A. Surgery based. These are
1. Na F
2. Stanous F
3. Low pH solutions and gels of acidulated F_ system
4. F_ prophylactic paste
5. F_ varnishes
B. Home based These are
1. Fluoride dentifrices
2. Fluoride mouth rinses
SURGERY BASED TOPICAL FLUORIDE SODIUM
FLUORIDE SOLUTION

Knutson Technique:
1. Thorough 20ppm cleaning and drying of the teeth
2. 3 Minute application of the 2% Na F solution at
weekly intervals (4 times a year) at ages 3 years, 7
years, 10 years and 13 years. The effectiveness of
this techniques in reducing caries experiences is
30%.
Stanous Fluoride: This method is more effective in
reducing caries experience than NaF solution.
Method 80ppm – 100% stanous fluoride is used after
thorough cleaning and drying of the teeth. However
stanous fluoride is associated with some major
advantages.
1. Chemical instability in solution which therefore
require a fresh mixture of solution for each
application.
2. Causes brown extrinsic stains to be formed on
the teeth especially in association with margins
of restorations and areas of enamel hypo
calcification.
Acidulated Agents: We have already mentioned
that a lower pH enhances fluoride uptake when
we talked about the mechanism of action of
F_. It has been confirmed (Brudevold et al
1963) that prolonged exposure of enamel to a
1.23% fluoride solution acidulated by means of
acid sodium phosphate enhanced the uptake
of fluoride by enamel.
The major Clinical problem in the use of topical
fluoride solutions in young children is the control
of salivary flow during the recommended 4
minutes period when the teeth have to remain
soaked in the fluoride solution. This is especially
difficult in the case of A.P.F. (acidulated
phosphate fluoride). Solutions which stimulates
profuse salivary flow because of its acidic
nature. Accidental swallowing of even small
volumes of solutions can initiate nausa or
vomiting. To overcome this modern technique
has been developed i.e the introduction of
gelling agents as based mixed the solution.
Gelling agents could be methyl or hydroxyl
cellulose.
This is brings us to A.P.F. gel
APF gel. Is an improvement on the already
mentioned A.P.F. solution. It has this tropic
properties and can be forced into the less
accessible areas of the teeth.
Phosphoric acid is used as acidulating agent
because the phosphate would depress
dissolution of enamel and formation of Ca F 2-
The A.P.F. gel is normally used in a personalized
tray but it can be used other-wise.
The concentration of fluoride in APF gel is 1.23%
i.e 12.3ppm
Advantages of the A.P.F. gel
1. Gel doesn’t spill
2. Gel which has a thixotropic properties can be forced
into the less accessible areas of the teeth e.g
approximal areas.
The success or the effectiveness of topical application of
fluoride depends on-
1. The age of the subjects
2. The quality of the technique employed
3. The duration of the study
4. The frequency of application
5. The level of disease experienced in the community
from which the subjects were taken.
There is 20-40% reduction with annual or semi-annual
applications.
FLUORIDE VARNISHES
Clinical trials have shown that Duraphat is
as effective as fluoride solutions and gels.
DURAPHAT varnishes are the most popular
and widely used fluoride varnishes. Other
fluoride varnishes are (a).Elmex protector
(b) Expoxylite 9070. Duraphat contains
50mg/ml suspended in a special base
which adheres to the long enough to allow
deep penetration of fluoride into enamel
and dentine.It can be removed by brushing
HOME BASED TOPICAL FLUORIDES
These are fluorides which are applied by the
individual at home (or at school under
the supervision of the school nurse) but
without the supervision of dental
personnels.
1. Fluoride dentrifices. They contain 1,200-
1,450ppm fluoride
2. Fluoride mouth-rinses. 230ppm of
fluoride
FLUORIDE DENTIFRICES
These days in countries where dentifrices are used 95% of
all dentifrices on sales contain fluoride compound.
Sodium fluoride used in some topical fluoride agents
combines with the usual abrassive base (i.e carbonate
and calcium phosphate) in dentifrices, inactivating the
sodium fluoride was the American Crest toothpaste. It
contained 0.4% stannous fluoride, but it was withdrawn
from the market because it causes staining of the teeth
especially around anterior fillings.
Now most dentifrices sold in the world today contain
SODIUM MONOFLUOROPHOSPHATE (Na MFP). It is
compatible with most commonly used chalked-based
abrasive systems.
Effectiveness of fluoride dentifrices in reducing caries
experience is 25%. Some authors attribute the falling
trends in dental caries in developing countries to the
wide use of fluoride dentifrices.
MOUTH -RINSES
Na F mouth rinses contain a concentration of
230ppm of F_. Children need to be supervised
when using this both at home, at schools and in
the surgeries. There have been cases where
children has died in the surgery after
accidentally drinking fluoride mouth rinses.
The current concept of demineralization and
remineralization. Its implication in the prevention
of dental caries.
Demineralization and remineralization (i.e
Constant exchange of minerals) is occurring all
the time on the tooth surface but when
demineralization predominates then caries
lesions are formed.
 Lactic acid Demineralization Ca ++ P04 = Plague

E Caries
N
A
M
E
L
Remineralization Ca ++ P04 =

Reversal of caries
Demineralization process in early lesions is seen as white
spot lesions often in areas of plague stagnation such as
(1). Pits
(2).Fissures (3) Occlusal surface of molars and premolars
(4) Approximal smooth surface just cervical to the
contact point
(5). Enamel of the cervical margin just coronal to the
gingival margin.
The early lesion is sometimes seen as brown spot lesions
(Murray, Nash & Kidd). Evidence has shown that in the
presence of F_the remineralization process is
accelerated (Experiments by Koulourides, Silversyone,
Backer Dirks). Backer-Dirks showed that out of 72
surfaces with white spot lesions in 8 years olds and 15
years olds, 37 of these lesions disappeared within a 4
year period.
Invitro experimental studies have shown that acid
softened enamel surface can reharden after
the application of cal. Phosphate. The small
lesion of enamel caries has been shown to
consist 4 histological zones / when examined
under polarizing microscope).
1. Translucent zone
2. Dark zone
3. Body on the lesion
4. Surface Zone
Dark zone and Surface zone are a result of
remineralization.
Translucent zone and body of the lesions are a
result of dermineralization
IMPLICATION OF THE CONCEPT IN THE PREVENTION
OF DENTAL CARIES

1. Early diagnosis of the early carious lesions is

very vital for the control of caries.
2. Use of the most sensitive method such as bite
wing X-rays etc transllumination etc is
necessary so as not to miss these early
lesions.
3. During examination blunt probes with diameter
of 0.5 – 0.6mm, tapering and with less
pressure should be used so as not to break
through the surface layer, because breaking
through this layer will accelerate the process of
caries
4. Since lesions can heal dentist should not be in
a hurry to use the drill. Preventive method
using F_ supplement in small concentrations
as well as topical application and diet control
should be the choice of treatment
5. Constant monitoring of the pt is important. This
potentates the relevance of the 6 monthly
recalls
6. Use of fissues sealants in combination with
systemic fluoride is useful
7. The significance of this discovery in screening
is that most early lesions are missed and
DMFT results are not representative of the
total caries experience.
IMMUNISATION OF THE HOST

CARIES VACCINE
In theory any disease of microbial origin could be prevented
by immunization of the susceptible host.
Specificity of antibacterial action is the basis of the immune
system of the body. These system have been used often
to control diseases that result from a single infection by a
single pathogenic strain or species of micro-organisms
by vaccination.
5. Acceptability of the vaccine will depend on the dental
health awareness (behaviour) of the community.
Now in Europe the public opinion is cautious about
vaccination against disease that are not life threatening.
CONTROL OF SUPRAGINGIVAL MICRO-
ORGANISMS

This can be divided into

1. Mechanical control
Fissure sealants
Maintaining stringent oral hygiene measures.
Detersive foods.
2. Substances that inhibit bacteria growth
Antibiotics
Chlorhexidine
Urea and Ammonia compounds
ChlorophyII
3. Introduction of competitors predators? Commensals
MECHANICAL CONTROL
FISSURE SEALANTS
In the early parts of the lecture we talked about the
morphology of the tooth (i.e fissure patterns etc)
as part of the host contributory factors to the
susceptibity to caries disease.
In the text we also mentioned that the effect of
fluoride is least on the pits and fissures. This
brings us to the question of how these problem
are overcome to prevent caries action in these
places.
It has been observed that 50% of caries in school
children are in pits and fissures.
What is Fissure Sealing?
It is a technique whereby pits and fissures that
occur principally on the occlusal surface of
molar and premola teeth are occluded by the
application of fluid materials, which are then
polymerised in situ.
Current used methods are based on the
principle that the adhesion of acrylic and
composite resins to enamel is greatly
increased if the tooth surface is 1st etched
with acid.
 OCCLUSAL SURFACE LOWER FIRST MOLAR

90
80
70
60
% 50
affected Fluoride Area
by 40
Non-Fluoride Area
decay
30
20
10
0
6 7 8 9 10 11 12 13
MESIAL SURFACES LOWER FIRST MOLAR

16
14
12
10
8 Non-fluoride area
6 Fluoride area

4
2
0
6 7 8 9 10 11 12 13
Fissure Sealants could be filled or unfilled clear or
limited or opaque .
Types of Curing – 1st generation fissure sealants
were ultraviolent light cured
2nd Generation fissure scalants were chemically
cured (auto-polymerized)
3rd generation fissure sealants were visible light
cured.
4th generation fissure sealants are those that
contain fluoride but studies are still going on.
The author does not see how F. releasing
sealant can exert their maximum effect as the
sealants are not known to penetrate the depte
of the fissure.
Most critical part of the application
procedure are:
 Rinsing of the etehed enamel
 Drying the tooth surface
 Maintaining the isolation of the teeth until the
sealant material has polymerized.
There are two main types of resin used.
1. Those that polymerise after mixing two
components
2. Those that polymerise only after exposure to
an appropriate light source. There was no
difference in retention rate between materials
that had been light cured or chemically cured.
 The majority of sealants are unfilled that is they not
contain filler particles as do compositeres in
restorative materials.
 Most if not all of the sealants currently marketed have
a base formulation of dimethacrylates which is a
reaction production of bisphenol and glycidyl
methacrylate (bis GMA)
Fissure sealants have a retention rate of 85% for 1 year
and 50% for 5 years. Its effectiveness in reducing
caries experience is 35%. It is an expensive
preventive measure and its use can only be justified in
the high risk approach to preventing dental caries. We
shall talk about it later. It was noticed that longer
curing time was needed than were generally
recommended by the manufactures.
CLINICAL GUILDELINES FOR THE
APPLICATION OF FISSURE SEALANTS
INDICATION:
A. Children with special needs e.g medically
compromised, mentally or physically
handicapped or from a disadvantaged
social background who might be at high
risk from developing dental caries.
B. Children with extensive caries in primary
teeth
C. Patient with caries in one of the molar
teeth
CONTRAINDICATION

A. In children with caries free primary

dentition, first permanent molars do not
need to be sealed routinely.
Rather these teeth should be reviewed at
regular intervals
B. Pt with rampant caries who are at high
risk to decay
Sealing of primary molars is not normally
adviced.
TOOTH SELECTION
A. It has the greatest benefit on the occlusal
surface of permanent molar teeth.
B. Sealants should be applied as soon as the
selected tooth has erupted sufficiently to
permit moisture control and certainly within 2
years of eruption. It is desirable to place
sealants on newly erupted teeth that have not
achieved their full clinical crown height.
Note: The period of etching should be extended for
120 sec in primary teeth.
c. Any child with occlusal caries in one 1st
permanent molar should have the
remainining sound 1st permanent molars
fissure sealed.
d. Teeth to be sealed should be free of
approximal caries Mechanical control of
supragingival plague micro-organisms by
maintaining strigent oral hygiene
measures.
For at least 500 years, clinicians have claimed that
removal of scrum slimmy stuff and scale, fulness
and food particles from surface of teeth will
prevent decay of the teeth and inflamation of the
gums. Such measures involves brushing the
teeth at least twice daily especially before going
to bed, flossing the proximal regions of the teeth,
use of tooth picks etc. Dental prophylatic
measures are also helpful in minimising caries
experience, though these methods are not as
efficient as other methods of controlling caries.
Detersive Foods: Dating far back into detersive
foods have been known to help in reducing the
occurrence of caries but just like the above it is
not a very efficient method of control.
Other materials containing F. Which have
been advocated for fissure sealing

Glass ionomer cements

Conventional glass ionomer cements
Silver cermet cement
Recents studies gave 93% full retention at 6
months 85% at 12 months and 83% at 24
months and no caries were observed with the
glass ionomer based materials at recall
New materials is combining glass ionomer and
resins are in the pipe line.
CONCLUSIONS
 90% of caries lesions occur in pots and fiisures
 Caries in pits and fissures increases with age
 Poor durability of restorations and unfortunate
consequences of replacement has generated a
need for a more preventive oriented approach to
these lesions.
 Auto polymerized sealants are well
recommended and have reported 15 years
results. Whilst visible light cured materials a
sensitive to operator technique and have
reported clinical results over 5 yrs.
 Fluoride releasing cement are in their infancy
but are showing promise.
Conclusion Contd.
 Glass ionomers as fissures sealants materials is
beginning to beginning to produce good results
in terms of retention of materials and they have
been encouraging result on caries inhibition
 There is a positive interaction between Fin
driking water and fissure sealants in preventing
caries ( Weintroub 1989)
 Both fissure sealing and some form of F-
supplement (Notal not topical) should be
employed in any programme designed to
prevent caries. The use of either measures in
isolation will provide partial benefits
COST EFECTIVENESS SEALANTS

 Note: The lower the incidence of caries the

less cost effective it became to use fissure
sealants
 Comparison with other preventive measures
which are less labour-intensive put fissure
sealants in a less favourable position.
A complete schedule of fissure sealing might
include molar and premolar fissures buccal
pits of lower molars and liquia pits upper
molars and coagulum pits of incisors.
 METHOD OF APPLICATION OF GLASS
IONOMER CEMENT

1. Unlike the resist fissure sealants there is

need to clean the tooth with pumice and
brush
2. Tooth is isolated and dried
3. It is then conditioned with polyacrylic acid
for 30s, dredging the pits and fissures
with a fine probes
4. Washing of the conditioned surface
5. Redry the surface of the tooth and
isolated
6. The glass ionomer material is mixed and
beads of sealant transferred to the tooth
with a probe and this is used to the entire
depths of the fissure.
7. The surface of the sealant is now
protected with cling film or articulating
wax. When it sets the wax can be
removed and the excess cement quickly
removed with a fire roubur.
8. Finally a thin layer of light curing resin is
applied and cement.
 SUBSTANCES THAT INHIBITS
BACTERIA GROWTH

ANTIBIOTICS: Some authors have attributed the

decline in caries partly to the use of antibiotics
e.g. Penicillin. Some few research work have
shown a decline in the level of caries experience
in their study group.
The disadvantage is that we may come across
hyper-sensitivity reaction from pt and micro-
organism may develop resistant strains and
proliferate.
UREA AND AMMONIA COMPOUNDS
AND CHLOROPHYL
These have not shown any remarkable reduction
in clinical trials
Chlorhexidine: It is used in concentration of 0.1 -
0.2%. It acts by damaging the cell membrane of
a wide variety of bacteria. It binds into the
enamel surface and plague components and it is
slowly released, thus inhibiting bacterial
colonization and plague formation.
Its use is highly indicated in children or patients
with special needs. e.g medically compromised,
mentally or physically handicapped children or
patients.
INTRODUCTION OF COMPETITORS OR PREDATORS
OR COMMENSALS
So far it is only veillonella spp, a gram negative
bacteria, sometimes found in the mouth, which
has been shown to have a protective effect
against caries. Although more studies have to be
caries out in this field.
HOW DOES IT ACT AGAINST THE PROCESS OF
CARIES
The require lactate for growth but are not able to
metabolize dietary carbohydrate. They use up
lactate produced by other micro-organisms and
concert it to weaker and less carcinogenic organic
acid. This kind of relationship with the caries
producing bacterial is more of commensalisms.
SUBTRATE AS A TOOL IN PREVENTIVE
DENTISTRY

Diet can affect the tooth in two ways, 1st

while the tooth has erupted into the mouth
and 2nd while the tooth is forming before
eruption. The relationship of diet to the
tooth during the pre-eruptive phase is
nutritional while once the tooth has
erupted into the oral cavity the relationship
to diet is environmental rather than
nutritional.
PRE-ERUPTIVE EFFECT
Vitamin A, vitamin C and Vitamin D deficiencies as
well as deficiencies and inbalance ratios of
calcium and phosphorus cause characteristic
malformations in histologival structure of the
developing tooth. Inadequate amounts of
vitamins D of calcium and phosphorus result in
imperfect calcification of the mineralizing enamel
matrix and dentin matrix, though only vit. D
deficiency during development is believed to
reseult in an increases susceptibility of the tooth
to caries in human populations. The others have
been proved to results in an increase caries
susceptibility of the tooth in animals.
POST-ERUPTIVE EFFECT
Evidence has shown that the post eruptive local
effect is very much more important than the pre-
eruptive effect.
There is a wealth of evidence which have shown
that sugar contributes to the initiation and
progress of caries
C.O.M.A (Committee on Medical Aspect of Food
Policy) report on dietray sugars and human
diseases has strongly implicated sugars as the
main causative factor in dental caries.
Throughout the discussion of this topic, sugar
means NON-MILK EXTRINSIC OR FREE
SUGARS.
Stable starchy foods, intrinsic sugars in
whole fruit and milk are negligible causes
of dental caries.
Studies reviewed have shown that when
annual sugar availability exceeds 10kg to
15kg per person per year, dental caries
increases. The World Health Organisation
has recommended that free sugar intake
should be below 10% of the total energy
intake.
PLAGUE Ph STUDY

Stuies which produce evidence about the

cariogenic effect of sugar have been
mentioned in the text.
Of interest is the plague pH study. This has
shown that cryogenics food depresses the
pH in the mouth (sign of acidity in the
mouth) and the fall in pH is proportional to
the carcinogenicity of the food. Fig 1
Illustrate stephans curve which is used to
illustrate the pH relationship of food.
8

5
Peanuts
4
Sugared Coffee
3

0
3 7 11 15 19 23 27
DIET THAT HAVE A PROTECTIVE EFFECT
AGAINST CARIES

Already in the text we have mentioned that some

diet have a deterrent effect on caries. Studies
of this have been based principally on
1. Animal experiments
2. Labouratory experiments
3. Human clinical trials
It has been shwon (Nizel and Harris 1964) that the
addition of organic and inorganic phosphate to
cariogenic diets reduce caries experience in
rodents and in humans.
PHYTATE: It was observed that addition phytate to
cariogenic diet resulted in marked reduction in
caries in monkeys. The mode of action is the
ability to absorb readily and firmly to enamel
surface and so perevent dissolution of enamel.
Phytate is found in unrefined carbohydrate e.g
Wheat bran.
DIETARY CONTROL: The prevention of caries by
dietray control can be directed at reducing the
intake of free sugars and substitutions of sugar
free foods. Also the public could be encourage
to take foods which prevent the process of
caries. The above could be achieved through
Dental Health Education and Dental Health
Promotion.
PREVENTION

Diet that have protective effect against

caries
Avoiding diet that enhance caries activity
All sugary containing food – diet chart for
children.
Selenium enhance caries activity.
OBSERVATION STUDIES
Hopewood house studies in new south wales in
Autralia conducted on 80 children on lacto-
vegetarian diet showed a low prevalence of
dental caries. Low severity of dental caries.
Much lower than children of the same age and
socio-economical background attending state
schools
Study on Patients with hereditary fructose
intolerance
A defect in which the patients do not process a
liver enzyme fructose phosphate spliting
aldolase. This make them intolerable to fructose
and sucrose products. Research on 27 patients
revealed they were caries free.
Studies by Olougba and Lennon: Over a
period of 6yrs 1977-1983 recorded an
increase in DMFT from 0.17 to 3.18 in
higher social class and 0.05 to 1.7 in
poorer children in Ondo state nigeria.
Tristan de Cuhians in 1937 had low caries
rate in 1937 when their diet was very low
in sugar. In 1940 when their diet was of
sugery food increased there was a
deterioration in their dental health.
The human intervention studies –
Vipeholm Studies: Revealed that:
1. Consumption of sugar even at high levels is
associated with only a small increase in caries
increment if the sugar is taken up to 4 times a
day at meals and non between meals
2. Consumption of sugar both between meals
and at meals is associated with marked
increase in caries increment
3. Increase in caries activity varies from person to
person, the increase in caries activities
disappears on withdrawal of the sugary food
and caries lesions occur despite the avoidance
of sugar.
4. Animal experiemental germ free rates when
introduced to carogenic diet caries did not
develop in them. This confirms the need for the
plaque micro-organism in the invitation and
progress of caries.
Enamel slab experiment: Koulerides et al – intra-
oral appliances have been made that hold slabs
of enamel. These remain in the mouth 1wk-6wk.
In some of the experiments the carnogenic food
is eaten. Lesion formation are tested by the
micro-hardness test or micro-radiography or
iodine dye permeably tets.
Starch: various studies have shown that the incidence
abd prevalence of peopla\e who eat starch and do not
consume sugar food is very low.
Human interventional studies (Turko Studies) has shown
that as the starch content of various food items was
not altered and sugar was substituted by Xylotal the
DM was 0.0 in the study group feed with sugar and
fruits the DMFS was 3.8.
Cooked starch or starchy food were to be capable of
causing caries but are far less cariogenic than sugar.
Tristan de cuhans: Before the influence of Western life
style ate only potatoes and their DMFT was very low.
But after their diet change to include sugar etc their
DMFT increase drastically.
AIM: To introduce the students to
prevention.
OBJECTIVES:
The student should be able to:
1. Define prevention in a broader perspective
2. To have a knowledge of what the medical
model is a critical appraisals of medicine and
dentistry and why there is world-wide
emphasis on prevention.
3. Describe strategies in prevention, aim of
prevention and methods of prevention.
Hypothiocyanite from salivary thiocynate is
claimed to have a significant effect on bacterial
growth
Lactoperoxidase in saliva catalyses formation of
hypitiocyanite in the presence of hydrogen
perioxinde produced by bacteria. This means
hydrogen peroxide H202 activates the
lactopixidase system.
The enzymes amyglocosidase and glucose
oxidase is used to produce sufficient hydrogen
keroxide in saliva.
This chemical reactions have been demonstrated
in labouratory presence in its plague.
IDENTIFICATION OF HIGH CARIES RISK CHILDREN

Methods available for identify caries high risk people are

Epidemiology – Deciduous caries experience
- Current or baseline caries experience
in permanent teeth.
A. Deciduous Dentition
Studies have shown that there is correlation between the
caries experience of the deciduous dentition and that
of the permanent dentition. Therefore screening
children on the basis of their caries levels at age 3 yrs
has little practice value in the identification of children
who will develop caries in their permanent dentition i.e
This does not have a high predictive value.
CURRENT BASELINE CARIES
EXPERIENCE IN PERMANENT

Studies have shown a higher correlation

than deciduous dentition between the
prevalence of caries in the permanent
dentition of a community with that of the
same children 3-4yrs later. The predictive
potential of this current baseline caries
experience is high. Indices used here are
DMFT dmft DMFS
Form arrangement of teeth and chemistry
entrance
 Number of teeth
 Fissure patterns
 Occlusion
 Enamel surface
 Characteristic
 Fluoride distribution
 Caries inhibition
 Caries inhibition
 Enamel solubility
 Identification of the early caries lesion.
A. Fluoride distribution: The distribution of fluoride
in dental enamel shows dearly that the
fluoride concentration falls steeply from the
enamel surface towards the dentino-enamel
junction. There is an inverse relationship
between the fluoride content of surface enamel
and caries experience i.e People with high
fluoride content in their enamel have lower
caries experience
B. When early caries lesion is identified early with
just the application of tropical fluoride the
lesion can reversed
BIOLOGICAL FACTORS IN PLAGUE
Dental plague can be considered an ecosystem
are the microflora, the teeth, saliva, diet and
dental care. Mutans streptococci are found in
man in high proportion in samples within the
area of an incipient carious lesions. In samples
from infant tooth sites the organisms are absent
(Association with disease). Elimination of the
organism ie antimicrobial measures directed at
mutans streptocci have led to significant
reduction of caries incidence both in animals
and man. Communicability: Mutans steptococci
are transmitted from parents to offspring in
animals. In humans, mothers are the most likely
source of for infection of children.
MICROBIOLOGICAL TEST: Strepmutans test and
Lactobaccillus test
In the Streptococcus mutans test a sample of
stimulated saliva is taken by chewing wax.
The sample of saliva is tested in the labouratory where
it is vortex mixed, diluted and cultured on Mitis
Salivasius bacitracin agar. The number of typical
colonies at a suitable dilution is recorded and the
count at a suitable dilution is recorded and the count
per ml of saliva is calculated. Values regarded as
high are those above 106 and values below 105 as
low. Using the same method the lactobacilly test is
carried out. But in this case Rogosa S.L agar is
used. For lactobacillus counts 105 are regarded as
high and 103 and below as low
These days for simplicity and easy use in the clinic
simple calorimetric test have been made.
Dip-Slide methods for strep mutan and lactoballus
a. Dinto cult Larmas (1995) This is a dip slide test
for lactobacilli. Illudiluted saliva is run over a
dip slide coated with a slightly modified
Rogasa S.L. agar. Growth of colonies is compared
with a standard illustration.
Dentocult S.M. A dip slide method for strep
muttans Undiluted saliva is run over a dip slide
coated with a slightly modified Mitis Salivarius
bacitrancin agar. Growth of colonies is
compared with a standard illustration.
TEST OF MICROBIOLOGICAL ACTIVITY
Shyders test: It is the best known test for microbiological
activity. It is dependant on the speed of acid formation
when a sample in saliva is insulated into acid glucose
agar/ Some researchers refer to its as simplified
lactobacillus count.
METHOD: Other test are Fosdicks test, Dewars test and
Rickles test which measure acid produced in mixture
of saliva and carbonhydrates
Salivary factors
Oral clearance
Buffering capacity
Antibacterial factors
Immunological aspects
BUFFERING CAPACITY OF SALIVA
The buffering capacity of saliva vary with caries
activities high pkacids such as acetic acid can
provide a buffering system which is able to
counter act the pH drop caused by the low pK
acids such as lactic and pyruvic acids measures
the amount
Dentobuff test (Frostal 1988) Measures the
amount of acid needed to lower the pH of saliva
through a fix interval. Have the saliva is added to
an acid solution containing a colour indicator
and the result is compared with a standard.
Buffering capacity is relates to salivary flow rate.
ORAL CLEARANCE
The physical removal of undesirable products by
saliva is a relatively simple protective
mechanism. A build up of bacterial can occur
when muscular clearing actions and salivary flow
rate are reduced during sleep, feverish illness,
after radiation affecting the salivary glands
ANTIBACTERIA FACTORS
1. Lysozyme is an enzyme which causes splitting
of bacterial cell walls. The effectiveness y this
process is affected by mucin which inhibits its
action. The viscosoty of saliva therefore is a
variant which besides reducing oral clearance
has other effects.
2. Lactoferrin: Has the ability of with holding
iron from invading bacteria
3. Lactoperoxidase: cause a reduction in
glycolysis and a subsequent in vivo
reduction in plaque accumulation
These enzyme studied relationship were not
good predictors of caries.
IMMUNOLOGICAL ASPECTS

Protection against dental caries can be achieved

either by systemic (serum) or secretary (Saliva)
immunity. Immunoglobulin A (IgA) sal. IgA
Immunoglobulin G.
These have not been good predictive test serum
antibodies proved to be a more useful predictor
of the resistance to caries experience. People
with low caries experience have been found to
have raised IgG antibodies to mutans strep and
not to other bacteria.
DEMOGRAPHY

 Oral hygiene
 Age
 Sex
 Socioeconomic status
 Family caries experience
 Ethnic group
SYSTEMIC CONDITIONS
 E.g Xerostomoia due to drugs symgrans syndrome
irradiation of the salivary glands diabetes mellitus?
 Cystic fibrosis phenylketonuria because of specific
dietary regions and life style
DIET
Fluoride intake
Cariogenic potential of food
Trace elements
Selenium, MO, AL, B
Normally a combination of predictive method are used.
Considering the fact that caries is a multifactorisl
disease.
DENTOCULT TEST FOR LACTOBACILLI
The dentocult test is based on a slightly modifed Rogosa – SL
agar cast on a special plastic dip slide.
Method: The slide is held under a running stream of saliva
which is collected by asking the patient to chew
unflavoured paroffin.
Note: Both slides of the slides are coated with the nutrient
agar (Rogosa-SL agar) and can be used for the count.
After inoculation (i.e with saliva) the dentocult slides are
incubated for 4 days at 370C and the density of the
microbial colonies can be compared against an
accompanying reference map to show the number of
bacteria in the test saliva.If the saliva is collected in test-
tubes graduated in millititres and the time of the collection
is taken into acount the mean salivary secretion rate of the
patient can be calculated. Also the pH of the saliva can
easily be measured using an indicator papers.
Growth > 104 microorganism/ml was taken as positive.
Test tube with Rogosa-SL agar
saliva
PREVENTION OF PERIODINTAL DISEASE

AIM: To equip the students with the methods of

preventing periodontal disease.
OBJECTIVES: The student would
1. Define periodontal disease
2. Be aware of the new classification and would
have a knowledge of the new concept and its
implication in preventing periodontal disease.
3. Have a knowledge of the aetiology of
periodontal diseases
4. Would have a knowledge of the normal oral
flora
5. Have a knowledge of the effect of plague
on the periodontium
6. Be informed on the current perceptions on
periodontal disease
7. Be informed on the prevention strategies
used for the prevention of periodontal
disease.
8. Have a knowledge of the prevention
methods used for the prevention of
periodontal disease.
LIST OF TITLES

1. Definition of periodontal disease

2. A brief anatomy and physiology of the
periodontium (brain storm) (i.e discussion)
3. Clinical appearance of a normal healthy
periodontium
4. Pathogenesis of periodontal disease
5. Current terminology and classification of
periodontal diseases.
6. Natural history of periodontal disease
1. Old Concepts 2. New Concepts
7. Implication of the new concepts in the prevention of
periodontal disease
8. Aetiology of periodontal disease.
9. Current perceptions on periodontal disease
10. Prevention strategies
11. Prevention method in the prevention of periodontal
diseases
 Methods used to increase tissue resistance
 Methods directed at the elimination of plague
 Elimination or control of condition that predipose
to periodontal disease.
DEFINITION:

Periodontal disease is the pathological conditions

of the periodontium. (i.e the gingiva and the
supporting structures of the tooth i.e cementum,
periodontal membrance and alveolar bone.
The periodontium consist of four different tissues –
gingiva, periodontal ligament, alveolar bone and
cementum. They are anatomically separate but
functionally they are all dependent on one
another in maintaining a viable healthy
supporting structure for the tooth
GINGIVITIS
It is an inflammatory response of the gingiva
without destruction of the supporting
tissues.
Periodontitis: is an inflammatory response of
the supporting tissues
Periodontium: Anatomically the periodontal
structures are described as the
1. Gingiva 2. Periodontal ligament
3. Periodontal ligament 4. Alveolar bone
GINGIVA: The gingiva is one of the soft
tissues that line the oral cavity. Together
with other soft tissues of the oral cavity
are known as the oral mucosa.
It is adjacent to the teeth and provides a
covering for the coronal portion of the
alveolar bone. It is divided into
a. Marginal gingiva
b. Attached gingiva
c. Interdental papilla
a. Marginal gingival is free or unattached, coronally
positioned and creates the soft tissue wall of the
gingival sulcus.
b. Attached gingival is firmly attached to the underlying
tooth and bone; it is apical to the marginal gingival; it is
stipled in texture, tapered in contour and firm in
consistency.
c. Interdental papilla is located between adjacent teeth,
generally triangular shaped. However, its shape
depends on the proximal contours of the teeth creating
the interproximal space.
In the bucco lingual dimension the interdental papilla
terminates coronally with separate buccal and lingual
peaks of tissues joined by a depression known as the
gingival col.
The gingival sulcus is the space created when the
marginal gingival is deflected away from the
tooth surface. It runs from the crest of the
marginal gingiva to the most coronal level of the
junctional epithelium.
The junctional epithelium is the portion of the
gingival epithelium closely adherent to the tooth
and it is located apical to the gingival sulcus.
Crevicular fluid: is continuously secreted into the
gingival sulcus
Periodontal Ligament; is the group of tissues that
surround the root of the tooth and serve as the
primary attachment of the tooth to the alveola
bone. It consist of bundles of continuous
intermigling collagen fibres. Average width of
the periodontal ligament is 0.18mm.
The principal collagen fibres are arranged in 4
groups.
a. Alveola crestal
b. Horizontal Transverse
c. Apical
d. Oblique
e. Transeptal intraodicular
In the periodontal ligaments are found blood
vessels and principal cells such as
1. Fibroblasts
2. Differentiated mesenchymal cells
3. Osteoblasts
4. Osteoclasts
5. Cementoblasts
6. Epithelial rest of malassez
Alveola Bone: Is made up of bony processes that
project from the basal portions of the mandible and
maxilla. These processes are composed principally
of cancellous or spongy bone, covered with harder
outer covering known as the cortical bone. The
spaces in the alveola bone that accommodate the
roots of the teeth are known as alveoli.
The alveoli are lined with a layer of bone known as
alveolar bone proper or cribriform plate. (It contains
small holes for sharpeys fibers and blood vessels). It
is depicted by a white line on the radiography and it
is called the lamina dura. It is also covers the crest
of the interproximal bone and it is known
radiographically as the crestal lamina dura.
CEMENTUM: It is the calcified tissue that covers the
root of the tooth and provides a means of
attachment for the periodontal ligament fibers to the
tooth.
NORMAL HEALTHY PERIODONTIUM
The colour of a healthy gingiva is uniformly coral pink,
however variations exist. In dark-skinned people it
may be dark blue or brown colour. In health the
marginal gingiva is knife-edged in contour, firm in
consistency, smooth in texture and bound epically
by the free gingival groove. Whilst the attached
gingiva is tapered in contour, stippled in texture and
firm in consistency.
The papillae are generally triangular shaped and
cover the interproximal spaces. The depth of the
histological cervice i.e the distance from the
crest of the free gingiva to the coronal extent of
the junctional epithelium is 0.5mm. Clinically the
crevice depth is the distance to which a blunt
probe will penetrate and this is 2mm. WHO
accepted depth is 3.5mm. In health the alveolar
process surround the roots to within 1 to 2mm of
cemento-enamel junction and the crestal bone
radiographically shows intact lamin dura.
CURRENT TERMINOLOGY AND
CLASIFICATION OF PERIODONTAL DISEASE
GINGIVITIES: Gingivitis is used to designate inflammatory
lesions that are confirned to the marginal gingival
regardless of the cause.
The types most frequently encountered are
1. Plague associated gingivitis
2. Acute ulcerative necrotising gingivities
3. Hormonal gingivitis
4. Drug induced and spontaneous drug occuring
hyperplastic gingivitis
Baer P.N. and Kaslick R.S. 1978
There is a general agreement that at least some forms of
periodontitis begin as gingivitis, although transient form
of gingivitis that may not progress to periodontitis do
occur. (Suomi et al. 1971)
PERIODONTITIS
A great deal of new information has recently become
available and based on it a new classification of
periodontitis into 5 distinct entities has been
proposed.
1. Prepubertal periodontitis
2. Juvenile periodontitis
3. Rapidly progressive periodontitis
4. Adult periodontitis
5. Acute necrotising ulcerative gingiro-periodontistis.
(Page R.C. et al. 1983)
The above classification is based on many
characteristics including age, pocket flora, leucocyte
function test. Serum antibodies, clinical and
radiographic features and progression and history of
the disease. (Page R.C. et al. 1989)
PERIODONTITIS
A great deal of new information has recently become
available and based on it a new clasification of
periodontitis into 5 distinct entities has been proposed:
1. Prepubertal periodontitis
2. Juvenile periodontitis
3. Rapidily progressive periodontitis
4. Adult periodontitis
5. Acute necrotising ulcerative gingiro-periodontis (page
RC et al. 1983)
The above classification is based on many characteristics
including age, flora, leucocyte function test, serum
antibodies, clinical and radiographic features and
progression and history of the disease. (Page R.C. et
al. 1989)
NATURAL HISTORY PERIODONTAL DISEASE

Recent research has led to the formation of new concepts

about the natural history of periodontal diseases and
disputting of the old concept. (Goodson & Socransky
1984).
The Old concept states that periodontal disease is a
progressive and destructive periodontal process. This
means that once the disease starts it progresses into
tooth loss and once disease starts only continuous care
will prevent invitable progress of destruction. It also gives
the impresison that once the disease start it is
mandatory to treat it and sampling disease site for
microbial at any time will yield a sample. (Goodson and
Socransky 1984)
THE NEW CONCEPTS
EVIDENCE FROM RECENT RESEARCH
1. Animal studies indicate that the disease does not
progress in all lesions (Lindhe et al 1975).
2. Obsevational studies have shown that large numbers
of gingival sites with or without prior loss of periodontal
attachment remain stable.
3. Attachment loss rates in individual surfaces are either
too fast or too slow.
The new concepts are therefore divided into two model:
A. Random burst model
B. Asynchronous multiple burst model of destructive
periodontal disease.
The random burst model state that certain
gingival sites are free of destruction for a
life time and other sites might experience
disease followed by episodes of remission
or repair. The asynchronous multiple burst
model states that, burst occur
asynchronously i.e multiple burst break
down within a short period followed by
prolonged period of remission.
EPIDEMIOLOGY
1. Evaluation of large populations reveals that older
people have more attachment loss reflecting the
duration of exposure to aetiological agents
2. Periodontal conditions are worst in males
3. Lower socioeconomic groups
4. Infrequent dental attender (Presumably because
these groups demonstrate poorer standards of
preventive health behaviour
It most be noted that difference in periodontal disease
can not be explained solely by the amount of plague
present. This is due to secondary etiology factors
such as pregnancy, smoking, inherited characteristic
immune function etc.
GINGIVITIS
The prevalence and severity of gingivities from
the deciduous dentition stage increases with
increasing age to reach a peak prevalence of
90-100% at puberty. Later there is a slight
dedcline in prevalence and severity during
adolescence and followed by a slight increase
in adult life.
Humonal changes may be responsible for the
peak at puberty or gingival sites at risk as the
permanent teeth develop.
PERIODONTITIS: Periodontitis have been
observed in deciduous dentition (Sjodin
and Matsson 1994). Both prevalence and
extent of clinically significant periodontitis
is low in early adulthood and increases
with age. Only a minority of teeth
affected progress to an advance stage of
the disease.
AETIOLOGY OF PERIODONTAL
DISAESE
Periodontal disease is a multifactorial disease and an
understanding of the cause of the disease requires
consideration of the followings:
1. The role of micro-organisms (plague)
2. Conditions that may produce or interfere with its
removal
3. Local and systemic or constitutional factors may
alter the resistance or susceptibility of the tissues of
the periodontium to bacterial and other noxious
substances.
4. Individual variation in the relative destructive and
protective aspects of the host defence mechanism.
Immunosorbent assay (ELISA) and flow cytometry
have identified 6 aspects of the 23 treponemes
found in the periodontal environments,
Actinobacillus Actinomycetecomitans (Aa)
Bacteroides gingivalis and Bacteriodes
intermedius as aetiologic agents in periodontal
disease.
These predominate in the adult form of
periodontitis whilst in juvenile periodontitis Aa
seems to be the most important etiologic agent.
PLAQUE

Bacterial plaque is a complex tenacioulsy

attached soft non-mineralized deposit
composed of a consistently organised
structure of
1. Micro-organisms
2. Epithelial cells
3. Leukocytes
4. Macrophages
5. An intermicrobial matrix
6. Water
Micro-organisms consitute 70% of the bulk
of plaque. The intermicrobial matrix
comprises of protein and carbonhydrate
substrate derived partly from saliva
epithelia cells, crevicular exudase and
the diet. The earliest deposit to form on a
clean tooth surface si the acquired
pellicle a structureless film of glyproteins.
Initially bacterial plaque is transparent and therefore not
clinically visible as plaque goes through maturation
process by the proliferation and addition of bacteria
and bacteria by products it becomes visible by its
mass and discolouration.
Plaque can be deposited on a cleaned tooth surface
within 6 hours with maximum accumulation achieved
in approximately 30 days. Loe found that as plaque
was allowed to form its flora gradually chnaged from
an early accumulation of strepto-cocci to a later
preponderance of gram negative anaerobic bacteria
and it was at this time (after 10 days) that gingivities
reached its peaks. In a subsequent study he showed
that gingival tissues can be kept clinically healthy
provided plaque is completely removed at least once
every two days thereby suggesting that early plaque is
less injurious than its more matured form.
The following micro-organism are representative of
numerous bacterial that are related to the
plaque microbiota and its various stages of
maturation:
1. Gram-positive Cocci-Streptococcus
2. Gram positive rods – Lactobacillus
Actinomyces
3. Gram-nagative rods – Bacteroides
fustobaterium
4. Spirochetes
Two types of plaque found at the gingival margin are
Supragingival and Subgingival
Supgingival plaque is always deposited first. The
bacteria component differ.
Subgingival plaque found on most surface periodontal
pockets.
FORMATION OF PLAQUE
Acquired pillicle with 3-8hrs strepticoccus (mitis,sangius
& millar, mutans) Granitirods Actininisus (Niscosus
Actinomyces naeslundii & Odontlyticus) after the 1st
24hrs changes take places in plaque micro-organism.
Strep decrease to 45% gram negative anaesthesic.
Coci e.g Veillonella alcalescous increase to round
20%. After 3 days proportion of gram cocci and rods
increase by 7 days the complex plaque flora emerges
consisting spirochaetes, fusiform bacilli.
Filamentous organism and large numbers of
gram(-) cocci and bacilli. During the next 3
weeks of undisturbed plaque formation further
changes occur. The growth of anaerobic
organism e.g porphyromonas (Bacteriodes)
species builds up.
Subgingival plaque form from established
supragingival plaque. The subgingival
environment with its low oxygen favours the
growth anaerobic bacteria and nutrient coem
from the crevidular fluid.
2-3 months plaque Plaque of pockets 2-
(Supragingival) 3months
contains Anaerobes 90%
Strep 25% Mainly Bacteroides
Actinomyces 25% fusobacteria
Anaerobicroid 25% nucleatum
spinocheates.
Fusobacteria,
porphyromes Constitute 50% of
(Bacteroides) micro-organisms
Walinella, campy present in deep
bacter spirocheste pockets.
2% not easily cultured
PLAQUE MATURATION
MECHANISM BY WHICH PLAQUE EXERT
THEIR DESTRUCTIVE ACTION CAUSING
TISSUE DAMAGE

1. Production of toxins (exotoxin & endotoxins)

2. Bacterial antigens
3. Production of enzymes (Collagenase and
proteases)
4. Bacterial waste products (ammonia, hydrogen
sulphide)
The above act as irritants that produce the
changes in the periodontal tissues.
CONDITIONS THAT MAY PRODUCE OR
INTERFERE WITH THE REMOVAL OF
BACTERIAL PLAQUE
1. Calcified deposits- calculus
2. Oral hygiene
3. Bad social behaviour – smoking
4. Deficient dental treatment
5. Local functional factors e.g unreplaced missing
teeth, malocclusion, unrestored caries teeth
especially approximal region.
6. Food consistency
7. Foor debris – orthodontic appliances material
alba, dental stains
Material Alba: It is a visible soft deposit
consisting of micro-organism leucocytes,
salivary proteins, desquamated epithelial
cells and food particles. It is easily
removed by the application of forceful
water spray. These is enough evidence to
show that material alba acts as favourable
environment to be production and growth
of diverse micro-organism with
pathological potential, capable of causing
gingival inflammation.
Food debris (retention and impaction)
Food debris consists of particles of food retained in the oral
cavity and should be differentiated form food impaction.
It is easier to remove than plaque. Factors that lead to
food impaction are:
Orthodontic appliances
Irregularities in tooth position or
Reduced height and blunted contour of the interdental
papillae.
Food consistency: A diet of soft stickly food tend to produce
more bacterial plaque because soft food tend to cling to
the tooth. It therefore creates a favourable environment
for plaque accumulation.
Dental strains: these are result of pigmentation of
the acquired pellicle by chromogenic bacteria,
food or chemical agents.
Calcified deposits: Calculus is bacteria plaque
which has been mineralised and can be formed
on all teeth surface and protheses. Calculus acts
as a nidus for the accumulation of plaque and it
acts as a mechanical irritant.
Local and systemic or constitutional factors may
alter the resistance or susceptibility of the tissue
of the periodontium to bacterial and other
noxious substances.
Microbial health is related to host resistance. There must
be a balance among the oral micro-organism and the
host. If the resistance of the host is reduced this
balanced is disturbed and this may result in disease.
Host resistance is tissue protection, provided by the
normal body, defence mechanism which include the
following:
1. Healthy intact epithelial tissue (the main function of
epithelial tissue is protection).
2. Keratinization of the epitherlium that covers the oral
aspects of the gingival (gingiva sulcular epithelia is not
keratinised)
3. Fluids from the gingival sulcus that contain antibodies
and provide a washing effect.
4. Antibacterial and self cleaning action of saliva.
5. Utilization of the muscles of mastication and
tongue provide a natural cleansing effect.
Systemic host resistance involves total body
health.
Degenerative processes can affect the resistance
of the tissues. If the host resistance is lowered
the periodontal tissue will have less defense
against the destructive aspects of the chronic
inflammatory lesion.
CURRENT PERCEPTIONS ON PERIODONTAL
DISEASE
1. The prevalence of perio dental disease is very high. It
afflicts almost the total population in the world.
2. Inspite of almost universal prevalence of periodontitis,
it progress to tooth loss in only 10-15 percent of the
population (schaub 1984)
3. Periosontitis is not a major cause of tooth loss in adults
(Burt B.A. 1988, J. Public Health Dentistry 48 (4) 252-
256
4. It is estimated that periodontal disease accounts for
20-30% of all extractions (contrary to previous
believes)
5. Most adults have some loss of bony support and less
of probing attachment
6. Gingivitis and periodontitis are asosciated with
different bacterial flora.
7. Gingivitis preceeds periodontitis but not all sites with
gingivitis later develop into periodontitis.
8. Although usually related to age in a population,
periodontitis is not a natural consequences of ageing
9. Failure rate of periodontal treatment is high Kerr. N.W.
1981 followed up 44 patient for 5 years. These was
45% failure rate 1981). Brot. Dent J. 150,222-224).
Studies have shown that with all procedures employed
in treatment, clinical attachment is slightly lost in sulci
of intial probing dept of 1-3mm. (N.P. lang 1984, Non –
surgical and surgical periodontal treatment, Fransden).
10. It has also been demonstrated that the clinical
severity of periodontitis is reduced significantly 1
month after the hygienic phase of periodontal
therapy and that need for surgical pocket
treatment cannot be assessed properly until
completion of the hygienic phase of treatment
(E.C Morrison, S.P. Ramford and R.W. Hill 1980.
Journal of clinical periodontology 7. 199-211).
11. Prevention is labour intensive. The dentist
based appraoch is very expensive e.g It will take
160 days per year of chair-time to treat 1000
patients using the conventional approaches that
are currently taught in the schools.
12. The criteria's for differentiating the high risk
group from those not at risk are not highly
predictive.
13. The most consistent finding in periodontal
research is that, people with more plaque have
more severe periodontal disease.
14. At a community level there is a level of plaque
which is compatible with no progress of
periodontal disease, but within populations and
mouths with low plaque scores some people or
some periodontal sites develop severe
periodontal disease that may lead to advanced
loss of tooth support by the age of 50.
WHO goal for dentistry is to maintain a natural
functioning dentition for life including all social
biological functions such as self esteem,
aesthetic appearance speech, chewing, taste
and absence of discomfort.
This objective doesn’t imply that all the 32 teeth
will have physiologoical and anatomically perfect
periodontal support with attachment at the
cemento-enamel junction. A certain level of
structural change can be tolerated. Some
change in periodontal support is acceptable if
that change does not affect the functioning of
the dentition and can be tolerated by the patient
and peers and does not deteriorate further.
PREVENTION AND PERIODONTAL DISEASES

PREVENTION STRATEGIES: In view of the above

current perceptions of periodontal disease,
strategies to prevent and control periodontal
disease is divided into:
1. Population strategy for altering life practuce and in
particular oral cleaning effectiveness to reduced
the dental plague level of the community.
2. A secondary prevention strategy to detect and
treat people with destructive periodontal disease.
3. A high risk strategy for bringing preventive and
therapeutic care to individuals at special risk
(Gottlieb and Orban 1988)
POPULATION STRATEGY: This strategy will consist
mainly of Health education and health promotion
methods, to alter variables that affect oral cleaning
behavior. The objective of health education is to
improve the effectiveness of tooth cleaning
bahaviour. Such a population program should
contain the following components:
1. Dental health education on oral hygiene should be
incorporated into health education
2. Involving community leaders or leaders of public
opinion who could act as role models in our health
education programme. Also use the management
and organisational skills to help implement
preventive strategies.
3. Public education to increase awareness and knowledge
of good hygiene behaviour by educating all age groups
in a continuining and consistence programme.
4. Mass-media methods to increase community awareness
of body hygiene and tooth cleanliness. Informing the
public of the availability of oral hygiene aids
5. Health promotion to encourage environmental changes
i.e instituting improvements in hygiene at schools and in
the workplace as well as providing washing facilities.
Introducing marketing practices that encourage the sale
of good hygiene aids at low cost.
6. Professional education to improve tooth cleaning
instruction by professional personnel e.g teachers
nursery school attendants, health visitors, doctors,
dentists etc.
SECONDARY PREVENTION STRATEGY
It will involve applying measure to influence the
course of detected periodontitis. This will be
directed at those who have the disease but in
whom the disease condition could be reversed.
The principal therapeutic strategy is to reduce
the amount of dental plague by scaling, root
planning and oral hygiene instructions on
maintaining minimal level of plague.
This will involve either screening in the community
or dental clinics and sending them for treatment.
However most methods currently used have
major short-comings.
High Risk Strategy: There is a small number of
people who will have severe progressive
destructive periodontal disease despite effective
tooth cleaning practices. This strategy will
consist of screening for high risk individuals
taking therapeutic measures e.g applying anti-
microbial paste or solutions into pockets etc.
Also screening for people with medical or socio-
psychological conditions that are affected by
periodontal disease.
 W.H.O GOALS
Age (yrs) Mean No of DMF Periodontal status
missing teeth

12 0 2 0 teeth with pockets

> 3mm
15 0 3 0 teeth with pockets
> 3mm
18 1 4 0 teeth with pockets
> 3mm
35-44 2 12 Fewer than 7 teeth with
pockets > 4.5mm

65-74 10 12 20 functional teeth

METHODS USED IN THE PREVENTION OF
PERIODONTAL DISEASE

Methods used in controlling plague micro-

organism
1. Mechanical removal
2. Antibacterial control
3. Chemical
4. Enzyme
METHODS USED IN INCREASING TISSUE
RESISTANCE TO PLAGUE BACTERIA

1. Nutrition
2. Vaccination
3. Drug to increase tissue health
METHOD TO ELIMINATE CONDITIONS THAT
INTERFERE WITH PLAGUE REMOVAL
The oldest approach to plague control is the use of
detersive food or its mechanical removal by
brushes or other aids. Mechanical removal of
plague Micro-organism.
METHODS USED IN CONTROLLING THE
PROLIFERATIVE OF PLAGUE MICRO-ORGANISM

The best and the most popular mechanical removal of

plague is by maintaining stringent oral hygiene
measures.
ORAL HYGIENE MEASURES: are method and procedures
for the removal of soft deposit plague from the teeth and
surrounding tissues. It can be divided into two types
natural and mechanical.
Natural means of removing soft deposit from teeth is by the
used of detersive foods. It has been assumed that hard
or detersive food have a valuable cleansing action and
remove plague and food debris from the teeth and
surrounding tissues. However it has been proved that
the chewing of determine food does not appear to have
any significant plague.
PREVENTING EFFECT IN MAN MECHANICAL
ORAL HYGIENE MEASURES

The classical method of cleaning the teeth is by

regular use of a tooth brush and tooth paste or
by the use of other devices such as chewing
sticks, wood points on dental floss. It has been
shown that careful tooth brushing can keep the
teeth free from plague and maintain the gingivae
in a state of clinical health. (Loe et al 1965,
Theilade et al 1966) As far as maintaining
gingival health is concerned the efficiency of
tooth brushing may be even more important than
its frequency. Since thorough cl,eaning once
every 2nd days will maintain gingival health
(Kelner et al 1973, Lang et al 1973)
METHODS OF TOOTH BRUSHING

1. The bass
2. Roll
3. Scrub brush
4. Charters methods
CHARACTERISTICS OF A TOOTH BRUSH
RECOMMENDED TOOTH BRUSH SPECIFICATION

There is a wide variation in toothbrush designs however

little evidence exist to support specific
recommendations.
For adults suitable head dimensions appear to be 22-
28mm x 10-13mm and for children 20mm x 10mm
filaments should preferably be nylon (better physical
properties and standardization) with diameter 0.15-
0.2mm to give a soft medium texture. The filament are
best packed density to give the type of construction
called multi-fluted. There is no convincing evidence
that electric toothbrushes are more effective than hard
operated brushes for people with normal dextority
Toothpaste
STILLMAUS METHOD

The bristles are placed at 450 angle with the

bristles directed epically on the gingival
and party on the cervical particle of the
teeth. Pressure is applied to blanch the
gingival and a gentle but firm rotary motion
is applied to the brush with the bristles
remaining in the same position.
A modification of stillmans method exist.
Here a rolling stroke is used after the
vibration.
DIAGRAM
Which method of brushing is indicated depends on various
factors
1. Patients clinical situation e.g state of gingival and
periodontal tissue in regards to health or disease e.g
1. Tissue state such as cantour, tone, texture ie
whether gingiva is normal fibrotic odematous or
enlarged.
2. Papillary cantour such as open or filled embrances
spaces
3. Pocket or sucular dept
2. Anatomical limitations – seize & contour of dental arch,
position inclination and contour of the Indus teeth.
3. Presence of edentulous areas and in the type of
replacement pursed for the missing teeth
4. Patients personal situation – Manual dexterity,
Motivational level
PLAGUE CONTROL

Most periodontal disease & tooth loss can be

prevented because they are caused by local
factors that are accessible, correctable and
controllable. There are no forms if periodic
disease in which the removal of local irritants &
prevention of their recurrence do not
1. Reduce the severity of the disease
2. Lesser the rapidity of the destructive process
3. Prolong the usefulness of the neutral dentition.
Preventive periodontics is a multifaceted co-
operative programme of procedures performed
by the dentist & patient to present the onset
progression and recurrence of periodontal
disease. Plague control ie retarding or
preventing the accumulation of dental plague
and other deposits on the tooth surface is the
keystone of preventive periodontics.
Supplements to Toothbrushing (Interdental
cleaning materials)
Dental floss, interdentally rubber, wooden
cleansers, water irrigation.
Periodontal disease is primarily due to bacterial
products causing breakdown of the periodontal
tissue.
Method of prevention can be directed towards
eliminating or controlling the bacterial which
produce the disease or increasing the resistance
of the periodontal tissues to these bacterial
products.
Methods of preventing periodontal disease are
directed at preventing or controlling plague
formation and or at increasing the tissue
resistance to disease.
The oldest approach to plague control are the use
of detersive foods its mechanical removal by
brushes or other ands definitions of oral
hygiene measures methods and procedure for
the removal of soft deposits from the teeth and
surrounding tissues it can be divided into two
types natural & mechanical. Detersive foods: It
has been assumed that hard or detersive foods
have a valuable chewing action & remove
plague and food debris from the teeth &
surrounding tissues.
However it has been proved that the chewing of
detersive food does not appear to have any
significance plague preventing effect in man.
Mechanical oral hygiene: The classic method of
cleaning the teeth is by regular use of a tooth
brush and tooth paste or other devices such as
chewing stickc, wood points or dental floss. It
has beem shown that careful toothbrushing can
keep the teeth free from plague and maintain the
gingivae in a state of clinical health (Loe et al
1965, Thailade et al 1966).
As far as maintaining gingival health is concerned
the efficiency of tooth brushing may be even
more important than its frequency since
thorough cleaning once every second day will
maintain gingival health (Kelner et al 1973,
Lang et al 1973)
METHODS OF TOOTH BRUSHING
BRUSHING SEQUENCE & TIMINIG 10 SEC PER AREA

1. The bass
2. The roll
3. The scrub-brush
4. Charters method of tooth brushing are
methods most commonly used.
5. Mini scrub method (technique)
Bass technique: The bristles are applied to the
tooth at a 450 angle point apically so that the
bristle tips enter the gingival sulars. The brush
is activated with a slight vibrating movements.
Roll Method: Bristles are pointed towards the apex
of the tooth on the overlying gingiva and
pressure is applied. The bristles a then swept
from the dental gingival on the tooth.
Advantages: Considerable pressure may be
applied to the tooth without the risk of gingival
recession and abrasion.
Disadvantages:
1. Require considerable manual dexterity and a
degree of wrist flexibility and therefore not
suitable for those with manual limitations e.g pt
with arthritis.
2. Does not clean the gingival area subgingival
region and considered the least effective of
current techniques.
CHEMICAL PLAGUE CONTROL
Antibacterial agents and Antibiotics
Antibacterial agents: Chlorhexidine was the most
effective & further studies have shown that twice
daily minses with 0.29. Chlorhexidine was the
most effective & further studies have shown that
twice daily minses with 0.29. Chlortexidine
gluconate will inhibit plague formation and the
development of gingivitis (Loe & Liott 1970)
(Stains the tongue) long term use has clinical
advantages without substantially undesirable
side effects the early hope that it might provide
the perfect panacea have largely warred. It is
used as a short term adjacent to periodontal
therapy.
ANTIBIOTICS
Penicillin & tetracycline have been shown to inhibit
plague formation in animals.
1. Broad spectrum antibiotics will eliminated all
plague microorganism whilst latest research as
shown that specific organisms are involved in
the initiation & progress of periodontal disease
2. Hypersensitivity to drugs
3. Developing resistant strains make antibiotics to
eliminate plague undesirable.
Enzymes: Matrix of dental plague consist of large
extra cellular poly saccharine.
The scrub technique is a modification of the
Bass method. The brustles are applied at
might angles to the tooth surface and
activated by a back and forth hospital
scrubbing strokes.
Charters techniques: Bristles are at right
angle to the long axis of the tooth, gently
forced interproximatally and vibrated to
clean and massage the gingival margin
and interproximal areas.
INTERDENTALLY CLEANING AGENTS
Periodontal disease occurs more commonly and
causes more destruction in the inter depend
areas than on the facial & lungual aspects of
the teeth.
1. Toothpick was the 1st recorded oral hygiene
and is still probably the most commonly used
device for interdental cleaning.
Devices for interdental cleaning include
a. Various types of toothpicks
b. Interdental brushes
c. Rubber & plastic tips of various size & shape
d. Waxed and unwaxed dental floss
NUTRITION: The soft tissue reflect the metabolic
stains of the body. Often in quick and more
dramatic ways than comparable tissue located
else where in the body. The temperature
humidity & food available to the oral cavity also
promote the prolific growth of varied types of
micro-organism. Pinborg et al in Bangalore
showed that Kiwashiorker children her more
periodental disease.
GINGIVAL MASSAGE
Has long been advocated as a means of
increasing local resistance and can be produced
with a toothbrush, wood sticks, cloth or various
special gadgets.
It increases the amount of keratinization of the
attached gingival epithelium. Merzel et al 1963)
and increases the rate of cell turnover in gingival
epithelium and connective tissue McHugh 1967).
Although massage has been shown to cause
specific changing in the gingivae its value is not
established.
NUTRITION
Divided into those related to soft tissue-oral
mucosa periodontal membrane sensory papillae
those related to mineralized tissue EDC. Scurvy,
Pellagra, ariboflaviousis & deficiency of Vit B
complex. In general are all states for which
classic descriptions of the oral signs have been
widely published in textbooks on nutrition and
oral medicine. Although nutritional deficiencies
with oral signs are still very common in
underdeveloped countries they do not occur
frequently in countries with higher economic
standing except in groups with extenuating
circumstances.
TWO METHODS
1. Interference with plague bacteria attachment
mechanism or to disaggregate established plague.
This is directed at the extra cellular poly sacharides.
Dextranase and mutanase used. Not successful.
2. To potentiate naturally present antimycrobial activity
of saliva. Lactoperoxidase is a saliva catalysis with
the help of H202 produced by bacterial.
3. Hypothio cynate from salivary thio cynate which is
claimed to have effect on bacteria growth. Enzyme
used is amyloglucosidase and glucose oxidase
produce sufficient Hydrogen peroside in saliva to
activate lactoperoxidase labouratory study effective
but clinical study inconclusive.
It has been thought that the enzyme dextranase will
sever the linkages in xtrans which are one type of
glucose polymers found in plague. Feeding this
enzymed in food to hamsters resulted in marked
reduced in plague formation and in caries. However
clinically it is not effective because of the high degree
of specificity of the enzyme.
Surface-Acting agents: (Sulphonated polystyrene or
silicone) Have not been successful.
Fluoride rinses (i.e Naf or SnF2) rinses have been shown
to inhibit plague formation. This property of the minses
have been attributed to reduction in adhension
between the bacteria & the tooth enamel.
INCREASING TISSUE RESISTANCE
Another way of preventing periodontal disease is
by increasing the tissue resistance. The
resistance of the periodontal tissues to disease
varies considerably between individuals and to
a lesser extent between certain racial & ethnic
groups. This differences have not been
satisfaction.
Plague control by oral irrigation by the use of water
irrigation devices. This may be useful as an
adjunct to toothbrush but on its own does not
prevent dental diseases. Solution
1. Oxygenating agent
2. Quaternary ammonium
PLAGUE CONTROL BY HARD
FIBROUS FOODY

Hard fibrous foods reduce plague

accumulate and tooth surface & gingivitis
exposed to their mechanical cleaning
action & mastication. Course fibrous foods
also provide functional stimulation required
for maintenance of the periodontal
ligament & alveola bone.
PLAGUE CONTROL BY LIMITATION OF
SUCROSE CONTAINING FOODS

Note: Digestion of sucrose increases plague

formation. This fact is of greatness clinical
importance.
The major component of the intercellular matrix of
plague is the poly sacharride dextran.
The bacteria require sucros to form dextran:
reducing sugar intake reduces plague formation.
OTHER PREVENTIVE MEASURES AGAINST
GINGIVAL PERIODONTAL DISAESE

Through supragingival and subgingival

cleaning & sealing should induce, removal
of plague, stain & calculus & the
smoothing & polishing of the surfaces of
the teeth, restovations and prostheses by
means of rubber cups, dental floss, and
prosthesis by means paste. Source of
local irritation over hanging improperly
contoured restorations races of food
impaction should be corrected.
NUTRITION: Dietary deficiencies affect the healthy of
the gingival tissues and the periodontal tissues
surrounding the teeth & lack of its most acute form.
Conditions that may affect or enhance accumulation &
growth of plague or that may interfere with its
removal will contribute to the progress of
periodoental disease.
LOCAL ENVIRONMENTAL EFFECT
a. Tooth anatomy & position
b. Anatomic conditions resulting in mouth breathing
c. Anatomic conditions resulting in food impractical
d. Soft tissue relationship
e. Prosthodatic restorative appliances
f. Occlusal traumalism
THE ROLE OF SYSTEMIC FACTORS
Many secondary etiologic factors exert their effect by causing
the periodontal tissues to be less resistant to the
challenge posed by the presence of micro-organism.
In induces it
1. Diabetes mellitus
2. Downs syndrome
3. Papillor – Latevre syndrome
4. Defect in the phagocyte cells
5. Pregnancy and puberty
6. Aging
7. Nutrition
8. Humans
9. Debilitating disease
10. Psychosomatic disorders
11. heredity
MICROBIAL PLAGUE (DEFINITION)
Is a product of microbial growth, tenaciously
attached to the surface of the tooth & adjacent
gingiva & exhibiting a definite microscope
architexture
CHEWING STICK
The chewing stick is widely used for cleaning teeth
in Africa. In Nigeria it is used by 90% of the
population.
It is cut from the stems of roots of a variety of
plants and the end of the stick is crushed
between the teeth to produce fray fibers. The
fubrice and of the stick which may have a spicy
taste is rubbed vigovously against the teeth and
gingivae often for prolonged periods.
TYPES IN NIGERIA
1. Fagara zanthoxyloides Lam (Ata orin)
2. Masslari accumulate (GiDon)
3. Bullock Hoyle (Pako Ijebu)
4. Vernonia amygdalina Ewuro)
5. Garcinia Kola (Orogbo)
6. Anogeissus schimperi (Pako Dudu)
Most of these chewing sticks have an antibacterial
effect. The fact the Fagara Zanthoxyloides
(Ata) inhibits the growth of streptococcus
mutans has aroused the interest of many
researchers. Akpata.
Also the chewing sticks have been found to
have a stabilizing effects in the red blood
cell membrane Isaac – Sodeye 1975,
Elwin-lewin 1982.
Its effectiveness in the removal of dental
plague has been proved by many research
work (Berit. Olsson) 1978 and even
recommended for use in preventive dental
program.
PREDICTORS OF CARIES
1. Baseline epidemiological factors & method
2. Morphology of the tooth – Occlusal surface,
fissue
1. Fissure retentiveness
2. Occlusal morphology
3. Biological factors methods
1. Microbial analysis & tests
2. Biochemical activity of plague microses
3. Salivary factors
4. Diet –Diet Chart
5. Age
6. Race
7. Sex
8. Socioeconomic factors opposite in Nigeria
DIP SLIDE METHOD USED IN THE CLINIC
Undiluted saliva is run over a dip slide exacted
with a slightly modified Rogosa S.L. agar for
lactobacilli. Growth of colonies is compared with
a standard illustrate (Dentocult).
DENTOBUFF TEST
Saliva is added to an acid of pH3 containing a
colour indicators and the result is compared with
a standard. Buffering capacity is related to
salivary flow rate and age.
FISSURE RETENTIVENESS
Four point scale
1. Well coalesced fissure allowing no penetration of an
explorer.
2. Slight or swallow penetration
3. Definition penetration to a considerable depth
4. A deep narrow fissure permitting penetration to the
base and providing resistance to withdrawal in
stickness.
If the penetration and resistance were sufficient to satisfy
the criteria for decay or if the surface is restored then
no score was assigned. All posterior teeth are
examined and the mean retentiveness is calculated
from individual surface scores.
MORPHOLOGY SCORES

1. Flat anatomy
2. Normal anatomy
3. Steep Cuspal indices
All posterior teeth were examined and the
mean retentiveness is calculated from
individual surface scores.
MINIMAL INTERVENTION DENTISTRY

A new approach in Dentistry

G.V Black 1st revolution – Standardized
instrumentation, Standardize material
Failure rate of an excellent amalgam is 15yrs
Public opinion on dentistry – Not happy with
dentists.
a. Drilling b. Infection c. Sound of the
drill d. Horizontal life.
They are not happy with the invasive procedure.
90% of patients interviewed will come often it
procedures are not associated with the abov
2nd Generation – Recognized a need to
change restoration dentistry

What is minimum Intervention (MI)

1. Disease risk assessment
2. Earliest disease detection
3. Minimal intervention
How do ART compare to amalgan
Amalgann requires cavity preparation and u need
equipment & electricity ART need non of
these.
HEALOZONE KAVO
Painless: This involves ozonisation of the caries
cavity. Ozone is very poisonous but the
equipment when titled around the tooth creases
a vacuum and it is only then that ozone will flaw,
so there is no danger of other tissue coming in
contact with the ozone.
Gloss ionomer needs a little moisture. It is good
and useful in time management.
Consideration: Lifestyle, General health, Socio
economic factors, patient compliance.
Minimal intervention considers the socioeconomic
factors and the where the pt hoes
Minimal intervention focus on the disease
EVIDENCE BASED PRACTISE (MI)

This is different from orthodox practice.

Systematic Review (Develop a protocol formulate
questions)
1. Gather all evidence
2. Steps Formulation the key glessting, define
inclusion and excleepsy, defining reach
strategy.
Teach (EB) evidence based practice
When we come across cases which are not to
clear to us. We should handle the case using EB
and we send the students especially post
graduates to do a search and fill the form below
them the lecturers have to sign the form. The
post graduate student should do literature
Diet log or Chart
Date Time Food Fluid
Amount

Any time we teach students before we teach them

they come with some knowledge of the topic.
Thank you for listening