Teeth and oral cavity disorders

22.3 Teeth and oral cavity disorders



Nicky Kilpatrick, Kerrod Hallett


The oral cavity can be considered the gateway to the body. It is the start of the alimentary tract and is integrally involved in the initial phases of digestion. The oral cavity consists of teeth sitting in sockets in the alveolar processes of the maxillary and mandibular bones supported by a fibrous sling known as the periodontal ligament. The oral cavity is lined by a combination of attached gingival tissue (gums) and more generalized mucous membranes. As with the rest of the body, the oral cavity is susceptible to both developmental and acquired disorders that can occur in isolation or as part of more general medical conditions or genetic syndromes.


It is becoming increasingly well recognized that oral health plays a significant role in maintaining good general health and wellbeing. This chapter will, therefore, summarize the key features of normal oral development and highlight the common disorders that affect both the teeth and their supporting structures. It will also identify the oral manifestations of some of the more common paediatric diseases.



Development


Teeth start to form from the fifth week in utero and may continue until the late teens or early twenties with the eruption of the third permanent molars (or wisdom teeth) (Table 22.3.1). The first tooth to erupt is usually a lower central incisor at around 7 months of age. By the age of 2.5 years most children will have a complete primary dentition consisting of 20 teeth: 8 incisors, 4 canines, 8 molars. At around the age of 6 years, the primary incisors become mobile and fall out. Most people have 32 permanent teeth, the first of which to erupt is usually the lower first permanent molars at around 6 years of age. The period that follows, referred to as the mixed dentition phase, is highly variable.



Table 22.3.1 Summary of the eruption times for primary and permanent teeth

image

Permanent upper incisors are usually more prominent than their predecessors; this allows the mandible to grow forward and encourages the development of what is described as a normal occlusion – a class I occlusion. Variations of the norm are common particularly in the anteroposterior dimension, and cause changes to the relationship between the upper and lower incisors. When the maxilla is forward relative to the mandible and the upper incisors protrude, creating an increase in ‘overjet’, this is known as a class II malocclusion. Conversely, in those cases where the mandible is relatively prognathic and the upper front teeth develop behind the lower ones, the result is a class III malocclusion, or reverse overjet.


These malocclusions may result from growth anomalies in either or both jaws and may be complicated further by the pattern of eruption of the dentition, size of the teeth and other external influences such as thumb-sucking. Recognizing malocclusions is important not only in determining the need for and nature of treatment, but also in diagnosing growth disorders and in syndrome identification, as jaw discrepancies are common in such conditions.



image Practical points




• Eruption times vary widely.


• Provided the sequence of eruption of the teeth is in order (central incisors before lateral incisors, etc.), delays per se are not a cause for concern.


• Asymmetrical eruption, particularly of the permanent incisors, should be reviewed by a dentist in order to check that there is no obstruction (such as an extra tooth) to the eruption of the appropriate tooth.


• The simultaneous presence of primary and permanent teeth during the mixed dentition phase is generally not a problem.


• Premature loss of primary teeth can be a sign of underlying systemic disease and should be reviewed by a paediatric dentist.



Teething


Teething is a normal process by which an infant begins to cut their first teeth (primary dentition). A variety of symptoms can accompany teething, including sensitive and painful gums, mouth ulceration, drooling, feeding difficulties, lack of sleep, fevers, diarrhoea and crying. There is no scientific evidence that any of these symptoms is directly related to tooth eruption; nevertheless, they are commonly reported and can cause significant distress to the child and anxious parent. Similarly there is no evidence base to support any particular management strategy. The use of chilled teething rings, hard sugar-free rusk biscuits and finger pressure appears to help. Over-the-counter teething preparations are of limited use. Not only do many contain choline salicylate and significant amounts of ethanol, which are contraindicated in very young infants, but also repeated use can cause ulceration of the gums. Some lidocaine-based gels are thought to be slightly more effective and may be mildly antiseptic. Mildly increased temperature can be managed with systemic oral medication, but temperatures of 38°C and above, or other serious symptoms (e.g. convulsions), should not be ascribed to teething and should be assessed independently.



Developmental anomalies


A few developmental anomalies occur in the newborn or very young child. As it is unusual for infants to be seen by a dental health professional, it is important that the medical practitioner examine the oral cavity periodically and refer to a paediatric dentist as appropriate. Amongst the more common are Epstein pearls, Bohn nodules, eruption cysts and natal teeth.



Oral alveolar developmental cysts



Epstein pearls




• Whitish-yellow nodules appear on the roof of the mouth in a neonate.


• Composed of trapped epithelial remnants during palatal fusion.


• The cysts usually burst and disappear by 90 days.



Bohn nodules




• Multiple 1–5-mm creamy nodules on the outer surface of the alveolar ridges (normally shed in utero).


• Composed of epithelial remnants.


• Sometimes mistaken for prematurely erupting teeth.


• No treatment indicated as the contents discharge spontaneously by the third month.



Eruption cysts




• A blue or clear swelling overlying the crown of an erupting tooth, most frequently in the incisor region of the maxilla.


• Eruption is slightly delayed and discomfort or pain may occur.


• Management is symptomatic only. Surgical intervention is contraindicated.



Natal and neonatal teeth




• Present in 1 in 3000 births, or erupt in the neonatal period – usually in the lower incisor region.


• Most are prematurely erupted normal primary teeth, but some may be ‘supernumerary’ or extra teeth.


• Can interfere with breastfeeding (nipple trauma).


• Can cause an ulceration under the tongue in breastfed infants, called Riga–Fede disease, that often necessitates tooth removal.


• Removal is commonly indicated to alleviate parental anxiety and is simple (using topical local anaesthesia and a haemostat). Suggest checking vitamin K-dependent coagulation factors before removing teeth.



Developmental defects of enamel


Teeth start forming from the fifth week in utero. Any disturbance in metabolism can cause damage to, or even the death of, the sensitive enamel-forming cells (the ameloblasts). Such a disturbance will leave a permanent developmental defect on the tooth surface which will be apparent as a loss of tooth substance (hypoplasia) or a deficiency in the quality of the enamel (hypomineralization) once the tooth erupts. Such defects in enamel have in the past been related to:



• prenatal events such as maternal rubella virus or cytomegalovirus (CMV) infection, maternal syphilis and pregnancy toxaemia


• natal events such as prematurity, hypoxia and hyperbilirubinaemia


• postnatal events – measles virus infection, gastrointestinal disease and hypoparathyroidism.


The first permanent molars (the so-called 6-year-old molars) and incisors are particularly susceptible to enamel defects as they are developing at the time of birth. Children with other health issues such as congenital heart disease or cerebral palsy are more likely to have developmental defects of their teeth, possibly as a result of systemic illness, fevers and periods of hypoxia in infancy and early childhood. Early identification of these defects is important as the quality of the tooth enamel is compromised; the teeth may be sensitive, particularly to oral hygiene measures, and more likely to develop decay.



image Clinical example


Miranda, now aged 2 years, was born normally at term with a normal birth weight. Since then she has demonstrated slow developmental milestones and mild hemiplegia with no obvious cause. Dental examination revealed a caries-free primary dentition, which, however, had chronologically distributed enamel hypoplastic (developmental) defects, affecting the teeth at 4–7 months in utero. On questioning, the grandmother had recorded in her diary the dates when her daughter had a severe viral infection and was in bed for several days.


Antibodies to CMV were detected on testing. CMV was the presumptive cause of the enamel defects and possibly also of the mild neurological defect and hemiplegia. This diagnosis helped early planning for future care. These enamel defects can increase the risk of developing dental caries as the surface of the teeth are often more porous and retain plaque, and they can be quite sensitive. Such teeth can be protected with a tooth-coloured adhesive material and the parents should be encouraged to assist Miranda with her oral hygiene and to maintain regular dental visits.



Acquired disorders of the teeth



Dental caries


Dental caries (decay) remains one of the most common chronic diseases in childhood, and recent epidemiological data show that disease prevalence and severity in childhood is increasing. As with many diseases, there are considerable inequalities in terms of caries experience with around 80% of all decay being experienced by just 20% of children. It is therefore important to identify children at high risk of developing decay and target them for proactive prevention. Given the fact that very few preschool-aged children are seen by a dental health professional, responsibility lies with medical and nursing professionals to identify infants at risk of developing decay and to refer to a paediatric dentist for appropriate anticipatory preventive advice.


Dental caries (or decay) is an infectious disease caused by the presence of certain bacteria, predominantly mutans streptococci (MS), in the oral cavity. The MS metabolize sugars and starches to produce acids; this lowers the pH of the oral cavity and promotes loss of minerals from the tooth surface. Minerals in the saliva, including calcium, phosphate and fluoride, are re-deposited on the tooth surface once neutral pH is restored (normally after about 20 minutes). This process is dynamic and as long as minerals are replaced the tooth surface remains sound and intact. If, however, the drop in pH is prolonged and/or frequent, there will be a net loss of minerals leading to a weakening and eventual breakdown (cavitation) of the tooth surface. The early sign of mineral loss is characterized by pre-cavitated or ‘white spot’ lesions (Fig. 22.3.1A), usually around the necks of the teeth where the MS tend to colonize the oral biofilm (known clinically as dental plaque) on the teeth. Early identification of these pre-cavitated lesions is important because they signal the need for proactive preventive measures to encourage remineralization. If the disease does progress to cavitation, restorations (fillings and crowns) are necessary to rehabilitate function and aesthetics.


image image

Fig. 22.3.1 (A) Typical appearance of an early carious lesion. The white spot lesion represents demineralization of the enamel caused by the presence of bacterial plaque creating an acidic environment. If left unmanaged, the white area will continue to demineralize until cavitation occurs (B) If identified early enough, remineralization of the enamel is possible through exposure to topical fluoride (particularly toothpaste) and other calcium-based products such as casein phosphopeptide–amorphous calcium phosphate (CPP-ACP).


Early childhood caries (ECC – historically also referred to as nursing-bottle caries, baby-bottle decay, and many other terms) is a distinct form of dental caries affecting preschool-aged children. ECC is particularly virulent, causing massive destruction to the primary dentition in children as young as 14 months of age (Fig. 23.3.1B). At birth, MS do not inhabit the oral cavity; however, the earlier colonization occurs, the greater the risk of ECC. The most common source for transmission of MS has been shown to be the primary caregiver, usually the mother. Poor maternal oral health coupled with inappropriate feeding behaviours such as prolonged on-demand breastfeeding, particularly through the night after 18 months of age, and putting a child to sleep with a bottle, places an infant at high risk of developing ECC. Medical practitioners, paediatricians and maternal child health nurses are all in a strategically good position to identify individuals at risk of developing ECC (Table 22.3.2).


Table 22.3.2 Common risk factors for dental caries
























Risk factor Influence
Fluoride exposure Exposure to fluoridated water source and the regular use of fluoridated toothpaste are two key factors that reduce caries risk
Sugar exposure Infant feeding habits are very important, with frequency of exposure being most relevant. High risk associated with prolonged bottle-feeding and on-demand night-time breast feeds (> 18 months of age)
Family oral health history Poor parental oral health places child at risk of decay as cariogenic bacteria can be transmitted to infants from their primary caregiver (usually the mother)
Social and family practices Poor, Indigenous, ethnic and migrant groups have higher levels of dental disease
Medical history Medically compromised children are at greater risk of dental decay, the impact of which on their general health can be considerable. They are also less likely to receive appropriate treatment
Saliva flow Children with reduced salivary flow are at significant risk of developing caries as the acids in the oral cavity cannot be diluted, buffered and cleared effectively. Examples of such children are those taking specific medications for management of asthma, those with ADHD, childhood cancer, or with certain head and neck tumours managed by radiotherapy

ADHD, attention-deficit/hyperactivity disorder.



Prevention of dental caries


Strategies to prevent dental caries should start as soon as the first primary teeth erupt (Table 22.3.3).


Table 22.3.3 Summary of caries preventive strategies


































Factor Strategy
Fluoride A smear of child’s fluoridated toothpaste should be applied regularly to an infant’s teeth within 6 months of their eruption
Teeth should be brushed twice a day with nothing to eat or drink after the night-time brushing
Parents should supervise tooth-brushing until around 8 years of age
The use of additional fluoride supplements (tablets or drops) is no longer recommended due to the risk of unsupervised ingestion
Diet Reduce the frequency of intake of sweetened foods and drinks, particularly between mealtimes
Avoid on-demand feeding through the night-time
Limit sugary snacks to meal times when salivary flow is optimal
Avoid sugary snacks close to bedtime
Increase water intake for hydration
Dental attendance Parents should be encouraged to take their infant to a dental professional within 6 months of the eruption of their first teeth
Regular monitoring by a dental professional should continue into adulthood
Remineralizing products Products containing fluoride concentrates and calcium phosphopeptides are available through dental practitioners. These promote remineralization of early carious lesions (e.g. Tooth Mousse®; GC Corporation, Itabashi-ku, Tokyo, Japan)


Fluoride


Fluoride is the single most effective way to protect teeth from decay. It acts in two ways: it can enhance the ability of teeth to resist demineralization caused by intraoral acids, and it can also inhibit oral bacterial enzymes to reduce the conversion of sugars to acids. However, the latter effect is relatively small in comparison to its biochemical modification of the structure of tooth enamel.


Fluoride can be delivered both systemically and topically. Fluoridation of the water supplies allows for both effects. Water ingested during development of the teeth allows fluoride to be incorporated into the developing dental enamel. However, it is as a topical agent that water has its most beneficial effect as low-dose fluoride comes into frequent contact with the teeth before being ingested. As such, water fluoridation is considered a very cost-effective public health intervention. However, many homes in rural and remote areas do not enjoy ‘town water’ and so miss out on the advantages of water fluoridation. The other common source of fluoride comes in the form of toothpaste. In Australia and New Zealand (and most parts of Europe) there are two common strengths of fluoride toothpaste; most adult toothpastes contain around 1000 parts per million (ppm) fluoride, whereas child toothpastes contain lower concentrations of fluoride, around 400 ppm. Early exposure to fluoridated toothpaste is very effective in preventing caries as the newly erupted immature tooth surface is highly susceptible to the beneficial maturation effect of fluoride. The use of additional fluoride supplements (tablets or drops) is no longer recommended in Australia and New Zealand, but varies around the world. Advice regarding the appropriate use of fluoride prescription should be sought from the local paediatric dentists and/or professional bodies.

Related posts:

  1. Sudden unexpected death in infancy
  2. Birth defects, prenatal diagnosis and teratogens
  3. Neural tube defects, large heads and hydrocephalus
  4. Surgical conditions in the newborn

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Aug 4, 2016 | Posted by in PEDIATRICS | Comments Off on Teeth and oral cavity disorders

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