nursing caries: literature review and report of a case managed under local anaesthesia

Australian Dental Journal 1994;39(6):373-81

Nursing caries: Literature review and report of a case managed under local anaesthesia

Timothy Johnston, BDSc* Louise Brearley Messer, BDSc, LDS, MDSc, P h D t

Abstract Although the prevalence of dental caries in children has fallen in recent years, significant numbers of children are still treated for nursing caries. This form of rampant caries affects the primary dentition and causes rapid destruction of normally resistant surfaces. The treatment of nursing caries is multi- factorial, involving the child, parents, dental team and other health care providers to ensure the restorative dental treatment is supported by parental education in caries prevention, oral hygiene and infant nutrition. This paper presents a literature review on the condition, followed by a case report of a child with nursing caries treated in the clinic under local anaesthesia.

Key words: Nursing caries, nursing bottle, local anaesthesia, case report.

(Received for publication March 1993. Revised September 1993. Accepted October 1993.)

Introduction Nursing caries (NC) is a specific form of rampant caries

in the primary dentition of infants and young children.’.’ Typically, the condition is found in an infant or toddler who frequently falls to sleep sucking a nursing bottle filled with sweetened fluids (including milk), a pacifier dipped in sweetener, or who has a prolonged demand breast feeding habit. In most cases, N C is a form of over- indulgence rather than The nursing bottle, as differentiated from the feeding bottle, is used to describe the ‘bottle’ given to a child in the crib before sleeping.’-3 Frequent intake, prolonged oral clearance, and the lowered circadian flow of saliva at night all appear critical to the development of NC.1.2*4,5

*Postgraduate student in Paediatric Dentistry, University of Melbourne. Honorary Dental Officer, Royal Children’s Hospital, Melbourne. fElsdon Storey Professor ofchild Dental Health, School ofDental Science, University of Melbourne.

Australian Dental Journal 1994;39:6

The features of the carious lesions are: 1) the many teeth involved; 2) rapidity of lesion development; and 3) location on usually caries-resistant surfaces, such as the labial of the maxillary incisors and the lingual surfaces of the mandibular primary molars. ’** Differentiating N C from classical rampant caries is the usual absence of caries in the mandibular incisors in NC.

Review of literature Terminology

The many synonyms for NC include Nursing Bottle Caries, Baby Bottle Caries and Baby Bottle Tooth Decay. These terms are useful since they describe the problem and ascribe a possible cause in a form understood by parents and the Although the ‘bottle’ has been described as the most frequent cause, the terms listed are not inclusive of all aetiological factors.’.’ The term ‘nursing caries’ has become accepted in the literature as more precise since it includes breast feeding, although it fails to include the sweetened pacifier which may be signifi-

Rampant caries in breast fed children can also occur in the absence of an abusive feeding habit. This pattern of rampant caries closely resembles bottle-induced NC.’

Pattern of caries The pattern of N C is characteristic. The pathogenesis

is related to the eruptive pattern of the primary teeth, the cariogenic feeding pattern, and the oral The four maxillary incisors are usually the most severely affected, since they are among the first teeth to erupt and therefore have the longest exposure to the cariogenic challenge.8 In caries severity, the maxillary incisors are followed by the first molars, second molars and canines, depending on the eruption sequence. The aggressive extension of the lesion may be due to heavy colonization of sound enamel adjacent to the lesion with mutans streptococci . ’

Teeth erupting after discontinuation of the cariogenic habit (for example, canines, second molars), are affected less than maxillary incisors.”’ Knowing eruption times, it may be possible to correlate the feeding history given by a parent with the pattern of lesions. Caries in teeth

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erupting after the stated time of habit discontinuation should alert the dentist to an incorrect feeding history, or a new cariogenic challenge related to a new dietary pattern. Further inquiry may be required to overcome possible denial and guilt feelings held by the parent(s), and to ascertain the true feeding practices of the child.

During suckling, the nipple (natural or artificial) rests against the palate, with the tongue extending anteriorly over the mandibular incisors to form an oral seal. The nursing liquid pools around the teeth present (except the protected mandibular incisors), particularly affecting the maxillary incisors.',z Fluid flow around the medial aspect of the tongue bathes the occlusal and lingual surfaces of the molar teeth. Frequent, prolonged nursing followed by periods of fluid stagnation in the mouth in association with reduced salivary clearance allows rapid cariogenesis. '.'

Mutans streptococci in young children The aetiology of N C is indistinguishable from other

coronal carious lesions, representing the interaction between pathogenic organisms, fermentable carbohydrate substrate, host susceptibility and time.'-3 Uniquely, lesions progress rapidly and the cariogenic challenge overwhelms the protective mechanisms.

Dental caries occurs in the presence of certain micro- organisms and ecological factors influence the initial col~nization.~ Typically, Streptococcus salivarius is established within a day of birth, on the dorsum of the t o n g ~ e . ~ . ~ As soon as teeth erupt, Streptococcus sanguis is detectable on the smooth coronal surfaces. Streptococcus sobrinus, reported to be involved in dental caries, was not detected by Matee et al. in a breast fed population with NC.7 Mutans streptococci are not detectable in the predentate baby but appear in the pits and fissures soon after tooth e r u p t i ~ n . ' . ~ . ~ Implantation of mutans streptococci occurs only when teeth are present to provide retentive, non shed- ding surfaces. Once established, mutans streptococci counts relate closely to the number of teeth e r u ~ t e d . ' , ~ Recent longitudinal studies following infants of caries active mothers found that in 75 per cent of test subjects infection of the child by mutans streptococci occurred within a specific 'window' period, 19 to 31 months of age.'O Vertical transmission was confirmed by DNA finger- printing of the mutans streptococci strains, cultured from mother and child plaque samples.'O

The mutans streptococci are implicated in the initiation of dental caries, and lactobacilli are implicated in lesion p r o g r e s s i ~ n . ~ ~ ~ ~ ~ ~ ~ Colonization of lactobacilli does not appear until 24 months of age and then only tran- siently.'.2 However, the organism is frequently a secondary inhabitant of established lesions. Lactobacilli counts were significantly higher within the lesion than on adjacent tooth surfaces,' suggesting that lactobacilli play a role in lesion progression, but not in lesion initiation. Mutans streptococci have been found in all children with rampant caries, and also in most caries-free ~ h i l d r e n . ~ The levels in plaque and saliva from children with N C were unusually high, representing up to 60 per cent of cultivat- able plaque flora, compared with 1.0 per cent in caries free ~hi1dren.l.~ Similar high numbers of veillonella and lactobacilli were found in N C lesions.',2

Colonization of mutans streptococci is thought to be associated with primary infection, usually transmitted from the primary caretaker, via saliva as a transport medium.'~2~10 A significant relationship between salivary mutans streptococci levels in the mother and the risk of infection to the infant has been described." The frequency of infant infection was 9 times greater when maternal salivary levels of mutans streptococci exceeded lo5 colony forming units (CFU) per mL of saliva, compared with levels of less than lo3 CFUs/mL.',2,'' Increased frequency of maternal salivary contact significantly increased the caries incidence of the infant, even when the maternal caries incidence was low."

Dietary factors Sucrose (disaccharide of glucose and fructose) is con-

sidered to be the major cariogenic substance in the dlet.1-3.9 Numerous NC cases implicate a nursing bottle containing either sweetened fluids or fluids with added saccharide sweetener.' Cariogenic contents of the nursing bottle include bovine and human milk, sweetened milk, fruit juices, carbonated and non-carbonated soft drinks, and nursing formulas. The frequency and duration of the habit practice, along with the ingestion of cariogenic solids (for example, biscuits) is an important aspect of this condition.

The cariogenicity of milk (bovine and human) presents a complex role in the aetiology of dental caries. Bovine and human milk both contain lactose, which in vitro can enhance the implantation of cariogenic bacteria and produce caries in laboratory animals. '.' In humans, the pH of dental plaque falls after frequent ingestion of lactose or milk.'.z Clinical evidence of children consuming milk (bovine or human) and developing N C has been established. 12,7 Under conditions conducive to NC, human milk can be more cariogenic than bovine milk due to its lactose content (7 per cent) which is approximately twice that of bovine milk.'.' Bovine milk has a higher concentration of calcium and phosphorous than human milk, bound in organic and inorganic molecules and also free in ionic form,'-3 These bio-available ions may favour remineralization. 1.3 Some infant nursing formulas are similar in lactose concentration to human milk. Although soya-based formulas are lactose-free, the carbohydrate used in manufacture may be a sucrose derivati~e. '-~

Milk contains several proteins including casein (phos- phoprotein) and whey (non-phosphorylated protein), which could provide a protective organic coating on enamel.',' Early studies reported enamel to be 20 per cent less soluble in an acidic buffer if initially exposed to bovine rnilk.l3,l4 Summarizing the evidence from many studies, Ripa concluded that under normal dietary conditions, milk is minimally cariogenic and may even be cariostatic.' This conclusion does not contradict the clinical evidence attributing N C to milk, as affected children may have abusive, rather than 'normal' dietary habits, in association with inadequate oral hygiene and fluoride exposure.

Fluid supplements considered 'natural health foods' may present a caries risk due to the intrinsic sugar content. The use of fruit juices is a common finding in N C and the low pH (3-4) also presents a potentially erosive effect.',' Syrup additives (for example, vitamin preparations) to the nursing fluid often contain a high sucrose content and

Australian Dental Journal 1994;39:6. 374

have been implicated in the development of NC. l . *

Vitamin supplementation in this form is common in England,l and may be of concern in Australia among immigrant families.

Host fuctors The characteristic absence of caries of the mandibular

incisors is due to physical protection by the tongue and the proximity of the submandibular and sublingual gland duct orifices, allowing mechanical cleansing and dilution and buffering of plaque acids.'f2 Salivary flow follows circadian patterns, affected by sleeping and wakening and many aspects of the individual's envir~nment .~ Salivation falls to a minimum during night sleep and reduces significantly during any sleep (for example, nap time).4*5 This affects mechanical cleansing and buffering following fermentation of cariogenic substrates. The nursing liquid then stagnates and has cariogenic potential. Therefore, the young child put to bed with a nursing bottle filled with a cariogenic substrate is at risk for caries.

Minimal evidence supports a morphological predis- position to NC, although disturbances such as hypo- mineralization and hypoplasia may increase caries susceptibility. The relative aggression of the lesions in NC may be related to the thin enamel in primary teeth. 1-3,1s

Time is an essential factor in the development of NC, and prolonged nursing, especially at night, is a major contr ibut~r . ' -~ Derkson and Ponti described several children diagnosed at 9 months of age with NC who nursed for up to 8.3 hours per day, compared with 2.2 hours for unaffected children.I6

Frequency of feeding may affect the development of NC. Demand feeding provides frequent intakes of fermentable substrate (up to 10 exposures per day), allowing plaque pH levels to fall for prolonged periods7 A time-response curve to milk ingestion and pH levels illustrated that frequent exposure of plaque to milk over 4-6 weeks led to a greater descrease in the plaque pH at each subsequent ingestion. 1-3 Recent recommendations of the Diarrhoea1 Disease Control Program of the World Health Organiz- ation, on feeding habits of children in the first six months,

Table 1. Prevalence of nursing caries

concluded that supplementing breast milk with non- nutritive fluids undermines the nutritional benefits of breastfeeding and substantially increased the risk of illness and morbidity, especially among infants living in unsani- tary conditions. l7 The recommendations made to foster breast feeding included encouraging 24-hour rooming and demand breastfeeding. l7 If 24-hour rooming is practised and baby sleeps with mother, demand breastfeeding could increase the frequency of substrate intakes during the quiescent period of salivary flow and therefore increase the potential for NC.'.' As breastfeeding is promoted, and wisely, it is prudent to also promote dental awareness.

Other predisposing factors In addition to biological factors, demographic factors

(such as age, oral hygiene, socio-economic and cultural characteristics) can affect the development of NC. Infants infected with mutans streptococci before 2 years of age tended to have greater caries experience than those infected later.3 As expected, most studies have found an inverse relation between oral hygiene status and the incidence of NC.'-3,'5 While reports suggest the lower socio-economic classes have a higher prevalence, a polarization is apparent, with a greater prevalence of NC at both socio-economic extremes rather than concentrating at the lower socio- economic end.1-3.6 This polarization is related to factors including high density housing and greater sibling number^.^,^,'^ Low parental education and family income, and single marital status may also predispose to NC.'-3.'5 Cultural and ethnic variables play an important role in the development of NC, as feeding habits and pacifier use differ between cultures.' For example, several English studies have found a increased caries prevalence in ethnic or minority immigrant p o p u l a t i o n ~ . ' ~ ~ ' ~

Prevalence The reported prevalence in western countries is less than

Determining the true prevalence of N C in a population is dificult since children most affected are of pre-school age and not accessible for exam- i n a t i ~ n . ' - ~ . ' ~ Also, data collected may be from biased

5 per Cent.l-3.12.15.20-34

Country Sample Nursing caries prevalence (70)

England 1967 1968 1966 1971 1982 1988

USA 1984 1987 1992

Canada 1982 Australia 1983

1985 1991

South Africa 1987 1978

1981

Goose'O Goose" Winter" Winter" ~ 0 1 t l 4

~ 0 1 t ' ~ Johnsonx6 Kelly*' Weinstein" DerksonI6 CalacheZ9 Brownlo Wyne" Cleaton-J~nes~~ Cleat~n-Jones'~

Richardson34

309 5549

100 60 1 555 565 200 514 125 594 202 112 160 499 439 192 437 192 468

1-2 year olds 1-2 year olds 1-5 year olds 2-60 month olds 12-60 month olds 12-60 month olds 3.5-5 year olds American Indians Mexican-American migrants 0.75-6 year olds 4 year old (Brunswick, Victoria) < 2 years old (Middle class Brisbane) 2 and 3 year olds (Adelaide) 1-5 year olds (Urban Whites) 1-5 year olds (Rural Blacks) 1-5 year olds (Urban Blacks) Rural Blacks Urban Blacks Urban Whites

6.8 5.9

12.0 8.0 3.1 7.3

11.0 53.1 29.6

3.2 6.4 5.4 2.6

10.0 11.4 3.1

11.7 4.0

12.2

Australian Dental Journal 1994;39:6. 375

samples. For example, children whose parents are aware of an existing dental problem are more likely to present for examination.'.'' Finally, differing diagnostic criteria may complicate the assessment of prevalence.

Table 1 summarizes prevalence figures from recent studies of NC from 5 countries. The 4 Australian studies reported prevalences ranging from 2.6 per cent to 18 per cent. 15.20-34 Higher values occurred in minority and indigenous populations, including American Indians (53.1 per Mexican-Americans (29.6 per cent)," and rural black South Africans (1 1.4 per cent; 11.7 per ~ e n t ) . ~ ~ . ~ ~ Although such studies suggest high risk groups, the figure of 12.2 per cent for a South African urban white population is u n e x p e ~ t e d . ~ ~ Therefore, high prevalences could occur in other western societies containing large migrant populations.

Management of nursing caries Discontinuation of habit

The treatment of NC must begin with removal of the deleterious habit, and only when preventive advice has been given and instituted, should restorative treatment commence.'.35 The treatment of children with NC depends on the severity of the caries, patient age and behaviour, and parental c o - ~ p e r a t i o n . ' ~ ~ ~ ~ ~ ~ ~ ~ Most impor- tantly, the initial treatment should include identifying and eliminating the aetiological factors. Surprisingly, Dilley found that of 78 parents with children treated for NC, 75 per cent were not instructed to discontinue the offending habit.37 This should be of concern to the dental profession if her sample is representative of the population. The restorative management of NC is only one phase of the treatment plan which should also address the modifi- cation of all four factors in the caries equation, that is, pathogenic organisms, fermentable substrate, host susceptibility and time (frequency) of exposure.

Parental instructions Decreasing the use of the nursing bottle, weaning to

a cup by twelve months, and avoiding sweetened pacifiers will all modify the cariogenic challenge. If a bottle is required prior to sleeping, gradual dilution over a few days of the offending fluid to 100 per cent water should be initiated. Pacifiers should not be sweetened; again a dilution method may be employed. Breast feeding habits can be modified with co-operation of the child's paediatrician, especially for children presenting in pain. Pain causing sleep disturbance and altered feeding patterns has been shown by Acs et al. to affect the N C child's general health, causing significantly lower body mass than unaffected ~hi ldren.~ ' It is suggested increased glucocorticosteroid production due to pain, decreased growth hormone secre- tion caused by disturbed sleep, and inadequate nutrition combine to retard the child's growth and de~elopment.~'

Fluoridated dentifrices can be introduced after 12 months of age, as long as the child can spit out reliably. This ability may not be well developed before three to four years of age. Wiping the teeth with gauze or a soft cloth is suggested to remove excess dentifrice from the mouth to prevent it from being swallowed. The dentifrice should be a low-fluoride product specially formulated for

376

children, for example, 400 ppm fluoride. For children aged 6 years and older at high caries risk, daily or weekly home use of 0.05 per cent sodium fluoride mouthrinse can be used for children capable of rinsing and A four-monthly application of topical fluoride (1.23 per cent APF gel) is beneficial to prevent further caries progression; this should be administered professionally in the dental surgery. Home use of APF gels is not recommended due to the high fluoride content (the 1.23 per cent APF gel contains 12 300 ppm fluoride; this is 12.3 times as concentrated as an adult fluoride dentifrice containing 1000 ppm fluoride). Inadvertent and repeated ingestion of fluoride during the preschool years may result in mild fluorosis of the anterior teeth.38 In addition, toxicity is a consideration, for example, the 'probably toxic dose' (5 mg F/kg) for an average 2 year old (1 1.3 kg) is 57 mg. This dose is contained in 57 g of a 1000 ppm fluoride-containing dentifrice, 248 mL of a 0.05 per cent fluoride mouthrinse, 57 2.2 mg sodium fluoride tablets or 4.6 mL of 1.23 per cent APF gel.39

Parental instruction on infant oral hygiene is imperative, encouraging careful cleansing (for example, wiping the gum pads with a gauze or face washer) after each feeding to minimize fluid stagnation. Primary infection by vertical transmission may be unavoidable, and measures to reduce the bacterial numbers transferred will be of use, for example, avoiding transfer by sharing spoons has been suggested.'.2*'o Toothbrushing by the parent should start as soon as the first primary teeth erupt. A gentle sideways scrub using a soft multi-tuft toothbrush and covering two teeth at a time, is employed. Dental flossing by the parent should commence as soon as any two teeth are in proximal contact. Reduction in proximal caries of 30 per cent (in the presence of fluoridated dentifrice) has been demon- strated by Wright et al. in controlled flossing studies of yound children.40 For parents, reducing the availability of infective organisms by effective oral hygiene and restoration of all carious lesions in their own mouths is indicated.

Anaesthetic management Patient behaviour, age, and the extent of restorative

treatment required are major determinants in selecting the mode of anaesthesia to be used. Although the N C patient usually has had little previous dental experience, general anaesthesia is not always necessary, and many such children can be treated successfully under local anaesthesia. Careful patient preparation, parental support, skilful behaviour management and efficient clinical techniques are required. While treatment under sedation is popular amongst US paediatric d e n t i ~ t s , ~ " ~ ~ this is not widely practised by Australian dentists. When appropriate informed' consent is sought for treatment under general anaesthesia, many parents prefer the reduced risks associated with local anaesthesia.

Dentition stabilization/tempottion in the young child

The restoration of a child's mouth affected by N C is challenging and rewarding, as all aspects of restorative and preventive dentistry are employed over an intense treatment time. In the very young child, where a general

Australian Dental Journal 1994:39:6.

Table 2. Treatment protocols for nursing caries Early carious and white spot lesions

Glass ionomer temporary restorations Fissure sealants Professionally applied professional topical fluoride therapy

Anterior teeth Carious lesions without pulp involvement

Composite resin restorations Glass ionomer restorations Composite crown restorations

Amalgam restorations Preventive resin restorations Class I glass ionomer restorations Ni-Cr (stainless steel) crowns

Carious lesions with pulp involvement

Posterior teeth

Pulpotomy or pulpectomy with full coverage coronal restoration Extraction with space maintenance where indicated

anaesthetic is contraindicated and local anaesthesia is not possible, the first step is dentition stabilization/temporization.

The child can be placed in the knee-to-knee position with the mother (child's head on the dentist's knee), across the mother's lap and shoulder in the dental chair, or in a bean-bag adapted to fit into the dental chair. Gross caries removal is performed atraumatically using large round burs (spoon excavators may provoke unexpected pulpal exposures) and anterior lesions are temporized with fluoride releasing, light-cured glass ionomer cement (for example, Vitrabondt, Photac-fils). Posterior lesions can be temporized with silver cermet (for example, Ketac Silvers). Remineralization of white spot lesions (for example, on labial surfaces), can be attempted with concentrated fluoride solution (for example, 20 per cent stannous fluoride) applied under cotton roll isolation. Susceptible pits and fissures on primary molars can be sealed with a rapidly polymerizing, light-cured sealant (for example, Deltonfl). Home application of 1.23 per cent APF gel cannot be recommended for the reasons stated previously; however, the applications can be performed professionally at three to four month intervals. These visits also provide an opportunity for the dentist to check if lesions have been arrested, to evaluate if the home care and dietary instructions are being followed, and to plan definitive treatment with the parent. Caries stabilization and temporization is indicated only for teeth free of signs and symptoms of pulp p a t h o l ~ g y . ' * ~ , ~ ~ . ~ ~ For children presenting with acute pain, abscess formation, a draining sinus or facial cellu- litis, immediate definitive treatment is required.'e2 Depending on the extent of caries and the ability to place a coronal restoration, endodontic or exodontic treatment is p e r f ~ r m e d . ' . ~ * ~ ~ . ~ ~ The recommended measures are summarized in Table 2.

Definitive restoration of the dentition For older children who are more easily managed under

local anaesthesia or who present a reduced general anaesthetic risk, endodontic treatment of pulpally involved teeth is the treatment of choice, aiming to maintain arch

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Australian Dental Journal 1994;39:6.

integrity. A pulpotomy is indicated for a tooth with a vital pulp, free from signs and symptoms of irreversible inflam- mation (for example, inability to achieve haemostasis). Pulpectomy and obturation with a resorbable material is indicated for teeth with necrotic or chronically inflamed pulps, and at least two-thirds of the normal root length. 1.2.36.43.44 Extensive internal and external root resorption, or periapical infection (which may involve the permanent tooth bud) contraindicate endodontic treatment. 1.2.40 Unresolved periapical and hrcal pathology and failure of bone deposition indicate the tooth for extraction. Space maintenance should be considered if posterior teeth are r e m ~ v e d . ~ , ~ , ~ ~ . ~ ~

All endodontically treated primary teeth, or those with extensive carious destruction, should be restored with full coverage restorations. Full coverage restorations offer complete protection of susceptible surfaces, increased retention, and placement of margins subgingivally into non caries-susceptible areas. The placement of crowns is often more time efficient, particularly in the operating theatre.36.4s*46 The use of full coverage restorations in the primary dentition, especially for teeth severely affected by caries, is supported by several i n ~ e s t i g a t i o n s . ~ ~ . ~ ~ - ~ ~ Stainless steel (SSC) and composite crowns have been shown to be significantly more reliable as restorations than large amalgam, composite or silver cermet restorations in the primary dentition. Comparative five-year success rates have reported 87-97 per cent for SSCs compared with 27-33 per cent for Class I and I1 amalgam restora- t i o n ~ . ~ ~ . ~ ~ The criteria for failure of the amalgam restorations were marginal ditching, fracture of tooth or restoration, secondary caries, or a new lesion. Loss of retention or perforation were the primary causes of failure of The success rate for SSCs was reported as approximately twice that of Class I1 amalgams for each year up to ten years of service.47 Secondary caries, loss of retention, and coronal fracture have all been implicated in the failure of amalgam restorations.

Composite crowns provide aesthetic restoration of anterior teeth. Using primary celluloid crown forms, hnc- tional restoration of anterior teeth can be readily achieved in a few minutes. As it is usual for all four maxillary incisors to be affected in NC, it is desirable to restore all four incisors, although not necessarily in the same appointment. One-visit appointments are feasible depending on patient behaviour and pulp

Teeth not indicated for endodontic treatment or coronal restorations for the reasons discussed above should be e ~ t r a c t e d . " ~ - ~ ~ * ~ ~ Investigations of post-treatment effects of N C on children, especially following incisor extraction, have found these children develop normally (socially and physically) and are free of permanent speech defects.49

The above recommendations are summarized in Table 2.

Prevention Prevention of N C is twofold: firstly, the education of

prospective parents, and secondly, the identification of 'high risk' infants. Concerning risk, the use of a nocturnal bottle and patient age were identified as two key factors in a recent Australian study.6 These 'at risk' children may then be targeted through dental, medical and paramedical

377

Table 3. Preventive measures for nursing caries in the primary dentition Dietary advice

Oral hygiene

Dietary counselling with parents, possibly involving child's physician, eliminating the cariogenic substrate

Oral hygiene instruction to parents Toothbrushing and flossing performed by parent General dental education

Fluoride supplements in non fluoridated water areas Professionally applied topical fluoride 3-4 monthly 'Well baby' examinations within 6 months of the

Regular recalls First and second primary molars Establishing parental dental health

Fluoride Fluoride dentifrices

Dental examination

Fissure sealants Parental dental

eruption of the first tooth

health education

services.6 Microbiological investigations to detect 'at risk' children may not be suficiently specific, since high levels of mutans streptococci and lactobacilli occur in caries free ~ h i l d r e n . ~ The investigations of bacterial transfer suggest parents should ensure their own dentitions are caries f~ee.~.'O Prima gravida mothers with mutans streptococci levels exceeding lo6 CFUs/mL of saliva, treated with intensive preventive and restorative treatment, can delay

the primary infection of newborns and hence reduce their caries e~perience.~ Dentists treating prospective parents need to provide early preventive education, in effect, 'treating the parent before the child'. '.'"' Minimizing the possibility of carrier vehicles (such as saliva transfer), early infant dental examinations, and maintenance of caries-free dentitions by parents are recommended.1~'2~'s

Preventive dental programmes implemented through 'well baby' examinations should involve dietary and oral hygiene advice (for the infant and parent), provide an understanding of the causes of NC, and introduce the infant to dentistry in a non-threatening e n ~ i r o n m e n t . ' ~ ' ~ ~ ~ ~ Routine use of examination protocols which involve the parents in the examination, encourage discussion and demonstration of caries preventive measure^.^' Recom- mended measures are summarized in Table 3.

Prognosis A few studies have addressed the post-treatment suscep-

tibility of NC children to dental caries. Johnsen et al. reported that children with a previous diagnosis of N C and receiving on-going dental care were more susceptible (three-fold) to proximal lesions in primary teeth than children who were initially caries free." This figure may

Fig. 1.-Pre-treatment labial view showing typical caries pattern and labial developmental defects of the enamel on 83. Fig. 2. -Pre-treatment maxillary occlusal view.

Fig. 3. - Pre-treatment mandibular occlusal view showing caries free incisors.

370 Australian Dental Journal 1994;39:6.

Fig. 4.-Pre-treatment maxillary anterior occlusal intraoral radiograph. Fig. 5. - Pre-treatment right bitewing radiograph. Fig. 6. -Pre-treatment left bitewing radiograph.

be even greater among children not receiving regular dental care. Therefore, it is imperative these children have regular dental examinations incorporating appropriate professional and home preventive programmes. In addition to treating the existing caries, prevention of future lesions is important. Continued clinical review, oral hygiene, use of fluoride, dietary counselling and fissure sealants should be employed to assist the child to have a caries free secondary d e n t i t i ~ n . ’ - ~ . ~ ~

Case report Presentation and history

A Filipino male child, 5 years 10 months old, was presented by his parents to the Children’s Department of the Royal Dental Hospital of Melbourne on a casualty basis, with the chief complaint of discoloured maxillary anterior teeth. On referral to the Paediatric Dentistry Post- graduate programme, N C was diagnosed. His medical history was unremarkable, apart from a week-old rhinovirus infection treated with an antihistamine- decongestant and a paracetamol elixir. The social history was of an immediate family unit of Filipino extraction. The father was a policeman and mother was a clerk. There were three siblings, an older boy (aged 10 years 6 months), and two girls (7 years 5 months; 3 years 5 months).

The patient’s dental history involved a single visit to a private dentist in Melbourne when two restorations were placed. There was no previous dental care prior to immigration. Dietary questioning revealed he was breast-


fed and bottle-fed to age 9 months, often being put to sleep with a nursing bottle containing milk, formula or fruit juices. His present diet appeared balanced and unremarkable in the use of refined dietary carbohydrates. His general appearance was of a well-nourished, well-presented child (height 114 cm, weight 19.7 kg).

Examination and treatment plan Extra-oral examination detected a right side subman-

dibular lymphadenopathy possibly associated with the viral infection; no other anomalies were detected. Intra-oral examination of soft tissues was unremarkable.

Dental examination revealed a complete primary dentition, an orthognathic skeletal pattern, primary second molars in Class I occlusion, 1 mm overbite, 1 mm overjet, and a midline deviation from the facial midline of 2 mm to the left in the maxilla and 1 mm in the mandible. Clinically unsatisfactory silver cermet disto-occlusal restorations were present in teeth 54 and 64. Dental caries was noted on teeth and surfaces as follows: 55, 65 (occlusal, palatal); 54, 64 (distal); 75 (occlusal, lingual); 74 (distal); 84 (occlusal); 51, 52, 61 and 62 (mesial, distal, labial). Small circular developmental defects of enamel were noted in the middle third of the labial surface of teeth 73 and 83. All teeth were asymptomatic (Fig. 1-3).

Intra-oral radiographic examination (two bitewings, one maxillary anterior occlusal film; Fig. 4-6), confirmed the diagnosis of dental caries. Possible pulpal exposures were noted on the pulpal walls of the cavity preparations in

379

Fig. 7.-Post-treatment labial view. Fig. 8. - Post-treatment maxillary occlusal view.

Fig. 9. - Post-treatment mandibular occlusal view.

54 and 64. Although the oral hygiene status was poor (O'Leary plaque index 100 per cent), there was no gingi- vitis. No other pathology was noted. Clinical photographs and study casts were prepared and a treatment plan was developed and discussed with the parents.

Management The preventive phase consisted of dietary counselling,

oral hygiene instruction (brushing and flossing), dental prophylaxis and topical fluoride administration (Thixo- Flur Gel, APF) 11 for four minutes accompanied by intraoral evacuation. Dietary counselling consisted of discussion with the parents of the cause of dental caries, particularly NC, and the ongoing need to limit the form and frequency of refined carbohydrate consumption.

The restorative phase was achieved in five appointments, treating each posterior quadrant followed by the maxillary anterior teeth. All restorations were performed under rubber dam using XylocaineTM** 2% with 1 :80,000 adrenaline as local anaesthesia. The treatment performed was as follows: Tooth 74: disto-occlusal

Vitrabondl-lined amalgam?? restoration; teeth 54, 64: formocresol$$ pulpotomies, IRMOO core and nickel chrome crowns11 cemented with Ketac Silver;§ teeth 55, 65, 75, 84: preventive resin restorations;lf 11 teeth 74, 85: fissure sea1ants;l teeth 52, 51,61 and 62: VitrabondII- lined composite crownsII 11 formed with strip crowns.$

The behaviour of the patient was most compliant throughout. One week after the last appointment, he presented with a minor luxation of 62, moving the tooth lingually and into supra-occlusion. The injury had occurred two days earlier in a fall on playground equip- ment. Head and neck examination indicated no other injuries.

All restorations were satisfactory. Following clinical and radiographic examination (periapical film of 61 , 62, 63), no treatment was indicated. Although in supraocclusion, tooth 62 was not in crossbite and due to the favourable position it was left to self-reposition. At the same appointment, clinical photographs (Fig. 7-9) and study casts were

~~

I Colgate-Orapharm, Mt Waverley, Vic., Australia. **Astra Pharmaceuticals, North Ryde, NSW, Australia.

380

tVDI Permite C. Southern Dental Industries, Vic., Australia. $$Formcam1 Mitis. Colgate-Orapharm, Mt Waverley, Vic., Australia. ##IRM CAPS. LD Caulk Division, Milford, DL, USA. ((Ion Ni Chro Crowns. 3M Dental Products Division, St Paul, MN, USA. I ISilux. 3M Dental Products Division, St Paul, MN, USA. Wnitck Crown Forms. 3M Dental Products Division, St Paul, MN, USA.


prepared, dietary counselling and oral hygiene instructions reviewed, a dental prophylaxis performed and topical APF 1.23%$ applied for four minutes. The O'Leary plaque index had improved to 10 per cent. Recalls (at one, two and four months) to monitor tooth 62 indicated all teeth were asymptomatic and tooth 62 had repositioned into acceptable occlusion. The patient is being reviewed on a four-monthly basis with attention to his diet, oral hygiene and caries status.

Conclusion A case of NC treated in the dental clinic and managed

under local anaesthesia had been presented. Prevention of N C requires appropriate dental education of new and prospective parents. Dental education of medical and paramedical colleagues is also important so they can assist in this education. The dental restoration of a child affected with NC can be challenging, utilizing all aspects of restorative, preventive and child management techniques. The restoration of the dentition to function and aesthetics, and even self confidence, is rewarding for the dental team.

References 1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

Ripa LW. Nursing caries: A comprehensive review. Pediatr Dent

Yiu CK, Wei SH. Management of rampant caries in children. Quin- tessence Int 1992;23: 159-68. Davenport ES. Caries in the preschool child: Aetiology. J Dent

Dawes C. Circadian rhythms in human salivary flow rate and composition. J Physiol 1972;220:529-45. Dawes C, Ong BY. Circadian rhythms in the flow rate and propor- tional composition of parotid to whole saliva volume in man. Arch Oral Biol 1973;18:1145-53. Ho GC, Messer LB. A prediction model of nursing caries. J Dent Res 1993;72:Abstr 69. Matee MI, Mikx FH, Maselle SY, Van Palenstein Helderman WH. Mutans streptococci and lactobacilli in breast-fed children with rampant caries. Caries Res 1992;26: 183-7. Bhaskar SN, ed. Orban's oral histology and embryology. 9th edn. St LOUIS: Mosby, 1980:383. Silverstone LM, Johnson NW, Hardie JM, Williams RA, eds. Dental caries: Aetiology, pathology and prevention. London: MacMillan Press,

Caufield PW, Cutter GR, Dasanayake AP. Initial acquisition of mutans streptococci by infants: Evidence for a discrete window period of infec- tivity. J Dent Res 1993;72:37-45. Berkowitz RJ, Turner J, Green P. Maternal salivary levels of Strep- tococcus muruns and primary oral infection of infants. Arch Oral Biol

Aaltonen AS. The frequency of mother-infant salivary close contacts and maternal caries activity affect caries occurrence in 4-year-old children. Proc Finn Dent SOC 1991;87:373-82. Weiss ME, Bibby BG. Effects of milk on enamel solubility. Arch Oral Biol 1966;11:49-57. Weiss ME, Bibby BG. Some protein effects on enamel solubility. Arch Oral Biol 1966;11:59-63. Kamp AA. Well-baby dental examinations: A survey of preschool children's oral health. Pediatr Dent 1991; 13:86-90. Derkson GD, Ponti P. Nursing bottle syndrome: Prevalence and aetiology in a non-fluoridated city. J Can Dent Assoc 1982;48:389-93.

1988;10:268-82.

1990; 18: 300-33.

1981 :49-69.

1981;26: 147-9.

17. Martines JC, Rea M, Zoysa I. Breast feeding in the first six months: No need for extra fluids. BMJ 1992;6834: 1068-9.

18. Silver DH. A comparison of 3 year olds' caries experience in 1973, 1981 and 1989 in a Hertfordshire town, related to family behaviour and social class. Br Dent J 1992;172:191-7.

19. Vermeulen M, Vinckier F, Vandenbroucke J. Dental general anesthesia: Clinical characteristics of 933 patients. J Dent Child 1991;58:27-30.

20. Goose DH. Infant feeding and caries of the incisors: An epidemiological approach. Caries Res 1967;l: 167-73.

21. Goose DH, Gittus E. Infant feeding methods and dental caries. Public Health 1968;82:72-6.

22. Winter GB, Hamilton MC, James PM. Role of the comforter as an aetiological factor in rampant caries of the deciduous dentition. Arch Dis Child 1966;417:207-12.


23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

36.

37.

38.

39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

51. 52.

Winter GB, Rule DC, Mailer GP, James PMC, Gordan PH. The prevalence of dental caries in preschool children aged 1 to 4 years. Br Dent

Holt RD, Joels D, Winter GB. Caries in preschool children. The Camden study. Br Dent J 1982;152:107-9. Holt RD, Joels D, Bulman J, Maddick IH. A third study of caries in preschool aged children in Camden. Br Dent J 1988;165:87-91. Johnson DC, Schultz OW, Schubot DB. Caries patterns in head start children in a fluoridated community. J Public Health Dent 1984;44:61-6. Kelly M, Bruerd B. The prevalence of baby bottle tooth decay among two native American populations. J Public Health Dent 1987;47:94-7. Weinstein P, Domoto P, Wohlers K, Koday M. Mexican-American parents with children at risk for baby bottle tooth decay: Pilot study at a migrant farmworkers clinic. J Dent Child 1992;59:376-83. Calache H, Wright FAC. The dental status of four year olds in the Brunswick Child Development Study. Aust Dent J l989;32: 126-31. Brown JP, Junner C, Liew V. A study of Streptococcus mutans levels in both infants with bottle caries and their mothers. Aust Dent J

Wyne AH, Spencer AJ, Szuster FSP. Prevalence and risk factors of Nun- ing caries in Adelaide pre-school children. J Dent Res 1991;70:Abstr 35. Cleaton-Jones P, Richardson BD, McInnes PM, Fatti LP. Dental caries in South African white children aged 1-5 years. Community Dent Oral Epidemiol 1978;6:78-81. Cleaton-Jones P, Richardson BD, Rantsho JM. Dental caries in rural and urban black preschool children. Community Dent Oral Epidemiol

Richardson BD, Cleaton-Jones PE, McInnes PM, Rantosho JM. Infant feeding practices and nursing bottle caries. J Dent Child 1981;48:423-9. Acs G, Lodolini G, Kaminsky S, Cisneros GJ. Effect of nursing caries on body weight in a pediatric population. Pediatr Dent 1992;14:302-5. O'Sullivan EA, Curzon ME. The efficacy of comprehensive dental care for children under general anaesthesia. Br Dent J 1991;171:56-8. Dilley GJ, Dilley DH, Machen JB. Prolonged nursing habit: A profile of patients and their families. J Dent Child 1980;47:102-8. Evans RW, Stamm JW. An epidemiological estimate of the critical period during which human maxillary incisors are most susceptible to fluorosis J Public Health Dent 1991;51:251-9. Whitford GM. The physiological and toxicological characteristics of fluoride. J Dent Res 1990;69:Spec 1 ~ 5 3 9 - 4 9 . Wright GZ, Feasbv WH, Banting DB. The effectiveness of interdental flossing with and without a fluoride dentifrice. Pediatr Dent

Roberts SM, Wilson CF, Seale NS, McWhorter AG. Evaluation of morphine as compared to meperidine when administered to the moder- ately anxious pediatric dental patient. Pediatr Dent 1992;14:306-13. Sams DR, Cook EW, Jackson JG. Roebuck BL. Behavioural assess- ments of two drug combinations for oral sedation. Pediatr Dent

Fuks AB, Eidelman E. Pulp therapy in the primary dentition. Current opinion in dentistry 1991;1:556-63. Kubota K, Golden BE, Penugonda B. Root canal filling materials for primary teeth: A review ofthe literature. J Dent Child 1992;59:225-7. Roberts JF, Sherrif M. The fate and survival of amalgam and preformed crown molar restorations placed in specialist paediatric dental practice. Br Dent J 1990;169:237-44. Dawson IR, Simon IF, Taylor PP. Use of amalgam and stainless steel restorations in primary molars. J Dent Child 1981;48:420-2. Messer LB, Levering NJ. The durability of primary molar restorations: 11. Observations and predictions of success of stainless steel crowns. Pediatr Dent 1988;10:81-5. Pollard MA, Curzon JA, Fenlon WL. Restoration of decayed primary incisors using strip crowns. Dent Update 1991;18:150-2. Koroluk LD, Riekman GA. Parental perceptions of the effects of maxillary incisor extractions in children with nursing caries. J Dent Child

Goepferd SJ. Infant oral health: A rationale. J Dent Child

Goepferd SJ. Infant oral health A protocol. J Dent Child 1986;53:261-6. Johnsen DC, Gerstenmaier JH, DiSantis TA, Berkowitz RJ. Suscepti- bility of nursing-caries children to future approximal molar decay. Pediatr Dent 1986;8: 168-70.

J 1971;130:271-7.

1985;30:96-8.

1978;6: 135-8.

1980;2: 105-9.

1993;15:186-90.

1991;58:233-8.

1986;53:257-60.

Address for correspondenceheprints: Timothy Johnston,

School of Dental Science, The University of Melbourne,

71 1 Elizabeth Street, Melbourne, Victoria 3000.

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nursing caries: literature review and report of a case managed under local anaesthesia

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