Baby Bottle Syndrome

Baby bottle syndrome, now known as early childhood caries (ECC), is defined as the presence of 1 or more decayed teeth or missing teeth (resulting from dental caries) or filled tooth surfaces in any primary tooth between birth and 71 months of age.

Tooth decay or dental caries is the single most common chronic childhood disease worldwide, 5 times more common than asthma, 7 times more common than hay fever, 4 times commoner than childhood obesity, and 20 times commoner than juvenile diabetes. According to the American Academy of Pediatric Dentistry, it is today an international public hazard in both developing and developed nations. It is an infectious disease that can begin as early as the teeth erupt, usually around 6 months, and can progress rapidly causing immense pain and discomfort to the child.[1][2][3]

The multifactorial nature of ECC encompasses but is not restricted to certain other terminologies such as "nursing caries," "comforter caries," and "baby bottle tooth decay," as improper nursing is not the only causative factor as they would suggest.[4][5][6] Presently, the term "early childhood caries" is used as the best description.[5][7] This term was coined at a workshop sponsored by The Center for Disease Control and Prevention 1994. The goal to comprehend the causative factors behind the genesis of this malady. Attention was drawn to various psychosocial, economic, ethnic, and cultural factors that contribute to the widespread increase in the incidence of this disease worldwide.[8]

In infants, ECC often follows a characteristic pattern of development. It affects maxillary incisors first, followed by the maxillary and then the mandibular molars, and because of the protective nature of the tongue, the mandibular incisors are often spared. Progression in infants depends on the chronology in which the dentition erupts and the dietary habits.

Actual causation is the interaction of microbes like Streptococcus mutans on sugary foodstuffs or fermentable carbohydrates producing lactic acid which erodes the tooth enamel causing demineralization.[9] Left untreated, the repercussions on the child’s health and quality of life, and can create serious social and economic consequences.

A multitude of factors contribute toward the genesis of early childhood caries, as listed below[10]:

• Cariogenic microorganisms: ECC is the commonest chronic infectious disease of childhood, Streptococcus mutans and Streptococcus sobrinus are the principal cariogenic bacteria involved.[11][12]
• Lactobacilli also play an important role in the progression of caries, but not in its initiation. The mechanism of action is the fermentation of carbohydrates like sucrose, fructose glucose and lactose by bacteria which adhere to the tooth enamel producing lactic acid.[13][14] This acid lowers the intraoral pH and causes demineralization of tooth enamel. Prolonged demineralization eventually leads to corrosion of dentin as well and cavitation.[15] It has been proved that there is a greater risk of acquisition of ECC with earlier infectivity with Streptococcus mutans, even before the eruption of the first tooth. This period is termed the window of infectivity wherein infection caused by Streptococcus mutans can be easily acquired causing caries. If protection is offered in this crucial period, the risk of caries developing is much lower. This can be explained by the colonization of the oral cavity by less pathogenic bacteria during this time.[16][17][18]
• Direct transmission of infection: Vertical transmission of the microbes is an important route of spread from the mother to the child, probably through infected saliva, sharing of food and utensils with the child or through poor oral hygiene or open carious lesions. Droplet infection through unclean habits in the mother such as tobacco or betel-nut chewing can also spread the infection. It has also been observed that babies delivered by Caesarian section had a greater propensity to develop caries than those delivered vaginally as the aseptic environs and atypical microbial environment increases the chances of opportunistic Streptococcus mutans colonization. Horizontal transmission between siblings and caregivers is a causative factor.
• Improper dietary and feeding practices: The underlying principle in the causation of ECC is the repeated availability of fermentable substrate which lowers the intraoral pH for a prolonged period, thus encouraging caries formation. Nocturnal breastfeeding after 12 months of age is to be discouraged as it causes a reduction in the salivary flow and higher lactose levels, predisposing to demineralization and caries.[19][20] Babies that are put to bed with a bottle of milk or formula or juice could develop caries faster due to early Streptococcus mutans colonization, and the establishment of high Streptococcus mutans counts.
• Sugary diets: Acid-producing bacteria ferment sugar molecules by salivary amylase producing lactic acid causing demineralization of teeth and caries[21][10] The duration of action of the acid on tooth enamel determines the extent of the damage caused which is proportional to the amount of sugar deposited on the tooth enamel. This includes chocolates, sweets, ice-creams, and other sticky food residues which linger on dental surfaces and crevices for prolonged periods.[22]
• Developmental and cCongenital disabilities: Enamel hypoplasia due to developmental disturbances in pregnancy like intrauterine growth retardation, preterm births and maternal smoking or drug abuse could increase the risk of plaque accumulation and caries. The enamel and dentin of primary teeth are thinner, and caries development can rapidly progress to the pulp. Hence, newly erupted teeth are at a far greater risk of developing caries till full maturation takes place. Leroy et al. showed a proportional correlation between maternal smoking and ECC.
• Systemic disease/medications: Chilrdren with juvenile diabetes due to high blood sugars, or children with special needs who may have to cope with reduced oral hygiene are more susceptible to caries. Cancers and patients undergoing radiotherapy need sugary lozenges to increase salivary flow which could pose a greater risk for caries.
• Socioeconomic and ethnic factors: ECC is commoner in children coming from a lower socioeconomic background due to antenatal and perinatal malnutrition predisposing to enamel hypoplasia and a higher propensity for caries development.[23][24][14][25][26] Poorer economic conditions are linked to lower levels of education and literacy with a lower understanding of the need to maintain proper oral hygiene and avoid sugary foodstuffs. One Canadian survey showed that children with parents who had higher incomes, dental insurance, and higher education levels had less severe caries than those whose parents came from opposite backgrounds.
• Lack of access to dental care: People living in poorer countries and developing nations with lack of medical infrastructure have no access to dental care.
• Lack of exposure to fluoride: Non-fluoridated sources of drinking water amongst other sources lowers the tooth immunity to attack by cariogenic pathogens.

Despite the best of dental care and awareness of dental hygiene in developed countries, ECC has remained an increasing problem today in both developing and developed nations. The incidence of the disease varies area-wide and country-wide, with varying prevalence depending on socioeconomic strata, ethnicity, and dietary patterns. In developed nations, it is between 1% to 12%; whereas, in economically backward nations it is as high as 70%. One study reported a prevalence of 11.4% in Sweden, 7% to 19% in Italy, 76% in Palestine and 83% in the UAE. In another study, a stark contrast was seen between incidences in Swedish children to being 2.1% as against 85.5% in their counterparts in rural China. National surveys of some nations have revealed the following prevalence: India 51.9%, Israel 64.7%, Brazil 45.8%, Greece 36%, and the United States 3% to 6%. Not many studies have demonstrated differences in gender ratios, but one study of 3- and 4-year-olds showed boys to be more prominently affected than girls.

The genesis of dental caries depends on a triad of essential factors, namely:

1. Cariogenic microbes: Streptococcus mutans and Streptococcus sobrinus
2. Fermentable substrate
3. Host tissue with diminished reserve: It is the ready availability of fermentable carbohydrates (sugars like fructose, sucrose, glucose, and lactose) on which microbes such as Streptococcus mutans act, releasing acid which brings about the systematic destruction of the host tissue (enamel and dentin of the tooth) with subsequent cavitation and caries.

Evidence has linked Streptococcus mutans to dental caries, and it has been proven that strains of this species can produce lactic acid which is implicated in the genesis of caries. Although the incidence is of Streptococcus sobrinus infection is lower, it is a closely-related, lactic-acid producing species linked to causing dental caries. Lactobacillus species also play a role in the progression of caries but not in its initiation. Actinomyces species, especially Actinomyces gerencseriae are thought to be responsible for root surface caries and deep-seated caries caused by Bifidobacterium species. Candida albicans is also said to cause dental caries. Molecular methods for bacterial identification now make it possible to pinpoint the specific microbes associated with dental caries, and DNA sequencing is used to identify closely-related species difficult to trace through traditional techniques. Bacteriocin typing studies were used to isolate Streptococcus mutans from mothers and infants, and results demonstrated identical patterns, proving the concept of vertical transmission from mother to offspring.[27][28][29] Chromosomal DNA patterns or identical plasmids are nowadays used to prove this theory.[30][31][32]