PEDIATRIC DENTISTRY AND

CHAPTER 10

ORTHODONTICS
Andrew L. Sonis and Isabelle I. Chase

PEDIATRIC DENTISTRY
1. What is the difference between natal and neonatal teeth?
Natal teeth are present at birth, whereas neonatal teeth emerge through the gingiva during
the first month of life.
2. How common are natal teeth?
There is a large range in the reported prevalence of natal teeth. One study used two meth-
ods of determining prevalence: method 1 prevalence was 1 in 3667 births and method 2
prevalence was 1 in 716 births. In previous studies, the prevalence ranged from 1 in 1000 to
30,000 births.
3. Summarize the characteristics of natal teeth.
• 
95% are the actual primary teeth; 5% are supernumerary teeth.
• 
All natal teeth observed in one study were mandibular central incisors.
• 
A family history of natal teeth has been established in previous studies; the incidence of
a positive family history ranges from 8% to 46%.
• 
When natal teeth erupt, the enamel is at the normal histologic age for the child. Because
the teeth erupt prematurely, the enamel matrix is not fully calcified and wears off quickly.
Once the gingival covering is lost, the enamel cannot continue to mature.
4. How are natal teeth managed?
In general, natal teeth are left alone unless they cause difficulty for the infant or mother.
Clinical complications include ulceration of the tongue, lingual frenum, or mother’s nipple
during breast-feeding. Because natal teeth are usually mobile, some people worry about
aspiration. Although no cases of aspiration have been reported, it is generally recommended
that highly mobile natal teeth be extracted. On non-mobile natal teeth, treatment may also
include grinding to smooth the incisal edge. In three reports, a breast-feeding splint was
fabricated. In one study, half of the natal teeth were removed or lost before 4 months of age.
If the teeth survive past 4 months of age, the prognosis for continued survival is good; most
natal teeth, however, are not aesthetically pleasing because of enamel dysplasia.
5. Are any syndromes associated with natal teeth?
Three syndromes have been associated with natal teeth: (1) chondroectodermal dyspla-
sia, or Ellis-van Creveld syndrome; (2) oculomandibulodyscephaly with hypotrichosis, or
Hallermann-Streiff syndrome; and (3) pachyonychia congenita, or Jadassohn-Lewandowski
syndrome.
6. What is the definition of early childhood caries (ECC)?
The disease of early childhood caries (ECC) is the presence of one or more decayed (non-
cavitated or cavitated lesions), missing (because of caries), or filled tooth surfaces in any
primary tooth in a child 71 months of age or younger. In children younger than 3 years, any
sign of smooth surface caries is indicative of severe early childhood caries (S-ECC). From
ages 3 through 5 years, one or more cavitated, missing (because of caries), filled smooth
surfaces in primary maxillary anterior teeth or a decayed, missing, or filled score of four or
more (age 3), five or more (age 4), or six or more (age 5) surfaces constitutes S-ECC.
7. What should be included in an infant dental health program?
1. Prenatal oral health counseling for parents
• 
Counsel parents about their own oral health habits and their effect as role models.
• 
Discuss pregnancy-related gingivitis.
228
 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS 229

• Review infant dental care: (1) clean gums daily before eruption of the first primary
tooth to help establish healthy oral flora; and (2) do not use dentifrice to avoid fluo-
ride ingestion.
• Review oral care for toddlers (1-3 years of age): (1) introduce soft toothbrush; (2) use
a small “smear” of fluoride-containing toothpaste, twice daily, with the eruption of the
first tooth, until 2 years of age, and a pea-sized amount of dentifrice beginning at age
2 years; (3) allow child to begin brushing with supervision (parents should remain pri-
mary oral caregiver); and (4) discuss timing of eruption of primary teeth and teething.
• Review of preschool oral care (3-6 years of age): (1) parents should continue to su-
pervise and help with oral hygiene; (2) continue with pea-sized amount of dentifrice;
and (3) start flossing if teeth are in contact with each other.
2. Discussion of early childhood caries (baby bottle tooth decay) and how it can be
prevented
• Avoid putting child to sleep with a bottle.
• Avoid on-demand nocturnal breast-feeding after the first primary tooth begins to
erupt.
• Always avoid giving sugar-sweetened beverages by bottle or sippy-cup.
• Limit sweetened beverages to 4 ounces daily and ideally only with meals.
• Encourage drinking from a cup around the first birthday.
3. Discussion of timing of first dental visit (see question 9)
8. What is meant by anticipatory guidance?
Anticipatory guidance is the deliberate and systematic distribution of information to
parents as a tool to help them know what to expect, how to prevent unwanted conditions
or events, and what to do when an anticipated or unexpected event occurs. Information
should include dental and oral development, fluoride status, non-nutritional oral habits (see
questions 10 to 12), injury prevention, oral hygiene, and the effects of diet on the dentition.
9. When should children have their first visit to the dentist?
Currently, the American Academy of Pediatric Dentistry (AAPD) and American Dental
Association (ADA) recommend an initial oral evaluation within 6 months of the eruption
of the first primary tooth and no later than the child’s first birthday. At this visit, the dentist
should complete thorough medical and dental histories (covering prenatal, perinatal, and
postnatal periods) as well as an oral examination. After completing these tasks, the dentist
can best formulate a tailored prevention care plan based on the patient’s risk of develop-
ing oral and dental disease. In addition, the dentist can use this appointment to provide
­anticipatory guidance (see question 8).
10. What are non-nutritional sucking habits?
Non-nutritional sucking habits are learned patterns of muscular contraction. The most
­common types are as follows:
•  Finger habit
•  Lip wetting or sucking
•  Abnormal swallowing or tongue thrusting
•  Abnormal muscular habits
Sucking is the best-developed avenue of sensation for an infant. Deprivation may cause
an infant to suck on the thumb or finger for additional gratification.
11. Are non-nutritional sucking habits harmful to the dentoalveolar structures?
If a child stops non-nutritional sucking habits within his or her first 3 years of life, the damage
usually is limited to the maxillary anterior segment and presents as an open bite. If the habit
continues past 3 years, the damage may be long-lasting and detrimental to the developing
dentoalveolar structures. After 4 years of age, a finger habit can become well established and is
much harder to stop. Oral structures can become further deformed by palatal constriction and
posterior crossbite.
Tongue and lip habits are often associated with a finger habit and produce added compen-
satory forces that can lead to full-blown malocclusion. Thumb and finger habits can cause an
anterior open bite, proclination of the upper incisors, lingual movement of the lower incisors,
and constriction of the maxillary arch. Lip sucking and lip biting can procline the maxillary
incisors, retrocline the mandibular incisors, and increase the amount of overjet.
230 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS

Table 10-1. Fluoride Supplementation

Fluoride Concentration in Local Water Supply (ppm)
AGE <0.3 0.3–0.6 >0.6
6 mo-3 yr 0.25 mg/day 0 0
3-6 yr 0.50 mg/day 0.25 mg/day 0
6-16 yr 1.00 mg/day 0.50 mg/day 0

Tongue thrusting and mouth breathing may also play a part in the creation of a malocclu-
sion. An anterior open bite is the most common dental problem associated with the anomalies.
12. Describe intervention therapy for non-nutritional sucking habits.
1. Ideally, the patient should understand the problem and want to correct it.
2. The timing of intervention is controversial. Some authors suggest that therapy should
begin around age 4 years to prevent irreversible changes, whereas others suggest waiting
until the patient is about 6 to 7 years old to ensure that he or she can understand the
intent of therapy.
3. Patients who decide to accept appliance therapy should have support and encourage-
ment from their parents to help them during treatment.
4. The dentist should know the patient well to provide intervention and advice at the cor-
rect time.
5. The dentist should be able to evaluate the deformity and extent of its effects so that it
can be treated in the best possible manner.
13. What is the current schedule of systemic fluoride supplementation?
See Table 10-1.
14. Summarize the scientific basis for the use of fluoride varnishes in caries
management.
1. When used appropriately, varnishes offer a 40% to 65% reduction in the incidence
of caries, with a 36% reduction in fissured caries and a 66% reduction in nonfissured
surfaces.
2. Varnish results in a 51% reversal of decalcified tooth structure and a reduction in enamel
demineralization of 21% to 35%.
3. Varnish application is effective in arresting and reversing active enamel lesions, reducing
the need for restorative treatment.
4. Varnishes are as effective as acidulated phosphate fluoride gels in controlling approximal
caries.
5. In primary teeth of preschool children, varnishes result in a 44% reduction in caries.
15. Is prenatal fluoride supplementation effective in decreasing caries rates in the
primary dentition?
No. No studies to date support the administration of prenatal fluorides to protect the
primary dentition against caries.
16. Do home water filtration units have any effect on fluoride content?
Absolutely. For example, reverse osmosis home filtration systems remove 84%, distillation
units remove 99%, and carbon filtration systems remove 81% of the fluoride from water.
17. Why has the prevalence of fluorosis increased in the United States?
The increased prevalence is likely because of three factors: (1) inappropriate fluoride
supplementation; (2) ingestion of fluoridated toothpaste (most children <5 years ingest all
the toothpaste placed on the toothbrush); and (3) high fluoride content of bottled juices.
For example, white grape juice may have a fluoride concentration greater than 2 ppm.
18. What are the common signs of acute fluoride toxicity?
Acute fluoride toxicity may result in nausea, vomiting, hypersalivation, abdominal pain,
and diarrhea.
 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS 231

19. What is the first step in treating a child who has ingested an amount of fluoride
greater than the safely tolerated dose?
In acute toxicity, the goal is to minimize the amount of fluoride absorbed. Therefore, syrup
of ipecac is administered to induce vomiting. Calcium-binding products, such as milk or
milk of magnesia, decrease the acidity of the stomach, forming insoluble complexes with
the fluoride and thereby decreasing its absorption.
20. Are children born with Streptococcus mutans?
Children are not born with Streptococcus mutans. Instead, they acquire this caries-causing
organism between the ages of about 1 and 3 years. Mothers tend to be the major source of infec-
tion. The well-delineated age range of acquisition is referred to as the window of infectivity.
Transmission of S. mutans may be vertical (e.g., from caregiver to child) or horizontal
(e.g., between siblings). Transmission may be decreased by reducing habits such as sharing
utensils or foods. Additonally, several studies have demonstrated decreasing maternal levels
of S. mutans decreases the transmission rate to the child.
21. What variable is the best predictor of caries risk in children?
Past caries rates are the single best predictor in assessing a child’s future risk.
22. Is milk a contributing factor to early childhood caries?
Several animal and in vitro studies have suggested that milk and milk components are not
cariogenic. Similarly, human breast milk by itself does not cause demineralization. However,
when mixed with a sucrose-containing substance, cow’s milk and human breast milk promote
caries.
23. What food components reduce the caries-inducing effects of carbohydrates?
Phosphates, fats, and cheese decrease caries susceptibility. Phosphates apparently have
a topical effect that aids in remineralization and improves the structural integrity of the
enamel surface. Although the mechanism is not entirely clear, fats may form a protective
barrier on the teeth or coat the carbohydrate. Cheese may contribute through a number of
mechanisms, including its fat, phosphorus, and calcium content.
24. Is there any dental health benefit to chewing gum?
One study found that children of mothers who chewed sugar-free gum sweetened with xyli-
tol (in addition to normal oral hygiene measures) had 70% less dental decay than children
of mothers who did not chew the gum.
25. Summarize the mechanisms of xylitol’s effect.
• 
Xylitol has a five-carbon chemical structure not recognized by oral bacteria.
• 
Because it is not fermented, no acid production results, and pH levels in the mouth do
not decrease (see question 27).
• 
Chewing xylitol-sweetened gum promotes stimulation of salivary flow, which in turn helps
rinse away excessive sucrose residues and neutralize acids from other foods. In addition,
saliva contains calcium and phosphate, which promote remineralization of early caries.
• 
Xylitol is a polyol that inhibits the growth of S. mutans, thereby reducing caries sus-
ceptibility. Continued use helps reduce the number of virulent bacteria in the plaque,
although xylitol is not bactericidal.
• 
Xylitol reduces plaque in the oral cavity and enhances the proportion of soluble to
insoluble polysaccharides.
• 
Xylitol complements fluoride in the oral cavity.
26. Who throws a meaner curve, Ryan or Stephan?
Undoubtedly Stephan! The Stephan curve describes the decrease in pH that occurs fol-
lowing a cariogenic challenge. Hall of Fame pitcher Nolan Ryan, on the other hand, is best
remembered for his fast ball, although did have a pretty good curve.
27. What is meant by critical pH?
Critical pH is the pH (∼5.5) at which enamel is demineralized.
28. What is the Vipeholm Study? What did it demonstrate?
In the Vipeholm Study (1954), adult institutionalized patients were followed for several
years on a variety of controlled diets. The following results were reported:
232 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS

• 
Caries increased significantly when sucrose-containing foods were ingested between meals.
• 
Sucrose in a retentive form produced more caries than forms that were rapidly cleared
from the mouth.
• 
Sucrose consumed with meals was the least detrimental form.
• 
Caries activity differs among people with the same diet.
29. Why does this CAT not have your tongue?
CAT stands for the Caries Risk Assessment Tool developed by the AAPD to aid in assess-
ing a child’s risk of caries (Table 10-2). Recommendations based on their guidelines are as
follows:
1. Dental caries risk assessment, based on a child’s age, biologic and protective factors, and
clinical findings, should be a routine component of new and periodic examinations by
oral health and medical providers.
2. There is not enough information at present to carry out quantitative caries risk assess-
ment analyses. However, estimating children at low, moderate, and high caries risk via a
preponderance of risk and protective factors will enable a more evidence-based approach
to medical provider referrals, as well as establish periodicity and intensity of diagnostic,
preventive, and restorative services.
3. Clinical management protocols, based on a child’s age, caries risk, and level of patient
and parent cooperation, provide health providers with criteria and protocols for
determining the types and frequency of diagnostic, preventive, and restorative care for
patient-specific management of dental caries.
30. Why might children with asthma be at higher risk of developing dental caries?
The two major classes of medications used to treat asthma are anti-inflammatory agents
(e.g., corticosteroids, cromolyn sodium) and bronchodilators (beta-adrenergic agonists,
such as ventolin and albuterol). Over the years, numerous studies have shown that all
these medications can impair salivary function, causing xerostomia (dry mouth) and thus
potentially increasing susceptibility to caries. Evidence suggests that children with asthma
may have double the risk of caries in their primary and permanent dentition. Therefore, it
is important to implement appropriate preventive measures in asthmatic patients, such as
routine fluoride application and giving extra attention to oral hygiene.
31. What is the earliest macroscopic evidence of dental caries on a smooth enamel
surface?
A white spot lesion results from acid dissolution of the enamel surface, giving it a chalky
white appearance. Optimal exposure to topical fluorides may result in the remineralization
of such lesions.
32. Which teeth are often spared in nursing caries?
The mandibular incisors often remain caries-free as a result of protection by the tongue.
33. Does an explorer stick necessarily indicate the presence of caries?
Several studies have demonstrated that an explorer stick may often be caused by the
anatomy of the pit and fissure and not the presence of caries (poor sensitivity). However,
the lack of a stick is a good indication of lack of caries (good specificity). It has been
suggested that sharp eyes are more important than sharp explorers in detecting pit and
fissure caries.
34. What are the indications for an indirect pulp cap in the primary dentition?
An indirect pulp cap is indicated in a deep carious lesion approximating the pulp but
without signs or symptoms of pulp degeneration. Long-term studies have indicated a higher
success rate for indirect pulp caps compared to pulpotomies.
Calcium hydroxide is a commonly used medication that is applied to the dentin,
followed by a restorative material that provides a complete seal.
35. What are the indications for a direct pulp cap?
A direct pulp cap maybe indicated when there is a small mechanical or traumatic exposure
of the pulp. Materials commonly used include calcium hydroxide, glass ionomer and, more
recently, mineral trioxide aggregate (MTA). According to one study, successful outcomes
are inversely related to the amount of bleeding.
 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS 233

Table 10-2. Caries Risk Assessment Tool (CAT)

CARIES RISK
INDICATORS LOW RISK* MODERATE RISK† HIGH RISK‡
Clinical conditions No carious teeth in Carious teeth in past Carious teeth in past
past 24 mo 24 mo 12 mo
No enamel demineral- One area of enamel More than one
ization demineralization enamel
No visible plaque; no Gingivitis Demineralization
gingivitis (enamel caries—
white spot lesion)
Visible plaque on
anterior (front)
teeth
Radiographic enamel
caries
High titers of Strepto-
coccus mutans
Wearing dental or
orthodontic appli-
ances
Enamel hypoplasia
Environmental Optimal systemic and Suboptimal systemic Suboptimal topical
characteristics topical fluoride fluoride exposure fluoride exposure
exposure with optimal topi- Frequent (i.e., 3 or
Consumption of cal exposure more) between-
simple sugars or Occasional (one or meal exposures to
foods strongly as- two) between-meal simple sugars or
sociated with caries exposures to simple foods strongly asso-
initiation, primarily sugars or foods ciated with caries
at mealtimes strongly associated Low-level caregiver
High socioeconomic with caries socioeconomic
status of caregiver Midlevel socioeco- status (i.e., eligible
Regular use of dental nomic status of for Medicaid)
care in an estab- caregiver (i.e., No usual source of
lished dental home eligible for school dental care
lunch program, Active caries present
CHIP) in the mother
Irregular use of dental
services
General health Children with special
conditions health care needs
Conditions impairing
saliva composition/
flow
CHIP, Children’s Health Insurance Program.
*Low risk: The child does not have moderate-risk or high-risk indicators.
†Moderate risk: The presence of at least one moderate-risk indicator and no high-risk indicators present results

in a moderate-risk classification.
‡High risk: The presence of a single risk indicator in any area of the high-risk category is sufficient to classify a

child as being at high risk.

Adapted from American Academy of Pediatric Dentistry: American Academy of Pediatric Dentistry Caries Risk Assess-
ment Tool (CAT). http://www.chcs.org/usr_doc/AAP_CAT.pdf. Accessed May 7, 2014.
234 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS

36. What medication shows the greatest promise for primary tooth pulpotomies?
Recent studies have suggested that MTA has great potential as a primary tooth pulpotomy
medication. It results in less internal root resorption and improved clinical and radiographic
outcomes compared with formocresol, ferric sulfate, or sodium hypochloride. (It also smells
a lot better than formocresol.)
37. What are the disadvantages of MTA as a primary tooth pulpotomy medication?
They are mainly cost considerations. It is at least 20 times more expensive than
formocresol.
38. Which branchial arch gives rise to the maxilla and mandible?
The first branchial or mandibular arch gives rise to the maxilla, mandible, Meckel’s carti-
lage, incus, malleus, muscles of mastication, and anterior belly of the digastric muscle.
39. How does the palate form?
The paired palatal shelves arise from the intraoral maxillary processes. These shelves,
originally in a vertical position, reorient to a horizontal position as the tongue assumes a
more inferior position. The shelves then fuse anteriorly with the primary palate, which
arises from the median nasal process, and posteriorly and with one another. Failure of fusion
results in a cleft palate.
40. When do the primary teeth develop?
At approximately 28 days in utero, a continuous plate of epithelium arises in the maxilla
and mandible. By 37 days in utero, a well-defined, thickened layer of epithelium overlying
the cell-derived mesenchyme of the neural crest delineates the dental lamina. Ten areas in
each jaw become identifiable at the location of each of the primary teeth.
41. After the eruption of a tooth, when is root development completed?
In the primary dentition, root development is complete approximately 18 months after
eruption; in the permanent dentition, the period of development is approximately 3 years.
42. Define ankylosis. How is it diagnosed?
Ankylosis is the fusion of cementum with alveolar bone and may occur at any time during
the course of eruption. Because affected teeth have retarded vertical growth, they appear
to be submerged below the occlusal plane. Diagnosis involves visual determination that a
tooth may be 1 mm or more below the height of the occlusal plane, radiographic evidence
of lack of a periodontal ligament, and/or lack of physiologic mobility. The ankylosed tooth
emits an atypical sharp sound on percussion. In addition, children with affected siblings are
twice as likely to have submerged teeth compared with the general population. Ankylosis
often occurs bilaterally; 67% of affected people have two or more submerged teeth.
43. What causes ankylosis? Which teeth are usually affected?
The definitive cause of ankylosis is unknown. Contributing factors cited in the literature
include local mechanical trauma, disturbed local metabolism, localized infection, chemical
or thermal irritation, and gaps in the periodontal membrane.
Mandibular first primary molars are usually affected, followed by second mandibular
molars, first maxillary molars, and second maxillary molars. The prevalence of infraclusion
peaks between 8 and 9 years of age, with a suspected range of 1.3% to 8.9%.
44. How is ankylosis treated?
The severity of submergence dictates the treatment protocol. Therefore, constant vigilance
at recall appointments is crucial. The age at which ankylosis begins determines the rate of
submergence. The younger the child at onset of ankylosis, the more quickly the tooth sub-
merges because of the increased rate of growth of alveolar bone height. In minor cases, in
which the occlusal surface is within 1 mm of the occlusal plane, the tooth needs only moni-
toring for exfoliation. In rare cases, the ankylosis is severe enough that the occlusal surface
meets the interproximal gingival tissue. In such cases, the affected tooth must be extracted,
with subsequent space maintenance. For moderate cases, stainless steel crowns or buildup
restorations can be used to prevent space loss or supraeruption. With mismanagement or
misdiagnosis, the sequelae of infraclusion include space loss, molar tipping, supraeruption of
antagonist teeth, and periodontal defects with decreased height of bone.
 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS 235

45. How should dosages of local anesthetic be calculated for a pediatric patient?
Because children’s weights vary dramatically for their chronologic age, dosages of local
anesthetic should be calculated according to a child’s weight. A dosage of 4 mg/kg of lido-
caine should not be exceeded in pediatric patients.
46. Should the parent be allowed in the operatory with the pediatric patient?
The debate continues. However, some studies have indicated that many pediatric dentists
allow the parent to be present in the operatory.
47. What is the treatment for a traumatically intruded primary incisor?
In general, the treatment of choice is to allow the primary tooth to re-erupt. Re-eruption
usually occurs in 2 to 4 months. If the primary tooth is displaced into the follicle of the
developing permanent incisor, the primary tooth should be extracted.
48. What are the potential sequelae of trauma to a primary tooth?
Potential sequelae include color changes, necrosis, infection and tooth loss. Color changes
include yellow (pulp canal obliteration or metamorphosis), pink (internal resorption), or
gray-black (hemosiderin or pulpal necrosis) color changes. Hemosiderin is not uncommon
within the first 30 days after the trauma. After 30 days, a gray or gray-black color change in
the crown typically indicates pulp necrosis. Necrosis may occur at any time after the injury
(weeks, months, years). No treatment is indicated unless other pathologic changes occur
(e.g., periapical radiolucency, fistulation, swelling, pain).
Damage to the succedaneous permanent tooth, including hypoplastic defects, dilacera-
tion of the root, or arrest of tooth development, has also been reported.
49. What are the indications for a lingual frenectomy?
Tongue-tie, or ankyloglossia, is relatively rare and usually requires no treatment. Occasion-
ally, however, a short lingual frenum may result in lingual stripping of the periodontium
from the lower incisors, which is an indication for frenectomy. A second indication is
speech problems secondary to tongue position as diagnosed by a speech pathologist. Inabil-
ity to latch on or breast-feed has been reported in some infants with a high lingual frenum.
Breastfeeding in these patients has been reported to improve following frenectomy.
50. If a child reports a numb lip, can you be certain that the child has a profoundly
anesthetized mandibular nerve?
Children, especially young ones, often do not understand what it means to be numb. The
mandibular nerve is the only source of sensory innervation to the labia-attached gingiva
between the lateral incisor and canine. If probing of this tissue with an explorer evokes no
reaction from the patient, a profound mandibular block is present. No other sign can be
used to diagnose profound anesthesia of the mandibular nerve.
51. Does slight contact with a healthy approximal surface during preparation of a
class II cavity have any significant consequences?
Even slight nicking of the mesial or distal surface of a tooth greatly increases the possibil-
ity for future caries. Placement of an interproximal wedge before preparation significantly
decreases the likelihood of tooth damage and future pathology.
52. Why bother with restoring posterior primary teeth?
Caries is an infectious disease. As at any location in the body, treatment consists of con-
trolling and eliminating the infection. With teeth, caries infection can be eliminated by
removing the caries and restoring or extracting the tooth. However, extraction of primary
molars in children may result in loss of space needed for permanent teeth. To ensure arch
integrity and reduce the risk of pain, infection, and loss of function, decayed primary teeth
should be treated with well-placed restorations.
53. What is the most durable restoration for a primary molar with multisurface caries?
Stainless steel crowns have the greatest longevity and durability. Their 4.5-year survival
rate is more than twice that of amalgam (90% vs. 40%).
54. How should a primary tooth be extracted if it is next to a newly placed class II
amalgam?
Three steps can be taken to eliminate the possibility of fracturing the newly placed amalgam:
236 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS

1. The primary tooth to be extracted can be disked to remove bulk from the proximal
surface. Care still must be taken to avoid contacting the new restoration.
2. Placing a matrix band (T-band) around the newly restored tooth offers additional
protection.
3. When luxating the primary tooth, ensure that the elevator is placed subgingivally so
that the forces are against alveolar bone rather than the adjacent amalgam.
55. Can composites be used to restore primary teeth?
If good technique is followed, composite material is not contraindicated. Interproximally,
however, it may be difficult to get the type of isolation required for optimal bonding. There
is no scientific advantage to using composite instead of amalgam for such restorations, and
one has to evaluate whether aesthetic effects justify the additional time required for the
composite technique in primary teeth.
56. List the indications and contraindications for pulpectomy in a primary tooth.
Indications
• Teeth with chronic inflammation or necrosis of the radicular pulp
• Often attempted on the primary second molar before eruption of the first permanent molar
Contraindications
• Teeth with advanced resorption (internal or external), loss of root structure, or evidence
of periapical infection involving the crypt of the succedaneous tooth
• Primary root canals that are difficult to prepare because of variable and complex morphology
• Proximity of succedaneous tooth bud (unwanted damage may result from instrumenta-
tion, medication, or filling materials)
57. How successful is pulpectomy in a primary tooth?
In primary teeth with zinc oxide–eugenol (ZOE) pulpectomies, the success rate is 77.7%.
Success rates as high as 100% have been reported with Vitapex (premixed calcium hydrox-
ide and iodoform; Neo Dental International). The most important preoperative predictor
of success is amount of tooth root absorption (>23% resorption reduces the success rate
to only 23%). If correctly done, pulpectomy does not cause adverse effects on succedane-
ous tooth formation, but it does involve a 20% chance of altering the eruption path of the
permanent tooth.
58. What filling materials may be used for pulpectomy in a primary tooth?
The ideal properties of the filling material for pulpectomy in a primary tooth include a
resorption rate similar to that of primary root, no damage or irritation of periapical tissues
or the permanent tooth bud, antiseptic nature, and no discoloring of teeth. The two most
commonly used materials are as follows:
• ZOE paste—different rate of resorption, potential underfilling, mild foreign body
reaction with overfilling
• Calcium hydroxide and iodoform paste—rapid resorption, no deleterious effects on
succedaneous tooth
59. Which syndromes or conditions are associated with supernumerary teeth?
Apert syndrome Gardner syndrome
Cleft lip and palate Hallermann-Streiff syndrome
Cleidocranial dysplasia Oral-facial-digital syndrome type 1
Crouzon syndrome Sturge-Weber syndrome
60. Which syndromes or conditions are associated with congenitally missing teeth?
Achondroplasia Incontinentia pigmenti
Ectodermal dysplasia Chondroectodermal dysplasia
Cleft lip and palate Oral-facial-digital syndrome type 1
Hallermann-Streiff syndrome Down syndrome
Crouzon syndrome Rieger syndrome
61. In the case of a congenitally missing second premolar, how long can the second
primary molar be retained?
Most second primary molars lacking succedaneous teeth can be retained indefinitely, pro-
vided there is adequate root support in the plane of occlusion.
 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS 237

62. What are the differences among fusion, gemination, and concrescence?
Fusion is the union of two teeth, resulting in a double tooth, usually with two separate pulp
chambers. Fusion is usually observed in the primary dentition.
Gemination is the attempt of a single tooth bud to give rise to two teeth. The condi-
tion usually presents as a bifid crown with a single pulp chamber in the primary
dentition.
Concrescence is the cemental union of two teeth, usually the result of trauma.
63. What is the incidence of inclusion cysts in the infant?
It is approximately 75%.
64. What are the three most common types of inclusion cysts and their cause?
1. Epstein’s pearls are caused by entrapped epithelium along the palatal rapine.
2. Bohn’s nodules are ectopic mucous glands on the labial and lingual surfaces of the
alveolus.
3. Dental lamina cysts are remnants of the dental lamina along the crest of the alveolus.

65. What are the most common systemic causes of delayed exfoliation of the
primary teeth and delayed eruption of the permanent dentition?
Achondroplasia Gardner syndrome
Apert syndrome Hypopituitarism
Chondroectodermal dysplasia Hypothyroidism
Cleidocranial dysplasia Ichthyosis
De Lange syndrome Osteogenesis imperfecta
Down syndrome Vitamin D–resistant rickets

66. What are the most common systemic causes of premature exfoliation of the
primary dentition?
Fibrous dysplasia Hypophosphatasia
Cyclic neutropenia Juvenile diabetes
Acatalasia Odontodysplasia
Chediak-Higashi disease Papillon-Lefèvre syndrome
Dentin dysplasia Prepubertal periodontitis
Gaucher disease Scurvy
Histiocytosis Vitamin D–resistant rickets
67. What are Murphy’s laws of dentistry?
1. The easier a tooth looks on radiograph for extraction, the more likely you are to fracture
a root tip.
2. The shorter a denture patient, the more adjustments he or she will require.
3. The closer it is to 5 pm on Friday, the more likely someone will call with a dental
emergency.
4. The cuter the child, the more difficult the dental patient.
5. Parents who type their child’s medical histories are trouble.
6. The more you need specialists, the less likely they are to be in their office.
7. When a patient localizes pain to one of two teeth, you will open the wrong one.
8. The less a patient needs a procedure for dental health, the more the patient will want it
(e.g., anterior veneer vs. posterior crown).
68. Give the appropriate splinting times for the following traumatic dental injuries:
luxation, avulsion, root fracture, and alveolar fracture.
Luxation: 3 weeks
Avulsion: Splinting times depend on the extraoral dry time. If the tooth is reimplanted
within 60 minutes of the trauma, it should be splinted for 2 weeks for teeth with open and
closed apices. Splinting for 4 weeks is recommended when the tooth has had an extraoral
dry time longer than 60 minutes. In either case, caution should be used because of the high
risk of ankylosis associated with excessive splinting times.
Root fracture and alveolar fracture: 4 weeks for alveolar fractures and root fractures
limited to the apical third and midroot. For cervical third root fractures, a longer splinting
time (up to 4 months) may be beneficial.
238 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS

In all cases, a flexible splint should be used to allow physiologic movement of the teeth.
In addition, sound clinical judgment should be exercised to help decide whether longer
splinting times are necessary. For example, an avulsed tooth with a closed apex that is still
+3 mobile after 1 week may need to be splinted for 2 weeks.
69. What can be done to prevent impaction of permanent maxillary canines?
Within 1 year after the total eruption of the maxillary lateral incisors the maxillary canines
should be palpable. Additionally, a panoramic radiograph or intraoral radiographs should
be taken to determine the axial inclination of the developing permanent canine. If mesial
angulation is noted with overlap of the maxillary lateral incisor root, extraction of the maxillary
primary canine and maxillary first primary molars may often eliminate the impaction of the
maxillary canine.
70. What is the most important technique of behavioral guidance in pediatric
dentistry?
It is “tell-show-do.” Tell the child what is going to happen, show the child what is going to
happen, and then perform the actual procedure intraorally. The major fear in pediatric den-
tal patients is the unknown. The tell, show, and do technique eliminates fear and enhances
the patient’s behavioral capabilities.
71. What pharmacologic agents are indicated for behavioral control of the pediatric
dental patient in an office setting?
With the exception of general anesthesia, there are no absolutely predictable pharmaco-
logic agents for controlling the behavior of pediatric dental patients. Unless the operator
has received specific training in sedation techniques for children, patients with anxiety or
behavioral problems are best referred to a specialist in pediatric dentistry.
72. Do hypertrophic adenoids and tonsils affect dental occlusion?
The incidence of posterior crossbite is increased in children with significant tonsillar and
adenoid obstruction. Of children with a grade 3 obstruction, 80% have a posterior crossbite.
73. What technique may be used if a pediatric patient cannot tolerate a
conventional bitewing radiograph?
To help reduce gagging and pushing the film out of the mouth with the tongue, try placing the
film while the patient watches in a small hand mirror. This distracts the child and allows her or
him to see that film is not going in the throat. A Snap-a-Ray film holder may also help the child
better tolerate the film position because it reduces the vertical height and minimizes discomfort
in the floor of the mouth. Digital sensors make it even more challenging due to their increased
bulk.
If these techniques don’t work, a buccal bitewing is taken. The tab of the film is placed
on the occlusal surfaces of the molar teeth, and the film itself is positioned between the
buccal surfaces of the teeth and cheek. The cone is directed from 1 inch behind and
below the mandible upward to the area of the second primary molar on the contralateral
side. The setting is three times that which is normally used for a conventional bitewing
exposure.
74. What are the morphologic differences between primary and secondary teeth?
How does each difference affect amalgam preparation?
1. The occlusal anatomy of primary teeth is generally not as defined as that of secondary
teeth, and supplemental grooves are less common. The amalgam preparation therefore
can be more conservative.
2. The enamel in primary teeth is thinner than in secondary teeth (usually 1 mm thick);
therefore, the amalgam preparation is shallower in primary teeth. A depth of 1.5 mm
from the occlusal surface will place the preparation 0.5 mm into dentin, which allows
for sufficient bulk of the amalgam. This depth is easy to approximate using a 330 bur
because the head length of this bur is 1.6 mm.
3. Pulp horns in primary teeth extend higher into the crown of the tooth than pulp horns
in secondary teeth; therefore, the amalgam preparation must be conservative to avoid a
pulp exposure. The most common pulp exposure is the mesial buccal pulp horn of the
mandibular first molar.
 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS 239

4. Primary molar teeth have an exaggerated cervical bulge that makes matrix adaptation
more difficult.
5. The generally broad interproximal contacts in primary molar teeth require wider proxi-
mal amalgam preparation than those in secondary teeth.
6. Enamel rods in the gingival third of the primary teeth extend occlusally from the denti-
noenamel junction, eliminating the need in class II preparations for the gingival bevel
that is required in secondary teeth.
75. What is the purpose of the pulpotomy procedure in primary teeth?
The pulpotomy procedure preserves the radicular vital pulp tissue when the entire coronal
pulp is amputated. The remaining radicular pulp tissue is treated with an agent such as
formocresol.
76. What is the advantage of the pulpotomy procedure on primary teeth?
The pulpotomy procedure allows resorption and exfoliation of the primary tooth but
preserves its role as a natural space maintainer.
77. What are the indications for the pulpotomy procedure in primary teeth?
1. Primary tooth that is restorable with carious or iatrogenic pulp exposure
2. Deep carious lesions without spontaneous pulpal pain
3. Absence of pathologic internal or external resorption but intact lamina aura
4. No radiographic evidence of furcal or periapical pathology
5. Clinical signs of a normal pulp during treatment (e.g., controlled hemorrhage after
coronal amputation)
78. What are the contraindications for pulpotomy in primary teeth?
1. Interradicular (molar) or periapical (canine and incisor) radiolucency
2. Internal or external resorption
3. Advanced root resorption, indicating imminent exfoliation
4. Uncontrolled hemorrhage after coronal pulp extirpation
5. Necrotic dry pulp tissue or purulent exudate in pulp canals
6. Fistulous tracks or abscess formation
7. Medical condition (e.g., immunosuppression, severe cardiac disease)
79. How does rubber dam isolation of the tooth improve management of pediatric
patients?
1. The rubber dam seems to calm the child because it acts as a physical and psychological
barrier, separating the child from the procedure being performed.
2. Gagging from the water spray or suction is alleviated.
3. Access is improved because of tongue, lip, and cheek retraction.
4. The rubber dam reminds the child to open the mouth.
5. The rubber dam ensures a dry field that otherwise would be impossible in many
children.
6. It helps prevent inadvertent swallowing and/or aspiration of materials.
80. When do the primary and permanent teeth begin to develop?
The primary dentition begins to develop during the sixth week in utero; formation of
hard tissue begins during the 14th week in utero. Permanent teeth begin to develop
during the 12th week in utero. Formation of hard tissue begins about the time of
birth for the permanent first molars and during the first year of life for the permanent
incisors.
81. Summarize the chronology of development and eruption of the primary and
permanent teeth.
See Table 10-3.
82. What is leeway space?
Leeway space is the difference in the total of the mesiodistal widths between the primary
canine, first molar, and second molar and the permanent canine, first premolar, and second
premolar. In the mandible, leeway space averages 1.7 mm (unilaterally); it is usually about
0.9 to 1.1 mm (unilaterally) in the maxilla.
 240 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS

Table 10-3. Chronology of Development and Eruption of Teeth*

TOOTH
GERM CALCIFICATION CROWN ERUPTION ROOT
TOOTH COMPLETED COMMENCES COMPLETED IN MOUTH COMPLETED
Primary
Incisor 3-4 mo i.u. 2-4 mo 6-8 mo 6 mo-2 yr
Canines 5 mo i.u. 9 mo 16-20 mo 2½-3 yr
First molars 12-16 wk i.u. 5 mo i.u. 6 mo 12-15 mo 2-2½ yr
Second 6-7 mo i.u. 11-12 mo 20-30 mo 3 yr
molars
Permanent
Central 30 wk i.u. 3-4 mo 4-5 yr Max, 7-9 yr 9-10 yr
incisors
Mand, 6-8 yr
Lateral 32 wk i.u. Max, 10-12 mo 4-5 yr 7-9 yr 10-11 yr
incisors
Mand, 3-4 mo
Canines 30 wk i.u. 4-5 mo 6-7 yr Max, 12-15 yr
11-12 yr
Mand,
9-10 yr
First 30 wk i.u. 1½-2 yr 5-6 yr 10-12 yr 12-14 yr
­premolars
Second 31 wk i.u. 2-2½ yr 6-7 yr 10-12 yr 12-14 yr
­premolars
First molars 24 wk i.u. Birth 3-5 yr 6-7 yr 9-10 yr
Second 6 mo 2½-3 yr 7-8 yr 12-13 yr 14-16 yr
molars
Third 6 yr 7-10 yr 12-16 yr 17-21 yr 18-25 yr
molars
Mand, Mandibular; Max, maxillary.
*All dates postnatal, except where designated intrauterine (i.u.).
Adapted from Bishara SE: Textbook of orthodontics, Philadelphia, WB Saunders, 2001.

83. What changes occur in the size of the dental arch during growth?
From birth until about 2 years of age, the incisor region widens, and growth occurs in the
posterior region of both arches. During the period of the full primary dentition, arch length
and width remain constant. Arch length does not increase once the second primary molars
have erupted; any growth in length occurs distal to the second primary molars and not in
the alveolar portion of the maxilla or mandible. There is a slight decrease in arch length
with the eruption of the first permanent molars and a slight increase in intercanine width
(and some forward extension of the anterior segment of the maxilla) with the eruption of
the incisors. A further decrease in arch length may occur with molar adjustments and the
loss of leeway space when the second primary molar exfoliates.
84. What is the pink tooth of Mummery?
It is the pink appearance of a tooth caused by internal resorption.
85. What intervention is indicated when permanent maxillary canines are observed
radiographically to be erupting palatally?
It is extraction of the primary maxillary canine. About 75% of ectopic canines show nor-
malization of eruption at 12 months.
 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS 241

86. Does teething cause systemic manifestations?

Although teething may be associated with drooling, gum rubbing, or changes in dietary
intake, no evidence indicates that it causes systemic illness (e.g., diarrhea, fever, rashes,
seizures, bronchitis). Fever associated with teething may be a manifestation of undiagnosed
primary herpes gingivostomatitis.
87. Should dental implants be placed in the growing child?
Generally, placing implants should be deferred until growth is completed. In a growing
child, the implant may become submerged or embedded. In addition, an implant that
crosses the midline may limit transverse growth.
88. Should an avulsed primary tooth be reimplanted?
No. The prognosis of reimplanted primary teeth is poor and may adversely affect the devel-
oping succedaneous tooth.
89. How should an avulsed primary tooth be managed?
Rinse the tooth with water, and place it under the child’s pillow.
90. What variable is most important in the prognosis of an avulsed permanent
tooth?
Time out of the mouth is most critical. With an extra-alveolar time less than 1 hour, partial
periodontal ligament (PDL) healing is possible; an extra-alveolar time longer than 1 hour
results in total PDL death and progressive root resorption.
91. What other factors affect prognosis?
They are an extra-alveolar storage medium and stage of root development.
92. If an avulsed tooth cannot be reimplanted immediately, which transport medium
is best?
In order of preference, they are Hank’s balanced salt medium, milk, saliva, and water.
93. How do closed versus open apices affect prognosis?
Closed apices
• 
Revascularization is not likely.
• 
Pulp extirpation occurs in 7 to 10 days.
• 
Pulpal necrosis (radiolucency) is usually noted as early as 3 to 4 weeks (usually, apical
third within 1 year).
Open apices
• 
Revascularization is possible.
• 
Pulp necrosis is evident after 2 to 4 weeks and presents with periapical pathology, some-
times with signs of internal root resorption (IRR).
94. What are the most common complications after reimplantation of an avulsed
tooth?
• 
Pulpal necrosis
• 
Inflammatory resorption, replacement resorption (ankylosis)
• 
Internal calcification with pulpal obliteration (common in non–endodontically treated
reimplants)
95. Describe the occurrence of ankylosis after reimplantation of an avulsed tooth.
• 
Irreversible and progressive
• 
More rapid progression with younger age
• 
Mobility and dull percussion noted as early as 5 weeks (on radiographs at 8 weeks)
• 
Small areas of ankylosis are reversible with functional mobility
• 
The tooth loss is rapid and typically occurs within 1-5 years.
96. What is the most reliable diagnostic test for ankylosis?
It is percussion.
97. Why must care be taken not to nick the adjacent interproximal surface when
preparing a class II restoration?
Damaged noncarious primary tooth surfaces are 3.5 times more likely to develop a carious
lesion and to require future restoration than undamaged surfaces. Damaged noncarious
 242 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS

permanent tooth surfaces are 2.5 times more likely to develop a carious lesion and to
require future restoration than undamaged surfaces.
98. Do all discolored primary incisors require treatment?
The gray discoloration of primary teeth is usually the result of a traumatic episode. This
discoloration is caused by hemorrhage into the dentinal tubules or a necrotic pulp. In the
case of hemorrhage into the dentinal tubules, the discoloration usually appears within 1
month of the injury. Often, the teeth return to their original color as the blood breakdown
products are removed from the site. Discoloration caused by a necrotic pulp may take days,
weeks, months, or even years to develop. It does not improve with time and may actually
worsen. A tooth that is light gray may progress to dark gray. A yellow opaque discoloration
is usually indicative of calcific degeneration of the pulp. Discolored teeth do not require
treatment unless there is radiographic and/or clinical evidence of pathology of the peri-
odontium (soft and/or hard tissues).
99. Which two dentists have appeared on the cover of Time magazine?
They are Dr. Harold Kane Addelson, the originator of the tell-show-do technique, and Dr.
Barney Clark, the first human recipient of a mechanical heart.

ORTHODONTIC TREATMENT
100. What is the relationship between overjet and dental trauma?
Because of the high prevalence of dental trauma involving maxillary incisors, it is impor-
tant to determine whether any interceptive treatment can lower a patient’s risk for trauma.
Children with class II malocclusions and increased overjet face a greater risk of maxillary
incisor trauma. A tendency to a skeletal open bite with a negative overbite and excessive
overjet predispose patients to dental trauma. Children with overjets more than 3 mm are
twice as likely to injure the anterior teeth as children with overjets less than 3 mm, and
a 6-mm overjet results in four times the risk of trauma. The risk of trauma increases with
increasing overjet measurements.
Although definitive guidelines are not available, high-risk children with a large overjet,
excessive maxillary incisor proclination, and high facial angle may benefit from an evalu-
ation for early orthodontic intervention. It is the dentist’s role to provide anticipatory
guidance about injury prevention and the use of a mouth guard.
Note: The American Association of Orthodontists recommends that all children be
seen by an orthodontist by age 7 years.
101. What are the advantages of fixed versus removable orthodontic appliances?
Fixed orthodontic appliances offer controlled tooth movement in all planes of space.
Removable appliances are generally restricted to tipping teeth.
102. What is the straight wire appliance?
The straight wire appliance is a version of the edgewise appliance with several features that
allow placement of an ideal rectangular arch wire without bends (a so-called straight wire).
These features include the following: (1) variations in bracket thickness to compensate
for differences in the labiolingual position and thickness of individual teeth; (2) variations
in angulation of the bracket slot relative to the long axis of the tooth to allow mesiodistal
differences in the root angulation of individual teeth; and (3) variations in torque of the
bracket slot to compensate for buccal-lingual differences in the root angulation of indi-
vidual teeth.
103. What are so-called functional appliances? Do they work?
Functional appliances are a group of fixed and removable appliances that are generally used
to promote mandibular growth in patients with class II malocclusion. Although these appli-
ances have been shown to be effective in correcting a class II malocclusion, most studies
indicate that their effects are mainly dentoalveolar, with little if any effect on the growth of
the mandible.
104. When should orthodontic therapy be initiated?
There is no one optimal time to initiate treatment for every orthodontic problem. For
example, a patient in primary dentition with a bilateral posterior crossbite may benefit from
 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS 243

palatal expansion at age 4 years. Conversely, the same-aged patient with a severe class III
malocclusion caused by mandibular prognathism may best be treated by waiting until all
craniofacial growth is completed.
105. What is the difference between a skeletal and dental malocclusion?
Skeletal malocclusion refers to a disharmony between the jaws in a transverse, sagittal, or
vertical dimension or any combination thereof. Examples of skeletal malocclusions include
retrognathism, prognathism, open bites, and bilateral posterior crossbites. Dental malocclu-
sion refers to malpositioned teeth, generally the result of a discrepancy between tooth size
and arch length. This discrepancy often results in crowding, rotations, or spacing of the teeth.
Most malocclusions are neither purely skeletal nor purely dental but rather a combination of
the two.
106. If a primary first molar is lost, is a space maintainer necessary?
Before eruption of the 6-year molar and its establishment of intercuspation, mesial migra-
tion of the second primary molar will occur, and a space maintainer is indicated to prevent
space loss.
107. When should a crossbite be corrected?
Whenever a crossbite is noted and the patient is amenable to intraoral therapy, correction
is indicated. Although a crossbite can be corrected at a later date, optimal time for correc-
tion is as soon as possible after diagnosis.
108. When is the proper time to consider diastema treatment?
A thick maxillary frenum with a high attachment (sometimes extending to the palate) is
common in the primary dentition and does not require treatment. However, a large midline
diastema in the primary dentition may indicate the presence of an unerupted midline super-
numerary tooth (mesiodens) and often warrants an appropriate radiograph.
The permanent maxillary central incisors erupt labial to the primary incisors and often
exhibit a slight distal inclination that results in a midline diastema. This midline space
is normal and decreases with the eruption of the lateral incisors. Complete closure of the
midline diastema, however, does not occur until the permanent canines erupt. Treatment of
residual midline space is addressed orthodontically at this time.
109. What is ectopic eruption? How is it treated?
Ectopic eruption occurs when the erupting first permanent molar begins to resorb the distal
root of the second primary molar. Its occurrence is much more common in the maxilla, and
it is often associated with a developing skeletal class II pattern. It is seen in about 2% to 6%
of the general population and 25% in patients with cleft lip and palate; it spontaneously
corrects itself in about 60% of cases. If the path of eruption of the first permanent molar
does not self-correct, a brass wire or orthodontic separating elastic can be placed between
the first permanent molar and second primary molar, if possible. In severe cases, one may
use a Halterman appliance to upright the ectopic tooth or the second primary molar may
exfoliate early because of severe resorption or require extraction, necessitating the need for
space maintenance or space regaining.
110. What is the effect of early extraction of a primary tooth on the eruption of the
succedaneous tooth?
If a primary tooth must be extracted prematurely, and 50% of the root of the permanent
successor has developed, eruption of the permanent tooth is usually delayed. If more than
50% of the root of the permanent tooth has formed at the time of extraction of the primary
tooth, eruption is accelerated.
111. Where are the primate spaces located?
In the maxilla, primate spaces are located distal to the primary lateral incisors. In the man-
dible, primate spacing is found distal to the primary canines.
112. What is the normal molar relationship in the primary dentition?
Historically, both the flush terminal plane and mesial step have been considered normal.
More recent studies have demonstrated that this may not be the case, because about 45%
of children with a flush terminal plane go on to develop a class II molar relationship in the
permanent dentition.
 244 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS

113. What is meant by the term pseudo–class III?

This term refers to the condition in which the maxillary incisors are in crossbite with the
mandibular incisors. Although the patient appears to have a prognathic mandible, it is
caused not by a skeletal disharmony but rather by the anterior positioning of the jaw as a
result of occlusal interference. The ability of the patient to retrude the mandible to the edge
to edge incisal relationship is often considered diagnostic.
114. What is the space maintainer of choice for a 7-year-old child who has lost a
lower primary second molar to caries?
The lower lingual arch (LLA) is the maintainer of choice. The 6-year-old molars are
banded. The connecting wire lies lingual to the permanent lower incisors in the gingival
third and prevents mesial migration of the banded molars. Unlike the band and loop space
maintainer, the LLA is independent of eruption sequence. (The band and loop serve no
purpose after the primary first molar exfoliates.) However, the LLA should not be used if
the permanent mandibular incisors are absent because the lingual arch may prevent the
eruption of these teeth.
115. What is the space maintainer of choice for a 5-year-old child who has lost an
upper primary second molar to caries prior to the eruption of the first permanent
molar?
The distal shoe is the appliance of choice. This appliance extends backward from a crown
on the primary first molar and subgingivally to the mesial line of the unerupted first perma-
nent molar, thus preventing mesial migration.
116. A 4-year-old child with generalized spacing loses three primary upper incisors
to trauma. What space maintainer is needed?
No space maintainer is necessary.
117. What is the best space maintainer for any pulpally involved primary tooth?
Restoring the tooth with pulpal therapy is the best way to preserve arch length and
integrity.
118. If a primary tooth is lost to caries but has no successor, is it necessary to main-
tain space?
Sometimes it is necessary to maintain the space, but not always. The decision is based on
the patient’s skeletal and dental development. Either way, orthodontic evaluation is of the
utmost importance to formulate the future plan for this space.
119. When do you remove a space maintainer once it is inserted?
The space maintainer can be removed as soon as the succedaneous tooth begins to erupt
through the gingiva. Space maintainers left in place too long make it more difficult for
patients to clean their teeth. Furthermore, it may be necessary to replace a distal shoe with
another form of space maintainer once the 6-year molar has erupted to prevent rotation of
the molar around the bar arm.
120. What are the various types of headgear and their indications?
There are four basic types of headgear. Each type of headgear has two major components,
intraoral and extraoral. The extraoral component is what generally categorizes the type of
headgear.
1. 
Cervical-pull headgear. The intraoral component of cervical-pull headgear is composed
of a heavy bow that engages the maxillary molars through some variation on a male-
female connector. The anterior part of the bow is welded to an extraoral portion con-
nected to an elasticized neck strap, which provides the force system for the appliance.
The force application is in a down and backward direction. This headgear is generally
used in a class II, division 1 malocclusion, in which distalization of the maxillary molars
and/or restriction of maxillary growth, as well as anterior bite opening, is desired.
2. 
Straight-pull headgear. The intraoral component is similar to the cervical-pull headgear.
However, the force application is in a straight backward direction from the maxillary
molar, parallel to the occlusal plane. Like cervical-pull headgear, this appliance is also
used for a class II, division 1 malocclusion. Because of the direction of force application,
this appliance may be chosen when excessive bite opening is undesirable.
 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS 245

3. 
High-pull headgear. The intraoral components of high-pull headgear are similar to
those described. However, the force application is in a back and upward direction.
Consequently, it is usually chosen for a class II, division 1 malocclusion in which a bite
opening is contraindicated (class II malocclusion with an open bite).
4. 
Reverse-pull headgear. Unlike the other headgears, the extraoral component of
reverse-pull headgear is supported by the chin, cheeks, forehead, or a combination of
these structures. The intraoral component usually attaches to a fixed appliance in the
maxillary appliance via elastics. Reverse-pull headgear is generally used for a class III
malocclusion, in which protraction of the maxilla is desirable.
121. What is the basic sequence of orthodontic treatment?
1. Level and align. This phase establishes preliminary bracket alignment, generally with a
light round wire, braided arch wire, or nickel-titanium arch wire.
2. Working arch wires. This phase corrects vertical discrepancies (e.g., bite opening)
and sagittal position of the teeth. A heavy round or rectangular arch wire is generally
used.
3. Finishing arch wires. This phase idealizes the position of the teeth. Generally, light,
round arch wires are used.
4. Retention. Retention of teeth in their final position may be accomplished with a fixed
or removable retainer.
122. What are the dental health benefits of orthodontic treatment?
Ironically, few studies have shown any dental health benefit to orthodontic treatment. Posi-
tive effects on caries susceptibility, periodontal disease, and temporomandibular disorders
(TMDs) are largely unsupported by the literature. The exception would be susceptibility to
trauma, for which studies have suggested a direct relationship between overjet and trauma
to the maxillary incisors.
123. What is a tooth positioner?
A tooth positioner is a removable appliance composed of rubber, silicone, or polyvinyl
material. Its appearance is not unlike that of a heavy mouth guard, except that it engages
both the maxillary and mandibular dentition. It is generally used to idealize final tooth
position at or near the completion of orthodontic therapy. The appliance is usually custom-
fabricated by taking models of the teeth and repositioning them to their ideal position. The
positioner is then fabricated to this ideal setup. The elasticity of the appliance provides
for minor positional changes of the patient’s teeth. After completion of treatment, the
positioner may be used as a retainer.
124. How stable is the orthodontic correction of crowding?
Approximately two thirds of all patients treated for crowding experience significant
relapse without some form of permanent retention. This relapse rate is about the same
whether the patient is treated with a nonextraction or extraction approach; whether
third molars are present, congenitally missing, or extracted; and whether treatment is
started in the mixed dentition or permanent dentition. Unfortunately, no variables that
correlate with relapse potential have been identified. Also, relapse potential continues
throughout life.
125. What is the best way to prevent relapse?
It is lifelong retention. The type of retainer appears less important than the length of
retention.
126. Does eruption of third molars cause crowding of the incisors?
No. The eruption of third molars with a real or perceived increase in crowding of the inci-
sors is coincidental. Studies have revealed that patients who are congenitally missing third
molars experience the same crowding phenomenon.
127. What is the ideal molar relationship in the primary dentition?
It is the mesia1 step. Although many pediatric dentistry and orthodontic texts suggest that
the mesial step relationship and the flush terminal plane are considered normal, a longitudi-
nal study has revealed that almost 50% of flush terminal plane relationships in the primary
dentition later develop into class II malocclusions.
 246 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS

128. Define early mesial shift and late mesial shift.

These terms date back to the work of Baume in the late 1950s. The early mesial shift refers
to the closure of the generalized spacing frequently observed in the primary dentition that
closes with the eruption of the permanent first molars, causing a shift of the primary molars
mesially. The late mesial shift occurs with the exfoliation of the second primary molars and
the mesial drift of the first permanent molars into the leeway space.

Bibliography
Aeinehchi M, Dadvand S, Fayazi S, Bayat-Movahed S: Randomized controlled trial of mineral trioxide aggre-
gate and formocresol for pulpotomy in primary molar teeth, Int Endod J 40:261–267, 2007.
Alavaikko S, Jaakkola MS, Tjaderhane L, Jaakkola JJ: Asthma and caries: a systematic review and meta analysis,
Am J Epidemiol 174:631–641, 2011.
Al-Zayer MA, Straffon LH, Feigal RJ, Welch KB: Indirect pulp treatment of primary posterior teeth: a retro-
spective study, Pediatr Dent 25:29–36, 2003.
American Academy of Pediatric Dentistry (AAPD): Guideline on infant oral health care, 2012. http://www.aapd
.org/media/Policies_Guidelines/G_InfantOralHealthCare.pdf. Accessed May 7, 2014.
American Dental Association: Baby’s first dental visit, ADA News, 2001.
American Dental Association: Guide to Dental Therapeutics, ed 2, Chicago, 2000, ADA Publishing. 341, 523.
Andreasen JO, Andreasen FM: Essentials of Traumatic Injuries to the Teeth, Copenhagen, 1990, Munksgaard.
Baccetti T, Antonini A: Dentofacial characteristics associated with trauma to maxillary incisors in the mixed
dentition, J Clin Pediatr Dent 22:281–284, 1998.
Bishara SE: Textbook of Orthodontics, Philadelphia, 2001, WB Saunders.
Bishara SE, Hoppens BJ, Jakobsen JR, Kohout FJ: Changes in the molar relationship between the deciduous and
permanent dentitions: a longitudinal study, Am J Orthod Dentofac Orthop 93:19–28, 1988.
Brown MD, Aaron G: The effect of point-of-use water conditioning systems on community fluoridated water,
Pediatr Dent 13:35–38, 1991.
Casamassimo PS, Fields HW, McTigue DJ, et al.: Pediatric Dentistry: Infancy Through Adolescence, ed 5, St. Louis,
2013, Saunders.
Caulfield PW, Cutter GR, et al.: Initial acquisitions of mutans streptococci by infants: evidence for a discrete
window of infectivity, J Dent Res 72:37–45, 1993.
Coll JA, Sadrian R: Predicting pulpectomy success and its relationship to exfoliation and succedaneous denti-
tion, Pediatr Dent 18:57–63, 1996.
Disney JA, Graves RC, Stamm JW, et al.: The University of North Carolina Caries Risk Assessment study:
Further developments in caries risk prediction, Community Dent Oral Epidemiol 20:64–75, 1992.
Douglas J, Tinanoff N: The etiology, prevalence and sequelae of infraclusion of primary molars, ASDC J Dent
Child 58:381–483, 1991.
Edelstein B: Evidence-based dental care for children and the age 1 dental visit, Pediatr Ann 27:569–574, 1998.
Einwag J, Dunninger F: Stainless steel crowns versus multisurface amalgam restorations: an 8-year longitudinal
clinical study, Quintessence Int 27:321–323, 1996.
Enlow DH: Facial Growth, 3rd ed., Philadelphia, 1990, WB Saunders.
Ericson S, Kurol J: Early treatment of palatally erupting maxillary canines by extraction of the primary canines,
Eur J Orthod 10:282–295, 1988.
Flores MT, Andreasen JO, Bakland LK, et al.: Guidelines for the evaluation and management of traumatic
dental injuries, Dent Traumatol 17:193–198, 2001.
Fuks AB: Pulp therapy for the primary and young permanent dentitions, Dent Clin North Am 44:571–596,
2000.
Gorlin RJ, Cohen Jr MM, Levin LS: Syndromes of the Head and Neck, New York, 1990, Oxford University Press.
Gustafson BE, Quensel CE, Lanke LS, et al.: The Vipeholm Dental Caries Study: The effect of different levels of car-
bohydrate intake on caries activity in 436 individuals observed for five years, Acta Odontol Scand 11:232–364, 1954.
Hupp J, Ellis E, Tucker MR: Contemporary and Maxillofacial Surgery, ed 6, St. Louis, 2014, Mosby.
Isokangas P, et al.: Occurrence of dental decay in children after maternal consumption of xylitol chewing gum, a
follow-up from 0 to 5 years of age, J Dent Res 79:1885–1889, 2000.
Kaban LB: Pediatric Oral and Maxillofacial Surgery, Philadelphia, 1990, W.B. Saunders.
Kates GA, Needleman HL, Holmes LB: Natal and neonatal teeth: a clinical study, J Am Dent Assoc 109:
441–443, 1984.
King DL, Steinhauer W, Garcia-Godoy F, Elkins CJ: Herpetic gingivostomatitis and teething difficulty in
infants, Pediatr Dent 14:82–85, 1992.
Marcum BK, Turner C, et al.: Pediatric dentists’ attitudes regarding parental presence during dental procedures,
Pediatr Dent 17:432–436, 1995.
Matsuo T, Nakanishi T, Shimizu H, Ebisu S: A clinical study of direct pulp capping applied to carious-exposed
pulps, J Endod 22:551–556, 1996.
McDonald RE, Avery DR: Dentistry for the Child and Adolescent, St. Louis, 1994, Mosby.
Messer LB, Cline JT: Ankylosed primary molars: results and treatment recommendations from an eight-year
longitudinal study, Pediatr Dent 2:34–47, 1990.
 CHAPTER 10 PEDIATRIC DENTISTRY AND ORTHODONTICS 247

Mortazavi M, Mesbahi M: Comparison of zinc oxide and eugenol, and Vitapex for root canal treatment of
necrotic primary teeth, Int J Paediatr Dent 14:417–424, 2004.
Moyers R: Handbook of Orthodontics, Chicago, 1986, YearBook.
Nguyen QV, Bezemer PD, Habets L, Prahl-Anderson B: A systematic review of the relationship between overjet
size and traumatic dental injuries, Eur J Orthodont 21:502–515, 1999.
Noorollahian H: Comparison of mineral trioxide aggregate and formocresol as pulp medicaments for pulpoto-
mies in primary molars, Br Dent J 204:E20, 2008.
Oulis CJ, Vadiakas GP, et al.: The effect of hypertrophic adenoids and tonsils on the development of posterior
crossbites and oral habits, J Clin Pediatr Dent 18:197–201, 1994.
Peng L, Ye L, Guo X, et al.: Evaluation of formocresol versus ferric sulphate primary molar pulpotomy: a system-
atic review and meta-analysis, Int Endod J 40:751–757, 2007.
Proffit WR, Fields HW, Sarver DM: Contemporary Orthodontics, ed 5, St. Louis, 2013, Mosby.
Resource Centre for Rare Oral Diseases, Department of Oral, Maxillo-Facial Surgery at the University Hospital
of Copenhagen: The dental trauma guide, 2014. http://www.dentaltraumaguide.org/Permanent_Root_fracture_
Treatment.aspx. Accessed August 14, 2014.
Ryburg M, Moller C, Ericson T: Saliva composition and caries development in asthmatic patients treated with
beta 2-adrenergic agonists: a 4-year follow-up study, Scand J Dent Res 99:212–219, 1991.
Sanchez DM, Childers NK: Anticipatory Guidance in Oral Health: Rationale and Recommendations, American
Academy of Family Physicians, 2001.
Schatz J-P, Hakeberg M, et al.: Prevalence of traumatic injuries to permanent dentition and its association with
overjet in a Swiss child population, Dent Traumatol 29:110–114, 2013.
Scully C, Welbury R: Color Atlas of Oral Diseases in Children and Adolescents, London, 1994, Mosby-Year Book
Europe.
Stephan RM: Changes in the hydrogen ion concentration on tooth surfaces in carious lesions, J Am Dent Assoc
27:718, 1940.
Tuna D, Olmez A: Clinical long-term evaluation of MTA as a direct pulp capping material in primary teeth, Int
Endod J 41:273–278, 2008.
Vaikuntam J: Fluoride varnishes: should we be using them? Pediatr Dent 22:513–516, 2000.
Vij R, Coll JA, Shelton P, Farooq NS: Caries control and other variables associated with success of primary
molar vital pulp therapy, Pediatr Dent 26:214–220, 2004.