Chapter 9 N Introduction to Public Health Dentistry
FUNCTIONS OF PUBLIC HEALTH DENTISTRY
The services provided to the community by public health dentist
include:
1. Preventive Services
a. Application of topical fluorides
b. Pit and fissure sealants application
c. Promotion of water fluoridation
d. Defluoridation
2. Public Health Training
a. School teacher training program.
b. Training of the health care worker about dental health
and oral hygiene measures.
3. School Dental Health Program
a. Topical fluoride application.
b. School mouth rinsing program.
c. Teaching of oral hygiene methods and importance of
dental health to children.
d. Education about safe play areas for children to school
authorities.
e. Knowledge about junk foods and effects of cold drinks
to children.
4. Dental Public Health Program
a. Examination and treatment of community through
dental health program.
b. Screening program for oral cancer.
c. Dental health check up and treatment like extraction,
filling, oral prophylaxis of industrial workers through
camps.
5. Dental Health Education
a. Education about dental health and its importance to
community, industrial workers and social
organizations.
b. Imparting knowledge about oral health to expectant
mothers.
c. Knowledge about injury to teeth and importance of
mouth guards.
d. Education to geriatric population about oral health.
e. Informing people about ill effects of tobacco and
smoking.
f. Educating public about methods of prevention of
dental diseases like dental caries, periodontal disease
and oral cancer.
g. educating care takers about maintenance of oral health
in special needs patients.
h. parent counseling for pre school and school children.
6. Program Administration and Promotion
a. Helping the State / Central agency in conducting
epidemiological studies regarding oral diseases.
b. Conducting surveys to determine dental needs of the
population.
c. Providing dental health knowledge to state agencies
or education department.
The economic costs of oral diseases are also considerable,
although difficult to quantify. They result from direct costs of
95
treatment within the health care systems and out-of-pocket co-
payments from patients, and from indirect costs such as work-
loss, absenteeism from school, travel expenses, and the total
societal burden through loss of economic productivity.
Besides dental decay, in a number of countries oral cancers,
trauma to teeth and craniofacial trauma, oral manifestations
of HIV-infection and noma (cancrum oris) are also important
oral public health problems. Oral cancer is one of the ten most
frequent cancers worldwide with great variability between
different regions. In some countries in Asia, oral cancer accounts
for up to 50 percent of all cancers. Three quarters of oral cancer
cases occur in developing countries. Noma shows the strongest
links to poverty and general medical and social deprivation
and has a large impact on the affected individuals.
Oral diseases are major public health problems on a global
level. Their most common effects, orofacial pain and tooth loss,
are known to almost every human being. Budget limitations,
lack of infrastructure, resources and knowledge, lack of capacity,
different priorities, or even unwillingness to act, are some of
the reasons for the widening gap between need, services
provided, and effective policies that address oral health
problems.
PUBLIC HEALTH MILESTONES IN
INDEPENDENT INDIA
1947: Ministries of health and Director-General of Health
Services established at the Center and States. The Indian
Nursing Council Act passed
1948: India joined the World Health Organization and
the Employees State Insurance Act passed. The Dental
Council of India established under the Dentist Act
1949: The Registrar-General India appointed in the
Ministry of Home Affairs. WHO opened its South East
Asia Regional Office in New Delhi. The Indian Pharmacy
Council and Family Planning Association of India
established
1950: India became a Republic in the Commonwealth.
The Planning Commission was set up by the Government
of India
1951: The beginning of the first Five Year Plan. The BCG
vaccination programme launched in the country
1952: The Community Development Programme
launched for the all-round rural development. The Central
Council of Health constituted. First Primary Health Center
set up
1953: The National Malaria Control Programme and
National Extension Service Programme for rural
development started. A nation-wide family planning
program started. A committee appointed to draft a Model
Public Health Act for the country
1954: The Contributory Health Service Scheme (Central
Government Health Scheme), the Central Social Welfare
96 Section 2 N Dental Public Health
Board, the National Water Supply and Sanitation
Programme and the National Leprosy Control Programme
started. The Prevention of Food Adulteration Act passed
by Parliament
1955: The National Filaria Control Programme
commenced. The National TB sample survey conducted.
1956: The Second Five Year Plan started. The Model
Public Health Act published and the Central Health
Education Bureau established in the Union Health
Ministry. The Indian Medical Council established
1957: Influenza pandemic swept the country. The
Demographic Research Centres established in Calcutta,
Delhi and Trivandrum
1958: The National Malaria Control Programme
converted into National Malaria Eradication Programme.
The National Development Council endorses Panchayati
Raj. The National TB survey completed
1959: The Mudaliar Committee appointed. A Central
Expert Committee recommended eradication of small pox
and cholera. Rajasthan introduces Panchayati Raj.
National Tuberculosis Institute at Bangalore established
1960: The School Health Committee and the National
Nutrition Advisory Committee constituted
1961: The Third Five Year Plan launched. The Mudaliar
Committee report published. The Central Bureau of
Health Intelligence established
1962: The Central Family Planning Institute established
in Delhi. The National Smallpox eradication Programme
and the School Health Programme initiated, the National
Goitre Control Programme and the District Tuberculosis
Programme launched
1963: The Applied Nutrition Programme was launched
with aid from UNICEF, FAO and WHO. The National
Institute of Communicable Diseases (formerly Malaria
Institute of India) inaugurated and the National Trachoma
Control Programme started. A Drinking Water Board and
the Chadah Committee established
1964: The National Institute of Health Administration and
Education opened
1965: Reinforced Extended Family Planning Programme
launched. The Mukherjee Committee set up
1966: A separate department of Family Planning created
under the Health Ministry. The Population Councils
International Postpartum Family Planning program started
in Delhi and Trivandrum
1967: The Central Council of Health recommended levy
of health cess on patients. The Jungalwalla Committee
set up
1968: The Small Family Committees Report submitted.
Govt. appointed the Medical Education Committee
1969: The Fourth Five Year Plan launched. The Nutrition
Research Laboratories became the National Institute of
Nutrition. The Central Births and Deaths Registration Act
promulgated
1970: The Drugs (Price Control) Order promulgated. All
India Hospital (Post-partum) Family Planning Programme
started. The Population Council of India and the Central
Council of Indian Medicine (Ayurveda, Unani and Siddha)
formed. VHAI (Voluntary Health Agency of India)comes
into being.
1971: The Family Pension Scheme (FPS) for industrial
workers came into force. The Medical Termination of
Pregnancy Bill passed by the Parliament. Uni-purpose
Health Workers converted into Multi-purpose workers.
1972: National Service Bill passed. The National Nutrition
Monitoring Bureau set up
1973: National Programme of Minimum Needs was
incorporated in the Fifth Five Year Plan. The Government
envisaged a scheme for setting up 30-bedded rural
hospitals; one such hospital for every 4 primary health
centres. The Kartar Singh Committee recommended a
new cadre of health workers called Multi-purpose Health
Workers. The Central Council of Homeopathy was set
up. The Kartar Singh Committee was established
1974: The Fifth Five Year Plan launched. Parliament
enacted the Water (Prevention and Control of Pollution)
Act
1975: India became smallpox-free. A Revised strategy for
NMEP accepted. The Integrated Child Development
scheme launched. The National Childrens Welfare Board
set up. The Cigarettes Regulation (Production, Supply and
Distribution) Act passed by the Parliament. The Srivastava
Committee set up
1976: The Equal Remuneration Act promulgated
providing for equal wages for men and women for equal
work. A new Population Policy introduced. A National
Programme for Prevention of Blindness formulated. The
Central Council for Yoga and Naturopathy established.
In 1975-76 National Cancer Control Programme was
launched.
1977: The National Institute of Health and Family
Planning formed. The Rural Health Scheme launched.
Community Health Volunteers (Guides) scheme taken up.
Population Control and Family Planning was put in the
concurrent list. WHO adopted the goal of Health for All
by 2000 AD
1978: A Bill on Air Pollution introduced in the Lok Sabha.
The Parliament approved the Child Marriage Restraint
(Amendment Bill fixing the minimum age of marriage 21
years for boys and 18 years for girls
1979: The World Health Assembly endorsed the
Declaration of Alma Ata on primary health care
 Chapter 9 N Introduction to Public Health Dentistry
1980: Smallpox officially declared eradicated from the
entire world by the World Health Assembly. The Sixth
Five Year Plan launched
1981: The census taken. WHO and Member countries
adopted the global strategy for Health For All. The Report
of the Working Group on Health for All, set up by the
Planning Commission, published.
1982: The Govt. of India announced the National Health
Policy. Amendment done on the Drugs and Cosmetics
Act of 1940. National Mental Health Programme was
started
1983: India launched a national plan of action against
avoidable disablement, known as IMPACT India. The
National Leprosy Control Programme became the
National Leprosy Eradication Programme. Guinea-worm
Eradication Programme launched
1984: The Bhopal Gas tragedy, the worst ever industrial
accident killing at least 2500 people and no fewer than
50,000 affected. The ESI (Amendment) Bill approved by
Parliament and the Workmens Compensation
(Amendment) Act came into force
1985: The Seventh Five year Plan launched. The
Universal Immunisation Programme started. The Lepers
Act, 1898 was repealed by the Parliament. A separate
Department of Women and Child development set up
under the newly created Ministry of Human Resource
Development
1986: The Environment (Protection) Act and the
Consumer Protection Act were promulgated. National
Drug Policy announced. 1st AIDS case detected in country
(India).
1987: The New 20 Point Programme launched. A
worldwide safe motherhood campaign was launched
by World Bank. National Diabetes Control Programme
and National AIDS Control Programme initiated. The
Mental Health Act passed. The Drugs (Price Control)
Order released
1988: Hospitals and Other Institutions (Redressal of
Grievances of Employees) Bill passed
1989: Blood Safety Programme was launched. The ESI
(Amendment) Act modified
97
1990: Control of Acute Respiratory Infection
(ARI) Program initiated as a pilot project in 14 districts
1991: India stages the last decadal Census of the Century.
Population of India was 844.32 million. Pre-natal
Diagnostic Techniques (regulation and prevention of
misuse) Act enacted
1992: Eighth Five Year Plan launched. Child Survival and
Safe Motherhood Programme (CSSM) launched in the
country. The Infant Milk Substitute, Feeding Bottles and
Infant Foods (Regulation of Production, Supply and
Distribution) Act passed. The State of Indias Health
Report by VHAI released. Indias first National AIDS
Control Programme (1992-1999) was launched, and
National AIDS Control Organization (NACO) was
constituted to implement the program
1993: The dentists (amendment) act, 1993 [2nd April,
1993]. An Act further to amend the Dentists Act, 1948.
The Indian Association of Public health Dentistry
established
1994: Return of Plague after 28 years of silence in few
parts of the country. The Transplantation of Human
Organs Bill passed. The first Heart Transplantation Surgery
in the country done at AIIMS, New Delhi. Malaria
epidemic strikes Rajasthan. Swaminathan Committee
Report submitted
1995: The revised Rational Drug Policy announced.
Malaria epidemic strikes Assam. The Persons with
Disabilities (Equal Opportunities, Protection of Rights and
Full Participation) Act passed
1996: Dengue epidemic in Delhi. Malaria strikes again
many northern States of India. The Central Govt.
publishes the list of essential drugs. The Revised National
TB Control Programme initiated. The Supreme Court
orders the government to set up the National Council of
Blood Transfusion
1997: The National Illness Assistance Fund launched.
Delhi government enacts Anti-Smoking Bill
2003: 1st National oral health survey and fluoride
mapping was published
2008: Ban on tobacco smoking act. Smoking in public
places banned.
 Epidemiology of Dental
10 Caries
Dental caries is a disease of civilization, i.e. the more developed
a country the greater the incidence of caries. Caries is a Latin
word meaning rottenness. In ancient humans, caries was located
mainly at cementoenamel junction or in the cementum, in
contrast to modern times where dental caries is primarily located
in pits, fissures and in smooth surfaces of teeth.
DEFINITION
It is defined as progressive, irreversible microbial disease of
multifactorial nature affecting the calcified tissue of the teeth,
characterized by demineralization of the inorganic portion and
destruction of the organic portion the tooth.
EPIDEMIOLOGY
Studies have shown that dental caries remained low until the
17th century. Skeletal data shows that skulls of men from Pre
Neolithic period [12000 BC] did not exhibit dental caries but
skulls from Neo-lithic period [12000-3000 BC] contained
carious teeth. The prevalence of dental caries increased
dramatically towards the end of 17th century, and continued
to increase until the early 1970. The only break in this increase
came during the mid 40 and early 50s and this coincided with
the reduced availability of sucrose as a result of food rationing
imposed during the World War II.
Dental caries is a universal disease affecting all geographic
regions, races, both the sexes and all age groups. The prevalence
of dental caries is generally estimated at the ages of 5, 12, 15,
35 to 44 and 65 to 74 years for global monitoring of trends
and international comparisons. The prevalence is expressed in
terms of point prevalence (percentage of population affected
at any given point in time) as well as DMFT index (number of
decayed, missing and filled teeth in an individual and in a
population).
Since the mid 1970s reports from developed countries world
wide have shown that the prevalence of dental caries in children
and adolescent has declined. WHO global data bank confirms
a decline in the prevalence of dental caries in children and
CM Marya
adolescents in developed countries, and there is an increase in
dental caries in some developing countries (Fig. 10.1).
There is now increasing evidence that incidence of caries
levels has declined in developed countries in the past 20 years.
Dental caries is now largely a disease affecting the deprived
section of society. Recent reports also confirm that in many
communities, 80 percent of dental caries is occurring in 20
percent of the population.
The incidence of dental caries has been studied in American
white populations. The results show dental caries to be most
prevalent chronic disease in this population. The disease affects
all regardless of location, sex, age, or social stratum. The disease
starts in young people just as soon as teeth erupt. About 90
percent of youngsters are affected by age 14. As mentioned
earlier however, the incidence of caries is decreasing in this
young population in the U.S. and in other Western countries.
This downward trend is explained by increased fluoridation of
community water supplies and by increased attention to regular
care at dental offices and at home.
Caries Incidence is Tied to Soft, Sugar-laden
Western Diets
Isolated populations who have not adopted eating habits of
the West have long been known to have decreased incidence
of dental caries. Eskimos, some African natives, and inhabitants
of rural India are examples of such immune populations.
Examination of teeth shows considerable abrasion of the
occlusal surfaces indicating consumption of a coarse, abrasive
diet. It is not uncommon to observe teeth abraded down to
the contact points between adjacent teeth. There is no doubt
to explain the fact that dental caries in these primitive
populations is restricted to the interproximal areas below contact
areas where food impaction may occur.
TRENDS IN DENTAL CARIES
Dental caries afflicts humans of all ages and in all regions of
the world. It is a disease that may never be eradicated because
 Chapter 10 N Epidemiology of Dental Caries 99
of complex interplay of social, behavioral, cultural, dietary and people are switching from traditional starchy staple foods to
biological risk factors that are associated with its initiation and refined carbohydrates. The caries rate in each of these individual
progression. countries also depends on the individuals cur rent
When we evaluate global distribution of caries in the socioeconomic status. The sophistication and development of
twentieth century, three patterns evolve: dental services depends on access and availability of dentists.
The first is seen mainly in rural China, and Africa and remote For most of these countries in rural areas dental care if available
areas of South America. In these societies, there is still high consists of palliative services and extraction, while replacement
mortality rate, there is poor infrastructure roads are nonexistent of lost teeth with a prosthesis is exceptional. Populations in
or poorly maintained. Water sources are not protected and urban areas have greatest access to care, but the quality and
medical care is available only in cities (Sugar is available in the sophistication of care depends on the socioeconomic status of
cities and caries is a problem as people age). The prevalence the individual seeking care.
and severity of dental caries are usually higher in urban areas The urbanized nations of Asia and Central and South
compared with the lower socioeconomic groups living in rural America need to develop national preventive programs to
communities as shown in Table 10.1. combat the rising caries rate. These preventive programs must
Sado-Infirri in a World Health Organization report not only present known scientific facts, but also confront the
commented that Zaire and Malavi had low caries rate and little deep seated beliefs of the people that have been handed down
tooth loss. Countries such as Tanzania, Ethiopia and Ghana
from folk lore.
can be included into this group (Table 10.1). Many persons
The third pattern is found in North America, Australasia,
from rural Africa and China have little access to dental care and
Europe and Japan where the peoples oral status is characterized
several studies have reported higher caries experience in urban
by a decreasing caries rate in children and increasing number of
as opposed to rural areas.
retained teeth in older adults.
The second pattern of dental caries is found in newly
This change is a relatively new phenomenon, however,
industrialized countries such as Taiwan, India, Chile, Uganda
and Thailand as given in Table 10.2. In these countries, there because at the turn of the century, most people regard dental
is evidence of an increasing caries rate in children and in adults. care as a luxury rather than a health service, and individuals
There is also an increasing rate of edentulousness in the older used dentists only when they were experiencing pain.
population. There are several factors that have attributed to decline in
The relationship between increased industrialization, dental caries in these industrialized countries Table 10.3. These
consumerism, consumption of refined carbohydrates and sugars include the availability of fluorides especially fluoride dentifrices,
and caries rates is well known with increasing urbanization, a demand for dental care associated with a changed attitude
towards preserving natural teeth and preventive approach by
Table 10.1: Caries rate in 12-year-old general dentist.
However, there are still substantial amount of caries in the
Year Country DMFT
population, but these high rates are found only in some high
1987 Sudan (Rural) 0.2 risk group as follows;
1994 Sudan (Urban) 1.7 Developmentally disabled
1991 Nigeria 0.7 Mentally retarded
1987 Zaire 0.4 Immigrant groups
1981 Botswana 0.5 Low socioeconomic group individuals
1986 Kenya 0.9
The World Health Organization Global Data Bank (1995)
1997 China 0.8
1986 Tanzania 0.7 shows that out of 178 countries for which data is available 25
percent were categorized as having very low levels of dental
caries (DMFT 0.0 to 1.1), 42 percent as low (DMFT 1.2 to
Table 10.2: Increase in caries rate in 12-year-old
2.6), 30 percent as moderate (DMFT 2.7 to 4.4) and 13 percent
Year Country DMFT Change as high (DMFT 4.5 to 6.5) and 2.1 percent countries as very
high, i.e. 6.6 as shown below in Table 10.3.
1979-1992 Taiwan 0.9 4.3 + 477%
1972-1994 Thailand 0.9 1.6 + 177%
1960-1991 Chile 2.8 5.3 + 189% Table 10.3: Decrease in caries rate in 12 years
1972-1992 Mexico 2.5 5.1 + 204% Year Country DMFT
1961-1993 Lebanon 1.2 5.7 + 475%
1962-1995 Jordan 0.2-3.3 +1650% 1973 - 1992 England 4.8 1.2
1965-1983 Peru 3.2-5.9 +184% 1975 1993 Japan 5.9 3.64
1967-1993 India 1.23.8 +316% 1971 1994 USA 6.65 3.08
1966-1972 Uganda 0.4-2.4 +600% 1960 1992 Switzerland 7.67 1.12
100 Section 2 N Dental Public Health

REASONS FOR CARIES DECLINE AND RISE European countries like the Netherlands, 5- to 6-year-old
children had 18 DMFS and 12-year-old children had 8 DMFT.
Common Factors Contributing to the Decline of Since the 1970s, a dramatic decrease in the prevalence of
Dental Caries dental caries has occurred in developed countries. During the
1. Fluoridation of water supplies 1990s in the Netherlands, the mean DMFS in 5-year-old
2. Use of fluoride supplements children was only 4, whereas > 50 percent of these children
3. Use of fluoride dentifrices were cavity free.
4. Availability of dental resources In this same population, the DMFT for the 12-year-old
5. Increased dental awareness children was only 1.1 percent and 55 percent of the children
6. Adoption of preventive approach by the practitioner were cavity free. The distribution of the children according to
7. Changes in diagnostic criteria their caries experience is skewed, and 60 to 80 percent of the
8. Widespread use of antibiotics decay is found in 20 percent of the population in both Europe
9. Herd immunity and the United States. However, evidence indicates that the
10. Decrease in sugar consumption. favorable trends in dental caries have stabilized.

Reasons for Rise in Dental Caries
1. Increase in sugar consumption in underdeveloped countries
2. Lack of dental resources
3. Socio economic factor
4. Lack of water fluoridation
5. Lack of preventive dental health programs
DENTAL CARIES PANDEMIC
Caries is both diet-dependent and fluoride-mediated and is
amenable to prevention and management at both the
individual and population levels. It is also readily treatable
through conventional surgical interventions and dental repair.
Therefore, the extent and severity of its consequence for
individuals, communities, and nations varies by the availability
and balance of these factors. As a result, there are marked
disparities in caries experience, treatment experience, and
disease consequences both between countries and within
countries. BL Edelstein (2006) justifies that term pandemic
is fitting because those who are affected by caries and have
little or no access to care number in the hundreds of millions,
reside on all continents and in most societies, and experience
significant consequences of pain and dysfunction that impair
their most basic functions of eating, sleeping, speaking, being
productive and enjoying general health as defined by the
World Health Organization.
CARIES INCIDENCE IN EUROPE
Caries is as old as mankind, and the prevalence of caries is
reported to increase temporarily in relatively affluent periods.
In Europe, for example, there was an increase in caries during
the Roman occupation, probably as a result of increased use
of cooked foods. These early increases were minor compared
to the dramatic increase that started from the time that sucrose
was imported from the Caribbean islands to Europe. This
increase continued until the 1960s, by which time dental caries
was considered rampant. At that time, in non-fluoridated
CARIES INCIDENCE IN THE UNITED STATES
Dental caries is one of the most common childhood diseases
in the United States. Studies have shown that in children aged
5 to 9 year, 51.6 percent have had 1 filling or caries lesion; of
those aged 17 year, the proportion is 77.9 percent; 85 percent
of adults aged >18 year have had caries. However, in the last
quarter of the 20th century, the percentage of adults with no
decay or fillings increased slightly from 15.7 to 19.6 percent in
that aged 18 to 34 year and from 12 to 13.5 percent in those
aged 35 to 54 year. Reasons for the decline can be partly
attributed to increased use and availability of fluoride. These
trends, however, were not found in older adults during this
period; in the older adult population, the percentage of teeth
free of caries and restorations declined from 10.6 to 7.9 percent
in that aged 55 to 64 year and from 9.6 to 6.5 percent in those
aged 65 to 74 years.
US findings by the Centers for Disease Control and
Prevention (CDC) released in August 2005 reveal high ongoing
prevalence of dental caries in children, with 27 percent of
preschoolers, 42 percent of school-age children, and 91 percent
of dentate adults having caries experience.
Caries is increasing in the Third World and in the US elderly.
While decreased incidence has been observed in the US young,
caries rates are increasing in Third World countries as they
adopt Western diets. It is also increasing in the US elderly. In
this population, retention of teeth into old age with
accompanying exposure of root surfaces, has led to an increase
in cemental caries.
INDIAN SCENARIO
Dental Caries has been consistently increasing both in prevalence
and severity since last five decades. In the year 1941, its
prevalence was reported between 40 to 50 percent with an
average DMFT of 1.5 (Table 10.4). In 1980s the point prevalence
increased to about 80 percent in children with an average DMFT
of 2 to 6 at the age of 16 years in different regions of the country.
The point prevalence in 10 to 15-year-old children of Delhi was
found to be 39.2 percent and DMFT was 2.61 in the year 1992
 Chapter 10 N Epidemiology of Dental Caries 101
Table 10.4: Prevalence of dental caries in India

Author Year Age Place Prevalence of caries (%)

Shourie K L 1941 12 Delhi (urban) 54.8

Kokil et al 1951 Gujrat 68.7
Sehgal 1960 4-18 Bombay 90.0
Dutta 1965 Less than 12 Dumdum 67.1
Gill et al 1968 12 Lucknow 99.0
Tiwari and Chawla 1977 15 Chandigarh 86.6
Damle et al 1982 15 Naraingarh (Rural) 77.2
Tiwari et al 1985 15 Bombay (Urban) 96.0
Mehta et al 1987 15 Dehradun 45.0
Thaper et al 1989 12 Rajasthan (Rural) 31.4
Gupta et al 1993 12 New Delhi 87.0
Chopra et al 1995 15 Delhi (Urban) 20.9
Gopinath et al 1999 12 Tamil Nadu 61.2
Singh et al 1999 12 Faridabad (rural) 33.1
Goel et al 2000 12 Puttur 59.6
Kulkarni and Deshpande 2002 11-15 Belgaum 45.12
Sudha P 2005 5-7 Mangalore 94.3
11-13 82.5
Joshi N 2005 6-12 Kanyakumari 77
Goyal A 2007 6 years Chandigarh 79.74
12 80
15 87

(Prakash et al, 1992). As per the WHO Oral Health Surveillance
1992, the DMFT index in 12-year-old Indian was 0.89 while in
1996 the point prevalence was 89 percent with DMFT ranging
between 1.2 to 3.8. In India, different investigators have studied
various age groups.
The potential for promoting the consumption of sugar is
greater in underdeveloped countries because they are low sugar
consumers and most developed countries have either reached
saturation levels of sugar consumption or switched to sugar
substitutes.

DENTAL CARIES IN UNDERDEVELOPED PROBABLE REASONS FOR THE MARKED

COUNTRIES
The pattern of dental caries in underdeveloped countries is
following the pattern of the disease which was observed in
Europe in the 18th and 19th centuries. An increase in the
prevalence and severity, first in the upper income groups then
in the urbanized populations followed by changes in disease
prevalence in the rural groups. The influence of social class is
strong. In Ethiopia, children from more affluent high social class
families had four times more caries in primary teeth than poorer
children and twice as many permanent teeth with caries.
Urbanized populations in underdeveloped countries are more
likely to consume refined sugars than those in rural areas.
Therefore, it is not surprising that caries rates are higher in urban
populations. In the Sudan, 15 to 19-year-old urban children had
seven times more caries than children in rural areas where the
sugar consumption was below 5 lbs/person/year.
Deteriorating dental health is seen as a necessary
consequence of a certain kind of economic growth because a
change to a more refined high-sugar diet is associated with
economic growth. Sugar consumption in underdeveloped
countries is rising; consumption is predicted to be higher than
in industrialized countries where consumption is falling.
DECLINE IN DENTAL CARIES IN MOST
WESTERN INDUSTRIALIZED COUNTRIES
No single factor has been found to account for the decline and
the most likely explanation is that a combination of factors is
responsible. Dental caries is a sugar-dependent infective
disease. The demineralizing effect of the cariogenic challenge
can be prevented or reduced depending on the strength of the
challenge and the availability of fluoride at the site of attack.
Fluoride reduces the enamels solubility in acid and it influences
the remineralization of lesions as well as the metabolism of the
oral bacteria. Some authors believe that the main mechanism
whereby fluoride acts in caries prevention is in promoting
remineralization. The factors to consider in relation to the
decline in caries are sugar consumption, fluorides in toothpaste,
fluoride-rinsing, systemic fluoride, improved oral hygiene and
the use of antibiotics.
Globally, WHO reports caries prevalence in school-age
children at 60 to 90 percent and as virtually universal among
adults in the majority of countries. Because so few countries
are spared high levels of this disease, caries maps typically
display disease severity rather than prevalence. Global data by
WHO (National oral health surveys) shows caries distribution
102 Section 2 N Dental Public Health
among 12 year olds by average numbers of teeth affected,
using the Decayed, Missing, and Filled Teeth (DMFT) index of
severity. The map shows a clear pattern of higher disease
experience in North and South America, Western Europe, and
much of Africa; more moderate disease experience in much of
South America, Russia, and the former Soviet Republics; and
low levels of disease in Eastern Africa, China, Australia and
Greenland. While the correlation between caries rates and
national development is not tight, WHO has observed that
developed countries have higher rates of caries experience,
while developing countries have lower rates. (Fig. 10.1) WHO
has attributed these differences to the relative availability of
simple sugars in diets, to fluoride, and to dental treatment (World
Oral Health Report 2003). Figure 10.2 shows the situation for
the ages 35 to 44 years.
THE CARIES PROCESS (PATHOGENESIS)
Bacterial Plaque and Acid Production
The mechanism of dental caries formation is essentially
straightforward. Plaque on the surface of the tooth consists of
a bacterial film that produces acids as a byproduct of its
metabolism. To be specific, certain bacteria within the plaque
are acidogenicthat is, they produce acids when they
metabolize fermentable carbohydrates. These acids can dissolve
the calcium phosphate mineral of the tooth enamel or dentine
Fig. 10.1: World map on dental caries 2003 (12 years old)
in a process known as demineralization. If this process is not
halted or reversed via remineralization (the redeposition of
mineral via saliva) it eventually becomes a frank cavity.
Dental caries of the enamel typically is first observed
clinically as a so-called white-spot lesion. This is a small area
of subsurface demineralization beneath the dental plaque. The
body of the subsurface lesion may have lost as much as 50
percent of its original mineral content and often is covered by
an apparently intact surface layer. The surface layer forms
by remineralization. The process of demineralization continues
each time there is carbohydrate taken into the mouth that is
metabolized by the bacteria. The saliva has numerous roles,
including buffering (neutralizing) the acid and remineralization
by providing minerals that can replace those dissolved from
the tooth during demineralization.
The critical pH value for demineralization varies among
individuals, but it is in the approximate range of 5.2 to 5.5.
Conversely, tooth remineralization can occur if the pH of the
environment adjacent to the tooth is high due to: (1) lack of
substrate for bacterial metabolism; (2) low percentage of
cariogenic bacteria in the plaque; (3) elevated secretion rate of
saliva; (4) strong buffering capacity of saliva; (5) presence of
inorganic ions in saliva; (6) fluoride; and (7) rapid food
clearance times. Whether dental caries progresses, stops, or
reverses is dependent on a balance between demineralization
and remineralization.
 Chapter 10 N Epidemiology of Dental Caries
Fig. 10.2: World map on dental caries 2003 (35-44 years old) (with permission from WHO)
However, if demineralization overtime exceeds remineral-
ization, an initial carious lesion (the so-called white spot
lesion) can develop and may further progress to a frank
cavity.
Demineralization can be reversed in its early stages through
uptake of calcium, phosphate, and fluoride. Fluoride acts as a
catalyst for the diffusion of calcium and phosphate into the
tooth, which remineralizes the crystalline structures in the lesion.
The rebuilt crystalline surfaces, composed of fluoridated
hydroxyapatite and fluorapatite, are much more resistant to
acid attack than is the original structure. Bacterial enzymes can
also be involved in the development of caries.
The cause of dental caries is the consumption of fermentable
carbohydrates (sugars). There is a dose- response relationship
between the quantity of the sugar consumed and the
development of dental caries. It is suggested, at levels below
10 kg/person per year dental caries will not develop. [15 kg/
person per year in fluoridated areas].
THEORIES OF DENTAL CARIES
The Legend of the Worm
Ancient Sumerian text known as The legend of the worm
gives reference of the tooth decay and tooth pain. It was
103
obtained from the Mesopotamian areas which date back to
about 5000 BC. According to the legend, toothache was caused
by a worm that drank the blood of teeth and fed on the root of
the jaws.
Endogenous Theories
Humoral Theory
The ancient Greek believed that a persons physical and mental
constitution was determined by four elemental humors of the
body: blood, phlegm, black bile and yellow bile. An imbalance
in these humors is the cause of all diseases including dental
caries.
According to Galen, the ancient greek physician and
philosopher, dental caries is produced by internal action of
acrid and corroding humors. Hippocrates referred to
accumulated debris around teeth and to their corroding action.
He also stated that stagnation of juices in the teeth was the
cause of tooth ache.
Vital Theory [Proposed during 18th Century]
According to this theory, the tooth decay originated like bone
gangrene, from within the tooth itself.
104 Section 2 N Dental Public Health
Exogenous Theories
Chemical Theory
Parmly (1819) proposed that an unidentified chemical agent
was responsible for caries. According to this theory, teeth are
destroyed by the acids formed in the oral cavity by the
putrefaction of protein which produced ammonia and was
subsequently oxidized to nitric acid. Robertson (1895) proposed
that dental decay was caused by acids formed by fermentation
of food particles around teeth.
Parasitic or Septic Theory
Dr Miles and Underwood proposed the so-called septic
theory. They claimed that dental caries is caused by direct
action of microorganisms that penetrate the dental tubules and
destroy the organic component of the dentine leaving the
inorganic parts to be broken down and washed away in fluids
of the mouth.
AREAS PRONE TO DENTAL CARIES
Bacterial plaque is the essential precursor of caries. Hence,
sites on the tooth surface which encourage plaque retention
and stagnation are particularly prone to progression of lesions.
These sites are:
Enamel in pits and fissures on occlusal surfaces of molars
and premolars, buccal pits of molars, and palatal pits of
maxillary incisors
Tooth surfaces adjacent to dentures and bridges which make
cleaning more difficult, thus encouraging plaque stagnation
Approximal enamel smooth surfaces just cervical to the
contact point
In patients where periodontal disease has resulted in gingival
recession, caries occur on the exposed root surface
The enamel of the cervical margin of the tooth just coronal
to the gingival margin
The margins of restorations, particularly those that are
deficient or overhanging.

Chemoparasitic Theory (WD Miller) IMPORTANCE OF DIAGNOSIS OF DENTAL

CARIES
It is a blend of chemical and parasitic theory, because it states
that caries is caused by acids produced by microorganisms of 1. It forms the basis for treatment decision. Active lesion
the mouth. According to this theory, microorganisms of the require some form of active management whereas arrested
mouth, by secretion of enzymes or by their own metabolism, lesions does not.
degrade fermentable carbohydrate food materials to form acids 2. Informing the patient: patient will control the process
which demineralize the enamel and the disintegrated enamel 3. Advising the health planners: epidemiological surveys
is subsequently mechanically removed by force of mastication. inform the health agency (Central /State) about the state
Miller summarized his theory as follows.- Dental decay is a of health and disease of the population. These surveys assist
chemoparasitic process consisting of two stages- decalcification them to take necessary action.
or softening of the tissue and dissolution of the softened residue.
CLASSIFICATION OF DENTAL CARIES
Proteolytic Theory (Gottileb- 1947)
Various Clinical Classification Systems for Caries
According to this theory, microorganisms invade the organic i. According to location
pathways (lamellae) of the enamel and initiate caries by (a) Pit and fissure
proteolytic action. Subsequently, the inorganic salts are (b) Smooth surface
dissolved by acidogenic bacteria. Pincus (1950) stated that (c) Root surface
initial caries process in dental caries was due to the proteolytic ii. According to clinical appearance
breakdown of the dental cuticle. (a) Incipient
(b) Cavitation
Proteolysis Chelation Theory (c) Gross destruction
iii. According to rate of disease progression
This theory proposed by Shalz et al implies a simultaneous (a) Acute
microbial degradation of the organic components (proteolysis) (b) Chronic
and the dissolution of the minerals of the tooth by the process (c) Arrested
of chelation. According to this theory, dental caries results from (d) Rampant
an initial bacterial and enzymatic proteolytic action on the iv. According to history
organic matter of enamel without preliminary demineralization. (a) Primary
This causes the release of a variety of complexing agents, such (b)Secondary or recurrent
as amino acids, polyphosphates and organic acids which then Lesions can be classified according to their anatomical
dissolves the crystalline apatite. (location) site. Thus, lesions may be found in pits and fissures
 Chapter 10 N Epidemiology of Dental Caries
or on smooth surfaces. Lesions may start on enamel (enamel
caries) or on exposed root cementum and dentine (root caries).
Primary caries denotes lesions on unrestored surfaces. Lesions
developing adjacent to fillings are referred to as either recurrent
or secondary caries. Residual caries is demineralized tissue left
in place before a filling is placed.
Primary lesion: Begins on a surface with no previous lesion or
restoration.
Secondary lesion: Begins on a surface which has already had
a lesion, i.e. around an existing restoration. May also be a new
lesion on a remaining part of an inadequately excavated and
filled lesion.
Rampant caries is the name given to multiple active carious
lesions occurring in the same patient, frequently involving
surfaces of teeth that are usually caries-free.
Early childhood caries is a term used to describe dental caries
presenting in the primary dentition of young children.
Bottle caries or nursing caries are names used to describe a
particular form of rampant caries in the primary dentition of
infants and young children. The problem is found in an infant
or toddler who falls asleep sucking a bottle (called a nursing
bottle) which has been filled with sweetened fluids (including
milk).
ENAMEL CHANGES DURING EARLY CARIES
LESION DEVELOPMENT
Dental caries develops where microbial deposits are allowed
to form biofilms that are not frequently removed or disturbed
by mechanical wear (mastication, attrition, abrasion, from
brushing, flossing or toothpicks). Caries of the enamel is
preceded by the formation of microbial dental plaque.
105
After 14 Days
With completely undisturbed plaque, the enamel changes are
visible after air drying as whitish opaque changes.
Smooth chalky white area.
A subsurface lesion starts forming.
After 3 and 4 Weeks
The outermost surface exhibits complete dissolution of thin
perikymate overlappings and more marked dissolution
corresponding to larger developmental irregularities such as pits
of tomes processes and focal holes.
HISTOPATHOLOGY OF DENTAL CARIES
Dental caries can involve enamel, dentine and root (Fig. 10.3).
CARIES OF THE ENAMEL
Smooth Surface Caries
Incipient caries is the appearance of smooth chalky white area.
The overlying enamel surface is smooth, hard and shiny.
Early lesion in enamel caries is conical in shape with its apex
towards the dentine and base toward the surface of the tooth.
Four zones are present with differing translucency.
The early enamel lesion consists of four zones of alternating
levels of mineralization. It illustrates the dynamic nature of the
caries process (Fig. 10.4). The surface zone blocks the passage
of calcium ions into the body of the lesion and may have to be
removed to allow the lesion to become arrested.

CHANGES RECORDED IN ENAMEL COVERED

BY DENTAL PLAQUE
After One Week Fig. 10.3: Histopathology of dental caries

Macroscopically no changes can be seen.

At the Ultrastructural Level

There are distinct signs of direct dissolution of outer enamel
surface.
The intercrystalline spaces are wider, indicating a partial
dissolution of the crystal surfaces.

Histological Examination
Histological examination in polarized light shows slight increase
in enamel porosity, indicating an extremely modest loss of
mineral to a depth of 20 to 100 micrometer from the outer
surface. Fig. 10.4: Various zones in enamel caries
106 Section 2 N Dental Public Health
Four zones are clearly distinguishable starting from the inner
advancing front of the lesion:
1. Translucent zone
2. Dark zone
3. Body of lesion
4. Surface zone
Translucent Zone
Lies at the advancing front of enamel lesion (not always
present)
This is the first recognizable zone of alteration from the
normal enamel.
In transmitted light the zone appears structure less.
This zone may vary from 5 to 10 micrometer in width.
Pore volume slightly more than one percent [in sound
enamel: 0.1%]
Slight loss of mineral; Mainly the minerals are lost from this
zone and not organic material
Translucent appearance: Initial dissolution of the enamel
mainly occurs along the gaps between the rods and interrod
enamel in the tissue; thus on examining ground sections
imbibed in clearing agent, Quinolone (suitable since
refractive index is similar to that of enamel). Quinolone is
assumed to penetrate more easily into these enlarged pores,
the final result looks like a structureless zone.
No evidence of protein loss seen.
Dark Zone
Lies adjacent and superficial to the translucent zone.
This zone is formed as a result of demineralization and
appears dark brown
Under polarized light the dark zone has a pore volume of 2
to 4 percent
Occurs in 90 to 95 percent of lesions
Represents a result of multitude of demineralization and
reprecipitation processes
When examined in transmitted light, after inhibition with
Quinolone, appears dark brown in ground sections, thus
called Dark zone; and shows positive birefringence in
contrast to negative of that of sound enamel. Therefore,
Positive zone.
The appearance of dark zone is due to remineralization
occurring at the advancing front of the lesion. It is broader
in arrested or remineralized lesion.
Body of Lesion
Lies between the relatively unaffected surface layer and
dark zone.
It is the area of greatest demineralization.
In polarized light- pore volume is five percent in spaces near
the periphery and nearly equals to 25 percent in the outer
of the intact lesion.
On examination, the ground section in Quinolone with
transmitted light, the body of the lesion appears relatively
translucent compared to sound enamel.
It forms the bulk of the lesion and extends from just beneath
the surface zone to dark zone
Striae of retzius are well marked.
Reduction of 24 percent in mineral per unit volume as
compared to sound enamel.
Increase in unbound water and organic content due to
ingress of bacteria and saliva.
Surface Zone
It represents the most important change in enamel caries
in terms of prevention and management
Partial demineralization 1 to 10 percent loss of mineral salts
has taken place. Pore volume is less than five percent of
spaces.
Surface zone retains a negative birefringence.
The surface is resistant due to greater degree of mineralization
and concentration of fluoride in the surface enamel. It remains
intact and well mineralized because it is a site where calcium
and phosphate ions, released by subsurface dissolution
become precipitated. This is called remineralization.
Cavitation is due to loss of this layer which allows the
bacteria to enter the lesion. It is of relatively constant width,
a little thicker in arrested or remineralizing lesions.
Pit and Fissure Caries
Carious lesion starts at both sides of the fissure, not at the base.
The enamel is thin in fissures so there is early dentine
involvement. The carious lesion forms a triangular or cone-
shaped lesion with its apex at the outer surface and base towards
the dentinoenamel junction (DEJ).
Lesion begins beneath plaque, with decalcification of enamel.
Pit and fissures are often deep, with food stagnation,
Enamel in the bottom of pit or fissure is very thin, so early
dentine involvement frequently occurs.
Here the caries follows the direction of the enamel rods. In
pit and fissure the enamel rods are said to flare laterally at
the bottom of the pit and caries is said to follow the path of
enamel rods hence a characteristic angular/inverted V
shaped lesion is formed.
It is triangular in shape with the apex facing the surface of
tooth and the base towards the DEJ.
When reaches DEJ, greater number of dentinal tubules are
involved.
It produces greater cavitation than the smooth surface caries
and there is more undermining of enamel.
CARIES OF THE DENTINE
The caries process in dentine involves the demineralization of
the mineral component and breakdown of the organic
 Chapter 10 N Epidemiology of Dental Caries
Fig.10.5: Infected and affected layers in dentine
component of collagen fibers. The caries process in dentine is
approximately twice as rapid as in enamel. Spread of caries is
more in dentine compared to enamel because of:
1. Decreased calcification (mineralization).
2. Existence of pathways (dentinal tubules).
Advanced carious lesions in dentine consist of two distinct
layers having different microscopic and chemical structures. The
outer layer is heavily infected by bacteria which are mainly located
in the tubule spaces. The collagen fibers are denatured and the
organic matrix is not being remineralized. The inner layer is
scarcely infected, but affected by plaque acid (Fig. 10.5). It still
contains high concentrations of mineral salts and can be
remineralized.
The initial dentinal changes are known as dentinal sclerosis
or transparent dentine. The dentinal sclerosis is due to
calcification of dentinal tubules. The change is minimal in
progressing caries and more in slow caries. In transmitted light
the dentine appear transparent. In reflected light sclerotic
dentine appear dark. In advanced lesions tiny liquefaction foci
are formed.
In secondary dentine the dentinal tubules are fewer and
irregular. Caries spread laterally at the junction of primary and
secondary dentine separating both.
Various zones are distinguished assuming the shape of
triangle with the apex toward the pulp and the base toward
the enamel.
VARIOUS ZONES OF CARIES OF DENTINE
Zone of Fatty Degeneration
1. Firstly the fatty degeneration of the tomes dentinal fibres
resulting in deposition of fat globules in the further end of
dentinal tubules.
It has been suggested that this fatty degeneration
contributes to the:
1. Impermeability of the dentinal tubule.
2. Also sclerosis of dentinal tubule.
107
Zone of Dentinal Sclerosis
The sclerotic zone is located beneath and at the sides of the
carious lesion. It is almost invariably present, being broader
beneath the lesion than at the sides and is regarded as a vital
reaction of odontoblasts to irritation. Sclerosed dentine has a
higher mineral content. Dead tracts may be seen running
through the zone of sclerosis. They are the result of death of
odontoblasts at an earlier stage in carious process. The early
dentinal tubules contain air and the remains of dead
odontoblastic process and such tubules cannot undergo
sclerosis. However, they provide ready access of bacteria and
their products to the pulp.
Zone of Demineralization
In the demineralized zone the intertubular matrix is mainly
affected by a wave of acid produced by bacteria in the zone of
bacterial invasion, which diffuses ahead of the bacterial front.
The softened dentine in the base of a cavity is therefore sterile
(affected dentine) but it cannot be distinguished from softened
infected dentine. It may be stained yellowish-brown as a result
of the diffusion of other bacterial products interacting with
proteins in dentine.
Zone of Bacterial Invasion
In this zone the bacteria extend down and multiply within the
dentinal tubules, some of which may become occluded by
bacteria. There are always, however, many empty tubules lying
among those tubules containing bacteria. The bacterial invasion
probably occurs in two waves: the first wave consisting of
acidogenic organisms, mainly, lactobacilli produce acid which
diffuses ahead into the demineralized zone. A second wave of
mixed acidogenic and proteolytic organisms then attack the
demineralized matrix.
The walls of the tubules are softened by the proteolytic
activity and some may then be distended by the increasing
mass of multiplying bacteria. The peritubular dentine is first
compressed, followed by the intertubular dentine, resulting in
elliptical areas of proteolysis-LIQUEFACTION FOCI.
Liquefaction foci run parallel to the direction of the tubules
and may be multiple, giving the tubule a beaded appearance.
Zone of Decomposed Dentine
In this zone the liquefaction foci enlarge and increase in number.
Cracks or clefts containing bacteria and necrotic tissue also appear
at right angles to the course of the dentinal tubules forming
TRANSVERSE CLEFTS. Bacteria are no longer confined to the
tubules and invade both the peritubular and intertubular dentine.
In acute, rapidly progressing caries the necrotic dentine is very
soft and yellowish-white; in chronic caries it has a brownish-
black color and is of leathery consistency.
108 Section 2 N Dental Public Health

CARIES IN DENTINE FACTORS AFFECTING THE EPIDEMIOLOGY OF

Zone 1: Zone of fatty degeneration of tomes fibers (next to
pulp)due to degeneration of the odontoblastic process. This
occurs before sclerotic dentine is formed and makes the tubules
impermeable.
Zone 2: Zone of dentinal sclerosis characterized by deposition
of calcium salts in the tubule.
Zone 3: Zone of decalcification of dentine, a narrow zone
preceding bacterial invasion.
Zone 4: Zone of bacterial invasion of decalcified zone but intact
dentine.
Zone 5: Zone of decomposed dentine due to acids and enzymes.
ROOT CARIES
Root caries as defined by HAZEN, is a soft, progressive lesion
that is found anywhere on the root surface that has lost its
connective tissue attachment and is exposed to the environment.
The root surface must be exposed to the oral environment
before caries can develop here.
Plaque and microorganisms are essential for the cause and
progression of the lesion, mostly Actinomyces.
Microorganisms invade the cementum either along the
Sharpeys fibers or between the bundles of fibers.
Spread laterally, since cementum is formed in concentric layers.
After decalcification of cementum, destruction of matrix
occurs similar to dentine with ultimate softening and
destruction of this tissue.
Invasion of microorganisms into the dentinal tubules, finally
leading to pulp involvement.
The rate is slower due to fewer dentinal tubules than in
crown area.
DENTAL CARIES
In the 1960s, the caries theory was depicted as three circles
representing the three prerequisites for dental caries (Keyes
Triad). Three indispensable factors for development of caries
were: (1) carbohydrate (diet), (2) bacteria (dental plaque), and
(3) susceptible teeth (the host) (Keyes and Jordan, 1963).
Since then, many modifying factors have been recognized,
resulting in a more complex model that includes saliva, the
immune system, time, socioeconomic status, level of education,
lifestyle behaviors, and the use of fluorides. An important
breakthrough in the understanding of dental caries was the
recognition of the remineralization process as a result of plaque
fluid and saliva at pH levels above a critical value being highly
saturated with calcium and phosphates. The caries process can
be described as loss of mineral (demineralization) when the
pH of plaque drops below the critical pH value of 5.5; the
critical value for enamel dissolution is 5 to 6, and an average
pH of 5.5 is the generally accepted value. Redeposition of
mineral (remineralization) occurs when the pH of plaque rises.
The presence of fluoride reduces the critical pH by 0.5 pH
units, thus exerting its protective effect.
It is now established that dental caries is a multifactorial
disease and results from a combination of four principal factors
(Fig. 10.6) (Newbrun).
1. Host and teeth factors:
2. Microorganism in dental plaque
3. Substrate [diet]
4. Time

SUSCEPTIBILITY OF DIFFERENT TEETH

The Hagerstown Study ranks the order of susceptibility of teeth
to caries as:
1. Mandibular 1st and 2nd molars.
2. Maxillary 1st and 2nd molars.
3. Mandibular 2nd bicuspids, maxillary 1st and 2nd bicuspids,
maxillary central and lateral incisors.
4. Maxillary canines and mandibular 1st bicuspids.
5. Mandibular central and lateral incisors, mandibular canines.
Third molar had not erupted in the children studied.

PATHOGENIC PROPERTIES OF CARIOGENIC BACTERIA

These cariogenic bacteria can:

Transport sugars and convert them to acid (acidogenic)
Produce extracellular and intracellular polysaccharides which
contribute to the plaque matrix. The intracellular polysaccharides
can be used for energy production and converted to acid when
sugars are not available Fig.10.6: Four principal factors in dental caries
Thrive at low pH (aciduric). (Adapted from Newbrun)
 Chapter 10 N Epidemiology of Dental Caries 109

FACTORS AFFECTING DEVELOPMENT OF B. Geographic variation

DENTAL CARIES (FIG. 10.7) C. Climate
D. Oral hygiene
Host and Teeth Factors E. Soil
F. Fluoride
A. Tooth
Composition
Morphology I. HOST AND TEETH FACTOR
Position.
A. Tooth
B. Saliva
Composition i. Composition: Number of studies on the relation of caries
Buffering capacity of saliva to the chemical composition have shown that there was
Quantity. no difference found in the calcium, phosphorus,
C. Sex magnesium and carbonate content of enamel from sound
D. Age and carious teeth. But there was a significant difference
E. Race and ethnicity in fluoride content of teeth, i.e. more in sound teeth.
F. Socioeconomic status It was also noted that surface enamel is more resistant
G. Heredity to caries than subsurface enamel. Surface enamel is more
H. Emotional disturbances highly mineralized and tends to accumulate greater
quantities of fluoride, zinc, lead and iron than the
Agent Factors underlying enamel. The surface is lower in carbon dioxide,
A. Microorganism dissolves at a slower rate in acids and has more organic
B. Plaque material than subsurface enamel. These factors contribute
to caries resistance.
ii. Morphology: Morphologic features which may pre dispose
Environmental Factors
to the development of caries are the presence of deep,
A. Diet narrow occlusal fissure or buccal or lingual pits. These
Total consumption of carbohydrate fissure trap food, bacteria and debris leading to
Frequency and form of carbohydrate development of caries.

Fig.10.7: Factors affecting development of dental caries

110 Section 2 N Dental Public Health
Attrition on other hand makes the tooth flattened,
hence less food entrapment in fissures, so less caries.
iii. Position: Malaligned, out of position, rotated teeth are
difficult to clean, favoring the accumulation of food and
debris. This may predispose to the development of caries.
B. Saliva
It can be considered as an environmental factor also as teeth
are constantly bathed by it. This influences the process of dental
caries. Saliva has a flushing action on teeth.
i. Composition: varies from person to person. Saliva is dilute
fluid; over 99 percent being made up of water.
1. Proteins: They include enzymes, immunoglobins and
other antibacterial factors, mucous glycoproteins and
certain polypeptides.
2. Enzymes: -Amylase
3. Immunoglobulins secretary IgA
4. Antibacterial proteins Lysozyme, Lactoferrin,
Sialoperoxidase.
5. Glycoproteins.
6. Polypeptides Statherin, Sialin (helps to regulate pH
of plaque).
7. Other Organic Compounds:
- Free Amino Acids
- Urea (it is hydrolysed by many bacteria with release
of Ammonia, leading to rise in pH).
- Glucose
8. In Organic Constituents:
- Major Ions [Sodium, Potassium, and Chloride and
Bicarbonate] contribute to osmolarity of saliva.
- Bicarbonates: Principal buffer in saliva.
- Thiocyanate: Has antibacterial action.
- Fluoride: Has anticaries action.
i. Saliva: It has a critical role to play in the development of
caries or its prevention. Saliva provides calcium,
phosphate, proteins, lipids and antibacterial substances
and buffers. Saliva buffering can reverse the low pH in
plaque.
ii. Buffering and neutralization: pH of saliva depends on the
bicarbonate concentration. Saliva is alkaline and is an
effective buffer system. These properties protect the oral
tissues against acids and plaque. After eating a sugary
food if saliva is stimulated by chewing substances such as
wax or sugar free chewing gum, the drop in pH in plaque
which would have occurred is reduced or even eliminated.
This salivary neutralization and buffering effect markedly
reduces the cariogenic potential of foods.
iii. Quantity: Rate of flow of saliva may be an additional factor
which helps contribute to caries susceptibility or caries
resistance. Mild increase or decrease in flow may be of
little significance, near total reduction in salivary flow
adversely affects dental caries. There is an inverse relation
between salivary flow and dental caries.
C. Sex
In young people caries has been seen to higher in the females
but some studies show no significant difference between the
sexes. Root caries is seen more in males. Girls may be more
prone to caries due to early eruption of teeth and hormonal
changes (puberty and pregnancy).
D. Age
Although present in all ages, it was believed that dental caries
was disease of childhood. WHO global data bank has shown a
decline in DMFT values in 12-year-old children. Some studies
indicate greatest intensity of dental caries occurs in 15 to 25
years of age.
Root caries is seen in over 60 years age group people,
mainly due to denuded root surface because of gingival
recession.
E. Race and Ethinicity
A number of studies indicate that blacks [Negroes] of
comparable age and sex have a lower caries scores than
Caucasians. Chinese population has shown to have a lower
caries rate than corresponding white population. These
differences are probably more due to environmental factors.
F. Socioeconomic Status
There is an inverse relationship between socioeconomic status
and dental caries experience in primary dentition. The relation
has not been established in adults, though some studies suggest
so.
G. Heredity
Environmental factors have a greater influence than genetic
factors but latter also contributes to the causation of caries.
H. Emotional Disturbances
Emotional disturbances, particularly transitory anxiety states
tend to increase the incidence of dental caries.
II. AGENT FACTORS
A. Microorganisms
The mouth has a diverse resident microbial flora. The normal
inhabitants become established early in life. There have been
a few epidemiological studies to investigate the link between
oral flora and dental caries. Streptococcus mutans was first
identified in 1924 by Clarke and subsequently Lactobacillus
acidophilus by Bunting (1930). These acid producing bacteria
were found to be associated with the formation of dental caries.
Streptococcus mutans is of interest because it has the ability to
 Chapter 10 N Epidemiology of Dental Caries
form an extracellular polymer of glucose, mutans from sucrose,
which aids the microorganism in adhering to the enamel surface
and in establishing a stable relationship there.
The absolute demonstration of a specific microorganism
as the causative agent of dental caries in man may be impossible
because of diverse organisms being always present in the oral
cavity and on the teeth.
L. acidophillus and other acidogenic microorganism in
plaque and carious lesion may be capable of producing caries
by themselves, or they may be able to act synergistically with
Streptococcus mutans in caries initiation.
Actinomyces are Gram-positive pleomorphic rods (GPPR)
which form a large proportion of the oral microflora of all
mammals. Actinomyces are also among the earliest colonizers
of dental surfaces and may constitute up to 27 % of the pioneer
bacteria. They have been implicated in root caries, although
their role in dental caries initiation and progression is not well-
understood.
B. Dental Plaque
Bacterial plaque is a dense non-mineralized, highly organized
mass of bacterial colonies in a gel-like intermicrobial, enclosed
matrix or slime layer. It is a transparent film that can be supra-
gingival, coronal to the gingival margin on the clinical crown
of the tooth and subsgingival, apical to the margin of the gingiva.
III. ENVIRONMENTAL FACTORS
A. Diet
According to acidogenic or chemoparasitic theory, dental caries
occurs when acid is produced by bacteria in dental plaque when
refined carbohydrates are eaten. The presence of refined
carbohydrate as sugar is essential for the majority of caries
development and sucrose is the most cariogenic of all sugars.
In human consumption, sucrose accounts for 60 percent of all
sugars eaten.
B. Geographic Variation
It is well documented that dental caries experience has been
decreasing in children in developed western [19731983]
countries. But this decrease is beginning to level out. Gradual
increase in caries in 5 years old have been found in some areas.
[Palmer & Pitts 1994].
C. Climate
Sunshine and high temperature areas seems to have lower
dental caries [inverse relationship]. Whereas areas with more
relative humidity and rainfall have shown increase dental caries.
D. Oral Hygiene
Inverse relationship has been seen between oral hygiene and
dental caries. Poor oral hygiene increases the rate of dental caries.
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E. Soil
Trace elements in soil have shown a relation with caries. An
increase in dental caries is seen in areas where selenium is
present in soil, whereas molybdenum and vanadium are said
to decrease dental caries.
F. Fluoride
Fluoride in water and soil decreases incidence of dental caries.
EARLY CHILDHOOD CARIES
Early childhood dental caries has been reported by the Centers
for Disease Control and Prevention to be perhaps the most
prevalent infectious disease of our nations children. Early
childhood dental caries occurs in all racial and socioeconomic
groups; however, it tends to be more prevalent in low-income
children, in whom it occurs in epidemic proportions. Human
dental flora is site specific, and an infant is not colonized until
the eruption of the primary dentition at approximately 6 to 30
months of age. The most likely source of inoculation of an infants
dental flora is the mother or another intimate care provider,
through shared utensils, etc. Decreasing the level of cariogenic
organisms in the mothers dental flora at the time of colonization
can significantly impact the childs predisposition to caries. To
prevent caries in children, high-risk individuals must be identified
at an early age (preferably high-risk mothers during prenatal care),
and aggressive strategies should be adopted, including
anticipatory guidance, behavior modifications (oral hygiene and
feeding practices), and establishment of a dental home by 1 year
of age for children deemed at risk.
ROOT CARIES
Root caries can be defined as a lesion which is initiated or
extends onto the part of the tooth apical to the cementoenamel
junction.
The term primary as it is used with root caries refers to
new dental caries occurring in the absence of a restoration.
Secondary (recurrent) root caries refers to caries occurring
adjacent to an existing restoration. There is general agreement
on this terminology.
Root caries most often occurs supragingivally, at or close
to (within 2 mm) the cemento-enamel junction.
This phenomenon has been attributed to the location of
the gingival margin at the time conditions were favorable for
caries to occur. The location of root caries has been positively
associated with age and gingival recession. This is consistent
with the concept that root caries occurs in a location adjacent
to the crest of the gingiva where dental plaque accumulates.
Root caries occurs predominantly on the proximal (mesial and
distal) surfaces, followed by the facial surface.
Early root caries tends to be diffused (spread out) and track
along the cementoenamel junction or the root surface. More
advanced root lesions enlarge toward the pulp.