paeds Flashcards

1
Q

compomer vs rmgic

A

command set, adhesive,
Aesthetic
Simple to handle
Radiopaque
BUT Technique sensitive
Less F release than GICs
vs

Adhesive
Aesthetic
Command set
Simple to handle
Fluoride release
BUT Water absorption
Significant wear

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2
Q

ECC

A

Presence of 1 or >
* Decayed (non)cavited /cavitated
* Missing dt caries/
* Filled

….In any primary tooth in a child 71 months of age or younger(<6yo)

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3
Q

considerations in mx of paeds pt?

A
  1. CRA (OHI, systemic!conditions, parental compliance)
  2. Child MX
    a. Behaviour MX
    b. ITR,ART!
  3. Need for restoration
    4.Proximalvsocclusal caries
  4. Deep proximal caries
  5. Longevity of restorations
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4
Q

FORMOCRESOL VS 1/5 dilution of
formocresol /buckley’s solution of formocresol vs FERRIC SULPHATE

A

high success rates; fixes tissues regarless infl/ not; concerns-toxicity,
potential mutagenicity
and carcinogenicity
Actual amount of
formaldehyde vapour
exposure(ppm) to a child
unkwn

vs

formalaldehyde19%,+
cresol35%+in distilled
water+glycerine
< tissue irritation and <cytotoxic; equally effective

vs

ferric ion complex,seals
cut blood vessel
mechanically producing
haemostasis; + form protective
metal protein-clot over
underlying vital radicular
pulp+ very acidic ; unable to fix; astringent 15.5%-shrinks tissues–> Int RR //Calcific metamorphosis

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5
Q

MTA efficacy vs formocresol/ferric sulphate

A

Clinical trials show that MTA performs equal to or
better than formocresol or ferric sulfate and may be the
preferred pulpotomy agent in the future.

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6
Q

Calcium silicate cement is

A

a bioceramic material- MTA AND BIODENTINE

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7
Q

Hall Technique

A

Hall technique (HT), the dentist does not remove
any decay
but cements a steel crown over the decayed primary tooth.
- deep decay over halfway into dentin/no irr p.

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8
Q

MTA adv 5

A

-Biocompatible → Less pulpal inflammation and/or hyperemia
● Antimicrobial activity (some facultative bacteria but no effect on strict anaerobic bacteria)
○ Initial pH 10.2 and rises to 12.5 after 3h
● Superior sealing properties
-Low solubility
● Setting ability uninhibited by blood or moisture
● Capacity to induce bone, dentin, and cementum formation and regeneration of periapical tissues (e.g., PDL)

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9
Q

MTA Disadvantages

A

● Cost
● Long setting time (around 3-4 hrs)
● Additional chair time (2nd appt to complete tx)
○placing MTA in 1 visit without external moisture is not recommended-affect flexural strenth.
● Discolouration (for both gray and white MTA) - as long as there is bismuth oxide (only those which use zirconia as radiopacifiers that don’t discolour

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10
Q

biodentine 8 adv

A

● Does not cause tooth discolouration-zirconium dioxide
● Complete in 1 appointment (sets in 12 minutes) dt presence of calcium carbonate and calcium oxide

● Biocompatible
● Antimicrobial activity (some bacteria)
● Good sealing ability
●Stimulate tertiary dentin formation

● Enhanced mechanical properties → reported that it penetrates through opened dentinal tubules to crystallize,
interlocking with dentin
● Good handling characteristics

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11
Q

biodentine disadv

A

cost and >clinical studies needed

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12
Q

ICDAS 4

A

Underlying dark shadow from dentine through intact enamel surface

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13
Q

icdas 5; 6

A

Distinct cavity with visible dentine involving less than half of tooth surface ; >1/2 if its 6

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14
Q

taurodontism

A

Apical extension of trunks of teeth-enlarged pulp chamber and
short roots
* Associated ectodermal*dysplasia- hav microdontia

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15
Q

1st appt of RET

A

LA, RDI, Access
2. Sodium hypochlorite (1.5-3%) irrigation for 5 mins
3. Sterile saline or EDTA irrigation for 5 mins
- Minimise cytotoxic effects of sodium hypochlorite on vital tissues
1. Dry with paper points
2. Intracanal medicament
- Antibiotic paste
➢ Triple- ciprofloxacin, metronidazole, minocycline 1:1:1 at concentration 1-5mg/ml
NOTE: Place below CEJ to minimise crown staining
➢ Double- without minocycline or substitute minocycline for other antibiotic
- Calcium hydroxide (for disinfection)
1. Interim coronal seal
- 3-4mm of Cavit/IRM/GI

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16
Q

2ND visit for RET

A

LA (*without vasoconstrictor), RDI
2. 17% EDTA irrigation
- Releases growth factors from dentine
1. Sterile saline irrigation
2. Dry with paper points
3. Induce bleeding
- Over-instrumenting ~2mm past apical foramen with a K- file
- Alternative: Platelet-rich plasma (PRP), Platelet-rich fibrin (PRF),
1. Scaffold
- Blood clot: Allow blood to fill canal until to level of CEJ
- Resorbable collagen matrix (CollaPlug, CollaCote, CollaTape) over blood clot if necessary
. Pulp space barrier
-White MTA or tricalcium silicate cement layer on top of blood clot/collagen matrix under CEJ
1. Coronal restoration
- RMGIC
- Refresh cavity walls with bur and seal with adhesive restoration

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17
Q

Tooth mousse

A

casein phosphopeptide - amorphous calcium phosphate

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18
Q

Amelogenesis Imperfecta (AI) 6 key facts not classification
What is it? Interfere with ?
Affects which dentition
Eruption?
Assoc with?
High incidence of
Appearance n implication

A

is a developmental disturbance that interferes with normal enamel formation without a systemic disorder.

It affects nearly all teeth in both the primary and permanent dentitions.

-may exhibit accelerated or late eruption.

Associated w-enlarged follicles, impacted permanent teeth, ectopic eruption, enamel resorption and ankylosis [unlikely].

-high incidence of anterior open bite.

-disfiguring appearance, impacting the individual’s self-esteem and social interactions.

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19
Q

Classify AI

A

Hypocalcified AI: Characterized by normal thickness but smooth surface and less hardness of the enamel.

Hypoplastic, pitted AI: Exhibits normal thickness with a pitted surface and normal hardness.

Hypoplastic, generalized AI: Has reduced thickness with a smooth surface and normal hardness.

Hypomaturation AI: Features normal thickness, chipped surface, less hardness, and opaque white coloration.

20
Q

Dentinogenesis Imperfecta (DI) 3 facts and radiographic feature

A

is a hereditary developmental disturbance of the dentin that can occur in isolation or in conjunction with Osteogenesis Imperfecta (OI), a systemic hereditary disorder of the bone-brittle and prone to #.

  • blue-gray to yellow-brown discoloration of teeth, which appear opalescent due to the defective, abnormally-colored dentin shining through the translucent enamel.
  • enamel often fractures from the teeth due to the lack of support from the poorly mineralized dentin, leading to rapid wear and attrition.

Radiographically, teeth may show bulbous crowns, cervical constriction, thin roots, and early obliteration of the root canal and pulp chambers.

COLIA 1 and 2 gene mutation

21
Q

Dental caries is a …

A

disease caused by an ecological shift in the
composition and activity of the bacterial biofilm when exposed
over time to fermentable carbohydrates, leading to a break in
the balance between demineralization and remineralization.

22
Q

Resin-based sealants are

A

urethane dimethacrylate, “UDMA,”
or bisphenol A-glycidyl methacrylate (also known as “bisGMA”) monomers polymerized by either a chemical activator and/or light of a specific wavelength and
intensity. Resin-based sealants come as unfilled, colorless,
or tinted transparent materials or as filled, opaque, toothcolored, or white materials.

23
Q
  • GI sealants are
A

cements that were developed and are used
for their fluoride-release properties, stemming from the acid-base reaction between a fluoroaluminosilicate glass powder
and an aqueous-based polyacrylic acid solution.
*

24
Q

Polyacid-modified resin sealants are..

A

referred to as compomers, combine resin-based material found in traditional
resin-based sealants with the fluoride-releasing and adhesive
properties of GI sealants.

-strontium fluorosilicate glass

25
Q

Resin-modified GI sealants are

A
  • essentially GI sealants with
    resin components. This type of sealant has similar fluoride release properties as GI, but it has a longer working time
    and less water sensitivity than do traditional GI sealants.
26
Q

bisphenol A (BPA) in dentistry

A

Bis-GMA, Bis-DMA, Bis-EMA [Bis-GMA – bisphenol A diglycidyl dimethacrylate
Bis-EMA – bisphenol A ethoxylated dimethacrylate
Bis-DMA – bisphenol A dimethacrylate] , commonly used monomers in dentistry, are derivatives from bisphenol A (BPA).
Small and transient increase in baseline BPA levels may be detected in patient’s urine and saliva following treatment with resin-based dental materials.

27
Q

how to reduce BPA exposure?

A

main source of BPA is believed to be the outer layer of sealants and resin composites that does not polymerize in the presence of oxygen.
1.Reading and following manufacturers’ instructions;
2. Ensuring proper curing light function (i.e. light intensity);
3. Reducing the distance between light curing tip and restoration surface;
4. Applying glycerin gel for the polymerization of the last resin layer;
5. Completing restorative material curing to help maximize the material’s monomer-to-polymer conversion.
6. by pt rinsing their mouths.
7. RDI

28
Q

moisture can trigger a reaction that
releases fluoride and buffers acidic environments in which dental filling

A

COMPOMER

29
Q

primary tooth eruption sequence

A

Starts with
lower A 5mo-8mo ->
upper A 6-10 mo +Lower B 7-10mo->
Upper B 8-12 mo ->
U+L D 11-18mo –>
U+L C 16-20mo ->
U+L E 20-30mo
No eruption until 5.5yrs

30
Q

permanent tooth eruption sequence

A

Mixed Dentition: followed by the loss of primary teeth and the eruption of permanent successors.

L6 5-7yr –>
upper 1st molar&lower central incisors 6-7yrs-> upper CI and L LatInc 7 -8yrs–>
U LInc 8-9yrs–>
L3 9-11 yrs–>
U4 10-11yrs->
L4 and U5 10-12yrs–>
L5 11-13yrs–>
U3 11-12yrs ->
U+L 7’s 12-14yrs –>
8’s 17-30 yrs

Permanent Dentition: By age 12 to 13, most children have lost all their primary teeth, and the permanent teeth, excluding the third molars, have erupted. The third molars, or wisdom teeth, typically erupt between 17 and 21 years of age.

31
Q

dental amalgam an alloy made of

A

silver[main], tin and mercury

32
Q

What happens to amalgam… and… strength when add high copper and spherical alloys?

A

higher early compressive and tensile strength

33
Q

measles -what virus, primary symptoms, transmission

A

paramyxovirus
Primary Symptoms: High fever, cough, malaise,and a dark red, maculopapular rash that originates behind the ears and spreads to the rest of the body. Koplik’s spots—tiny white spots on the buccal mucosa —are a key diagnostic indicator/pathognomonic.

Koplik’s spots can precede the rash and are useful for early diagnosis.

Transmission: Highly contagious through respiratory droplets.

34
Q

Mumps-Primary Symptom:
Transmission:

A

Mumps Virus
Swelling of the parotid salivary glands-usually bilateral, but unilateral swelling can occur, which can cause pain and discomfort in the jaw and neck area, low-grade fever, malaise, headache, and possibly swelling of other salivary glands.

Oral Impact: Dry mouth due to salivary gland involvement, difficulty swallowing-self limiting

Transmission: Respiratory droplets and direct contact with saliva.

35
Q

Rubella (German Measles)

Primary Symptom+ transmission

A

Rubella virus.
fever; less commonly, enlarged lymph nodes. Conconfluent, pink, maculopapular rash, which, like measles, extends from behind the ears to the rest of the body.Forchheimer spots are tiny red spots on the soft palate in rubella. They sometimes precede the skin rash of rubella.
self limiting as well
Transmission: Respiratory droplets.

36
Q

Roseola infantum

A

Roseola infantum (sixth disease)HHV-6 human herpes virus -6: Three days of high fever are followed by a sudden decrease in temperature and development of a patchy, rose-pink, macular rash. The rash originates on the trunk and neck, and may spread to the face and extremities in some cases.

37
Q

Varicella infection in children

A

varicella zoster virus (VZV) (chickenpox): The intensely pruritic rash affects the whole body.

Characterized by sequential clusters of papules, vesicles, and pustules in various stages of development; which leads to the characteristic clinical finding known as “starry sky.”

The rash may be preceded by a prodrome of constitutional symptoms.

38
Q

VIT D deficiency lead to ..in cren, … in adolescent / adults

essential for …. + … absorption

A

low vitamin D can lead to soft bones- rickets in children and osteomalacia in adolescents and adults.
Vit D essential for the absorption of calcium and phosphate from the diet-which are critical for the normal mineralization of tooth enamel and dentin.

39
Q

MIH is definied as…
appear as…
prone to.. 3x+ problems 4x

A

HYPOmineralisation of systemic origin, presented as demarcated opacities , qualitative defects of enamel of one to 4 FPM w/w/o incisors involvement.
Appear white, creamish, yellow or brown defects- assoc with PEB-post eruptive breakdown.
prone to decay, sensitivity and esthetic issues + problems to anaesthesize, b’vioral mx prob, tooth loss, financial concerns.

40
Q

mild MIH vs Severe MIH

what is predictor of MIH in 1* tooth? vs SECC

A

mild - demarcated enamel opacities without PEB, induced sensitivity air/water, mild asthetic issue

severe, breakdown and carious, spontaneous HS, strong esthetic concern

may be seen in 2nd 1* molar and tips of permanent canine - predictor of MIH [localised] vs generalised in secc

41
Q

etiology of MIH

qs to ask to diff with Fluorosis/ AI/ enamel hypoplasia - Turner’s tooth/ White spot lesion

A

Not fully understood
SYSTEMIC AND MEDICAL H/O
Pre natal period -medical issue/abx h/o / high fever -third trimester
Perinatal - prolonged delivery/ induced delivery/ spontaneous vagina delivery/ Cesarean
Post natal first 3 yrs of life - newborn- admitted ?/ VZV-chickenpox/ URI freq/ high fever
Any insult during period cause MIH.

MIH have genetic defect in Enam, amelix and MMP 20

Fluorosis - h/o of excessive fluoride ingestion when younger ; geographical area near hotspring, HIGH CONTENT OF FLUORIDE in water

Enamel hypoplasia - h/o Trauma /localised abcess infection

VS MIH with PEB -LACK VIT D -Def affect the development of teeth - affect calcium absorption -> in country lack of sunlight- eg in UK ->hypomineralised

AI - hypomineralized, hypomaturation, hypoplastic
-ask if same defect in primary dentition as permanent dentition
-familial history - related to genetics

WSL - early sign of caries - area of plaque is stagnant - proximal and cervical areas dt Poor OH+caries and high sugary diet

42
Q

Condition + Key Features

1 Fluorosis
2Enamel Hypoplasia
3Amelogenesis Imperfecta
4 white spot lesion
5 Traumatic Hypomineralisation
6 MIH

A

1.Associated with fluoride ingestion during enamel development and caries resistant. Presents as diffuse, linear, patchy/ confluent white opacities without a clear boundary bilaterally+symmetrical.
2.Quantitative developmental defect with reduced enamel thickness. Regular and smooth lesions. Often results in pre-eruptive enamel breakdown+increased caries risk.
3 Genetic condition resulting in enamel that is hypoplastic, hypomature, or hypomineralized. Affects both 1* and permanent teeth. Familial history often present.
4 Early sign of caries, appearing as chalky, matte or opaque than the adjacent sound enamel. Typically found near the cervical/proximal margin of the tooth.
5 Occurs due to trauma/PERIapical infection to the primary predecessor tooth, affecting the mineralisation of the permanent tooth. Presents uniquely in shape, outline, and color, often limited to one tooth and asymmetrical.
6. MIH with post-eruptive enamel breakdown
are sharp and irregular due to post-eruptive
shearing of weakened enamel; caries prone, assymetrical [vs fluorosis]; smooth cm2 vs WSL presentation.

43
Q

mx of MIH considerations for pain mx
why hard to give LA?
what LA technique and which LA ?

A

Hard to anaesthesize because pulp v inflamed and hard to give LA + sensitive during filling/cleaning ; may hv acute pulpitis- better ID block and buccal block
Lidocaine and articaine -> IADN -> NO DIFF
ARTICAINE FOR INTRAOSSEOUS MORE EFFECTIVE and intradental and intraligament > profound

Take PREEMPTIVE ANALGESIC
N20 help reduce pain
R dam isolate and reduce sensitivity during tx
Suction, avoid high volume suction dt air stimulation
Behaviour prob- kiv GA

44
Q

silver diamine fluoride
Composition
MOAction:
Application by:

benefits: 6x
Effectiveness by …
cost < than….
complexity?

A

Silver Diamine Fluoride [usually 38%] is composed of silver, fluoride, and ammonia.
colorless/blue-tinted liquid with pH between 10 and 13
Silver acts as an antimicrobial ions disrupt membranes and inhibit DNA replication; fluoride promotes remineralization; ammonia stabilizes the solution for treating dentin sensitivity.
Application: Requires professional application.

Benefits of SDF:
1increase in mineral density of treated carious tissue.
2Cost-Efficiency: Significantly less expensive< atraumatic restorative tx (ART) but same efficacy.
4 Ease of Use: Simple application process, minimal training required.
5 Non-Invasive: Does not require removal of sound tooth tissue.
6 Restorative Compatibility: Does not impair bonding of glass ionomer cements; limited evidence on resin composite performance post-SDF application.

45
Q

Clinical Application SDF

disadvantages:

recommendad usage:

A

1 Caries Arrest: Effective in arresting caries in primary and permanent teeth.
2 Sensitivity Treatment
3 Special Populations: Useful for patients who are uncooperative or have limited access to care.

1 Permanent black staining of treated carious lesions,limits use in visible areas st silver ions.
2 Unpleasant metallic taste.
3 Tissue Irritation: Potential irritation to gingival and mucosal tissues if contacted.
2x/yr application

46
Q

paper to quote for SDF

A

2019 systematic review found that once-yearly SDF application was more effective in preventing caries than more frequent application (i.e., 2 to 4 times yearly) of fluoride varnish. Add, FS perform better as SDF may need freq reapplication.