National Board Dental Examination / Integrated National Board Dental Examination (INBDE) Preventive, Pediatric, and Orthodontic Dentistry Syllabus

Preventive, Pediatric, and Orthodontic Dentistry syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Preventive, Pediatric, and Orthodontic Dentistry in National Board Dental Examination / Integrated National Board Dental Examination (INBDE), not a summary of it.

1. 1

   Preventive Dentistry and Cariology

   4 topics

   • Caries process and remineralization
     • Demineralization-remineralization balance
     • Caries detection and management by risk
   • Fluoride: mechanisms, delivery, and toxicity
   • Sealants and preventive resin restorations
   • Diet counseling and behavioral prevention
2. 2

   Pediatric Dentistry

   4 topics

   • Child growth, development, and behavior guidance
     • Non-pharmacologic behavior management
     • Eruption sequence and chronology
   • Restorative and pulp therapy in primary teeth
     • Pulpotomy and pulpectomy
     • Stainless steel crowns
   • Pediatric trauma and space management
   • Special health care needs in children
3. 3

   Orthodontics and Dentofacial Development

   4 topics

   • Normal occlusion and malocclusion classification
     • Angle classification
     • Skeletal versus dental discrepancies
   • Craniofacial growth and development
   • Orthodontic diagnosis and cephalometric analysis
   • Interceptive orthodontics and appliance therapy

Preventive, Pediatric, and Orthodontic Dentistry flashcards for National Board Dental Examination / Integrated National Board Dental Examination (INBDE)

20 of 51 cards from the Preventive, Pediatric, and Orthodontic Dentistry deck — real questions with worked answers.

1. What is the critical pH at which hydroxyapatite enamel begins to demineralize?

   Approximately pH 5.5. Below this, enamel hydroxyapatite dissolves; fluorapatite has a lower critical pH (~4.5), making it more acid-resistant.

2. Describe the dynamic balance underlying the caries process.

   Caries results from repeated cycles of demineralization (acid from bacterial fermentation dissolving mineral) and remineralization (mineral redeposition from saliva). Net mineral loss occurs when demineralization exceeds remineralization over time.

3. What are the primary cariogenic bacteria, and what is each one's role?

   Streptococcus mutans initiates caries (acidogenic, aciduric, adheres to enamel/produces glucans). Lactobacillus species are associated with progression/dentinal caries. Both ferment carbohydrates to organic acids.

4. What is the histologic structure of an incipient (white spot) enamel caries lesion from surface to deep?

   Four zones (deep to surface): translucent zone (advancing front), dark zone, body of the lesion (largest demineralization), and a relatively intact surface zone. The intact surface layer allows remineralization.

5. Which ions are required for remineralization of enamel?

   Calcium, phosphate, and fluoride. Saliva supplies calcium and phosphate (supersaturated with respect to enamel), and fluoride drives precipitation of the more stable fluorapatite/fluorhydroxyapatite.

6. What is the difference between hydroxyapatite and fluorapatite in caries resistance?

   Fluorapatite [Ca10(PO4)6F2] replaces hydroxyl ions with fluoride, creating a denser, more acid-resistant crystal with a lower critical pH (~4.5 vs ~5.5), making it more resistant to dissolution.

7. List the three main topical mechanisms by which fluoride prevents caries.

   1) Inhibits demineralization (incorporates into enamel surface forming fluorapatite). 2) Enhances remineralization (drives precipitation of fluoride-rich mineral). 3) Inhibits bacterial metabolism/enolase and acid production. Topical (post-eruptive) effect predominates.

8. What is the role of calcium fluoride (CaF2) reservoirs after topical fluoride application?

   High-concentration topical fluoride forms CaF2-like globules on enamel that act as a pH-controlled reservoir, releasing fluoride during acid challenges to promote remineralization.

9. What is the optimal fluoride concentration in community water fluoridation (current US recommendation)?

   0.7 mg/L (ppm). This single level (updated 2015 from the prior 0.7-1.2 range) balances caries prevention with minimizing dental fluorosis.

10. What is the probably toxic dose (PTD) and the certainly lethal dose (CLD) of fluoride?

    PTD = 5 mg F/kg body weight (dose at which symptoms appear and treatment is needed). The estimated lethal dose is ~32-64 mg F/kg (often cited CLD ~5-10 g sodium fluoride in an adult).

11. What is acute fluoride toxicity management for ingestion of less than 5 mg/kg vs more than 5 mg/kg?

    <5 mg/kg: give oral calcium (milk) and observe. >5 mg/kg: induce emesis, give calcium/magnesium/aluminum (milk, milk of magnesia, antacids) to bind fluoride, and seek emergency care/hospitalization.

12. What is dental fluorosis and during what period does it develop?

    Fluorosis is hypomineralization of enamel from excess fluoride during enamel formation (amelogenesis), appearing as white opacities to brown staining/pitting. It occurs only while teeth are developing (roughly birth to age 6-8), not after eruption.

13. What concentration of fluoride is in professionally applied vs over-the-counter products?

    Professional: APF gel 1.23% (12,300 ppm), 5% sodium fluoride varnish (22,600 ppm). OTC: toothpaste 1,000-1,500 ppm, OTC mouthrinse 0.05% NaF (230 ppm) daily or 0.2% weekly.

14. How are pit-and-fissure sealants different in mechanism from fluoride?

    Sealants provide a physical barrier that occludes pits and fissures, preventing bacterial colonization and substrate access. Fluoride works chemically on smooth surfaces; fluoride is least effective on occlusal pits/fissures, which is where sealants excel.

15. What is the most critical step for sealant retention, and what contaminant most commonly causes failure?

    Acid etching to create micromechanical retention, with maintenance of a dry field. Salivary (moisture) contamination of the etched surface is the most common cause of sealant failure.

16. What is a preventive resin restoration (PRR) and when is it indicated?

    A PRR (sealant restoration) combines a conservative composite restoration of a small carious pit/fissure with sealant placement over the remaining intact fissures. Indicated for incipient/minimal occlusal caries not warranting a full Class I prep.

17. Compare resin-based vs glass ionomer sealants.

    Resin-based sealants have superior retention and are preferred when moisture control is achievable. Glass ionomer sealants release fluoride and tolerate moisture better, useful as transitional sealants on partially erupted teeth or uncooperative patients despite lower retention.

18. What is the Stephan curve?

    A graph of plaque pH over time after a carbohydrate exposure: pH drops below the critical level (~5.5) within minutes due to bacterial acid, then recovers over ~30-60 minutes via salivary buffering. Frequent eating keeps pH below critical longer.

19. Why is frequency of sugar intake more important than total quantity for caries risk?

    Each carbohydrate exposure triggers a Stephan curve acid drop lasting ~20-40 minutes. Frequent intake produces repeated/prolonged acid exposure, giving less time for remineralization, so frequency is a stronger caries determinant than total amount.

20. What is xylitol and how does it reduce caries?

    Xylitol is a 5-carbon sugar alcohol that is non-fermentable by S. mutans. It cannot be metabolized to acid, reduces S. mutans levels, stimulates salivary flow, and (via mother's use) reduces transmission to infants.

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