Pediatric Module on Oral Health: Key Terms and Definitions

Infancy through toddlerhood (0-3 years)

Emotions undiscerned

• Behavior changes - crying

• Separation anxiety

• Second year - language skills

• Third year - NO! Why?

An initial oral evaluation visit should occur within 6 months of eruption of the first primary tooth and no later than 12 months of age.

Preschool (3-6 years)

Developing:

• Process of self control

• Frustrations

• Fears

• Power of reasoning

• Attention Span:

• 3-year-old: 4-8 minutes

• 4-year-old: 8-12 minutes

• 5-year-old: 12-28 minutes

School Age (6-12 years)

Literate

Body image / establish self-identity

Ability of independence

Influence of peers in school

Why are primary teeth important?

Help children speak clearly.

Help children chew naturally and eat.

Space holder for permanent teeth (maintain arch length).

Guide path for permanent teeth eruption.

Severe early childhood caries

1) Any sign of smooth-surface caries in a child < 3 years of age.

OR

2) From ages 3-5 years, 1 or more cavitated, missing

(due to caries), or filled smooth surfaces in primary maxillary anterior teeth.

OR

3) A decayed, missing, or filled score ≥ 4 (age three), ≥ 5 (age four), or ≥ 6 (age five).

Comprehensive clinical examination

Components of a comprehensive clinical examination include:

• general health/growth assessment (e.g., height, weight, BMI calculation, vital signs);

pain assessment;

extraoral soft tissues examination;

temporomandibular joint assessment;

intraoral soft tissues examination;

oral hygiene and periodontal-risk assessment;

intraoral hard tissue examination;

assessment of the developing occlusion;

radiographic assessment, if indicated;

caries-risk assessment; and

assessment of cooperative potential/behavior of child.

facial symmetry

facial profile

positions of maxilla/mandible

vertical facial relationships

airway assessment

arch form

symmetry

spacing

crowding

presence/absence of teeth

midline discrepancies or posterior crossbones

overbite/overjet

Facial profile

Class I: slightly convex

Class II: truly convex

Class III: straight or concave

Mallampati score

Brodsky classification system

Deciduous teeth

Primary teeth morphology

Crowns are smaller and more bulbous

Greater cervical constriction

Narrow occlusal table with anatomy not well defined

Thinner enamel & dentin

Larger pulp chamber and higher pulp horns

Enamel rods in cervical area directed occlusally

Broad and flat proximal contacts

Whiter in color

Primary teeth eruption sequence

calcification starts in utero

Permanent teeth eruption sequence

Maxilla: 61245378 Mandible: 61234578

6 months - First primary tooth

• 3 years - Complete primary teeth eruption

• 6 years - Permanent lower incisors and permanent first molars • 6-12 years - Mixed dentition

• 6-9 years - Early Mixed Dentition

• 10-12 years - Late Mixed Dentition

• 12 years - Permanent second molars

Radiograph by caries risk (0-5 years old)

Primary dentition: 2 BW, anterior occlusal, PAs as needed

Radiograph by caries risk (> 6 y/o)

Mixed dentition:

2-4 BW

PAs as needed

Panoramic

Anterior PA

caries/pulpal pathology

evaluate previous treatment

trauma, follow-up

evaluate resorption of primary teeth and development of permanent teeth

detect dental anomalies

use a size 2 sensor

lay the sensor flat and have patient gently bite down on the sensor between their teeth (horizontal sensor)

Early childhood caries

≥1 dmft (noncavitated or cavitated) in

children ≤71 months (

Main caries causing bacteria

Mutans streptococci

use sucrose to make extracellular polysaccharides stick the plaque together

Lactobacilli

produce predominantly lactic acid from fermentable carbohydrates

Bacteria transmission

Children can acquire cariogenic bacteria from anyone who is in close contact with them.

From birth to 3 year old - the critical time for caries causing bacterial transmission but can last life-long

Children with early cariogenic bacteria colonization before 4 years are four times more likely to get caries than those don't or get later

The transmission of the bacteria - saliva-sharing activity

Special Health Care Needs oral health conditions

Dental caries

o Orally defensive/behavior problems, diet, brushing - autism

o Sweetened medication and dry mouth

Enamel hypoplasia - young cancer patients, infancy infections

Calculus build-up/periodontal disease - G-tube fed

Dental crowding/malocclusion/dental anomalies

Bruxism and wear facets

Fracture of teeth or trauma - seizure

Poor cooperation

High risk to dental caries and periodontal diseases

Limited access to dental careAdvanced behavior management tools such as general anesthesia is

need to treat if advanced diseases developed (dental caries and

excessive dental calculus build up).

High risk for undergoing general anesthesia.

Anti-caries therapy for children

1. Current antimicrobial treatment: Broad spectrum antibiotics: PVPI, SDF(in-office)

2.Natural sugar substitute: xylitol, erythritol etc. Inhibits MS transmission and colonization

Xylitol 2g 3-4 times/day

¡ Wipes or syrup for infants

¡ Mints/candy/lolipops for children >3 yrs old

¡ Gums for children >6 yrs old

3. Modify oral and plaque pH environment:

Sodium bicarbonate (baking soda)

¡ Add to toothpaste

Wipeteeth (1/4TSP in 1OZ of water/rinse)

High and extreme risk

Pediatric patients with one (or more) white spot and/or cavitated lesion(s) are high- risk patients.

POE every 6 month

CRA every 3-4 months or at each operative treatment

Fluoride varnish every 3 month

Active caries found à Caries arrest/control: Silver

diamine fluoride/ GIC for cavitated caries lesions

Sealants for pits/fissure at risk

Pediatric patients with one (or more) cavitated lesion(s) and hyposalivary or special needs are extreme-risk patients.

Sealants

Up to 90% of caries in school-aged children occurs in pits and fissures

The teeth at highest risk are permanent first and second molars

Fluoride has least preventive effect on the pits and fissures

Fuji Triage sealants

Fuji Triage Sealants

Not as strict isolation requirement

Especially useful for:

ü Patient with behavior

management problems

ü Patient with special care needs

ü Partially erupted molars with high caries risk (enamel hypoplasia)

Piaget's 4 stages of cognitive development for children

Sensorimotor Stage (0-3yrs)

§Separation anxiety §Egocentric

Preoperational Stage (3-6yrs)

§Limited ability to

reasoning

§Love pretend play

Concrete Operational Stage (7-11yrs) Understand some logic and reasoning

Formal Operational Stage (12+yrs)

Abstract reasoning, hypotheticals

Sensorimotor stage

Emotional/Cognitive Development

§Build basic trust with parents and separation anxiety §Start to build simple concepts but limited language ability

§Fear of unfamiliar objects/noise

üKnee-to-knee exam or laying on parent in chair

üBest to have parents present

üBe calm, playful, positive and effective üPre-cooperative (

Preoperational stage (3-7 years)

Emotional/cognitive development

Curious to learn new things and start to express themselves

Understand/loves fantasy world & pretend play

Teachable, improved but limited ability to reasoning

React dramatically to real or perceived fears

✓ Require firm but kind handling

✓ Make fun and pretend play can be effective

✓ Allow child to have a sense of accomplishment from

successful appointment - positive reinforcement

Concrete operational stage (7-11 years)

Emotional/cognitive development

Expose to education and social development in schoo

l Decreased parental influence and increasing influence from peers

Develop abstract concepts and logical thinking/reasoning

✓ Motivate patient with reasoning

✓ Educate with fantasy, facts and respects

✓ Motivate patient using competition as reward

AAPD Behavior guidance techniques

non-verbal comunication

tell-show do

positive/negative reinforcement

positive and smart commands

effective communication

distraction

involve parents in the process

voice control/modulation

desensitization

Protective stabilization

Indications:

- Quick procedure: exam, extraction

- Autism/Developmental delay

- Sedated

- NOT just because parents want it

• Mandatory documentations

- Informed consent

- Indication and type of restraint

- Duration of restraint

- Behavior evaluation/rating during stabilization

¡ A patient cannot be restrained safely because of underlying medical or systemic problems

¡ Check tightness and duration of stabilization at regular intervals

¡ Extremities or the chest must not actively restrict circulation or respiration

¡ For patient's safety, terminated ASAP when a patient is experiencing severe stress

Why do we treat primary teeth?

1. Prevent odotogenic pain

2. Prevent infection

3. Preserve the space for the adult tooth (space loss)

Space maintenance of primary anterior teeth

The canines serve as an anchor

There is non-significant space loss after loss of primary anterior teeth

Space maintenance: One primary molar, between two teeth (in a quadrant)

can happen in primary or mixed dentition

Unilateral band/loop space maintainer

Space maintenance: One primary molar, the most distal tooth in the quadrant

Primary dentition only

Unilateral distal shoe space maintainer

Space maintenance: Two primary molars, adjacent to each other in the quadrant

Primary and mixed dentition

mandibular: lower lingual holding arch

maxillary: nance, transpalatal arch

Odontogenic Infection in Primary Teeth

Localized:

Pain

Swelling

Redness

Parulis

Sinus tract

Percussion sensitivity

Systemic

Fever

Lymphadenopathy

Malaise

Elevated white blood cell count

Treating odontogenic infection

Extraction is often the best treatment, but primary tooth pulpectomy or

antibiotic therapy is indicated in certain clinical situations.

Antibiotic treatment is not indicated:

- If tooth is extracted

- If dental infection is contained within the pulpal tissue or the immediate

surrounding tissue

Antibiotic Therapy for odontogenic infection

Antibiotic therapy is indicated:

- patient has a concurrent systemic medical problem

- patient has cellulitis, spreading of infection from localized area

- Systemic manifestations (e.g. fever)

Rapidly increasing signs of infection

- Fever and chills, malaise, fatigue, weakness

Involvement of anatomical danger zones

Large or rapidly progressing abscess/cellulitis

Factors to consider :

- Severity of infection

- Medical status of child

- Ability to obtain adequate anesthesia

- Feasibility for treatment

Antibiotics

Bactericidal (killing potential)

Penicillin

Amoxicillin

Augmentin

C lindamycin @ high dose

Bacteriostatic (growth inhibiting)

Clindamycin

Erythromycin

Tetracycline

Cellulitis

Definition: "A painful swelling of the soft tissue of the mouth and face resulting from a diffuse spreading of

purulent exudate along the fascial planes that separate

the muscle bundles." (Sapp)

Patient may be febrile with red and/or swollen face

Child appears acutely ill

Treatment

- extraction of the infected tooth

- antibiotic therapy

- Hospitalization if signs and symptoms indicate

serious systemic infection

- IV antibiotics may be indicated!

Indications for extractions

Extensive caries & unrestorable tooth

- Apical periodontitis

- Abscess

- Fractured root/ crowns

- Over-retained primary teeth

- Supernumerary teeth

Assessing trauma

medical history

¡Allergies to medications

Bleeding disorders e.g. Hemophilia, Von Willebrand ¡Cardiac disease (requires SBE prophylaxis?) ¡Current medications

Neurological disorders e.g. seizures

Status of tetanus prophylaxis

do no harm

Can the patient tell you...

What is your name?

What place is this?

Is it morning, afternoon, or night time?

Always ask questions sensitive to the child's age and cognitive development

Neurological assessment of a child with head trauma

signs of neurological issue:

Nausea

Vomiting

Drowsiness

Blurred vision

Loss of consciousness

Headache or neck ache

Blood or clear fluid from the nose (rhinorrhea) or ears (otorrhea)

Numbness

Amnesia

Was there LOC?¡Head exam: laceration, hematoma, skull fracture ¡Temperature, pulse, RR, BP

¡CN III: are pupils equal, round, responsive to light and accommodate (PERRLA)

¡CN III, IV, VI: extraocular movements intact (EOMI)

¡CN VII (Facial): close eyes, smile, frown, look for symmetry

Tetanus

Typically part of the DTAP (diphtheria-tetanus- pertussis) immunization series completed at age 5

¡Booster of tetanus toxoid at 11-12 years and every 10 years after.

¡If a child sustains a "dirty wound", the booster should be administered if it has been >5 years since his/her last booster.

EO exam for trauma

Neurologic concern

Blood or clear fluid from the nose (rhinorrhea) or ears (otorrhea) §Facial asymmetry

Hemorrhage

Wounds

Bruising (ie Battle sign) ¡Deviated/limited opening ¡Palpation of facial skeleton ¡ROM of mandible

¡ Soft tissue injury § Contusion

Abrasion

§ Laceration

IO exam for trauma

Crown fracture

¡ Pulp exposure

¡ Displacement

¡ Disturbance in

occlusion

¡ Tooth mobility

¡ Percussion

¡ Pulp vitality

Type of fractures

Uncomplicated crown fracture ¡Enamel

¡Enamel + Dentin

¡Treatment: Restore

Complicated crown fracture

¡Enamel, Dentin Fracture with Pulp Exposure

¡Treatment: Pulp treatment or extraction

¡ Root fracture ¡Monitor or Extraction

¡Alveolar fracture

Classification of dental trauma

Concussion (jolt, but no mobility, tender but appear normal)

monitor

Subluxation (trauma to teeth with class I, II mobility, but no displacement from the socket, sulcular bleeding)

monitor

Extrusion (extrude out of tooth socket, elongated crown and mobile)

Primary: extraction

Permanent: reposition/splint

Intrusion (intrude inward, into the tooth socket, shorten crown)

primary: monitor for future spontaneous re-eruption

permanent: re-eruption, surgical reposition/splint, ortho later

Luxation (lateral, facial, and lingual displacement)

primary: ext if severe

permanent: reposition/splint

Avulsion (completely out of socket)

primary: discard tooth

permanent: replant and splint

Tooth fracture:

-Uncomplicated fracture (only enamel or dentin exposure)

-Complicated fracture (pulpal tissue exposure).

Traumatized primary tooth consequences

¡Discoloration

§Yellow (calcific metamorphosis)

§Grey (hemosiderin deposit)

¡PCO (pulp canal obliteration) ¡Pulpal necrosis with abscess ¡Early exfoliation

¡Internal resorption ¡Ankylosis

Trauma permanent developing teeth sequelae

Determining factor - age at the time of trauma

¡Possible sequelae: ¡Discoloration of the enamel

blood pigment in dentinal tubules

¡Enamel hypoplasia (Turner's tooth)

¡Disturbances in eruption

¡Root dilaceration

¡Complications/arresting of tooth development

3 weeks post trauma= abscess and fistula develops --> RCT

Pathological sequelae of dental trauma

Pulpitis

} PDL (periodontal ligament cells) infection

} Pulp necrosis & infection

} Coronal discoloration

} Inflammatory resorption

◦ Internal resorption

◦ External resorption: root or surface resorption

} Replacement resorption (ankylosis)

} Pulp canal obliteration

} Damage of the developing permanent tooth buds

(primarily due to intrusion of primary tooth trauma)

Crown fractures with pulp exposure

Pulp exposure

¡Objectives: Maintain pulp vitality, restore normal esthetics and function

¡ Options:

§Direct pulp capping

§CaOH (DyCal) §Pulpotomy or Cvek

§MTA (preferred), or CaOH

§Pulpectomy (if pulpal necrosis development later on)

Lateral luxation

Tooth displaced laterally

¡Crown palatal/lingual

¡Tooth may be locked firmly into place

¡Usually not mobile nor tender to touch

¡Radiographic Findings:

¡Increased PDL space

¡Apex displacement toward or through the labial bony plate

Reposition as soon as possible and stabilize with flexible

wire splint for 2-3 weeks

¡Prognosis:

¡Dependent on stage of root development and amount of displacement

¡Damage to the PDL can lead to inflammatory and replacement resorption (ankylosis).

Intrusion

Apical displacement ¡Shortened/missing crown ¡Discontinuous PDL

Apex open:

Avulsion

The sooner the replantation, the better the prognosis

§A high percentage of teeth replanted within 5 minutes will have the PDL restored within a few weeks.

¡RCT is an important component of long term survival of the tooth

storage media:

} Milk

} Saliva

} Physiologic saline

} Hank's buffer solution (HBSS)

Not desirable media: water, causes rapid lysis of cells and increases inflammation on replantation

Every effort should be made to replant 15-20 min - acceptable, PDL healing is expected.

} Less than 60 min of extra oral dry time or in proper storage media, the chance for periodontal healing exits, and the chance of less severe inflammatory response.

} Greater than 60 min, PDL cells are not expected to survive

Extraoral dry time >60 minutes: PDL non viable

§Clean PDL cells off in 1% doxycycline solution

§Soak 15-20 min 2% NaF gel to slows osseous replacement §Flexible splint for 1-2 weeks

§Rx Antibiotic (Penicillin or Amoxicillin for 10 days)

§Tetanus update

¡Initiate RCT 7-10 days post injury (endo procedure such as apexification, revascularization, or obturation with gutta percha, depending on open or close apex)

Indications for N2O use

•Reduce anxiety and stress

•Mildly apprehensive, fearful child

•Control gagging (due to breathing through the nose)

•Mild to moderate asthma (not while having active wheezing attack)

•Reduce aware of time and fatigue

•When specifically requested by the patient

•Safe with several types of medically compromised children:

•Epilepsy and seizure disorders

•High function autistic and Down's syndrome pts

•Sickle Cell Anemia (Need to keep oxygen high)

Contraindications to N2O

•Psychiatric Disorders

•Developmental delayed

•Claustrophobic patients

•Severe behavioral problems, very apprehensive patients

•Pulmonary disease (COPD)

•Respiratory infections, otitis media, active coughing

•Any nasal obstruction

•Chronic mouth breathers

•First trimester pregnancy (toxicity to cellular mitosis of fetus)

•Drugs users (may experience traumatic, frightening and unpredictable pt's reaction)

•Methylenetetrahydrofolate reductase (MTHFR) deficiency (increase plasma homocysteine , thus increase venous thrombosis, stroke), and treatment with bleomycin sulfate (high concentration of oxygen may cause lung damage in patients with this therapy)

Disadvantage to N2O

•High Cost of equipment and refill of gases

•Potentiation (synergistic effects)- Combination with other sedative meds into deep sedation

•Staff training (required CPR or BLS training)

•Weak agent (lack of potency), not good for moderate to severe anxious patients

•Inconvenience-when working on maxillary anterior teeth with nasal hood

•Patient must breathe through the nose

•Potential toxicity due to chronic exposure (spontaneous abortion, congenital malformation, liver and kidney damage, neurological diseases, thus important to check for scavenger system)

•Pregnancy contraindicated

•Bioenvironmental pollution (contribution to greenhouse effect)

Mechanisms of N2O

•Anxiolytic effect:

- involves activation of GABAA receptor through benzodiazepine binding site.

•Analgesic effect:

-Initiated by neuronal release of endogenous opioid peptides and activation of opioid receptors

•Rapid uptake and absorbed quickly from alveoli, passing down a gradient into other tissues/cells (CNS), and excreted quickly from the lung.

Stages of inhalation sedation

•10-20% concentration, nitrous oxide will begin to produce some sedation

•Described as warm tingly feeling

•20-30% concentration

•Numbness of extremities

35-50% concentration

•Enhanced sedation and some analgesic effects

•Feeling heavy

•Trance-like eyes

•Room noise distinct but distant

•Numbness in hand, feet, and thighs

Symptoms of N2O sedation

BEarly to ideal sedation:

ØLight dizziness

ØIncrease in heart rate and peripheral vasodilation

ØTingling and numbness of hands and feet

ØWave of warmth

ØFeeling of euphoria

ØFeeling of lightness or heaviness of extremities

Diffusion Hypoxia

•If oxygen is turned off and the patient re-breathes room air or air in mask, Diffusion Hypoxia can occur

•

•Rapid release of N2O from blood stream into alveoli, thus diluting the concentration of oxygen

•Symptoms

•Headache

•Disorientation

•Nausea

•Lethargy

•5 minutes of 100% oxygen flow should be administered at the end

LA mechanism

•Diffuse (uncharged) through cell plasma membrane

•Bind intracellular receptor

•Close Na+ channel

•Inhibit depolarization/action potential to propagate, thus no nerve impulse

•Why in acute infection would inhibit the effectiveness of L.A.?

Types of LA

•Ester (benzocaine, novocaine, tetracaine): tendency for allergic reaction

•Amide (lidocaine, mepivacaine, prilocaine, bupivacaine, articaine): less allergic reaction greater potency

Properties of LA

1.Potency

2.Toxicity

3.Onset time (time required for complete conduction blockage)

4.Duration (increase protein binding capacity, vasoconstrictor epià increase duration)

CNS reactions to LA toxicity

•CNS excitation

•Signs of numbness or tingling

•Dizziness, disoriented

•Drowsiness, transient loss of consciousness, seizure

•Muscle twitching, tremors,

•Slurred speech, shivering

•Respiratory depression

Cardiovascular reaction to LA toxicity

•Increase HR and BP initially, then followed by

•Vasodilation, fall in BP

•Bradycardia, cardiovascular collapse, cardiac arrest.

WHY PEDIATRIC PTS ARE VULNERABLE TO L.A. TOXICITY?

•Agents absorbed more rapidly from tissues into blood stream (due to higher cardiac output and higher tissue perfusion)

•Liver enzyme system less mature, thus detoxify at slower rate

•Immature CNS and cardiovascular systems are more susceptible to toxicity

Very important to know maximum safe dosage

Consideration for special needs patients and LA

•Cardiac patients (ie. VT, hypoplastic left ventricle, arrhythmia, uncontrolled hypertension, PAH):

1.Epinephrine increases heart rates (tachycardia), increase BP

2.Lidocaine overdose suppresses cardiac function and CNS activity, seizure, and pulmonary depression.

3.Avoid block injections for patients on multiple anti-coagulants (direct infiltrations instead to avoid potential bleeding. This also applies to patients with bleeding disorders such as Hemophilia A and B).

•Patients with liver diseases:

1.Metabolized by liver (via cytochrome P450 3A4 dealkylation)

2.Prolonged half-life of lidocaine by 3-4 times (normal time is 1.5 to 2 hrs)

3.Increase potential drug toxicity and drug interactions.

•Patients undergo oral sedation with the use of diazepam (Valium):

1. Diazepam inhibits cytochrome P450, thus increases plasma lidocaine levels; predisposes pts to lido toxicity and respiratory depression.

Mepivacaine

•Mild vasodilation = long duration

•Good for post-op pain control in pediatric dentistry

Recommended for pulpal revascularization procedure

Articaine

•Better penetration, more effective numbness = controversial

•Contraindication for pt < 4 years old

Bupivacaine

•Very long duration (4-5 hrs)

•Good for post-op pain control for G.A. patients

HOW MANY MG OF ANESTHETIC IN 1 CARPULE OF 1.8 ML OF 2% LIDOCAINE?

•First step of calculation, 2% = 2/100 (g/mL). Then 2nd step is to multiple by the volume:

•2/100 (g/mL) x 1.7 (mL) = 0.034 g = 34 mg {multiply by 1000 to convert g to mg)

•100% of epi = 100/100 (g/mL) = 1 (g/mL)

•You then dilute 100% of epi by 100,000 times:

1 (g/mL) x 1/100,000

•The volume is 1.7 mL in one carpule:

1 (g/mL) x 1/100,000 x 1.7 (mL) = 0.000017 g = 0.017 mg of epi