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Figure2.Viciouscircleof treatment andre-treatment andits’complicationsin theabsenceofaneffectivepreventivestrategy. Dental Tribune Middle East & Africa Edition | 5/2016 25 paediatric cayed, missing, or filled score of ≥4 (age three), ≥5 (age four), or ≥6 (age five) surfaces constitutes S-ECC [10]. Dental decay in infants and young children has several names includ- ing: “nursing caries”, “nursing bottle caries”, “nursing bottle syndrome”, baby bottle caries” and “baby bottle tooth decay” [4]. These terms are of- ten used interchangeably in dental literature. They describe the condi- tion and the possible etiological fac- tors of the decay as understood by parents, public and professionals. However, none include the concept of a sweetened pacifier, which may be a significant cause in infants. Tinanoff and O’Sullivan used the term “Early Childhood Caries” which has been introduced in the USA to describe caries in infants and young children. This term has been widely acceptedasthecorrecttermbymost dentalcliniciansandeducators[11]. Pattern and Clinical Appear- anceofECC ECChasaspecificpatternandclinical picture. It is a specific form of ram- pant caries with the only feature dif- ferentiatingitfromgeneralizedram- pant caries being the usual absence of decay of the mandibular incisor teeth (Figure 1). The most commonly affected teeth are the maxillary inci- sors. Involvement of other teeth (the canines, first and second primary molars) depends on how long the carious process remains active but usually the severity of the lesions in these teeth is less than in the maxil- lary incisors. The mandibular inci- sors are usually not affected because the teat of the bottle is usually held above the tongue during sucking, so the lower incisors are protected by thetongueandalsobytheflowofsa- liva from the submandibular ducts [4]. The role of the innate infantile physiological tongue thrust pattern during deglutition is thought to be important in protecting the lower incisors[4]. In most cases of ECC, the first clinical sign is a band of dull white demin- eralization along the gingival line of the maxillary incisor teeth. As the lesion progresses, the white bands develop into cavities. This results in a brown or black collar around the necks of the incisors. In advanced cases, the lesions may become so severe that the crowns of the teeth are amputated leaving only decayed brownish-black root stumps (Figure 1). The commonly involved surfaces arethelabial,palatal,mesial,distalof maxillary incisors and of the maxil- lary and mandibular canines. In the first and second primary molars, the occlusal surface is commonly affected [12]. According to Ripa [4], the reason for this unique distribu- tion is related to three factors: 1) the chronology of tooth eruption; 2) the duration of the deleterious habit; and3)themuscularpatternofinfant sucking. PrevalenceofECC The prevalence of ECC varies greatly in different studies. The prevalence worldwide has been reported to vary between 3% and 94%. This wide range may be due to several factors such as: 1) children studied; their age and the accessibility for examina- tion;2)socio-economicstatus;3)eth- nicandculturalfactorsand4)criteria usedfordiagnosis. The prevalence of ECC in one coun- try usually cannot be compared with another [13]. Richardson et al reported that even results from one ethnic group cannot be extrapolated beyond that group, even within the same country [13]. In western socie- ties, approximately 80% of caries is present in 20% of the population commonly in children from low socio-economic groups, certain im- migrants, patients with learning difficulties and those with physical and medical disabilities. The den- tal survey of children aged one and half to four years in Great Britain [14] showed that the proportion of children affected increased with age: 4% of one and half to two and half year olds, 14% of two and half to three and half year olds and 30% of thoseagedthreeandhalftofourand half years had some experience of dental caries. In contrast, in the city of Abu Dhabi in the UAE, ECC in 2, 4 and 5 year olds is 35.5%, 85.7% and 93.8% respectively [6]. Hashim et al. (2006) in Ajman, UAE studied car- ies prevalence and severity of ECC in 5–6-year-old children. They reported high caries prevalence (76.1 %) and an average decayed, missing and filled surfaces (dmfs) score of 10.2 and that the Emirati (local) children hadhighercariesseveritythanother children [15]. Al-Hosani and Rugg- Gunn (1998) examined 5-year-old children in Alain city and reported a mean decayed, missing and filled teeth(dmft)scoreof8.6[6].Recently, Kowash (2015) in a cross sectional study in the same city reported a higher mean dmft of 10.9 [16]. The aforementioned ECC prevalence re- sults are clearly a cause of concern for this continuing problem in the UAE especially when comparing it with the internationally accepted definitionofsevereECC(S-ECC). EtiologyofECC The exact etiology of dental caries is still obscure. However, there is good scientific evidence to show that, for dental caries to occur, four main factors and some other minor or predisposing factors have to be pre- sent. Thus dental caries has a multi- factorial etiology [17]. The four main factors are a susceptible host (teeth and saliva), a substrate (fermentable carbohydrate), micro-organisms (mainly streptococci and lactoba- cilli) and time. Predisposing factors include: feeding habits, oral hygiene practices, general health and nutri- tional status. Socio-economic factors (parental education and occupation, family income, number of siblings, parental attitude and knowledge of dental health) and demographic fac- torssuchasrace,age,gender,soiland mater aspects are also contributing factors. These factors are often used as indicators to identify caries risk in children. The aetiology of ECC is indistinguishable from other coro- nal carious lesions in older children and adults. However, the lesion pro- gresses rapidly and the cariogenic challenge overwhelms the protec- tive mechanisms [18]. The etiology of the condition is a combination of frequent consumption of ferment- able carbohydrates as drinks, espe- cially at night time, with on-demand breast- or bottle-feeding because during sleep, salivary flow is greatly reduced. Other contributing factors include oral colonization by cari- ogenic bacteria (especially mutans streptococci) and poor oral hygiene [4]. In most cases of ECC, the etiology will be a combination of several of thesefactors. There is a considerable debate in the literatureregardingtheeffectofmilk on teeth. Several studies considered it to be cariogenic under certain conditions [19, 20, 21]. Others have shown it to be anti-cariogenic [22, 23, 24]. Storey [25] reported that the reasons for this controversy are due to: 1) the difficulty of studying the effect of one item of food on dental health in human, 2) the difficulties of designing definitive nutrition experiments even in animals, 3) the different effects of food processing procedures on milk and 4) basic dif- ferences in the composition of milk of different species. The lactose (a di- saccharide composed of glucose and galactose) content of human and bovine milk aids the implantation of cariogenic bacteria and produces enamel demineralization and caries when fed to animals [19]. The effects of milk on teeth depend upon the typeofmilkfeeding,feedingpractice andtimeofweaning. Itisdifficulttoidentifywhichtypeof microorganisms are responsible for causingdentalcariesduetothecom- plexity of plaque micro-organisms. However, mutans streptococci (MS) and lactobacilli (LB) are considered to be the most important cariogenic bacteria [26]. MS and LB can grow at an intracellular pH value lower than 6 (high aciduricity) and unlike most other bacteria, they can also produce lactic acid when exposed to high concentrations of sugars [27]. MS is responsible for initiation of carious lesion, whilst LB is responsible for the progression of the lesion and is the predominant microorganism of the cavitated carious lesion. The major source from which infants ac- quire cariogenic bacteria, especially MS, is the mother's saliva (vertical transmission). MS can also be ac- quired from other family members includingchildmindersandnannies (horizontal transmission) [5]. Teeth provide a non shedding surface for colonization of MS and its counts are related to the number of erupted primary teeth [28]. However, recent studies have also shown that MS can colonize the mouth of pre-dentate infant[29,30]. Consequences and complica- tionsofECC Depending on the severity and the extentofdentaldecay,ECCmaylead to a significant impact on the child’s oral and general health. Deep un- treated carious lesions lead to pain and discomfort, inability to prop- erly chew food and the child may avoid eating because of pain which may lead to weight loss and failure to thrive [31]. In severe cases, pulpal necrosis in primary teeth may lead to a dental abscess formation which can cause pain and damage the de- velopingpermanenttooth.Ifthereis anecessityforprematureextraction, primary tooth loss may result in various orthodontic complications (Figure 2). Premature extraction of primary maxillary incisors may also lead to problems in speech, normal development of language and aes- thetic which may affect the person- ality and self- esteem of the child. Untreated ECC lesions may cause abscess, cellulitis and spread of in- fection, which may result in serious andfatalcomplicationssuchasbrain abscess and Ludwig’s angina (Figure 2). Management of ECC complica- tions requires increased emergency room visits and hospitalization. The socio-economic consequences of ECC manifest in increased treatment costsandmissingschooltimeaswell as time off from employment for parents[32,33]. Management ofECC Prevention is the solution for the continuing problem of ECC. Despite following a high quality method for proper restoration of decayed teeth, recurrence of decay and its com- plications are very common in the absence of an adequate prevention program and follow up visits (Figure 2). ECC is an infectious and transmis- sible disease but it is preventable. There are two main preventive pro- grams: individual-based interven- tions and community-based inter- ventions. Individual-based preventive programmes This approach is used for high-risk populations because it is simple and does not require much effort from the parent or caregiver. The disad- vantages of an individual-based approach are twofold. Firstly, it re- quires identification of at-risk chil- dren and secondly, it can be costly as it requires professional or auxiliary personnel. Studies have used this approach by treating the mother by counselling, toothbrushing and use of fluoride to reduce the number of maternal micro-organisms trans- mitted to her child. Restoration of the mother’s open cavities and the use of anti-microbial agents can pre- vent or delay bacterial transmission toherinfant[8]. TheAmericanAcademyofPaediatric Dentistry(AAPD)[34]recommended dental health education program for parents with young children to improve their dental awareness and attitude toward dental health. The AAPD recommendations for the in- fant’soralhealthinclude. Establishment of a dental home: a dental consultation visit no later than one year of age is rec- ommended to educate parents and provide anticipatory guidance for prevention of dental diseases. The initial visit should include thorough medical (infant) and dental (parent and infant) histories, a thorough oral examination, performance of an age-appropriate tooth brushing demonstration and prophylaxis and fluoride varnish treatment if indi- cated. Oral hygiene:oral hygiene meas- uresshouldbeimplementednolater than the time of eruption of the first primary tooth. Twice-daily use of fluoridated toothpaste using a soft toothbrush of age-appropriate size. Parents should assess and super- vise their preschool-age child tooth brushing. Infant’s newly erupted teeth may be cleaned using a cloth. Flossing of child’s teeth is recom- mended when adjacent tooth sur- facescannotbecleanedwithatooth- brush. Diet: Human breast milk has not been epidemiologically associated with caries. Frequent night time bot- tle feeding with milk is associated with but not consistently implicated in ECC. Breastfeeding greater than seven times daily after 12 months of age is associated with increased risk for ECC. Night time bottle feeding with juice, repeated use of a no-spill cup and frequent in between meal consumption of sugar-containing snacks or drinks (e.g. juice, formula, soda) increase the risk of caries. [35, 36]. Therefore, it is recommended that infants should not be put to sleep with a bottle after the primary toothbeginstoerupt.Parentsshould be encouraged to have infants drink from a cup after one year of age. Repetitive consumption of any liq- uid containing fermentable carbo- hydrates from a bottle should be avoided. Fluoride: Optimal exposure to fluoride is important to all dentate infants and children [37]. Decisions concerning the administration of fluoride are based on the unique needs of each patient [38]. The use of fluoride for the prevention and controlofcariesisdocumentedtobe bothsafeandeffective[39]. Community-based preventiveprogrammes To solve the problem of ECC there shouldbecollaborativeeffortsofcar- egivers,healthprofessionals,andthe community [40, 41]. Weinstraub [41] believed that public health or com- munity approaches are more neces- sary and effective than individualis- tic or behavioural approaches. Oral health professionals like dentists and hygienists should be trained for skills, as necessary, for developing community-based initiatives and dental programs. These skills would include maintaining knowledge of social beliefs, culture and practices and establishing and implementing dental prevention programs [42]. A successful long-term dental health Figure 3. General anaesthesia full dental rehabilitation of a child with severe ECC: pre- treatment (A)andpost- treatment (B). ◊Page24 ÿPage 22 Dental Tribune Middle East & Africa Edition | 5/201625