NURSING CARIES AND RAMPANT CARIES

INTRODUCTION

Throughout the history of man, diseases have come and diseases have disappeared. For most of the major diseases. It has been possible to clearly identify the reasons why the disease was bought under control. Such reasons may include nation wide or even global vaccination programmes, change in living condition with improved nutrition and non-contaminated drinking water.

HISTORICAL BACKGROUND 

Caries in infant and young children have long been recognizable as a clinical syndrome, which was described as early as middle of last century. Beltrami characterized this pattern of early caries in young children in 1930’ & as “les dents noire de tout petis” or literally translated “black teeth of the very young”. In 1962 Dr. Elias Fass published the first comprehensive description of caries in infants, which he termed as nursing bottle mouth.

The first sentence of his paper begins “nothing is so shocking to dentist as examination of child patient suffering from rampant caries. Since first description is 1962 the term. Nursing bottle mouth has been succeeded by many names but recently in 1994 conference at centres for disease control and prevention recommended. Use of a less specific term such as early childhood caries [ECC] because it was the consequences of the attendees that the link both habits and caries was not absolute nursing caries is an unique pattern dental caries in very young children due to molonged and improper feeding habits. Even as first primary tooth starts erupting the oral environment can be condusive to initiation of demineralization. Inspite of the fact that dental caries is diminishing in our youth there are still a large no of children with advanced multiple carious lesion victims of parental ignorance of nursing caries which is distinct clinical entity.

Important terminology and their definitions are as follows:-

TERMINOLOGIES

AUTHOR AND YEAR

DEFINITION

Nursing caries

Nursing Bottle mouth

Nursing bottle syndrome bottle propping caries labial caries, comforter caries.

Night bottle syndrome.  baby bottle syndrome.

Nursing mouth.

Baby bottle mouth

Nursing mouth decay

Nursing bottle caries

Milk bottle

Syndrome

Infancy caries

Circular caries  

Rampant caries

Early childhood caries [ECC]

Winter et al 1966

Kroll et al, 1967

Shelton et al, 1977

Dilley et al, 1980

Croll, 1989

Tsam tsouris, 1986

Ripa, 1988

Massler (1945)  

Defined as presence of 1or more decayed,

A unique pattern of dental decay in young children due to prolonged nursing habit.

A syndrome characterized by a severe caries pattern beginning with max ant teeth in a healthy bottle fed-infant or toddler.

A devastating condition that may render young children denteelly crippled.

A unique pattern of dental caries in young children.

A very destructive carious process, which can affect.

Infants and toddlers.

Caries caused by prolonged use of bottle filled with any liquid other than water.

A specific from of rampant decay of primary teeth of infants.

Rampant caries is defined as suddenly appearing widespread, rapidly spreading, burrowing type of caries resulting in early involvement of pulp and affecting those teeth, which are usually regarded as immune to decay.

Epidemiology – missing or filled tooth surface in any 10 tooth in a child 71 months of age or younger.

PREVALENCE OF NURSING CARIES

Country                            Year of Publication                   Prevalence (%)

England                           1967 – 82                                   3.1 – 12%

United states                    1976 – 87                                   1 – 53.1%

Canada                             1982                                           3.2%

Australia                          1985                                           3.1+2.2%

Indonesia                         1979                                           48.0%

India (Manipal)               1996                                           65.5%

DEVELOPMENTAL STAGES OF ECC

Stage                                          Clinical stage                                       Age

Stage I                              Initial reversible                        10 – 18 month

Stage II                            Damaged carious stage             18 -24 month

Stage III                           Deep lesion                                          24 – 36 month

Stage IV                           Traumatic stage                         36 – 48 month

CLASSIFICATION OF ECC - BY WAYNE H

Type I ECC            -                   Mild to moderate

Type II ECC          -                   Moderate to severe

Type III ECC         -                   Severe.

ETIOLOGY OF ECC –

Dental decay in infects and toddlers is now collectively known as early childhood caries. Although the etiology of ECC is similar to other types of coronal. Smooth surface caries the biology may differ. The bacteria’s flora and host defense systems in young infant are in process of being established, in addition to tooth surfaces that are newly erupted and immature and may show hypoplastic defects its thus, in ECC there may be a unique. Risk factor in infants young children.

1. DENTAL PLAQUE –

Although there are few studies on formation and development of plaque in young children relevant information may be extra polated from in vivo studies in young adults besides modulation of the oral flora the acquired pellicle has functions such as lubrication, protection from acid attack prevention of crystal growth on enamel surfaces and a role in enamel remineralization. In the absence of fermentable carbohydrates, organic acid such as acetate, propionate, and butyrate are produced.

In contrast when fermentable carbohydrate are present, lactate is mainly produced, which coincides with a ph drop in plaque bacteria and their alkaline products provide major contributions to  the PH rise in plaque and the base generating metabolism of plaque bacteria is considered by many to be a significant determinant for cariogenecity of plaque.

2. MUTANS STREPTOCOCCI –

The main bacteria indicated in ECC are termed “mutans streptococci.” Of which the species S mutans and S – robrinus are most commonly isolated is human dental caries.

v   Mutans streptococci produces insoluble glucans from sucrose  these glucans increase thickness of plaque, and acid production at deeper plaque layers.

v   Synthesize intra cellular polysaccharide which support continual acid production during periods of low   arch of exogenous substrate.

v   Mutans streptococa producer large amt of lactic acid which causes tooth demineralization.

v   Acid tolerance of bacteria is high, thus allowing colonization and persistence of under cariogenic conditions.

v   Production of dextranase allows invation of  mutans streptococci to replace earlier colonizing bacteria.

3. SALIVARY FACTORS –

Saliva provides the main host defense system against caries has major role in clearance of foods and buffering of acid generated by plaque. Saliva contain anti microbial.

Proteins – lactofernin, lysozymes, saliva also contain several organic compounds – mucin  glycoprotein fibronectin, flow rates of saliva are important.

4. IMMUNOLOGICAL FACTORS –

Host immune mechanism include specific  immune factors derived from saliva [secretory IGA] and gingival crevicular  fluid [IgG]. And non – specific antimicrobial systems, derived mainly from saliva secretory IgA may inhibit bacterial adherence as well as neutralization of bacterial enzymes.

5. TOOTH MATURATION AND DEFECTS –

Tooth  is most susceptible to caries in the period immediately after eruption and prior to final maturation thus in many infants, a ambination of recently impted immature enamel in an environment of cariogenic flora with frequent ingestion of fermentable carbohydrates would render  tooth susceptible to caries.  

6. CARIOGENECITY OF SUCROSE –

Sugars, glucose, fructose found in fruit juices and vitamins and foods are probably the main sugars associated infant caries. Sugars is most important as it is only substrate. Used for bacterial generation of plaque dextrans. This is essential for bacterial adherence and facilitates implantation of cariogenic bacteria in the oral cavity.

7. FREQUENCY OF CONSUMPTION OF SUGARS –

Children with ECC have a high frequency of sugar consumption, not only of fluids, given in nursing bottle but also of sweetened solid food increased frequency of eating sucrose acidity of plaque and enhances the establishment and dominance of S. mutans the increased total times sugar is in mouth increases the potential for enamel demineralization and there is inadequate time of remineralization lization by saliva. As a result demineralization because predominant.

8. ORAL CLEARANCE OF CARBOHYDRATES –

In infants with ECC, the sleep time consumption of sugars is another common characteristic the low salivary flow during sleep decreases the oral clearance of sugars and increases length of contacted between plaque and substrates thus increasing the cariogenicity of substrate         

9. BOVINE MILK –

The cariogenecity of milk is often questioned because plain bovine milk is the common fluid placed in feeding bottle in many cases of ECC and also because prolonged breast feeding has been putatively  associated with ECC.

But most of studies show that milk is not cariogenic and exert some cariostatic effect. In vitro studies shows that milk decreases the solubility of enamel and results have been extended by intra oral cariogenecity test (ICT) which demonstrated that cheese extracts prevented enamel softening  caused by sucrose. The mechanisms of protection by milk appear to work are decreasing demineralization and increases remineralization of enamel, increasing the calcium and phosphorous concentration in plaque and increased acid buffering capacity of plaque.

10. HUMAN MILK –

Compared to bovine milk human breast milk has a lower mineral content higher concentration of lactose and less protein  the relationship breast feeding and dental caries are likely to be complex  and confounded by many biological variables such as mutans streptococcus infection enamel hypoplasia in take of sugars as well as social variables.

11. ACID FRUIT DRINK –

Acid in fruit juices and soft drinks many decrease the oral PH. In presence of sugars in the drinks, this fall is pH is likely to enhance the fermentation of carbohydrate thus causing enamel demineralization.

12. FLUORIDES –

There is minimal information cariostatic effect of topical fluorides is prevention of ECC. The topical effect of fluorides are complex and include changes in mineralization phase as well as modulation of metabolic effects of mutans streptococci and other bacteria in dental plaque.

13. OTHER RISK FACTORS –

A significantly high % of children rampant decay have history of medical conditions in infancy. The reason that chronically sick children have an increased risk of developing dental caries is likely to be related to predisposition to enamel hypoplasia of such children or to the possibility that many chronically sick infants are comfasted   with bottle containing sweet fluid or have frequent infestations of sweetened  medication.

PHYSCOSOCIAL AND BEHAVIOURAL ISSUES IN ECC

Prolonged use of the baby bottle, especially use of bottle at bed time is believed to be associated with increased risk of caries. But it is not only factor with caries development.

Infant feeding pattern – use of bottle is predominant is children with ECC but it is not sole factor. Greater length of bottle contact appears to be positively associated with caries. Another behaviour is development of maxillary anterior caries is use of bottle beyond the age of 1 year. It is seen that children caries eliminate both are 4-7 months later than those without caries. Use of bottle beyond age of 1 year is major risk factor. Children who are exclusively breast fed are also susceptible to caries.

RACE AND ETHNICITY –

Children living in ethnic areas demount an extremely rate of ECC ranging from 70% to 80% some of the factors for incidence of ECC are.

v   Increased risk that would be associated with cultural norms including concern for oral health.

v   Prenatal diet that contribute to enamel hypoplasia  

v   Care of 10 teeth.

v   Child learning practices

v   Access to dental and medical care.

v   Minorities may experience significant barriers to dental care including cost of care.

SOCIO – ECONOMIC STATUS

Social class may influence caries risk several ways- individuals from lower socio – economic status experience financial social and material disadvantage that compromise their ability to care for services and live in healthy environment all of which leads to reduced resistance to diseases.

TOOTH BRUSHING

As ECC starts on tooth surface that can be easily accessed by routine tooth brushing, oral hygiene levels may be associated with caries risk. Increase pregnancy and better oral hygiene are associated with decrease caries levels in preschool children.

DENTAL KNOWLEDGE

Dental knowledge is regarded as in important variable in etiology of ECC because understanding the relationship between microbiology of caries, the role of cariogenic foods, the use of baby bottle is necessary for prevention of ECC.

 STRESS

One of the underlying mechanisms that could account for effects of social class on oral health status is increased stress experienced in families with financial and social instability related to lower socio economic status.

PATHOPHYSIOLOGY

CLINICAL FEATURES

The intra oral decay pattern of nursing caries is characteristic and pathognomic of the conditions. It affects primary teeth in following sequence.

1. Maxillary lateral incisor – Facial, lingual, mesial and distal surfaces.
2. Maxillary lateral incisor – Facial, lingual, mesial and distal surfaces.
3. Maxillary first molar - Facial, lingual, mesial and occlusal, prominent surface
4. Maxillary canine and second molar – Facial, lingual and proximal surfaces.
5. Mandibular molars – At later stages.

Mandibular anteriors are spared because of

1. Protection by the tongue.
2. Cleaning action of saliva due to presence of the orifice of the duct of sublingual glands very close to incisors.

This unique pattern and unequal severity of lesion is due to

-      Chronology of primary tooth eruption

-      Duration of deleterious habits of feeding

IMPLICATIONS

The child who has nursing caries has an increased risk of developing caries even in permanent dentition.

The child with caries is also susceptible to other health hazards.

The treatment of nursing caries may prove to be financial burden for some parents.

MANAGEMENT

AIMS –

Management of existing emergency

Arrest and control of carious process

Institution of preventive procedures

Restoration and rehabilitation

Factors affecting management

Extent of the lesion

Age of the patient

Behavioral problems of the child due to young age of child

TREATMENT PROPER –

It can be divided into 3 visits –

FIRST VISIT –

This phase of treatment constitutes treatment of the lesion, identification of causes for counseling the parent

All lesions should be excavated and restored

Indirect pulp capping or pulp therapy procedures can be evaluated by further investigation. 

If abcesses is present it can be treated through drainage.

X-rays are advised to access the condition of the succedeous teeth.

Collection of saliva for determining salivary flow and viscosity

Also, application of fluoride topically

PARENT COUNSELLING

The parent should be questioned about the child’s feeding habits, specially use of nocturnal bottles, demand the breast feeding, pacifiers dipped in sweetening agents.

The parent should be asked to try to stop the child from using the bottle as pacifier while in bed.

In case of considerable emotional dependence on bottle suggest use of fluoridated water.

The parents should be instructed to clear child’s teeth after every feed.

Parents are advised to maintain teeth ache record of the child for 1 week include time, of food given to the child, type of food and number of sugar exposures.

SECOND VISIT –

Should be scheduled 1 week after first visit.

Analysis of diet chart and explanation of disease process of child’s teeth should be undertaken by simple equation.

Isolate the sugar factors from diet chart and control sugar exposure.

Reassess the restoration and redo if necessary

Caries activity tests can be started and repeated at monthly intervals to monitor success of treatment.

 THIRD AND SUBSEQUENT VISIT –

Restoring all grossly decayed teeth

In case of unrestorable teeth extractions can be done followed by space maintainers.

Crews can be given for grossly decayed or endodontically treated teeth   

Review and recall after every 3 months.

PREVENTION

The main strategies for the prevention of nursing caries should be create awareness and alert prospective parents and new parents about the condition and its cause.

Information on nursing caries can be distributed to new parents though obstetricians or gynecologist, pediatricians, paramedical staff, health workers and maternal and child health care centers.

Sealing of all caries free pits and fissures.

Professional fluoride programs

Use of antimicrobial therapy topically

Supervised home care should be taught.

Systemic fluoride program if there is sub-optimal F concentration in drinking water.

Parents should be educated

How and when to feed the child during the earliest stages of the child

When and how to introduce solid foods.

Breast feeding should be encouraged as human breast milk is highly adapted to the human and is almost a complete source of all required nutrients.

Broadly based committees at good level to adverse the issue of caries and risk factors in young children and how to recognize early signs of the condition and promote early intervention.

 BARRIERS IN ECC –

Any proposal to improve social, mental and physical health of children can not be successful without adequate funding, political leadership and support. Some of the potential barriers in providing optimum care for children are:-

Lack of involvement and commitment from dental and other health organization. The dental community lacks a shared vision of the definition of the problem, how to present it and who is responsible for planning and implementation.

There is no integrated plan to fight the social, economic and nutritional tissues facing people in low socio economic group.

There is weak direct support for research on epidemiology, etiology and prevention of ECC.

Dental health is not a priority of most programs and insurance packages.

RECENT ADVANCES

Role of salivary carbonic anhydrase isoenzyme VI

In humans, immunohistochemical studies have demonstrated the location of CA VI exclusively in the secretory granules of the acinar cells of the parotid and submandibular glands from where it is secreted into saliva.

The importance of saliva for dental health is demonstrated by the rampant caries seen in patients with grace salivary hypofunction.

Recent research has indicated that CA VI binds to the enamel pellicle and retains its enzyme activity on dental surfaces. In the enamel pellicle, CA VI  is located at the optimal site to catalyse the conversion of salivary bicarbonate and micro-delivered hydrogen ions to carbon dioxide and water. Protect teeth by catalyzing the most important buffer system in the oral cavity, thus removal of acid from the local microenvironment of the tooth surface.