Histopathology of Dentinal caries

  1. As the carious lesion invades dentin, dentinal tubules become involved.
  2. As dentin is part of the dentin pulp complex, it leads to reparative dentine formation.


  1. Zone 1: Zone of fatty degeneration of Tomes fibers.
    1. Starts at pulp
    2. No fat degeneration (misnomer name)
    3. Alteration by dentin by fat deposition leads to impermeability of tubules which leads to sclerosis 
    4. Sclerosis is reaction between vital pulp and vital dentin
    5. It is the calcification of tubules against further penetration of microorganisms.
  2. Zone 2: Zone of dentinal sclerosis characterized by deposition of calcium salts in dentinal tubules.
    1. Sclerotic zone is minimum in rapidly advancing caries and prominent in slow/chronic caries.
    2. This is a translucent zone due to the vital reaction of odontoblasts
    3. High mineral content
    4. Reflected Light: Appears Dark
    5. Transparent Light: Appears White
  3. Zone 3: Zone of Decalcification of dentin
    1. Tubules are made of pure microorganisms such as pioneer bacteria (Cocci and Bacilli etc)
    2. Intertubular matrix is mainly affected by waves of acid produced by bacteria in the zone of bacterial invasion
    3. Initial decalcification occurs in the wall of tubules. 
    4. Softened infected dentin cannot be differentiated with sterile soft dentine, clinically.
    5. Appears yellow-brown
  4. Zone 4: Zone of bacterial invasion of decalcified but intact dentin.
    1. Bacteria multiply within dentinal tubules.
    2. Acidogenic microorganisms: Seen in early caries
    3. Proteolytic organisms—predominate in deeper layers
    4. It supports the hypothesis that initiation and progression are two distinct processes and must be differentiated
  5. Zone 5: Zone of decomposed dentin.
    1. Bacteria invade both peritubular and intertubular dentin. Hence, Little architecture of dentin remains
    2. Liquefaction foci of miller enlarge and increase in number.
    3. Transverse Clefts: Perpendicular to tubules
    4. Acute Caries: necrotic dentin is very soft and yellowish-white
    5. Chronic Cases: Dentin is leathery and brownish-black


  1. Xylitol
    1. its 5 carbon sugar
    2. comes from birch trees. 
    3. preferential binding to Mutans strep but it cant ferment xylitol to acid
    4. Hence, no decrease in pH
  2. Sorbitol = caloric sweetness
  3. Aspartans = non caloric sweetener = 4Kcal/g = 200 times sweeter than sugar 

Caries activity tests

  1. Lactobacillus Count Test
    1. It was introduced by Hadley in 1933.
    2. It estimates the number of bacteria in the patient’s saliva by counting the number of colonies appearing on tomato Peptone Agar at ph 5
    3. Interpretation of caries activity
      1. Immune: less than 1000 
      2. Slight: 1000 – 5000
      3. Medium: I5000 – 10,000
      4. High: more than 10000.
  2. Snyder Test 2m
    1. The rapidity of acid formation by cariogenic bacteria
    2. Stimulated saliva + Glucose in Agar Medium containing bacto peptone, sodium chloride, and bromocresol green 
    3. Dye changes from blue-green to yellow
    4. Interpretation of color change with caries activity 
  • High—24 hours
  • Medium— 48 hours
  • Slight—72 hours
  • Immune—no color change
  1. Streptococcus mutans Level in Saliva
    1. The number S.Mutans colonies per ml of saliva is indicative of caries activity.
    2. Saliva samples obtained by using tongue blades are incubated on MSB agar (Mitis Salivarius Bacitracin Agar).
  2. Buffer Capacity Test
    1. The test evaluated the quantity of acid required to lower the pH of saliva using an arbitrary pH interval
    2. Buffering Capacity is inversely proportional to the process of caries
  3. Swab Test
    1. Oral swab- the buccal surface of teeth and placing it in Snyder media. 
    2. This is incubated for 48 hours and the pH changes are read and correlated with caries activity.
  4. Fosdick Calcium Dissolution Test
    1. Patient saliva is mixed with glucose and powdered enamel
    2. Measuring of powdered enamel dissolved in 4 hours by acid formed
    3. This is not a single test and requires trained personnel
  5. Reductase Test
    1. Measures the activity of salivary enzyme reductase. 
    2. Stimulated Saliva + diazo resorcinol, which colors the saliva blue. 
    3. The change in color from blue to red is measured after 30 seconds – 15 minutes and this is taken as a measure of caries activity.
    4. Interpretation
      1. Non-Conducive: Remains blue after 15 minutes
      2. Slightly conducive: Orchid after 15 minutes
      3. Moderately conducive: Red after 15 minutes
      4. Highly conducive: immediately to red
      5. Extremely conducive: Changes to pink or white


DEFINITION = American Academy of Paediatric Dentistry (AAPD) defines early childhood caries as ‘the presence of one or more decayed (non-cavitated or cavitated lesions), missing (due to caries) or filled tooth surfaces in any primary tooth in a child 71 months of age or younger.

A window of infectivity 2M**:

  1. Caufield (1996) stated that there is a window of infectivity between 19 and 33 months during which teeth get infected with S. mutans 
  2. The most beneficial time for vaccination against dental caries would be in infancy before the eruption of teeth. 
  3. This would promote the induction of adherence inhibiting salivary IgA thus delaying colonization of S. mutans
  4. With the establishment of early colonizers, there would be a synergistic effect of suppressing the colonization of S.mutans during the period of the window of infectivity. 
  5. A booster dose of vaccination may be required at the time of eruption of first permanent molars 


  1. Early colonization of MS is the most imp risk factor for developing ECC – MS transmission can be through the mother or from peers [ other kids] 
  2. MS Colonization of pre dentate children is mostly associated with maternal factors [ high level of MS in the mother, poor OH, and active caries ] 
  3. How is nocturnal bottle feeding/breastfeeding related to ECC? 
    1. When a child is laid to rest, the bottle or breast nipple rests against the palate and the tongue covers the lower incisors [ that’s why they are not affected] – 
    2. As the child becomes sleepy, saliva flow and swallow reflex are reduced
    3. Sugar remains stagnant around the neck of the teeth 
  4. what practices increase the chance of developing ECC?
    1. Prolonged nighttime bottle feeding
    2. On-demand breastfeeding after the age of 1
    3. Frequent snacking with sugary foods
    4. Frequent sipping of sugary drinks throughout the day


  1. ECC = also known as nursing bottle caries, baby bottle tooth decay 
  2. Seen in infants and preschool children [ below the age of 6
  3. Demineralization at the necks of the upper incisors – mandibular incisors are not affected
  4. Decay pattern:
  1. Maxilla: incisors, canines, first molars 
  2. Mandible: canines, first molars
  1. Lesion progresses to the necks of the teeth and in advanced cases, only a root stump is left
  2. Why does ECC follow this specific pattern? 
    1. Chronology of primary tooth eruption
    2. Duration of the deleterious habit [ bottle feeding]
    3. A muscular pattern of infant sucking
    1. Very mild: slight demineralization usually at the gingival crest and no cavitation.
    2. Mild: demineralization in a gingival third of tooth and moderate cavitation.
    3. Moderate: frank cavitation on multiple tooth surfaces.
    4. Severe: Widespread destruction of tooth and loss of the clinical crown 


  1. Identify the cause and stop the habit
  2. Give parental instruction on proper oral hygiene measures + diet counseling
  3. Decide if the case can be managed in the clinic [ with regular LA or nitrous sedation ] or the child needs GA
  4. If the case is treated in the clinic: full assessment of all affected teeth to know 
    1. which teeth can be restored
    2. which need pulp therapy
    3. which need extractions
First visitSecond visitThird visit
Immediate excavation of caries followed by temporization Dietary chart Caries activity doneTopical fluoride application doneParent counsellingExamine diet chart Caries activity done again Replace any temporary restoration with permanent restorationPulpul procedures Extractions Space maintersRecall the pt every 3 months

What instructions would you give the parents to a child with ECC? 

  1. STOP NIGHT TIME BOTTLE FEEDING / stop breastfeeding at will after the first tooth erupts
  2. Feed the child while being held + burp the infant after feeding
  3. Clean the teeth after each feeding [ wipe the teeth with a wet gauze]
  4. regularly lift the upper lip to check for signs of demineralization of the upper Interiors
  5. OH should start with the eruption of the first tooth – wipe the teeth with gauze and for ages 2- 6 brush with low fluoride tooth past [ 400-500 ppm] – parental supervision until the child can properly spit
  6. Children are encouraged to drink from a cup as they become 1 year old
  7. Avoid frequent snacking and have regular meals instead
  8. First dental visit should be combined with immunization dates [ at or before 6 months]

Prevention of ECC ideally begins prenatally: 

  1. give the mother information about diet and OH
  2. treat the mother’s own oral diseases and lower MS count by mouth rinses and restorative care
  3. educate the mother on modes of transmission of MS [ don’t lick spoons or pacifiers etc..]

Composite resin strip crowns

Composite is the material of choice for the restoration of primary anterior teeth. An anterior strip crowns with composite resin provides an aesthetic and durable restoration.


  1. Local anaesthesia and rubber-dam isolation should be used if possible. Alterna- tively, because of age and poor cooperation of younger children, the restorative work may be completed under general anaesthesia.
  2. Select the correct celluloid crown form depending on the mesiodistal width of the teeth.
  3. Remove the caries using a slow-speed round bur.
  4. Using a high-speed tapered diamond or tungsten carbide bur, reduce the incisal
    height by around 2 mm, prepare interproximal slices and place a labial groove at
    the level of gingival and middle thirds of the crown.
  5. Protect the exposed dentine with a glass ionomer lining cement.
  6. Trim the crown form and make two holes in the incisal corners by piercing with
    a sharp explorer.
  7. Etch the enamel for 20 seconds, and wash and dry.
  8. Apply a thin layer of bonding resin and cure for 20 seconds, ensuring all surfaces
    are covered equally.
  9. Fill the crown form with the appropriate shade of composite and seat with gentle,
    even pressure, allowing the excess to exit freely. The use of small wedges may be
    helpful in avoiding interproximal excess.
  10. Light cure each aspect (labially, incisally and palatally) equally.
  11. Remove the celluloid crown gently, and adjust the form and finish with either composite finishing burs or abrasive discs.
  12. Check the occlusion after removing the rubber dam.

Source: Handbook of Pediatric Dentistry, Third Ed



Anaesthetics – local & genral

Used as

👉 Percutaneous infiltration anaesthesia ,

👉 peripheral nerve block

👉Sympathetic nerve block
👉retrobulbar block ,

👉Cadual block

👉Lumbar epidural block

Brand names.

🙏Buloc by celon
Inj – 0.25 % & in 0.5 % ( 20ml )
🙏Bupivan by Sun pharma
Inj :- 0.25% (20ml)
0.5% ( 20ml )
0.5% ( 4ml )
🙏 Marcain by AHPL
Inj:- 0.5 % ( 20ml )
Inj :- 1 % ( 2ml )

  1. Halothane
    Inhalation anesthesia

👉 used in Induction & maintenance of general anaesthesia
🙏Fluothane by AhPL
I:vap :- 100% in ( 200 , 250 , 30, 50 ml ) soln
Inhalation anaesthesia

👉 Induction & maintenance of general anaesthesia
🙏 Forane by abbott
Inhalant :- 100% in ( 100, 250 ml )

🙏Isorane by AhPL
I:sol :- 5mg/5ml in ( 100,250,30 ml )

  1. Ketamine
    & Intravenous anesthesia

,🙏Ketam by sun
Inj 10mg/ ml (10ml )
Inj 50mg / ml ( 2ml )
🙏Ketmin by Themis medicare
Inj 50mg /ml ( 10 ml )
Inj 50 mg/ ml ( 2ml )
🙏Ketsia by celon
Inj 100mg ( 2ml )
Inj 500mg ( 10ml )

I sol :- inhalation solution
Ivap :- inhalation vapour

  1. Lidocaine ( used as )
    👉 as Epidural anesthesia
    👉Pulp dilatation during phaco-emulsification cataract surgery
    👉Spinal anaesthesia
    as Intravenous
    👉Intravenous regional anaesthesia
    👉 Sympathetic nerve block
    👉 Peripheral Nerve Block
    👉 Percutaneous infiltration anaesthesia
    👉Surface anesthesia
    Mouth / throat
    👉Surface anesthesia
    as for Opthalmic region
    👉Surface anesthesia
    Rectal & topical / cutaneous
    Company names


🙏Gesican 2% gelly by AHPL ( 30ml )

🙏Lidopatch by zydus cadila
T:patch- 5%

🙏Xylocaine by AstraZeneca
T:sol:- 2% 100ml
Oint :- 5% w/w ( 20mg )
Jelly :- 2% w/w ( 30mg )

🙏Xylocard 2 % by AstraZeneca
Inj (21.3mg/ml ) 50ml soln

🙏 Xylocaine viscous by astra zeneca
T:sol :- 21.3mg/ml ( 100ml )

🙏 Xylocaine topical 4% by AstraZeneca
T:sol :- 42.7mg/ml ( 30ml )

🙏Nummet by icpa
Spy :- 15% w/w ( 100g )

Some Combinations
Lidocaine + epinephrine

🙏 Lignosafe by stedman
( Lignocaine hcl 21.3mg & adrenaline 0.0125mg/ml )
Inj in 30ml

🙏 Xylocaine with adrenaline 2% by AstraZeneca
( Lidocaine hcl 21.3mg , adrenaline 0.005mg , nacl 6mg /ml )
Inj 30ml

Some other combination
🙏 Xylocaine 5% heavy ( lignocaine hcl 53.3mg/ml , Dextrose 75mg ) inj in 2ml

& Xylocaine soln ( same dosage as above ) T:Sol 100ml by AstraZeneca

🙏 Xylocaine spray by AstraZeneca
( Lidocaine hcl 100mg , ethanol 28.29% ) 500ml
🙏Xicaine by icpa
( Lignocaine 2 percent , adrenaline 0.022mg) inj 30ml
( Lignocaine hcl 2% , adrenaline 0.009 mg ) inj 30ml
🙏Asthesia by unichem
( Lidocaine 2.5% w/w , prilocaine 2.5% )
CRM (15,30,5 )g
Crm :- cream
Tsol :- topical solution