Chapter 9 N Introduction to Public Health Dentistry 95

FUNCTIONS OF PUBLIC HEALTH DENTISTRY treatment within the health care systems and out-of-pocket co-
payments from patients, and from indirect costs such as work-
The services provided to the community by public health dentist loss, absenteeism from school, travel expenses, and the total
include: societal burden through loss of economic productivity.
1. Preventive Services Besides dental decay, in a number of countries oral cancers,
a. Application of topical fluorides trauma to teeth and craniofacial trauma, oral manifestations
b. Pit and fissure sealants application of HIV-infection and noma (cancrum oris) are also important
c. Promotion of water fluoridation oral public health problems. Oral cancer is one of the ten most
d. Defluoridation frequent cancers worldwide with great variability between
2. Public Health Training different regions. In some countries in Asia, oral cancer accounts
a. School teacher training program. for up to 50 percent of all cancers. Three quarters of oral cancer
b. Training of the health care worker about dental health cases occur in developing countries. Noma shows the strongest
and oral hygiene measures. links to poverty and general medical and social deprivation
3. School Dental Health Program and has a large impact on the affected individuals.
a. Topical fluoride application. Oral diseases are major public health problems on a global
b. School mouth rinsing program. level. Their most common effects, orofacial pain and tooth loss,
c. Teaching of oral hygiene methods and importance of are known to almost every human being. Budget limitations,
dental health to children. lack of infrastructure, resources and knowledge, lack of capacity,
d. Education about safe play areas for children to school different priorities, or even unwillingness to act, are some of
authorities. the reasons for the widening gap between need, services
e. Knowledge about junk foods and effects of cold drinks provided, and effective policies that address oral health
to children. problems.
4. Dental Public Health Program
a. Examination and treatment of community through
PUBLIC HEALTH MILESTONES IN
dental health program.
b. Screening program for oral cancer.
INDEPENDENT INDIA
c. Dental health check up and treatment like extraction, 1947: Ministries of health and Director-General of Health
filling, oral prophylaxis of industrial workers through Services established at the Center and States. The Indian
camps. Nursing Council Act passed
5. Dental Health Education 1948: India joined the World Health Organization and
a. Education about dental health and its importance to the Employees State Insurance Act passed. The Dental
community, industrial workers and social Council of India established under the Dentist Act
organizations.
b. Imparting knowledge about oral health to expectant 1949: The Registrar-General India appointed in the
mothers. Ministry of Home Affairs. WHO opened its South East
c. Knowledge about injury to teeth and importance of Asia Regional Office in New Delhi. The Indian Pharmacy
mouth guards. Council and Family Planning Association of India
d. Education to geriatric population about oral health. established
e. Informing people about ill effects of tobacco and 1950: India became a Republic in the Commonwealth.
smoking. The Planning Commission was set up by the Government
f. Educating public about methods of prevention of of India
dental diseases like dental caries, periodontal disease 1951: The beginning of the first Five Year Plan. The BCG
and oral cancer. vaccination programme launched in the country
g. educating care takers about maintenance of oral health
1952: The Community Development Programme
in special needs patients.
launched for the all-round rural development. The Central
h. parent counseling for pre school and school children.
Council of Health constituted. First Primary Health Center
6. Program Administration and Promotion
set up
a. Helping the State / Central agency in conducting
epidemiological studies regarding oral diseases. 1953: The National Malaria Control Programme and
b. Conducting surveys to determine dental needs of the National Extension Service Programme for rural
population. development started. A nation-wide family planning
c. Providing dental health knowledge to state agencies program started. A committee appointed to draft a Model
or education department. Public Health Act for the country
The economic costs of oral diseases are also considerable, 1954: The Contributory Health Service Scheme (Central
although difficult to quantify. They result from direct costs of Government Health Scheme), the Central Social Welfare
96 Section 2 N Dental Public Health
Board, the National Water Supply and Sanitation 1969: The Fourth Five Year Plan launched. The Nutrition
Programme and the National Leprosy Control Programme Research Laboratories became the National Institute of
started. The Prevention of Food Adulteration Act passed Nutrition. The Central Births and Deaths Registration Act
by Parliament promulgated
1955: The National Filaria Control Programme 1970: The Drugs (Price Control) Order promulgated. All
commenced. The National TB sample survey conducted. India Hospital (Post-partum) Family Planning Programme
1956: The Second Five Year Plan started. The Model started. The Population Council of India and the Central
Public Health Act published and the Central Health Council of Indian Medicine (Ayurveda, Unani and Siddha)
formed. VHAI (Voluntary Health Agency of India)comes
Education Bureau established in the Union Health
into being.
Ministry. The Indian Medical Council established
1971: The Family Pension Scheme (FPS) for industrial
1957: Influenza pandemic swept the country. The
workers came into force. The Medical Termination of
Demographic Research Centres established in Calcutta,
Pregnancy Bill passed by the Parliament. Uni-purpose
Delhi and Trivandrum
Health Workers converted into Multi-purpose workers.
1958: The National Malaria Control Programme
1972: National Service Bill passed. The National Nutrition
converted into National Malaria Eradication Programme.
Monitoring Bureau set up
The National Development Council endorses Panchayati
Raj. The National TB survey completed 1973: National Programme of Minimum Needs was
incorporated in the Fifth Five Year Plan. The Government
1959: The Mudaliar Committee appointed. A Central
envisaged a scheme for setting up 30-bedded rural
Expert Committee recommended eradication of small pox
hospitals; one such hospital for every 4 primary health
and cholera. Rajasthan introduces Panchayati Raj. centres. The Kartar Singh Committee recommended a
National Tuberculosis Institute at Bangalore established new cadre of health workers called Multi-purpose Health
1960: The School Health Committee and the National Workers. The Central Council of Homeopathy was set
Nutrition Advisory Committee constituted up. The Kartar Singh Committee was established
1961: The Third Five Year Plan launched. The Mudaliar 1974: The Fifth Five Year Plan launched. Parliament
Committee report published. The Central Bureau of enacted the Water (Prevention and Control of Pollution)
Health Intelligence established Act
1962: The Central Family Planning Institute established 1975: India became smallpox-free. A Revised strategy for
in Delhi. The National Smallpox eradication Programme NMEP accepted. The Integrated Child Development
and the School Health Programme initiated, the National scheme launched. The National Childrens Welfare Board
Goitre Control Programme and the District Tuberculosis set up. The Cigarettes Regulation (Production, Supply and
Programme launched Distribution) Act passed by the Parliament. The Srivastava
1963: The Applied Nutrition Programme was launched Committee set up
with aid from UNICEF, FAO and WHO. The National 1976: The Equal Remuneration Act promulgated
Institute of Communicable Diseases (formerly Malaria providing for equal wages for men and women for equal
Institute of India) inaugurated and the National Trachoma work. A new Population Policy introduced. A National
Control Programme started. A Drinking Water Board and Programme for Prevention of Blindness formulated. The
the Chadah Committee established Central Council for Yoga and Naturopathy established.
In 1975-76 National Cancer Control Programme was
1964: The National Institute of Health Administration and
launched.
Education opened
1977: The National Institute of Health and Family
1965: Reinforced Extended Family Planning Programme
Planning formed. The Rural Health Scheme launched.
launched. The Mukherjee Committee set up
Community Health Volunteers (Guides) scheme taken up.
1966: A separate department of Family Planning created Population Control and Family Planning was put in the
under the Health Ministry. The Population Councils concurrent list. WHO adopted the goal of Health for All
International Postpartum Family Planning program started by 2000 AD
in Delhi and Trivandrum
1978: A Bill on Air Pollution introduced in the Lok Sabha.
1967: The Central Council of Health recommended levy The Parliament approved the Child Marriage Restraint
of health cess on patients. The Jungalwalla Committee (Amendment Bill fixing the minimum age of marriage 21
set up years for boys and 18 years for girls
1968: The Small Family Committees Report submitted. 1979: The World Health Assembly endorsed the
Govt. appointed the Medical Education Committee Declaration of Alma Ata on primary health care
 Chapter 9 N Introduction to Public Health Dentistry 97
1980: Smallpox officially declared eradicated from the 1990: Control of Acute Respiratory Infection
entire world by the World Health Assembly. The Sixth (ARI) Program initiated as a pilot project in 14 districts
Five Year Plan launched 1991: India stages the last decadal Census of the Century.
1981: The census taken. WHO and Member countries Population of India was 844.32 million. Pre-natal
adopted the global strategy for Health For All. The Report Diagnostic Techniques (regulation and prevention of
of the Working Group on Health for All, set up by the misuse) Act enacted
Planning Commission, published. 1992: Eighth Five Year Plan launched. Child Survival and
1982: The Govt. of India announced the National Health Safe Motherhood Programme (CSSM) launched in the
Policy. Amendment done on the Drugs and Cosmetics country. The Infant Milk Substitute, Feeding Bottles and
Act of 1940. National Mental Health Programme was Infant Foods (Regulation of Production, Supply and
started Distribution) Act passed. The State of Indias Health
1983: India launched a national plan of action against Report by VHAI released. Indias first National AIDS
avoidable disablement, known as IMPACT India. The Control Programme (1992-1999) was launched, and
National Leprosy Control Programme became the National AIDS Control Organization (NACO) was
National Leprosy Eradication Programme. Guinea-worm constituted to implement the program
Eradication Programme launched 1993: The dentists (amendment) act, 1993 [2nd April,
1984: The Bhopal Gas tragedy, the worst ever industrial 1993]. An Act further to amend the Dentists Act, 1948.
accident killing at least 2500 people and no fewer than The Indian Association of Public health Dentistry
50,000 affected. The ESI (Amendment) Bill approved by established
Parliament and the Workmens Compensation 1994: Return of Plague after 28 years of silence in few
(Amendment) Act came into force parts of the country. The Transplantation of Human
1985: The Seventh Five year Plan launched. The Organs Bill passed. The first Heart Transplantation Surgery
Universal Immunisation Programme started. The Lepers in the country done at AIIMS, New Delhi. Malaria
Act, 1898 was repealed by the Parliament. A separate epidemic strikes Rajasthan. Swaminathan Committee
Department of Women and Child development set up Report submitted
under the newly created Ministry of Human Resource 1995: The revised Rational Drug Policy announced.
Development Malaria epidemic strikes Assam. The Persons with
1986: The Environment (Protection) Act and the Disabilities (Equal Opportunities, Protection of Rights and
Consumer Protection Act were promulgated. National Full Participation) Act passed
Drug Policy announced. 1st AIDS case detected in country 1996: Dengue epidemic in Delhi. Malaria strikes again
(India). many northern States of India. The Central Govt.
1987: The New 20 Point Programme launched. A publishes the list of essential drugs. The Revised National
worldwide safe motherhood campaign was launched TB Control Programme initiated. The Supreme Court
by World Bank. National Diabetes Control Programme orders the government to set up the National Council of
and National AIDS Control Programme initiated. The Blood Transfusion
Mental Health Act passed. The Drugs (Price Control) 1997: The National Illness Assistance Fund launched.
Order released Delhi government enacts Anti-Smoking Bill
1988: Hospitals and Other Institutions (Redressal of 2003: 1st National oral health survey and fluoride
Grievances of Employees) Bill passed mapping was published
1989: Blood Safety Programme was launched. The ESI 2008: Ban on tobacco smoking act. Smoking in public
(Amendment) Act modified places banned.
 Epidemiology of Dental
10 Caries
CM Marya

Dental caries is a disease of civilization, i.e. the more developed adolescents in developed countries, and there is an increase in
a country the greater the incidence of caries. Caries is a Latin dental caries in some developing countries (Fig. 10.1).
word meaning rottenness. In ancient humans, caries was located There is now increasing evidence that incidence of caries
mainly at cementoenamel junction or in the cementum, in levels has declined in developed countries in the past 20 years.
contrast to modern times where dental caries is primarily located Dental caries is now largely a disease affecting the deprived
in pits, fissures and in smooth surfaces of teeth. section of society. Recent reports also confirm that in many
communities, 80 percent of dental caries is occurring in 20
DEFINITION percent of the population.
The incidence of dental caries has been studied in American
It is defined as progressive, irreversible microbial disease of white populations. The results show dental caries to be most
multifactorial nature affecting the calcified tissue of the teeth, prevalent chronic disease in this population. The disease affects
characterized by demineralization of the inorganic portion and all regardless of location, sex, age, or social stratum. The disease
destruction of the organic portion the tooth. starts in young people just as soon as teeth erupt. About 90
percent of youngsters are affected by age 14. As mentioned
EPIDEMIOLOGY earlier however, the incidence of caries is decreasing in this
young population in the U.S. and in other Western countries.
Studies have shown that dental caries remained low until the This downward trend is explained by increased fluoridation of
17th century. Skeletal data shows that skulls of men from Pre community water supplies and by increased attention to regular
Neolithic period [12000 BC] did not exhibit dental caries but care at dental offices and at home.
skulls from Neo-lithic period [12000-3000 BC] contained
carious teeth. The prevalence of dental caries increased
Caries Incidence is Tied to Soft, Sugar-laden
dramatically towards the end of 17th century, and continued
to increase until the early 1970. The only break in this increase Western Diets
came during the mid 40 and early 50s and this coincided with Isolated populations who have not adopted eating habits of
the reduced availability of sucrose as a result of food rationing the West have long been known to have decreased incidence
imposed during the World War II. of dental caries. Eskimos, some African natives, and inhabitants
Dental caries is a universal disease affecting all geographic of rural India are examples of such immune populations.
regions, races, both the sexes and all age groups. The prevalence Examination of teeth shows considerable abrasion of the
of dental caries is generally estimated at the ages of 5, 12, 15, occlusal surfaces indicating consumption of a coarse, abrasive
35 to 44 and 65 to 74 years for global monitoring of trends diet. It is not uncommon to observe teeth abraded down to
and international comparisons. The prevalence is expressed in the contact points between adjacent teeth. There is no doubt
terms of point prevalence (percentage of population affected to explain the fact that dental caries in these primitive
at any given point in time) as well as DMFT index (number of populations is restricted to the interproximal areas below contact
decayed, missing and filled teeth in an individual and in a areas where food impaction may occur.
population).
Since the mid 1970s reports from developed countries world TRENDS IN DENTAL CARIES
wide have shown that the prevalence of dental caries in children
and adolescent has declined. WHO global data bank confirms Dental caries afflicts humans of all ages and in all regions of
a decline in the prevalence of dental caries in children and 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 CARIES INCIDENCE IN THE UNITED STATES
1. Increase in sugar consumption in underdeveloped countries Dental caries is one of the most common childhood diseases
2. Lack of dental resources in the United States. Studies have shown that in children aged
3. Socio economic factor 5 to 9 year, 51.6 percent have had 1 filling or caries lesion; of
4. Lack of water fluoridation those aged 17 year, the proportion is 77.9 percent; 85 percent
5. Lack of preventive dental health programs 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
DENTAL CARIES PANDEMIC
that aged 18 to 34 year and from 12 to 13.5 percent in those
Caries is both diet-dependent and fluoride-mediated and is aged 35 to 54 year. Reasons for the decline can be partly
amenable to prevention and management at both the attributed to increased use and availability of fluoride. These
individual and population levels. It is also readily treatable trends, however, were not found in older adults during this
through conventional surgical interventions and dental repair. period; in the older adult population, the percentage of teeth
Therefore, the extent and severity of its consequence for free of caries and restorations declined from 10.6 to 7.9 percent
individuals, communities, and nations varies by the availability in that aged 55 to 64 year and from 9.6 to 6.5 percent in those
and balance of these factors. As a result, there are marked aged 65 to 74 years.
disparities in caries experience, treatment experience, and US findings by the Centers for Disease Control and
disease consequences both between countries and within Prevention (CDC) released in August 2005 reveal high ongoing
countries. BL Edelstein (2006) justifies that term pandemic prevalence of dental caries in children, with 27 percent of
is fitting because those who are affected by caries and have preschoolers, 42 percent of school-age children, and 91 percent
little or no access to care number in the hundreds of millions, of dentate adults having caries experience.
reside on all continents and in most societies, and experience Caries is increasing in the Third World and in the US elderly.
significant consequences of pain and dysfunction that impair While decreased incidence has been observed in the US young,
caries rates are increasing in Third World countries as they
their most basic functions of eating, sleeping, speaking, being
adopt Western diets. It is also increasing in the US elderly. In
productive and enjoying general health as defined by the
this population, retention of teeth into old age with
World Health Organization.
accompanying exposure of root surfaces, has led to an increase
in cemental caries.
CARIES INCIDENCE IN EUROPE
Caries is as old as mankind, and the prevalence of caries is INDIAN SCENARIO
reported to increase temporarily in relatively affluent periods. Dental Caries has been consistently increasing both in prevalence
In Europe, for example, there was an increase in caries during and severity since last five decades. In the year 1941, its
the Roman occupation, probably as a result of increased use prevalence was reported between 40 to 50 percent with an
of cooked foods. These early increases were minor compared average DMFT of 1.5 (Table 10.4). In 1980s the point prevalence
to the dramatic increase that started from the time that sucrose increased to about 80 percent in children with an average DMFT
was imported from the Caribbean islands to Europe. This of 2 to 6 at the age of 16 years in different regions of the country.
increase continued until the 1960s, by which time dental caries The point prevalence in 10 to 15-year-old children of Delhi was
was considered rampant. At that time, in non-fluoridated 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 The potential for promoting the consumption of sugar is
1992, the DMFT index in 12-year-old Indian was 0.89 while in greater in underdeveloped countries because they are low sugar
1996 the point prevalence was 89 percent with DMFT ranging consumers and most developed countries have either reached
between 1.2 to 3.8. In India, different investigators have studied saturation levels of sugar consumption or switched to sugar
various age groups. substitutes.

DENTAL CARIES IN UNDERDEVELOPED PROBABLE REASONS FOR THE MARKED

COUNTRIES DECLINE IN DENTAL CARIES IN MOST
WESTERN INDUSTRIALIZED COUNTRIES
The pattern of dental caries in underdeveloped countries is
following the pattern of the disease which was observed in No single factor has been found to account for the decline and
Europe in the 18th and 19th centuries. An increase in the the most likely explanation is that a combination of factors is
prevalence and severity, first in the upper income groups then responsible. Dental caries is a sugar-dependent infective
in the urbanized populations followed by changes in disease disease. The demineralizing effect of the cariogenic challenge
prevalence in the rural groups. The influence of social class is can be prevented or reduced depending on the strength of the
strong. In Ethiopia, children from more affluent high social class challenge and the availability of fluoride at the site of attack.
families had four times more caries in primary teeth than poorer Fluoride reduces the enamels solubility in acid and it influences
children and twice as many permanent teeth with caries. the remineralization of lesions as well as the metabolism of the
Urbanized populations in underdeveloped countries are more oral bacteria. Some authors believe that the main mechanism
likely to consume refined sugars than those in rural areas. whereby fluoride acts in caries prevention is in promoting
Therefore, it is not surprising that caries rates are higher in urban remineralization. The factors to consider in relation to the
populations. In the Sudan, 15 to 19-year-old urban children had decline in caries are sugar consumption, fluorides in toothpaste,
seven times more caries than children in rural areas where the fluoride-rinsing, systemic fluoride, improved oral hygiene and
sugar consumption was below 5 lbs/person/year. the use of antibiotics.
Deteriorating dental health is seen as a necessary Globally, WHO reports caries prevalence in school-age
consequence of a certain kind of economic growth because a children at 60 to 90 percent and as virtually universal among
change to a more refined high-sugar diet is associated with adults in the majority of countries. Because so few countries
economic growth. Sugar consumption in underdeveloped are spared high levels of this disease, caries maps typically
countries is rising; consumption is predicted to be higher than display disease severity rather than prevalence. Global data by
in industrialized countries where consumption is falling. 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, in a process known as demineralization. If this process is not
using the Decayed, Missing, and Filled Teeth (DMFT) index of halted or reversed via remineralization (the redeposition of
severity. The map shows a clear pattern of higher disease mineral via saliva) it eventually becomes a frank cavity.
experience in North and South America, Western Europe, and Dental caries of the enamel typically is first observed
much of Africa; more moderate disease experience in much of clinically as a so-called white-spot lesion. This is a small area
South America, Russia, and the former Soviet Republics; and of subsurface demineralization beneath the dental plaque. The
low levels of disease in Eastern Africa, China, Australia and body of the subsurface lesion may have lost as much as 50
Greenland. While the correlation between caries rates and percent of its original mineral content and often is covered by
national development is not tight, WHO has observed that an apparently intact surface layer. The surface layer forms
developed countries have higher rates of caries experience, by remineralization. The process of demineralization continues
while developing countries have lower rates. (Fig. 10.1) WHO each time there is carbohydrate taken into the mouth that is
has attributed these differences to the relative availability of metabolized by the bacteria. The saliva has numerous roles,
simple sugars in diets, to fluoride, and to dental treatment (World including buffering (neutralizing) the acid and remineralization
Oral Health Report 2003). Figure 10.2 shows the situation for by providing minerals that can replace those dissolved from
the ages 35 to 44 years. the tooth during demineralization.
The critical pH value for demineralization varies among
THE CARIES PROCESS (PATHOGENESIS) individuals, but it is in the approximate range of 5.2 to 5.5.
Conversely, tooth remineralization can occur if the pH of the
Bacterial Plaque and Acid Production environment adjacent to the tooth is high due to: (1) lack of
The mechanism of dental caries formation is essentially substrate for bacterial metabolism; (2) low percentage of
straightforward. Plaque on the surface of the tooth consists of cariogenic bacteria in the plaque; (3) elevated secretion rate of
a bacterial film that produces acids as a byproduct of its saliva; (4) strong buffering capacity of saliva; (5) presence of
metabolism. To be specific, certain bacteria within the plaque inorganic ions in saliva; (6) fluoride; and (7) rapid food
are acidogenicthat is, they produce acids when they clearance times. Whether dental caries progresses, stops, or
metabolize fermentable carbohydrates. These acids can dissolve reverses is dependent on a balance between demineralization
the calcium phosphate mineral of the tooth enamel or dentine and remineralization.

Fig. 10.1: World map on dental caries 2003 (12 years old)
 Chapter 10 N Epidemiology of Dental Caries 103

Fig. 10.2: World map on dental caries 2003 (35-44 years old) (with permission from WHO)

However, if demineralization overtime exceeds remineral- obtained from the Mesopotamian areas which date back to
ization, an initial carious lesion (the so-called white spot about 5000 BC. According to the legend, toothache was caused
lesion) can develop and may further progress to a frank by a worm that drank the blood of teeth and fed on the root of
cavity. the jaws.
Demineralization can be reversed in its early stages through
uptake of calcium, phosphate, and fluoride. Fluoride acts as a Endogenous Theories
catalyst for the diffusion of calcium and phosphate into the
tooth, which remineralizes the crystalline structures in the lesion. Humoral Theory
The rebuilt crystalline surfaces, composed of fluoridated The ancient Greek believed that a persons physical and mental
hydroxyapatite and fluorapatite, are much more resistant to
constitution was determined by four elemental humors of the
acid attack than is the original structure. Bacterial enzymes can
body: blood, phlegm, black bile and yellow bile. An imbalance
also be involved in the development of caries.
in these humors is the cause of all diseases including dental
The cause of dental caries is the consumption of fermentable
caries.
carbohydrates (sugars). There is a dose- response relationship
between the quantity of the sugar consumed and the According to Galen, the ancient greek physician and
development of dental caries. It is suggested, at levels below philosopher, dental caries is produced by internal action of
10 kg/person per year dental caries will not develop. [15 kg/ acrid and corroding humors. Hippocrates referred to
person per year in fluoridated areas]. accumulated debris around teeth and to their corroding action.
He also stated that stagnation of juices in the teeth was the
THEORIES OF DENTAL CARIES cause of tooth ache.

The Legend of the Worm Vital Theory [Proposed during 18th Century]
Ancient Sumerian text known as The legend of the worm According to this theory, the tooth decay originated like bone
gives reference of the tooth decay and tooth pain. It was gangrene, from within the tooth itself.
104 Section 2 N Dental Public Health
Exogenous Theories AREAS PRONE TO DENTAL CARIES
Chemical Theory Bacterial plaque is the essential precursor of caries. Hence,
Parmly (1819) proposed that an unidentified chemical agent sites on the tooth surface which encourage plaque retention
was responsible for caries. According to this theory, teeth are and stagnation are particularly prone to progression of lesions.
These sites are:
destroyed by the acids formed in the oral cavity by the
Enamel in pits and fissures on occlusal surfaces of molars
putrefaction of protein which produced ammonia and was
and premolars, buccal pits of molars, and palatal pits of
subsequently oxidized to nitric acid. Robertson (1895) proposed
maxillary incisors
that dental decay was caused by acids formed by fermentation
Tooth surfaces adjacent to dentures and bridges which make
of food particles around teeth.
cleaning more difficult, thus encouraging plaque stagnation
Approximal enamel smooth surfaces just cervical to the
Parasitic or Septic Theory contact point
Dr Miles and Underwood proposed the so-called septic In patients where periodontal disease has resulted in gingival
theory. They claimed that dental caries is caused by direct recession, caries occur on the exposed root surface
action of microorganisms that penetrate the dental tubules and The enamel of the cervical margin of the tooth just coronal
destroy the organic component of the dentine leaving the to the gingival margin
inorganic parts to be broken down and washed away in fluids The margins of restorations, particularly those that are
of the mouth. 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 105
or on smooth surfaces. Lesions may start on enamel (enamel After 14 Days
caries) or on exposed root cementum and dentine (root caries).
With completely undisturbed plaque, the enamel changes are
Primary caries denotes lesions on unrestored surfaces. Lesions visible after air drying as whitish opaque changes.
developing adjacent to fillings are referred to as either recurrent Smooth chalky white area.
or secondary caries. Residual caries is demineralized tissue left A subsurface lesion starts forming.
in place before a filling is placed.
Primary lesion: Begins on a surface with no previous lesion or After 3 and 4 Weeks
restoration. The outermost surface exhibits complete dissolution of thin
Secondary lesion: Begins on a surface which has already had perikymate overlappings and more marked dissolution
a lesion, i.e. around an existing restoration. May also be a new corresponding to larger developmental irregularities such as pits
lesion on a remaining part of an inadequately excavated and of tomes processes and focal holes.
filled lesion.
HISTOPATHOLOGY OF DENTAL CARIES
Rampant caries is the name given to multiple active carious
lesions occurring in the same patient, frequently involving Dental caries can involve enamel, dentine and root (Fig. 10.3).
surfaces of teeth that are usually caries-free.
CARIES OF THE ENAMEL
Early childhood caries is a term used to describe dental caries
presenting in the primary dentition of young children. Smooth Surface Caries
Bottle caries or nursing caries are names used to describe a Incipient caries is the appearance of smooth chalky white area.
particular form of rampant caries in the primary dentition of The overlying enamel surface is smooth, hard and shiny.
infants and young children. The problem is found in an infant Early lesion in enamel caries is conical in shape with its apex
or toddler who falls asleep sucking a bottle (called a nursing towards the dentine and base toward the surface of the tooth.
bottle) which has been filled with sweetened fluids (including Four zones are present with differing translucency.
milk). 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
ENAMEL CHANGES DURING EARLY CARIES
of calcium ions into the body of the lesion and may have to be
LESION DEVELOPMENT removed to allow the lesion to become arrested.
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.

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 On examination, the ground section in Quinolone with
advancing front of the lesion: transmitted light, the body of the lesion appears relatively
1. Translucent zone translucent compared to sound enamel.
2. Dark zone It forms the bulk of the lesion and extends from just beneath
3. Body of lesion the surface zone to dark zone
4. Surface zone Striae of retzius are well marked.
Reduction of 24 percent in mineral per unit volume as
Translucent Zone compared to sound enamel.
Increase in unbound water and organic content due to
Lies at the advancing front of enamel lesion (not always ingress of bacteria and saliva.
present)
This is the first recognizable zone of alteration from the
Surface Zone
normal enamel.
In transmitted light the zone appears structure less. It represents the most important change in enamel caries
This zone may vary from 5 to 10 micrometer in width. in terms of prevention and management
Pore volume slightly more than one percent [in sound Partial demineralization 1 to 10 percent loss of mineral salts
enamel: 0.1%] has taken place. Pore volume is less than five percent of
Slight loss of mineral; Mainly the minerals are lost from this spaces.
zone and not organic material Surface zone retains a negative birefringence.
Translucent appearance: Initial dissolution of the enamel The surface is resistant due to greater degree of mineralization
mainly occurs along the gaps between the rods and interrod and concentration of fluoride in the surface enamel. It remains
enamel in the tissue; thus on examining ground sections intact and well mineralized because it is a site where calcium
imbibed in clearing agent, Quinolone (suitable since and phosphate ions, released by subsurface dissolution
refractive index is similar to that of enamel). Quinolone is become precipitated. This is called remineralization.
assumed to penetrate more easily into these enlarged pores, Cavitation is due to loss of this layer which allows the
the final result looks like a structureless zone. bacteria to enter the lesion. It is of relatively constant width,
No evidence of protein loss seen. a little thicker in arrested or remineralizing lesions.

Dark Zone Pit and Fissure Caries

Lies adjacent and superficial to the translucent zone. Carious lesion starts at both sides of the fissure, not at the base.
This zone is formed as a result of demineralization and The enamel is thin in fissures so there is early dentine
appears dark brown involvement. The carious lesion forms a triangular or cone-
Under polarized light the dark zone has a pore volume of 2 shaped lesion with its apex at the outer surface and base towards
to 4 percent the dentinoenamel junction (DEJ).
Occurs in 90 to 95 percent of lesions Lesion begins beneath plaque, with decalcification of enamel.
Represents a result of multitude of demineralization and Pit and fissures are often deep, with food stagnation,
reprecipitation processes Enamel in the bottom of pit or fissure is very thin, so early
When examined in transmitted light, after inhibition with dentine involvement frequently occurs.
Quinolone, appears dark brown in ground sections, thus Here the caries follows the direction of the enamel rods. In
called Dark zone; and shows positive birefringence in pit and fissure the enamel rods are said to flare laterally at
contrast to negative of that of sound enamel. Therefore, the bottom of the pit and caries is said to follow the path of
Positive zone. enamel rods hence a characteristic angular/inverted V
The appearance of dark zone is due to remineralization shaped lesion is formed.
occurring at the advancing front of the lesion. It is broader It is triangular in shape with the apex facing the surface of
in arrested or remineralized lesion. tooth and the base towards the DEJ.
When reaches DEJ, greater number of dentinal tubules are
Body of Lesion involved.
It produces greater cavitation than the smooth surface caries
Lies between the relatively unaffected surface layer and and there is more undermining of enamel.
dark zone.
It is the area of greatest demineralization.
In polarized light- pore volume is five percent in spaces near CARIES OF THE DENTINE
the periphery and nearly equals to 25 percent in the outer The caries process in dentine involves the demineralization of
of the intact lesion. the mineral component and breakdown of the organic
 Chapter 10 N Epidemiology of Dental Caries 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.
Fig.10.5: Infected and affected layers in dentine
Zone of Demineralization
In the demineralized zone the intertubular matrix is mainly
component of collagen fibers. The caries process in dentine is
affected by a wave of acid produced by bacteria in the zone of
approximately twice as rapid as in enamel. Spread of caries is
bacterial invasion, which diffuses ahead of the bacterial front.
more in dentine compared to enamel because of:
The softened dentine in the base of a cavity is therefore sterile
1. Decreased calcification (mineralization).
(affected dentine) but it cannot be distinguished from softened
2. Existence of pathways (dentinal tubules).
infected dentine. It may be stained yellowish-brown as a result
Advanced carious lesions in dentine consist of two distinct
of the diffusion of other bacterial products interacting with
layers having different microscopic and chemical structures. The
outer layer is heavily infected by bacteria which are mainly located proteins in dentine.
in the tubule spaces. The collagen fibers are denatured and the
organic matrix is not being remineralized. The inner layer is Zone of Bacterial Invasion
scarcely infected, but affected by plaque acid (Fig. 10.5). It still In this zone the bacteria extend down and multiply within the
contains high concentrations of mineral salts and can be dentinal tubules, some of which may become occluded by
remineralized. bacteria. There are always, however, many empty tubules lying
The initial dentinal changes are known as dentinal sclerosis among those tubules containing bacteria. The bacterial invasion
or transparent dentine. The dentinal sclerosis is due to probably occurs in two waves: the first wave consisting of
calcification of dentinal tubules. The change is minimal in acidogenic organisms, mainly, lactobacilli produce acid which
progressing caries and more in slow caries. In transmitted light diffuses ahead into the demineralized zone. A second wave of
the dentine appear transparent. In reflected light sclerotic mixed acidogenic and proteolytic organisms then attack the
dentine appear dark. In advanced lesions tiny liquefaction foci
demineralized matrix.
are formed.
The walls of the tubules are softened by the proteolytic
In secondary dentine the dentinal tubules are fewer and
activity and some may then be distended by the increasing
irregular. Caries spread laterally at the junction of primary and
mass of multiplying bacteria. The peritubular dentine is first
secondary dentine separating both.
compressed, followed by the intertubular dentine, resulting in
Various zones are distinguished assuming the shape of
elliptical areas of proteolysis-LIQUEFACTION FOCI.
triangle with the apex toward the pulp and the base toward
Liquefaction foci run parallel to the direction of the tubules
the enamel.
and may be multiple, giving the tubule a beaded appearance.
VARIOUS ZONES OF CARIES OF DENTINE Zone of Decomposed Dentine
Zone of Fatty Degeneration In this zone the liquefaction foci enlarge and increase in number.
1. Firstly the fatty degeneration of the tomes dentinal fibres Cracks or clefts containing bacteria and necrotic tissue also appear
resulting in deposition of fat globules in the further end of at right angles to the course of the dentinal tubules forming
dentinal tubules. TRANSVERSE CLEFTS. Bacteria are no longer confined to the
It has been suggested that this fatty degeneration tubules and invade both the peritubular and intertubular dentine.
contributes to the: In acute, rapidly progressing caries the necrotic dentine is very
1. Impermeability of the dentinal tubule. soft and yellowish-white; in chronic caries it has a brownish-
2. Also sclerosis of dentinal tubule. black color and is of leathery consistency.
108 Section 2 N Dental Public Health

CARIES IN DENTINE FACTORS AFFECTING THE EPIDEMIOLOGY OF

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

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, C. Sex
hence less food entrapment in fissures, so less caries.
iii. Position: Malaligned, out of position, rotated teeth are In young people caries has been seen to higher in the females
difficult to clean, favoring the accumulation of food and but some studies show no significant difference between the
debris. This may predispose to the development of caries. 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).
B. Saliva
It can be considered as an environmental factor also as teeth D. Age
are constantly bathed by it. This influences the process of dental
caries. Saliva has a flushing action on teeth. Although present in all ages, it was believed that dental caries
i. Composition: varies from person to person. Saliva is dilute was disease of childhood. WHO global data bank has shown a
fluid; over 99 percent being made up of water. decline in DMFT values in 12-year-old children. Some studies
1. Proteins: They include enzymes, immunoglobins and indicate greatest intensity of dental caries occurs in 15 to 25
other antibacterial factors, mucous glycoproteins and years of age.
certain polypeptides. Root caries is seen in over 60 years age group people,
2. Enzymes: -Amylase mainly due to denuded root surface because of gingival
3. Immunoglobulins secretary IgA recession.
4. Antibacterial proteins Lysozyme, Lactoferrin,
Sialoperoxidase. E. Race and Ethinicity
5. Glycoproteins. A number of studies indicate that blacks [Negroes] of
6. Polypeptides Statherin, Sialin (helps to regulate pH comparable age and sex have a lower caries scores than
of plaque). Caucasians. Chinese population has shown to have a lower
7. Other Organic Compounds: caries rate than corresponding white population. These
- Free Amino Acids differences are probably more due to environmental factors.
- Urea (it is hydrolysed by many bacteria with release
of Ammonia, leading to rise in pH). F. Socioeconomic Status
- Glucose
8. In Organic Constituents: There is an inverse relationship between socioeconomic status
- Major Ions [Sodium, Potassium, and Chloride and and dental caries experience in primary dentition. The relation
Bicarbonate] contribute to osmolarity of saliva. has not been established in adults, though some studies suggest
- Bicarbonates: Principal buffer in saliva. so.
- Thiocyanate: Has antibacterial action.
- Fluoride: Has anticaries action. G. Heredity
i. Saliva: It has a critical role to play in the development of
Environmental factors have a greater influence than genetic
caries or its prevention. Saliva provides calcium,
factors but latter also contributes to the causation of caries.
phosphate, proteins, lipids and antibacterial substances
and buffers. Saliva buffering can reverse the low pH in
plaque. H. Emotional Disturbances
ii. Buffering and neutralization: pH of saliva depends on the Emotional disturbances, particularly transitory anxiety states
bicarbonate concentration. Saliva is alkaline and is an tend to increase the incidence of dental caries.
effective buffer system. These properties protect the oral
tissues against acids and plaque. After eating a sugary II. AGENT FACTORS
food if saliva is stimulated by chewing substances such as
wax or sugar free chewing gum, the drop in pH in plaque A. Microorganisms
which would have occurred is reduced or even eliminated.
This salivary neutralization and buffering effect markedly The mouth has a diverse resident microbial flora. The normal
reduces the cariogenic potential of foods. inhabitants become established early in life. There have been
iii. Quantity: Rate of flow of saliva may be an additional factor a few epidemiological studies to investigate the link between
which helps contribute to caries susceptibility or caries oral flora and dental caries. Streptococcus mutans was first
resistance. Mild increase or decrease in flow may be of identified in 1924 by Clarke and subsequently Lactobacillus
little significance, near total reduction in salivary flow acidophilus by Bunting (1930). These acid producing bacteria
adversely affects dental caries. There is an inverse relation were found to be associated with the formation of dental caries.
between salivary flow and dental caries. Streptococcus mutans is of interest because it has the ability to
 Chapter 10 N Epidemiology of Dental Caries 111
form an extracellular polymer of glucose, mutans from sucrose, E. Soil
which aids the microorganism in adhering to the enamel surface
and in establishing a stable relationship there. Trace elements in soil have shown a relation with caries. An
The absolute demonstration of a specific microorganism increase in dental caries is seen in areas where selenium is
as the causative agent of dental caries in man may be impossible present in soil, whereas molybdenum and vanadium are said
because of diverse organisms being always present in the oral to decrease dental caries.
cavity and on the teeth.
L. acidophillus and other acidogenic microorganism in F. Fluoride
plaque and carious lesion may be capable of producing caries Fluoride in water and soil decreases incidence of dental caries.
by themselves, or they may be able to act synergistically with
Streptococcus mutans in caries initiation. EARLY CHILDHOOD CARIES
Actinomyces are Gram-positive pleomorphic rods (GPPR)
which form a large proportion of the oral microflora of all Early childhood dental caries has been reported by the Centers
mammals. Actinomyces are also among the earliest colonizers for Disease Control and Prevention to be perhaps the most
of dental surfaces and may constitute up to 27 % of the pioneer prevalent infectious disease of our nations children. Early
bacteria. They have been implicated in root caries, although childhood dental caries occurs in all racial and socioeconomic
their role in dental caries initiation and progression is not well- groups; however, it tends to be more prevalent in low-income
understood. children, in whom it occurs in epidemic proportions. Human
dental flora is site specific, and an infant is not colonized until
B. Dental Plaque the eruption of the primary dentition at approximately 6 to 30
Bacterial plaque is a dense non-mineralized, highly organized months of age. The most likely source of inoculation of an infants
mass of bacterial colonies in a gel-like intermicrobial, enclosed dental flora is the mother or another intimate care provider,
matrix or slime layer. It is a transparent film that can be supra- through shared utensils, etc. Decreasing the level of cariogenic
gingival, coronal to the gingival margin on the clinical crown organisms in the mothers dental flora at the time of colonization
of the tooth and subsgingival, apical to the margin of the gingiva. can significantly impact the childs predisposition to caries. To
prevent caries in children, high-risk individuals must be identified
III. ENVIRONMENTAL FACTORS at an early age (preferably high-risk mothers during prenatal care),
and aggressive strategies should be adopted, including
A. Diet anticipatory guidance, behavior modifications (oral hygiene and
feeding practices), and establishment of a dental home by 1 year
According to acidogenic or chemoparasitic theory, dental caries of age for children deemed at risk.
occurs when acid is produced by bacteria in dental plaque when
refined carbohydrates are eaten. The presence of refined ROOT CARIES
carbohydrate as sugar is essential for the majority of caries
development and sucrose is the most cariogenic of all sugars. Root caries can be defined as a lesion which is initiated or
In human consumption, sucrose accounts for 60 percent of all extends onto the part of the tooth apical to the cementoenamel
sugars eaten. junction.
The term primary as it is used with root caries refers to
B. Geographic Variation new dental caries occurring in the absence of a restoration.
Secondary (recurrent) root caries refers to caries occurring
It is well documented that dental caries experience has been adjacent to an existing restoration. There is general agreement
decreasing in children in developed western [19731983] on this terminology.
countries. But this decrease is beginning to level out. Gradual Root caries most often occurs supragingivally, at or close
increase in caries in 5 years old have been found in some areas. to (within 2 mm) the cemento-enamel junction.
[Palmer & Pitts 1994]. This phenomenon has been attributed to the location of
the gingival margin at the time conditions were favorable for
C. Climate caries to occur. The location of root caries has been positively
Sunshine and high temperature areas seems to have lower associated with age and gingival recession. This is consistent
dental caries [inverse relationship]. Whereas areas with more with the concept that root caries occurs in a location adjacent
relative humidity and rainfall have shown increase dental caries. 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.
D. Oral Hygiene
Early root caries tends to be diffused (spread out) and track
Inverse relationship has been seen between oral hygiene and along the cementoenamel junction or the root surface. More
dental caries. Poor oral hygiene increases the rate of dental caries. advanced root lesions enlarge toward the pulp.