Baby Bottle Syndrome

Article Author:
Sujata Tungare
Article Editor:
Arati Paranjpe
Updated:
12/27/2018 7:38:36 AM
PubMed Link:
Baby Bottle Syndrome

Introduction

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.

Etiology

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.

Epidemiology

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.

Pathophysiology

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.

Histopathology

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]

History and Physical

A typical history depends on the age of the child and the extent of dental damage. Usually, a child with dental caries suffers from severe pain which hinders eating or speaking. As a result, there may be a history suggestive of delayed milestones due to malnutrition and inability to concentrate on studies, poor memory, stunted growth, difficulties in speech and articulation, and lowered self-esteem.[33][34][35][36]

On physical examination, typically dull white or brown spots on the demineralized enamel on the maxillary incisors along the gingival margin are seen. This progresses to destruction of the crown. White spots or pits or fissures on the enamel close to the gingival margin could be precursors of caries and should be examined with an index of suspicion.[37][38] In later stages, spread to maxillary and mandibular molars occurs, leaving stumps or a large yellow-brown cavity. In an older child with fully erupted primary dentition, extensive dental destruction may be evident.

Evaluation

Every child with ECC has to be evaluated and examined in detail. Poor dental health often extends beyond the oral cavity. As caries can affect the child’s mastication and phonetics, the ability to eat, drink, speak, or gain acceptance of peer groups may affect physical, mental, and psychosocial development. Manifesting as severe nutritional deficiencies and growth retardation, a lowered immune status predisposes the patients to a multitude of infections throughout the body. A thorough dental examination is carried out with IOPA radiography, or an OPG if required, and other investigations like a complete blood count (CBC), x-ray of the chest, among others.

Treatment / Management

The treatment of ECC is complex and is determined by a multitude of factors, including the age of the child, the extent of dental damage, co-existence of other complications, and the financial capacity of the parents.

In low-risk cases of white spots and enamel proximal lesions, extensive restoration may not be needed, and the clinician can prevent further decay and spread through parent education, diet counseling, and counseling the patient on the use of preventive agents such as topical chemotherapeutic agents. Topical fluoride is very popular in this regimen as a varnish with a resin base.[39] Toothpaste, foams, gels, rinses, and drops containing fluoride have a brief effect; whereas, fluoride varnish hardens on the tooth enamel after application and remains intact for about a week, longer on demineralized tooth surfaces than on healthy teeth.[40] This offers excellent protection against demineralization.[41] Chlorhexidine varnish can also be applied to protect the tooth surface. Likewise, bimonthly application of 10% povidone-iodine has been recommended by some for its antimicrobial effect against most cariogenic Streptococcus mutans.

Application of CPP or casein phosphopeptide stabilizes the calcium and phosphate and preserves them in an amorphous or soluble form called ACP (amorphous calcium phosphate). In the presence of CPP, calcium, and phosphate form highly insoluble complexes. These CPP-ACP complexes enhance fluoride action and improve remineralization of enamel.

In moderately severe to advanced cases or those at great risk, restoration with surgical extraction of teeth with pulpotomy or pulpectomy is required. In these cases, deep sedation or general anesthesia with its inherent complications is needed due to lack of compliance with the age group involved. Restoration is done with prefabricated stainless steel crowns for primary or permanent teeth with caries.[42][43]

Other conservative techniques used are the removal of carious tooth tissues and restorations with adhesive restorative materials like GIC, composites or traditional amalgams.[44] These are inexpensive, quick, and easy to perform. They obviate the need for general anesthesia and its inherent risks, so the safety profile is higher, and the cost of treatment suits the majority of the population involved which comes from a lower socio-economic background.[45][46][47][48]

Complications

Poor dental health translates into unhealthy teeth and gums and has far-reaching ramifications. The child’s inability to eat, chew, drink, and swallow food because of the pain and disfigured teeth can leave them malnourished and stunted. This may alter the appearance and disturb interactions with peers, leaving patients socially and psychologically affected. The condition may affect scholastic performance, and patients may be socially ridiculed due to disfigurement.[33][34][35][36] Often, these are children of poor, uneducated parents who are grappling with finances and cannot pay for the treatment, subjecting the child to further neglect.[49][50] Unchecked, neglected caries can progress to pulpitis and severe dental abscesses, which can affect erythropoiesis by affecting inflammation induced metabolic pathways leading to chronic anemia and growth retardation.[51][52][53] In children with special needs, who are already physically or mentally challenged, ECC may pose further health issues. In severe cases, it serves as a potential nidus of streptococcal infection which could cause the potentially lethal endocarditis if it spreads to a defective heart valve. It could also spread to other organs causing fever, pneumonia, and urinary tract infection.

Consultations

Given the levels of ignorance about the importance of dental hygiene and oral health worldwide, many times, children have never visited a dentist until medical problems arise. A child should visit a dentist, preferably a pediatric dentist for an early evaluation by the first birthday. The pediatric dentist will screen the child and counsel parents about preventive measures against caries. After this initial visit, an annual checkup is recommended.

Deterrence and Patient Education

ECC is the commonest chronic, infectious, childhood disease globally, and a health matter of highest concern. The disease is the product of a lack of education, low hygiene levels, and concurrent poverty and malnourishment. Certain socio-cultural and ethnic dietary practices encourage the growth of cariogenic microorganisms. Healthcare professionals should adopt the following measures in the systematic prevention of ECC:

  1. Health education: According to the American Academy of Pediatrics (AAP), infants should never be put to bed with a bottle of milk, juice, or other fermentable carbohydrates. Breastfeeding at night is to be discouraged after 12 months of age. Pacifiers are not to be dipped in sweetened liquids. Brushing with fluoride toothpaste twice a day is recommended.[54][55]
  2. Government bodies should implement fluoridation of drinking water to an optimum level.
  3. Professional usage of tooth varnishes like fluoride varnish or 10% povidone-iodine varnish to susceptible teeth to be promoted to prevent demineralization.
  4. Prevention of vertical and horizontal transmission of infections: Screening pregnant women for dental caries and treating them to prevent vertical transmission from mother to the child. Unhealthy practices such as sharing of utensils, toothbrushes, food, and licking of pacifiers are strongly condemned.
  5. Adoption of healthy eating habits and teaching the importance of a balanced diet is important in promoting dental health.

Enhancing Healthcare Team Outcomes

Since ECC is the world’s largest chronic infectious disease of childhood, it is an international health hazard with a grave prognosis. Despite the increasing awareness of dental care, ECC is a problem of global concern.

The etiological basis of ECC is multifactorial and has nutritional, socioeconomic, cultural, and educational foundations. The virulent form of dental caries is an entirely preventable disease. It begins soon after dental eruption, affects the smooth enamel of the tooth and progresses rapidly, permanently impacting the upcoming dentition. As dental health involves having healthy teeth, it is important to note that poor dental health translates into a child’s inability to eat, chew, drink, and gain proper nourishment. All this may manifest as physical malnutrition and stunted growth, deficiencies, poor scholastic performance, and disfigurement that may lead to a negative body image, psychological trauma, and social ridicule.[33][34][35][36] It can affect the family adversely, as a child who lives in a lower socioeconomic and educational background suffers further if the family cannot afford the expensive treatment needed.[49][50][56][57]


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