Infants are usually born completely edentulous (without teeth), but there are rare exceptions. Natal teeth are those that are present at birth, and neonatal teeth erupt within 30 days of birth [1]. These usually occur in the anterior mandible, particularly the early eruption of the mandibular deciduous incisors. Natal and neonatal teeth exhibit minimal root formation and may have a variable range of mobility. This can cause complications during breastfeeding, and sharp edges of the exposed teeth can even traumatize the oral mucosa of the infant. Although these are deciduous teeth, they must be cleaned gently with plain cotton gauze or a cotton swab, as they are subject to colonization by bacteria that can initiate the carious process. Consultation with a dentist or pedodontist can determine the best protocol by which this is accomplished. These teeth are extracted if the mobility presents a risk of aspiration, but this is rare.

The chronology of the eruption of the 20 deciduous teeth will vary widely among children. The mandibular central incisors are usually the first teeth to erupt at 6 to 10 months of age. The maxillary and mandibular second molars complete the sequence and usually appear at 23 to 33 months of age [2]. The lateral incisors, canines, and first molars erupt in the intervening interval. Genetics, systemic illness, and developmental problems are among the many factors that can delay the eruption of the deciduous teeth.

Unlike their permanent counterparts, deciduous teeth have no premolars. The permanent premolars replace the first and second deciduous molars and are the only permanent teeth to have less length in a mesial-to-distal (anterior-to-posterior) dimension than their deciduous predecessors. The permanent molars are the only permanent teeth that do not replace a pre-existing deciduous tooth.

When the roots of the deciduous teeth lose their normal means of attaching to the bone via the periodontal ligament and become fused directly to the bone, this is called ankylosis [5]. Although ankylosis can affect any deciduous tooth, the molars are most often involved. Ankylosis interferes with the normal process of deciduous root dissolution to allow for the normal sequence of shedding of the deciduous teeth and replacement by the permanent teeth. Ankylosed teeth have a dull sound when they are percussed with an instrument and a submerged appearance when adjacent non-ankylosed deciduous teeth are shed and the permanent successors erupt into their proper position. They can delay the eruption of their permanent successor and allow for the unintentional drifting of the adjacent teeth or hypereruption of the opposing tooth. These problems can lead to functional and cosmetic problems that require orthodontic correction. Ankylosed teeth can be difficult extractions because they are fused directly to the bone and excessive pressure can lead to fracture of the deciduous roots, the supporting alveolar bone, and the developing permanent tooth.

Early childhood caries (ECC) are lesions that occur in deciduous teeth between birth and 71 months of age. Deciduous teeth that have been restored or extracted due to extensive caries are also included in this definition [8]. The restoration of carious deciduous teeth or permanent teeth with incompletely formed roots and larger pulp chambers requires different restorative techniques and materials than those used to treat the permanent teeth of adults.

An initial clinical and radiographic examination will reveal the presence of caries and the risk of developing future caries. Statistics have shown that decay in the pits and fissures causes about 80% to 90% of all caries in the permanent posterior teeth and cause approximately 44% of all caries in deciduous teeth [9]. Pits and fissures are more plentiful and pronounced in the premolars and molars, although pits of varying sizes and depths are also common on the lingual aspects of the maxillary central and lateral incisors as well. These narrow invaginations in the enamel are areas in which bacterial plaque can congregate and into which toothbrush bristles may not reach.

The preparation of the tooth and placement of an amalgam restoration will depend on whether the carious lesion occurs in the deciduous tooth of a child, the permanent tooth of a child, or the permanent tooth of an adult. Amalgam does not have the capacity to self-adhere to enamel or dentin, and the form of the cavity may not be enough to retain the amalgam restorations. In these cases, auxiliary means of retention (i.e., small slots or grooves placed at the junction of the enamel and dentin) may be necessary. While this is not a problem in the permanent teeth of adults, careful placement is necessary to avoid pulpal involvement in children and adolescents.

A primary advantage of amalgam over composite resins is that it is not as technique-sensitive in its placement. If blood or saliva contaminates a tooth surface, the bond strength of a composite restoration will decrease, causing microleakage and ultimately failure. While a similar circumstance is not ideal for the placement of amalgam, the material is not dependent on a bonding process and contamination will not interfere with its setting.

Amalgam is durable under compressive strength, but its inclusion does not strengthen the tooth. It is a restorative material, not cosmetic, and its appearance will worsen over time as intra-oral oxidation reactions cause it to darken. Larger amalgam restorations can also impart a gray or black discoloration to the adjacent enamel.

Composite resin material was first introduced as a choice for the restoration of class III (interproximal lesions in anterior teeth), class IV (carious lesions or traumatic fractures of anterior teeth that involve the interproximal surface and the incisal edges), and class V lesions of both deciduous and permanent teeth. Numerous composite resin materials have now been developed to restore class I and class II lesions in deciduous and permanent posterior teeth. Beyond the cosmetic benefit, the use of etchants and bonding agents allows a chemical and mechanical bond to develop and secure the composite resin to enamel and dentin. Thus, less tooth structure is removed compared to amalgam, which cannot bond to enamel or dentin and relies on the reduction of additional tooth structure and retentive grooves or slots for mechanical retention.

The primary considerations in the use of composite material for the restoration of posterior deciduous teeth are the additional time required in their placement, the additional cost, and the ability to isolate the tooth. As noted, the placement of composite resin restorations requires that the tooth be isolated from saliva and blood with a rubber dam. While this device provides excellent isolation, some patients will find it uncomfortable, feeling that it is confining and a barrier to communication with dental staff during the procedure. Children can be especially fearful of the rubber dam and may be uncooperative during its placement, which can jeopardize the successful placement of the restoration. Children may also become restless and uncooperative during the longer time required for the placement of composite restorations. If confronted with any of these situations, consider the placement of amalgam restorations in posterior deciduous or permanent teeth or referral to a pedodontist capable of sedating the patient for restorative procedures.

Carious lesions that are left untreated will eventually cause necrosis of the coronal and radicular pulp. Necrotic (non-vital) immature permanent teeth present a unique challenge, as the non-vital radicular pulpal tissue cannot contribute to further development of the root and apexogenesis. In these cases, an apexification procedure is used. Conventional root canal therapy cannot be completed because the root of the immature permanent tooth has an open apex that cannot provide a definitive stop for obturation material. The apexification procedure is designed to create a definitive calcified stop in the apical region of the root, which would then allow gutta percha to be used to complete definitive root canal therapy. The initial appointment consists of the debridement and removal of the necrotic remnants of the pulpal tissue. A thick paste of calcium hydroxide is placed into the cleansed and debrided canal to stimulate the formation of the calcified stop in the apical region of the root. Whether calcium hydroxide is placed during the initial or second appointment, it is covered with a temporary filling material and left within the canal for approximately six months. If a calcified stop near the apical region of the tooth is confirmed by radiographs and is tactilely encountered by endodontic instruments such as files or reamers, conventional endodontic treatment can be completed [22]. If the stop is not encountered, the canal is retreated with calcium hydroxide paste. The complete loss of pulpal tissue in an immature permanent tooth precludes the continued thickening and developing of the root canal walls even if the apexification technique and subsequent endodontic therapy are successful [23]. This makes the tooth more susceptible to fractures of the crown or the root. A full-coverage crown can decrease, but not eliminate, the potential for coronal fractures. Patients should be reminded to minimize pressure to treated teeth and should be instructed to wear protective mouth guards during athletic activities.

Fluoride is the negatively charged ionic form of the element fluorine, and it is able to form stable bonds with positively charged ions, such as sodium and calcium, to promote remineralization of teeth. Virtually all water naturally contains fluoride, but usually at a concentration that is not sufficient to prevent tooth decay. The use of community water fluoridation began in late 1940s [25]. In 2010, the U.S. Department of Health and Human Services decreased the recommended optimal concentration of fluoride in drinking water for reduction of dental caries from 0.7–1.2 mg per liter of water to 0.7 mg per liter [30]. This change was the result of the widespread availability of fluoride-containing foods, water, beverages, toothpastes, and mouth rinses and to some degree was a response to concerns of overexposure to fluoride, which is neurotoxic at higher doses and can also cause dental and skeletal fluorosis [72]. This recommendation was finalized in 2015, with studies showing that 0.7 mg per liter of fluoride in drinking water maintained decreases of up to 35% of caries in children, while minimizing the risk of skeletal fluorosis [30,81]. Fluoride is slightly more toxic than lead and slightly less toxic than arsenic and has a narrow therapeutic window that can be difficult to control when all potential sources are considered [74]. Excessive ingestion of fluoride can cause fluorosis, a condition in which the enamel exhibits subtle changes (e.g., white spots) and potentially extensive areas of pitting and discoloration. Swallowed fluoridated toothpaste and drinking water are the primary sources of excessive fluoride intake and are considered the leading causes of fluorosis [71]. To prevent this, parents should receive instructions regarding toothbrushing technique and the amount of toothpaste that is appropriate for children to minimize the unnecessary ingestion of fluoride.

Fluoride's preventive effects are principally topical, rather than systemic, as was previously thought. Fluoride disrupts the activity of cariogenic bacteria (e.g., Streptococcus mutans) by decreasing its metabolism of carbohydrates in dental plaque, the action responsible for acidification of the oral environment that causes the demineralization [27]. Acid excreted by cariogenic bacteria stimulates the release of fluoride that is then incorporated into enamel that has undergone initial demineralization. However, mutated strains of Streptococcus bacteria resistant to fluoride are known to inhabit the oral cavity (and the environment) in response to fluoride exposure [70]. Fluoride is nonselective and also kills many species of beneficial bacteria.

Topical fluoride inhibits the demineralization of sound enamel and promotes the remineralization of damaged enamel, particularly in the context of dietary fluoride, calcium, and phosphorus deficiency [26]. Fluoride, calcium, and phosphate strengthen the crystal structure of enamel [28]. Beyond a topical effect, ingested fluoride will become incorporated into the enamel and dentin of unerupted teeth and thus increase their resistance to susceptible cariogenic bacteria [22]. New research indicates another important caries-preventing action of topical fluoride is to weaken the ability of bacteria to adhere to tooth enamel [73].

Fluoride concentrations in community water supplies in the United States are not standardized, and some communities have opted not to include fluoride in their water at all. The American Academy of Pediatric Dentistry recommends age-dependent fluoride supplementation only if the fluoride concentration in a child's water supply is less than 0.6 parts per million (ppm) [31]. No fluoride supplement is recommended for children from birth to 6 months, even if community water fluoridation is lacking. A 0.25-mg fluoride supplement is advised for children 6 months to 3 years of age if the fluoride concentration in available water is less than 0.3 ppm. Children 3 to 6 years of age should receive 0.50 mg fluoride if the water fluoride concentration is less than 0.3 ppm or 0.25 mg fluoride if the concentration range is 0.3–0.6 ppm. Children 6 to 16 years of age should receive 1 mg fluoride supplement if the fluoride concentration in the community water supply is less than 0.3 ppm or 0.50 mg if the fluoride concentration is 0.3–0.6 ppm [31]. The American Dental Association Council on Scientific Affairs encourages healthcare providers to evaluate all potential fluoride sources and to conduct a caries risk assessment before prescribing fluoride supplements [74]. Parents should consult with their pediatrician, pedodontist, or general dentist to determine if fluoride supplementation is required for their child.

Dental professionals who rarely treat or prescribe medications to pediatric and adolescent patients may give little thought to the profound differences in their ability to metabolize and excrete medications compared with adults. The dosage and frequency of administration may require significant adjustments. History of an adverse reaction to any medication should be discussed with the parent or guardian, as should the presence of pre-existing illness and other medication use. Age and weight should be considered before a medication is recommended or prescribed. For example, a child who is 3 years of age and weighs 30 pounds is often categorized generally as "pediatric," as is an adolescent who is 17 years of age and weighs 200 pounds. But their ability to absorb, distribute, metabolize, and excrete medications will be vastly different. Given these issues, it is not possible to recommend a single dose of any analgesic, antibiotic, or local anesthetic for all pediatric patients. Consultation with a pediatrician is necessary if there is any concern about the type, dose, or frequency of administration of a given medication.

Carious involvement of the pulp, localized infections, and trauma to the teeth or surrounding structures may all lead to the use of analgesics for pediatric patients. Acetaminophen is the most frequently used analgesic in this population for mild-to-moderate pain [33]. It is preferred over aspirin, which causes irritation to the gastric mucosa and may cause Reye syndrome. Acetaminophen has analgesic and antipyretic (fever-reducing) capabilities. It blocks the production of prostaglandins in the central nervous system and the generation of pain impulses peripherally [34]. Some younger children and adolescents may have difficulty swallowing tablets or capsules, and acetaminophen is available as a chewable tablet, elixir, or liquid.

Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and naproxen may also be used to relieve pain of odontogenic origin. NSAIDs have analgesic, antipyretic, and anti-inflammatory properties. The mechanism of action is twofold, as they decrease prostaglandin synthesis peripherally and decrease the accompanying inflammatory response. In the central nervous system, NSAIDs decrease the synthesis of prostaglandins in the critical pain processing regions and inhibit the ability for pain impulses to be transmitted or received.

The half-life of naproxen is 12 to 15 hours, which allows for it to be taken twice daily. The two- to four-hour half-life of ibuprofen requires that it be administered more frequently [35]. The gastrointestinal side effects that can occur with NSAIDs are decreased if they are taken with food; however, this practice will decrease their systemic absorption. To facilitate easier administration in the pediatric population, ibuprofen is available as infant drops, suspension, or chewable tablet, and naproxen is available as a suspension.

Patients who have experienced an aspirin-induced asthma attack should avoid the use of NSAIDs, as there is a high potential for cross-sensitivity [36]. This group of medications inhibits platelet aggregation and should not be used in patients with a bleeding disorder. NSAIDs are also contraindicated in patients who have gastrointestinal diseases such as inflammatory bowel disease or peptic ulcer.

Oral infections that develop from grossly carious teeth require prompt antibiotic treatment before definitive treatment is completed. The rise of resistant bacteria mandates that a conservative approach for the use of antibiotics is used. The extent of the infection, the immunocompetence of the patient, and the age of the patient should be considered before any antibiotic is prescribed. Dental infections contained within the pulpal or gingival tissues immediately adjacent to the tooth and fistulous tracts without signs of systemic involvement generally do not require antibiotic therapy; more extensive involvement and symptomatic presentations do [37]. Dental infections can advance rapidly among pediatric patients, especially younger children, and those who present with signs of systemic involvement should be referred to a pedodontist, oral surgeon, or an emergency department, as intravenous antibiotics and surgical drainage may be required.

Penicillin VK remains the empiric antibiotic of choice for the treatment of odontogenic infections [37]. It is effective against the gram-positive anaerobes commonly associated with these infections. Amoxicillin-clavulanate, a derivative of penicillin VK, is absorbed more rapidly and is more effective against gram-negative bacteria [38,75]. Both medications are available in suspension formulations, with amoxicillin also available as a chewable tablet. Clindamycin is the alternative antibiotic of choice when a patient is allergic to penicillin VK or amoxicillin, but the development of pseudomembranous colitis is a potential risk when this agent is used. Consultation with the patient's pediatrician is recommended prior to prescribing this medication. Cephalosporins should be considered, particularly if the patient has had a previous course of penicillin or amoxicillin [37].

As with all medications, the choice of local anesthetic for a pediatric patient must consider the age, weight, medical history, and type and duration of the planned procedure. The margin of safety will be less in smaller, younger children. One can ascertain the safe limit for a pediatric patient by determining the dose (in mg) of a given local anesthetic per kilogram of body weight (mg/kg), which will establish the maximum cumulative dose per appointment. If the maximum dose of lidocaine is 4.5 mg/kg for an entire appointment, a child who weighs approximately 16 kg should not receive more than two carpules of 2% lidocaine per appointment [39]. This is only a guide, as other factors (e.g., hepatic or renal impairment) can decrease a patient's ability to metabolize or excrete a local anesthetic.

Other local anesthetics, such as mepivacaine, prilocaine, and articaine, have established guidelines for the maximum allowable dose per appointment, also expressed as mg/kg. In general, the younger the age and the lower the weight of the pediatric patient, the lower the maximum allowable dose of local anesthetic. Clinicians should begin with these guidelines and use less if the medical history dictates or if a minimal amount of treatment is required.

The vasoconstrictor epinephrine is added to local anesthetics to prolong the duration of anesthesia and to aid in hemostasis in surgical cases. Preservatives such as sodium bisulfite or sodium metabisulfite are also added to local anesthetics that contain epinephrine in order to prolong their shelf life. Patients with allergies to sulfite compounds could develop an allergic reaction if a local anesthetic with epinephrine is used. For these patients, alternative anesthetics, such as mepivacaine plain, are reasonable alternatives.

The use of local anesthetics carries with it the responsibility of heightened safety. Before any local anesthetic is used, the dentist and staff should be fully trained in cardiopulmonary resuscitation for pediatric patients. Equipment and medications necessary in the event of a medical emergency should be easily accessible and all staff members should be trained in their appropriate use. Periodic emergency drills will define the role each staff member should assume during a medical emergency. Clinicians who infrequently use local anesthetics for pediatric patients should be cognizant of the differences in the safe maximum allowable dose of a given anesthetic among different patient populations.

Several systemic diseases that affect children and adolescents can present with oral and facial lesions. But the most common cause of oral ulcerations in children is an initial infection with herpes simplex virus-1 (HSV-1). Primary herpetic gingivostomatitis (PHG) usually occurs after 6 months of age and has the highest incidence between 12 and 18 months of age [16]. In children with PHG, the gingival tissues appear red and edematous, with small vesicular lesions and ulcerations on the oral mucosa. Patients will have pain, malaise, and headache and may be febrile. Liquid nutritional supplements and a soft, bland diet may be necessary during this period. Healing occurs spontaneously within 7 to 14 days with no residual scarring from the herpetic lesions. Although this initial attack will resolve, it is not cured. The virus will migrate to a regional nerve ganglion and can become reactivated in the future as recurrent herpes labialis. These recurrent lesions usually occur at the mucocutaneous junction of skin and lips, and unlike PHG, the oral mucosa and gingival tissues are typically uninvolved. Lesions of recurrent attacks heal in 10 to 14 days without scarring. Pediatric patients who are immunocompromised can have a more aggressive course of HSV-1 infection and a protracted healing period. Antiviral medications such as acyclovir can accelerate the healing time. Acyclovir is available as a cream, capsule, tablet, or suspension, with the dosage and frequency of administration adjusted according to the patient's age, weight, and medical history.

The measles virus causes cutaneous, red, maculopapular lesions. Oral manifestations of measles include grayish-white macules surrounded by an erythematous halo, known as Koplik spots. These lesions precede the eruption of the cutaneous lesions [45].

Hand, foot, and mouth disease is usually caused by coxsackievirus A16, although other coxsackievirus genotypes can serve as etiologic agents [32]. The disease primarily affects children during the summer and early fall. It usually begins with fever, loss of appetite, fatigue, and sore throat, followed within one or two days by oral sores.

While there is no single injury to the head, neck, oral, or perioral region that is absolutely indicative of child abuse, some injuries and patterns should be viewed with more suspicion than others. Injuries or bruises in the shape of a distinguishable object, such as a belt buckle, strap, rope, electrical cord, clothes iron, or hand, are cause for concern [49]. The cheeks and lips are the most common site of intentionally inflicted injuries in the oral and perioral region, with injuries to the oral mucosa, teeth, gingival tissues, and tongue following behind [49,50]. Beyond the oral and perioral region, the neck should be included as a part of the comprehensive examination of the child. Bilateral bruise marks or rope burns on the neck may be the result of an attempt to strangle the child; bilateral bruising on a child's arms may be indicative of shaking injury. Bruising and lacerations of the ears and the adjacent skin may be related to abuse; bilateral lesions and traumatic injuries to the ears are rarely accidental in nature. However, this may not be easily visible if hair extends over the ears. Hematomas within the oral cavity and in the perioral area can develop if a child is struck by a hand or a blunt object. Fractures or loss of multiple permanent or deciduous teeth may be the result of being slapped, punched, or struck.

Patients with anorexia nervosa have an extreme obsession with their body weight and the restriction of food intake. Women comprise 90% to 95% of anorexia cases, and it is estimated that 1% of all women between 12 and 25 years of age have anorexia, with the onset usually occurring during the adolescent years [60]. Anorexic patients often view themselves as overweight even though most are 15% or more below ideal weight.

Patients with anorexia go to extreme measures to lose weight and prevent weight gain. The most common mechanism is restricting or halting eating. Other patients may exercise excessively. Some patients with anorexia will use laxatives, enemas, or self-induced vomiting as a supplemental means to control their weight. These behaviors can lead to severe acute and chronic medical problems. Patients may appear emaciated but refuse to acknowledge the serious nature of the problem and do not consider the potential medical consequences of the disease.

Women who are anorexic often have irregular menstrual cycles. The skin can become dry and thin and at greater risk for traumatic injury. The restriction of caloric intake can stunt the physical and mental development of children and adolescents, and cognitive damage is possible in all patients. Problems with the cardiovascular system, including hypotension, bradycardia, and cardiac arrhythmias, are very common. Self-induced vomiting and use of laxatives can cause a severe disturbance in the body's mineral and electrolyte balance, and a drastic reduction of the minerals potassium, sodium, and calcium can interfere with the conduction of nerve impulses and the contraction of smooth, skeletal, and cardiac muscle. Failure of multiple organs and systems can lead to death. If part of the disease process, repeated episodes of self-induced vomiting can cause ulceration of the esophageal lining, with the subsequent development of esophageal varicosities and bleeding. Oral effects are generally limited to those caused by extreme starvation and malnutrition.

Enamel is the hardest substance in the human body, but the repeated exposure to the hydrochloric acid in regurgitated gastric contents over an extended period of time can lead to a unique pattern of enamel erosion called perimylolysis. Perimylolysis features the loss of enamel on the lingual, occlusal, and incisal surfaces of the teeth. As opposed to attrition, which is the loss of enamel from repetitive tooth-to-tooth contact or abrasion via an external source (e.g., excessive or overly forceful tooth brushing), the gradual dissolution of the enamel matrix in patients with bulimia leaves a glossy, smooth surface, most commonly on the lingual surfaces of the maxillary anterior teeth [63]. Any lost enamel cannot be regenerated. The underlying matrix of dentin is then exposed; it will wear faster than enamel and is more prone to caries. While enamel is devoid of any neural element, dentin contains dentinal tubules whose odontoblastic processes can perceive thermal stimuli as a source of pain. This can cause patients to neglect oral hygiene and increase the risk of caries and periodontal disease. The irreversible loss of enamel will also cause a change in the occlusion, decreasing the vertical dimension of occlusion. The loss of tooth structure requires that more complicated and expensive restorative options, such as crowns, be utilized. The loss of enamel support around composite or amalgam restorations can lead to their weakening and ultimate loss. The amount of time necessary for the enamel to be eroded in such fashion can range from six months to two years [64].