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A 2 year old boy is brought to the office by his mother, who is concerned that her child has not been eating normally and has many dark spots on his teeth. He might be having dental pain, but she is not sure. Acetaminophen has been given, and this might be helping to some degree. His mother reports trying to wean him off the bottle. She typically feeds him at night, and he refuses to go to sleep without a bottle of milk or apple juice. She doesn't brush his teeth because he doesn't like it. She has never taken him to a dentist due to financial reasons. His past medical history and family history are unremarkable.
Exam: VS T 37.5, P 85, R 25, BP 95/55. Height and weight are at the 75th percentile. He appears alert and active in no apparent distress. His physical exam is normal, except for findings in the oral cavity. Intraorally, there are opaque brown and grey specks on the enamel surface of several upper primary teeth. The upper central and lateral incisors show extensive decay and are slightly loose. The gingival tissues above the upper right central incisor are slightly swollen. Moderate lesions are visible in the upper canines, upper first molars, and lower first molars. The upper and lower second molars are just emerging through the gingiva. The lower canines and incisors are all intact, with no signs of dental decay.
A diagnosis of early childhood caries (ECC) is made, and he is referred to a dentist. His mother is told to wean him off the bottle and to brush his teeth at least twice a day.
Pediatricians and primary care family physicians play a vital role in promoting good oral hygiene as a life long habit that begins during infancy. They are the first and most frequent health care providers seen by infants and young children, during the formative years of oral health care. Beginning from the newborn period, they are also the first to provide information and guidance to infants and their parents. The key to oral health promotion and disease prevention lies in anticipatory guidance and education of parents, early detection, and timely referral for appropriate intervention.
A general knowledge of basic dental anatomy and tooth eruption patterns enables the primary care physician to evaluate a child's general oral health. The primary structures of the tooth are the: 1) enamel (outermost protective layer), 2) dentin (calcified tissue layer deep to the enamel), 3) gingival margin (region of the gum surrounding the tooth), 4) pulp (soft tissue at the core of the tooth which contains blood vessels, nerves and lymphatics), 5) cementum (layer of bony tissue covering the tooth root surface), 6) periodontal ligament (membrane around tooth attaching it to alveolar bone), 7) alveolar bone (bone that surrounds the root and forms the socket for the tooth), 8) neurovascular bundle (nerves, arteries, and veins in the dental pulp that exits at the root of the tooth).
Teeth can be named by their anatomic shape or by a letter/number convention used by dentists to describe the upper/lower and left/right teeth. Letters refer to primary teeth and numbers refer to permanent teeth. There are 20 primary teeth (described by positions A through E) and 32 permanent teeth (described by positions 1 through 8). From the center proceeding posteriorly: central incisor (#A, #1), lateral incisor (#B, #2), canine (#C, #3), first premolar (#4), second premolar (#5), first molar (#D, #6), second molar (#E, #7), third molar (#8).
The formation of human dentition begins as early as the 6th week in utero, during which, tooth buds of the primary (deciduous) teeth develop at 10 specific sites in the developing maxilla and mandible (1,2). Primary teeth begin to calcify at about 3 to 4 months in utero, and the enamel of all crowns is completed by 10 months after birth. From the midline of the oral cavity, anteriorly to posteriorly, the primary central incisors are the first to erupt at about age 6 to 7 months, followed by the lateral incisors at 7 to 9 months, the first molars at 12 to 14 months, the canines at 16 to 18 months, and the second molars at 20 to 24 months. By the time the child is 2 years old, all 20 primary teeth should be evident in the oral cavity (1,2,3).
Beneath the primary teeth, 20 permanent (succedaneous) teeth develop. As root development takes place in the permanent teeth underneath, this causes exfoliation of the primary teeth. Osteoclast formation is stimulated, which results in the resorption of the roots of the primary teeth and their subsequent loss. In addition, 12 permanent molars develop distally in sequential order: 3 upper and 3 lower on each side of the oral cavity (2).
With the exfoliation of primary teeth and replacement by permanent teeth, the child enters a mixed-dentition stage. Permanent teeth erupt in the following sequence: lower central incisor and first molars at about age 6 to 7, followed by the upper central incisor and lateral incisors, the canines and premolars, second molars, and finally third molars (wisdom teeth) during late teens up to the early twenties (1,2).
Disorders of tooth eruption and positioning are common pediatric dental problems that present clinically as malocclusion or abnormal alignment of the dentition. Delayed eruption of all teeth is indicative of developmental delay, hormonal abnormalities, and nutritional or systemic disturbances (e.g., hypothyroidism, trisomy 21, rickets, type I osteogenesis imperfecta, cleidocranial dysostosis, Albright osteodystrophy, progeria, or incontinentia pigmenti). Failure of eruption of single or small groups of teeth suggests local causes such as malpositioning of teeth, supernumerary (extra) teeth, retained primary teeth, or cysts (2,3). In contrast, premature eruption of all teeth is associated with precocious puberty or hyperthyroidism. Early emergence of single or small groups of teeth can arise from early loss of a primary tooth from trauma or extraction caused by caries and infection. An example of premature eruption is the presence of natal or neonatal teeth (at or within the first month of life) which are often rudimentary in form and appear as mere scales of enamel or shells of tooth crowns. They represent supernumerary teeth in approximately 15% of cases, and are frequently associated with other conditions (e.g., cleft palate, chondroectodermal dysplasia, pachyonychia congenita, Hallermann-Streiff syndrome) (2,3).
Other common pediatric dental issues related to developmental disorders of the dentition are abnormalities of tooth number, size, shape, structure, and color. Anomalies in tooth number are due to hereditary patterns producing extra or missing teeth, physical disruption of the dental lamina, and overactive dental lamina or failure of dental lamina induction, leading to an excess or failure of tooth initiation, respectively (3,4). For example, if the dental lamina produces an increased number of buds or if there are physical disruptions in the embryonic dental lamina, supernumerary teeth occur and the condition is termed hyperdontia. The extra teeth erupt most often in the maxillary midline between the central incisors. In contrast, when no tooth buds form (e.g., in congenital tooth absence) or when a normal site of initiation is disturbed (e.g., in cleft palate), the resultant reduction in number of teeth is termed hypodontia. The teeth that are most commonly absent are the third molars, the maxillary lateral incisors, and the mandibular second premolars (2,3,4).
Abnormalities in tooth size and shape occur as a result of disturbances during the morphodifferentiation stage of tooth development. Common examples are macrodontia, microdontia, and twinning. Macrodontia describes teeth that are larger than normal. Regional macrodontia is associated with hemifacial hyperplasia while diffuse macrodontia, a rarer condition, is associated with pituitary gigantism (2,5). Microdontia refers to a reduction in teeth size that is of hereditary genetic etiology. Localized microdontia is common, most frequently affecting the maxillary lateral incisors which may become slender and tapered (peg-shaped). Diffuse microdontia, which occurs rarely, is associated with pituitary dwarfism (2,3,5). Twinning is the phenomenon in which two teeth are joined together, and may result from fusion (the union of two separate tooth buds due to pressure, trauma, or crowding, creating a tooth of increased size or a reduction in number), germination (the incomplete division of a single tooth bud resulting in malformed teeth), or concrescence (joining of the roots of adjacent malpositioned teeth) (2,3,4).
Abnormalities in tooth structure, namely defects in the enamel or dentin layers, result from disruption during the histodifferentiation, apposition, and mineralization stages of tooth development. Common pathologies that affect the teeth surfaces and alter their appearances clinically are amelogenesis imperfecta (AI) and dentinogenesis imperfecta (DI). AI is a hereditary enamel defect that manifests as hypoplasia or hypocalcification, in which either insufficient quantities of enamel are formed during the histodifferentiation state of tooth development or the calcification stage of enamel formation is defective (4). Because there is faulty production of organic matrix, the teeth are covered by only a thin surface of malformed enamel which is susceptible to fracture and abrasion. The clinical appearance could range from the teeth being small and discolored as the yellow underlying dentin layer is seen, to the surfaces being pitted, rough, and worn down by attrition (3,6). Some nutritional and systemic disorders that can adversely affect enamel formation are vitamin A, C, and D deficiencies, exanthematous diseases, congenital syphilis, birth injury, prematurity, Rh hemolytic disease, local infection or trauma, and ingestion of chemicals (e.g., fluoride and tetracycline) (2). The treatment of AI varies depending on the extent of enamel involvement. The main concern is the loss of tooth structure due to attrition, thus full prosthodontic coverage with crowns is usually recommended for the preservation of the teeth in function. For patients without sufficient tooth structure remaining, over-dentures are recommended to prevent further erosion of the teeth. A physician who recognizes AI in a patient should make the proper referral to a dentist.
DI is an analogous condition in which the hereditary defect is in the dentin layer and dentinal organic matrix. It may be seen alone or occur with osteogenesis imperfecta, an inherited defect in collagen formation resulting in osteopenic bones, bowing of the limbs, bitemporal bossing, and blue sclera (4,6). During the histodifferentiation stage of tooth development, odontoblasts fail to differentiate normally, leading to poorly calcified dentin. The defect in dentin structure alters the junction between enamel and dentin. The enamel layer tends to flake away easily from the underlying dentin, exposing it, leading to rapid attrition. The typical clinical finding of DI is a bluish, brown translucent discoloration. Unless the crowns of these teeth are covered early and completely, the abrasion of chewing often reduces them to the level and contour of the supporting alveolar bone (3,6). Additional causes of dentin abnormalities are systemic disorders that impair normal absorption and circulating levels of calcium and phosphorous, such as Vitamin D-resistant rickets and hypoparathyroidism. Regional vascular abnormalities may also arrest calcification of both dentin and enamel and hinder tooth development (4). Depending on the morphology of each tooth, the size and shape of the crowns and root canals, full coverage prosthesis or full dentures are recommended. In the long run, these patients may be candidates for dental implants as well (6).
Tooth color abnormality is another commonly encountered dental problem that can result from intrinsic or extrinsic staining. Intrinsic staining is due to the incorporation of foreign substances into the developing enamel, while extrinsic staining is superficial and due to adherence of plaque or other discoloring substances to the teeth. Causes of extrinsic stains include a variety of foods and beverages (e.g., coffee), chromogenic bacteria, and iron found in infant formulas and vitamin supplements. In contrast, intrinsic stains are caused by blood borne pigments (e.g, congenital porphyria, cholestatic disorders, anemias, hemolysis) which produces red-brown discoloration, neonatal hyperbilirubinemia which produces blue-black discoloration of primary teeth, drug administration during enamel formation (e.g. tetracyclines) which causes brown-yellow discoloration, and hypocalcified-hypoplastic disease states which manifest as opaque white patches on the tooth or pitted areas devoid of enamel (2,3,4). At concentrations higher than 2.0 parts per million (ppm), fluoride content in drinking water can also cause a variety of discoloration, ranging from small white patches to severe brownish mottled enamel when concentrations exceed 5.0 ppm (3,4). The discoloration of intrinsic stain requires bleaching to remove, whereas extrinsic stains, which are developmental in nature, can be removed with abrasive agents used in dental cleanings.
Dental emergencies are a common occurrence, with the majority of cases due to trauma or pain (e.g., from dental decay and infection). As many as 10% of children may suffer significant tooth trauma requiring emergency management. Dental trauma tends to occur in toddlers (ages 1-3) from falls or child abuse, in school-aged children (ages 7-10) from bicycle, scooter and playground accidents, and in adolescents (ages 16-18) from fights, athletic injuries, and vehicle accidents (3). Facial trauma may loosen, avulse, or fracture teeth. If the family has a regular dentist, this dentist can be called for advice and many will provide after hours emergency care in their office. Without a family dentist, the patient will probably seek care in an emergency room, most of which are not optimally equipped for dental care. A frequently encountered dental emergency is tooth avulsion. If it is a permanent tooth, it should be rinsed and immediately inserted back into the gum socket (unless the patient is too young to be cooperative); alternatively, it can also be stored in saliva, saline, or milk. The tooth should not be scrubbed. Immediate dental consultation should be obtained.
Dental decay (caries) is the most common chronic disease of childhood, particularly in children of low socioeconomic backgrounds, minority groups, and developing countries who have limited access to dental care. The prevalence of dental decay is 30% to 50% among poor and minority children, and as high as 70% in some Native American groups (3). Beginning at an early age, cavities affect nearly 20% of 2 to 4 year olds, more than 50% of 8 year olds, and greater than 75% of 17 year olds according to CDC surveys.
The decay process of dental caries is characterized by demineralization and breakdown of tooth organic matrix. The development of caries is a complex, multifactorial process dependent on the presence of dental plaque, specific acidogenic bacteria (primarily Streptococcus mutans), fermentable carbohydrates, and a susceptible host. Host factors that increase the risk of caries include decreased salivary flow rate and pH, as well as areas of defective tooth maturation (e.g., enamel developmental dysplasia) where incremental layers have been disturbed and become susceptible to decay (2,7).
Caries formation is precipitated by specific oral bacteria that utilize dietary carbohydrates, primarily sucrose, as a substrate for acid production via fermentation. The acidic metabolic products in turn demineralize the tooth by reducing the pH of the surrounding dental plaque. The acidogenic bacteria most commonly associated with dental caries is Streptococcus mutans. S. mutans is a gram-positive bacteria with the ability to adhere to dental enamel, survive at low pH, and produce abundant acid. Carious lesions first appear as opaque white to brown specks, but gradually progress to cavitations of the enamel surface, invasion by other acidogenic bacteria (e.g., Lactobacilli) that worsen the decay, and eventual loss of the tooth if the damaging course is not halted (2,3).
A key determinant of dental decay is the frequency of carbohydrate consumption, and not necessarily the quantity consumed. In other words, retaining sweets orally for prolonged periods or drinking sweetened beverages constantly is more cariogenic than consuming the same amount of sugar in a single meal (3). Hence, the terms baby bottle syndrome and nursing bottle caries have been used to describe the phenomenon of early childhood caries (ECC), which is rampant decay that arises from the poor habit of bed time bottle feeding in infants and toddlers (< age 3) combined with concurrent S. mutans infection. ECC usually damages the upper primary teeth, due to the child's prolonged sucking on a bottle containing sweet juice or milk during sleep hours. The mandibular (lower) anterior dentition are usually spared because of their proximity to major salivary glands which help to neutralize the bacterial acid by-products (2,8).
Children with ECC are at increased risk for developing further caries with age. Furthermore, long standing untreated caries may lead to dental abscesses, resultant soft tissue swelling intraorally and/or facial swelling. Therefore, early diagnosis and prevention can help eliminate significant dental complications in toddlers and reduce the risk of decay in later childhood. Bottle feeding should be discontinued at 12 months. This may be unrealistic for some families, but it should certainly cease by 15 months of age. A physician who notices signs of baby bottle caries during a routine examination should refer the child to a dentist.
All parents should receive anticipatory guidance regarding dental development, oral hygiene, fluoride use, diet and feeding habits. Experienced primary care physicians can also perform a basic dental exam to screen for problems such as baby bottle caries, other caries, abnormal eruption sequence, and malocclusion. The American Academy of Pediatric Dentistry recommends an oral examination for all infants within 6 months of the eruption of the first tooth and no later than 12 months of age (9). Children at high risk for dental disease (e.g., low socioeconomic background, poor feeding habits) should receive checkups as often as every 3 months. While low risk children can be seen yearly, most children are recommended to receive periodic dental exams at 6 month intervals.
The use of fluoride represents the most promising approach to caries control. Fluoride plays a key role in altering the composition of the calcifying tooth structure, which changes the tooth's susceptibility to caries. The only mineral component in tooth is hydroxyapatite, a form of calcium phosphate easily substituted by other chemicals. When a high fluoride content is incorporated into the tooth structure, it becomes less soluble to the acid by-products of cariogenic bacteria. The American Dental Association recommends supplemental fluoride based on the concentration of fluoride ion (ppm) in drinking water (10). No supplemental fluoride is needed in newborns until age 6 months. For children between ages 6 months to 3 years, if the water fluoride concentration is less than 0.3 ppm, the supplement dose should be 0.25 mg/ day. No supplement is needed if the water fluoride concentration is greater than 0.3 ppm. In children between ages 3 to 6 years, if the water fluoride concentration is less than 0.3 ppm, the supplement dose should be 0.5 mg/day. If the water fluoride concentration is between 0.3 to 0.6 ppm, the supplement dose should be 0.25 mg/day. No supplement is needed if the fluoride concentration is greater than 0.6 ppm. In children between ages 6 to 16 years, if the water fluoride concentration is less than 0.3 ppm, the supplement dose should be 1.0 mg/ day. If the water fluoride concentration is between 0.3 to 0.6 ppm, the supplement dose should be 0.50 mg/ day. No supplement is needed if the fluoride concentration is greater than 0.6 ppm.
Community water fluoridation provides the most effective means for fluoride supplementation during the formative years of a child's growth. The water supplies for most communities in Hawaii are not fluoridated which is a major reason why children in Hawaii have one of the highest per capita rates of dental caries in the U.S. If community water fluoridation is not available, two other delivery systems of fluoride are available. Systemic fluoride can be prescribed for the child, usually in the form of sodium fluoride drops or tablets. Systemic fluoride incorporates itself into the developing teeth long before eruption. Topical fluorides are also available by prescription. Neutral sodium fluoride gel 1.1% or stannous fluoride 0.4% can be brushed on teeth or placed in a fluoride tray and applied to teeth for 3 to 5 minutes once a day. Excessive fluoride, however, can result in fluorosis which most commonly presents as dental discoloration (white and brown spots). Fluorosis may occur from excess fluoride intake due to swallowed fluoridated toothpaste or overaggressive fluoride administration.
Since good eating habits can be established in early childhood, parents should be educated and informed of the importance of limiting a child's consumption of foods with high sugar content, such as candies, honey, cookies, jam, chewing gum, jellies, sugary drinks and other adhesive carbohydrates. The child's frequency of eating is also an important contributing factor to the formation of carious lesions, especially the habit of eating in between meals and at bedtime. In addition to a sensible restriction of the child's sugar intake, the role of plaque in the caries process should also be discussed with the parents. Dental plaque is composed of densely packed microbial structures, insoluble salivary glycoproteins, microbial extracellular products, and epithelial and dietary debris which adhere firmly to teeth. It houses various bacterial populations. Dental plaque resists displacement by the forces of aqueous rinsing, but are readily removable by the mechanical actions of brushing, flossing and dental prophylaxis.
Brushing should begin as soon as teeth erupt, and reinforced by parents until children develop enough coordination required for adequate oral hygiene (usually until age 8). Unfortunately, it is common for parents to stop brushing their child's teeth when faced with a non-compliant youngster who throws a temper tantrum to avoid toothbrushing. Such parents must be taught that yielding is reinforcing the wrong behavior, as children soon realize that they can get away with brushing simply by crying. Instead, the opposite message should be conveyed. Children must understand that no matter how hard they resist, they will still need to get their teeth brushed. As long as parents are firm in enforcing toothbrushing routines, children will usually learn to accept it.
Prevention is optimized by regular dental examinations. Periodic dental visits familiarize the child with the dental office and offer the chance to develop a healthy rapport with the dentist, minimizing fear during future dental visits. More importantly, regular checkups enable early caries detection, application of topical fluorides, and reinforcement of home dental care instructions. Together, these preventive strategies help ensure the maintenance of good oral hygiene.
1. True/False: Normally, there are 20 deciduous teeth and 32 succedaneous teeth.
2. Name some developmental disorders of the dentition.
3. True/False: Amelogenesis imperfecta (AI) is a hereditary dental disease that can occur with osteogenesis imperfecta.
4. Which microorganism initiates the development of dental caries?
5. What are some preventive measures against dental caries?
6. At the 2 year old well child check, a child is noted to have severe decay of his anterior upper teeth. His mother claims that he stopped drinking from the bottle at age 12 months. His other teeth appear be normally formed. What is your comment to his mother?
7. A 10 year old boy falls off his bicycle and is struck in the mouth as he falls. His mother calls you for advice. He lost his front tooth and she has put it in a cup of milk. He did not loose consciousness. He is awake and alert and he does not appear to have other facial injuries. You advise her to call their family dentist to see if he can reimplant the tooth. In the meantime, what should his mother do with the avulsed tooth?
1. Ash MM. Development and Eruption of the Teeth. In: Ash MM (ed). Wheeler's Dental Anatomy, Physiology and Occlusion, 7th Ed. 1993, Philadelphia: W.B. Saunders Company, pp. 24-45.
2. Dock M, Creedon RL. The Teeth and Oral Cavity. In: Rudolph CD, Rudolph AM (eds). Rudolph's Pediatric Textbook, 21st edition. 2002, New York: McGraw-Hill, pp. 1283-1304.
3. Johnsen D, Tinanoff N. The Oral Cavity. In: Behrman RE, et al (eds). Nelson Textbook of Pediatrics, 16th edition. 2000, Philadelphia: W.B. Saunders Company, pp. 1108-1118.
4. Dummett CO. Anomalies of the Developing Dentition. In: Pinkham JR, Casamassimo PS, Fields HW, McTigue DJ, Nowak A (eds). Pediatric Dentistry: Infancy Through Adolescence, third edition. 1999, Philadelphia: W.B. Saunders Company, pp. 43-54.
5. Lunin M. Oral Pathology of the Child. In: Forrester DJ, Wagner ML, Fleming J (eds). Pediatric Dental Medicine. 1981, Philadelphia: Lea & Febiger, pp. 172-197.
6. Neville BW, Damm DD, Allen CM, Bouquot JE. Development and Eruption of the Teeth. In: Neville BW, Damm DD, Allen CM, Bouquot JE (eds). Oral & Maxillofacial Pathology. 1995, Philadelphia: W.B. Saunders Company, pp. 44-95.
7. Adair SM. Epidemiology and Mechanisms of Dental Disease. In: Pinkham JR, Casamassimo PS, Fields HW, McTigue DJ, Nowak A (eds). Pediatric Dentistry: Infancy Through Adolescence, third edition. 1999, Philadelphia: W.B. Saunders Company, pp. 174-177.
8. Johnsen D. Early Caries: The Importance of Recognition for Prevention and Treatment. In: Pinkham JR, Casamassimo PS, Fields HW, McTigue DJ, Nowak A (eds). Pediatric Dentistry: Infancy Through Adolescence, third edition. 1999, Philadelphia: W.B. Saunders Company, pp. 178-179.
Answers to Questions
2. Disorders of tooth eruption and positioning (premature, delayed, or failure of eruption, malocclusion or abnormal alignment), abnormalities of tooth number (supernumerary tooth), size and shape (macrodontia, microdontia, or twinning), structure (AI or DI), and color (intrinsic or extrinsic staining).
3. False. Dentinogenesis imperfecta is the condition that may occur with osteogenesis imperfecta.
4. Streptococcus mutans
5. Fluoride supplementation, good oral hygiene that includes brushing and flossing, limiting the amount but more importantly the frequency of intake of sweets (especially the habit of bedtime bottle feeding, eating in between meals and at bedtime), regular dental visits.
6. It is very likely that this history is not correct. These appear to be baby bottle caries, which is the most likely cause. It may be that mother feels guilty that she is not following your advice so she is denying that the child continues to go to bed with a bottle. Another possibility is that she is giving the child juice in a bottle at night and does not consider this to be "bottle feeding". Grandparents living in the same household will often interfere with childhood rearing practices, since they may insist on letting the child have a bottle to prevent the child from crying.
7. The best thing to do with the tooth is to push it back into its original location after a gentle rinse, if the child is cooperative. Otherwise, the tooth can be placed in saline gauze or milk. The tooth should not be scrubbed.