3) early caries - developmantal anamolies

8/13/2019 3) Early Caries - Developmantal Anamolies

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A warning: the script is about 26 pages. No worries it's

a piece of cake! Enjoy it

early childhood carries(ECC):-dental caries:1Part

We are going to talk about a specific type of dental caries ,which

happened in children which is called early childhood carries (ECC) ,it's a

clinical entity and we are going to discuss how this happens ; the

biological mechanisms ,the risk factors in children make it happen.

So the definitions according to AAPDAmerican academy of pediatric

dentistry- define it as the presence of one or more decayed teeth (non-

cavitated or cavitated lesion), missing teeth (due to carries),or filled

tooth surface on any primary tooth in children up to 71 months of age

,which mean less than 6 years.

The severitycan be rated any child who is less than 3 years has onesurface has sever early child carries.

Any child between 3-5 years who has DMF(D or M or F smooth surface)

one or more has also sever type.

Or DMF more than four in child who is 3 years old.

Or DMF is more than 5 in child who is 4 years old.

Or DMF more than 6 in childs who is 5 years old.

Terms of ECC:

These are the earlier terms have been used in the past , these are called

: labial caries, caries of incisors , rampant caries, nursing bottle caries,

nursing caries ,baby bottle tooth decay, maxillary anterior caries

,rampant infant and early childhood dental decay.

Nowadays we just use ECC.


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Now what are the characteristics of this type of decay?

Decay most often:

1-involves maxillary incisors.

2-usually doesnt affect mandibular incisors.

3-may progress to involve other teeth according to their date of eruption

the canines of molar of both arches (of course it affect the max. before

the man. because they erupt before) so it will affect the

ABDCE, so it depends on the age which detected the teeth

which will be affected.

**This is an example of early child with carries who has all the ant. teeth

are affected ,but the lower are not.

**This is another example of child who has the A and B are affected and

then the D are affected, the C and E still not affected, because the A,B,D

erupt before the C&E.


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** This is another example of rampant caries or ECC.

Epidemiology:

1- in developed countries like Australia ,America, United kingdom There

are increased rates of ECC within native& immigrant groups ( this is a

study in Australia) , for example in America the red Indians will be more .

In immigrant groups which they people who immigrate to those

countries, because of war or because other financial or economicreasons.

2- Increased among disadvantage to those from lower socio-economic

status (SES).

3-increased in special needs patients (SPNP).

Now the biological mechanesimsjust like any caries it requires:

1-cariogenic micro-organisims

2-fermentable carbohydrates

3-susceptible tooth and host

4-over time.


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These are the rings of teeth,(do u remember them??:P

These are the 3 cycles of keys , the person that give us this model he said

that caries occur when these 3 cycles come together. Nowadays we have

a 4th cycle which is atime or we can encircle all of these 3 cycles by big one and say they arehappened overtime.

Concepts of dental caries:

The fermentation of carbohydrates by the micro-organisims will producelactic acid which will demineralize the tooth surface and cause the

cavitation.

Caries etiology:

View has been around of caries etiology since MILLER first proposed the

chemo-parasitic theory for etiology of caries.

biology is modified by factors which are specific in these

young children.

What make it so rampant and so sever in these children?


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1- The implantation of the cariogenic bacteria in the infant are being

established, so these micro colonies and bacteria are starting to

establish them selves in the mouth of the young child.

2- You suppose to have an immune response ,but in young child theimmune response is immature so there is no immune response so these

micro-organisms will establish themselves strongly.

3- The behavior pattern will be associated with feeding, the feeding

patterns and oral hygiene in early childhood, many people think that

children dont need to have their teeth cleaned and many people will

keep feeding their children by bottle even they are not hungry just to

quiet them , so the children will get exposed to high amount of sugarand the teeth will not cleaned , so this is control its behavior of pattern .

4-Tooth surfaces are newly erupted and you know that newly erupted

tooth surfaces are always week , they are still not fully mineralized they

are hypo-mature , usually the enamel mineralization is still not complete

in these teeth and may show hypoplastic defects, so this will also

exacerbate the problem.

**Etiological factors:

A)CARIOGENIC MICRO-ORGANISMS:

If we come to the micro-organisms the main bacteria are the mutan

streptococci (MS), this is a wide group of bacteria which has many

variance especially S.mutan and S.sobrinus they are the main ones that

start colonizing.

Here study shows that only a small infective dose of M.S are required

for implantation and then the colonies will get bigger and bigger over

time .


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Now where do we get these micro-organisms??

From the primary carrier (father, mother, siblings, or nanny, but most of

the time from mother).

Lactobacilliare highly indicated in dentinal caries y3ne when the

cavity reaches the dentine.

Actinobacilli- indicated in root carries.

previous studies show that M.S usually are not found in the oral cavity

prior to eruption of teeth , this is what we always learn that there are no

bacteria in the mouth if there are no teeth because the bacteria need

the teeth to colonize on, but the recent studies have shown that theydont need the teeth to colonize the bacteria ,and they found the age at

which M.S are first acquired in infant is equal to the susceptibility of

caries , so the earlier you get these bacteria you have a higher risk of

dental caries .

in a study of 78 month = 4 years children ,they found that 89% of those

colonized by bacteria at the age of 2 years had DFT= 5,

but the ones who dont colonize at that age (2 years ) has small DFT=0.3

the earlier you get these bacteria you get a higher DFT.

In another study the found 50% of pre-term and 60% of full term who

are at the age of 6 months old had S.M and these children didnt have

teeth they were predentate and have the bacteria, which denies the

theory that said that you have to have teeth for the bacteria to colonize.

Another study showed that 30% of predentate children at the age of 3

months even younger they were infected by the bacteria and at the ageof 6 months they became more, over 60% showed presence of S.M in

the mouth.

So they showed that SM will increase with age, so that by the age of 24

months, 84% harbored the bacteria.


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The idea is that you can still get the bacteria when you dont have teeth

because they can colonize in the oral mucosa which means that we must

start prevention very early even before arrival of the child just to make

this mother aware, in the developed countries the nurse visits the

pregnant mother during pregnancy and even after delivery of the babyfor a while until this mother is able to take care of her baby, among the

things that get educated about dental caries.

Virulence of MS:

This bacteria in particular so special because it's highly indicated withdental caries in human.

1- It's able to synthesis Alpha-1-3 rich; water-insoluble glucans, theysynthesis them from sucrose and these will mediate irreversible

adhesion & colonization of MS to teeth, they are very sticky

increase thickness of plaque , which result in enhanced rates of

sugar diffusion & acid production at deep plaque layers.

2- S.mutans will also synthesize intracellular polysaccharide , thisintracellular polysaccharide is like keeping sugar for the day /

night when there is no sugar, its like when you stuck on some

chocolate and keep them in your jaws, they hide this kind of sugar

for the night when you are not having any sugar and they start

synthesizing it produce energy.

this activity maintains acidogenecity and tooth demineralization

during periods of low salivary secretion specially during sleep.

so what the problem during sleep?

they have their sugar ( ), and we dont have anyprotector factor specially with low salivary rate, the teeth are dry

even we brush our teeth they will keep synthesizing the acids and

demineralizing the teeth thats why brushing teeth before sleep is

very important, and the other one which is during the day after

breakfast, but before sleep is mandatory!!.


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3- They produce large amount of acid; they are very able to producelactic acid and cause teeth demineralization.

4- Aciduricity- is the term to indicate acid tolerance in very highlyacidic environment (low PH), which allowing colonization &persistence under cariogenic conditions.

5- Production of dextranase ; its a type of enzyme which allowsinvasion of MS to replace early colonizing, because at the

beginning when plaque forms we will have bacteria like :S.mitis &

S.sanguris they come and take place by dextranase.

B)FERMENTABLE CARBOHYDRATES:

1- Substrate:

1) Sweetened solid foods: so you give them sucrosemain sugar-,

fructose & glucose and they are cariogenic as sucrose.

Also we give them rise and bread (raw starch),this will causes small

drop plaque PH, but all the time the teeth are not cleaned they can stillcause caries.

2)Bottle content; it can be human or bovine milk or formula or juice.

So milk is not cariogenic because it contain caseinits main component

involved in reducing demineralization and increasing remineralization ,

but if u add sugar to the milk it will be cariogenic.

If you compare between human milk to bovine milk you will find that

human milk contain sugar 7% which is more than bovine milk= 4%.

But why did it have this amount of sugar? Because the child need energy

at this young age.

Milk formulas = cariogenic potential to sucrose because it contain sugar.

And the acid drinks in addition to sugar they decrease PH and cause

erosion.


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2- Frequency of consumption:this is our main problem, the children are

being given the bottle or the breast all the time just to quiet them even

if the child is not hungry they given the milk which increases their sugar

exposure.

3- Oral clearance of carbohydrates:children are highly give the bottle

especially at night because the parents want to sleep and the child will

enjoy it :D even they are not hungry , so this will increase sugar

exposure.

C)Susceptible tooth and host:

when the tooth is susceptible y3ne immature because it has been

demineralized enough,also you have other factors that make the teeth

weaker such as :

1)Medical conditions they will cause enamel hypoplasia.

So Enamel hypoplasia with sweetened medication, sweet fluids, sweet

milk & xerostomic side effect of medication, it will all cause ECC.

2)Malnutrition- will lead to alternations of salivary conditions & volume

which will lead to enamel defectsenamel hypoplasia.

This is a pt. with sickle cell anemia, she has to take antibiotics in a form

of syrup( very sweetened), she had to take it every day of her life to

avoid sickle cell crisis, because if she get an infection this will lead to

crisis.

So the sweetened antibiotic along with sweetened food intake and with

enamel hypoplasia because of her conditionincrease risk of dental

caries.


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So the risk factors:

1. Medical history

2. Feeding habits

3. SES and ethnicity

4. Family variables such as: single parent , young mom


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-So for the posterior teeth we usually prefer SSCs as 1st option

, 2nd

option is amalgam,composite , GIC, RMGI.

-For anterior teeth: composite, GIC &RMGI.

-For multiple surface caries we use strip crowns & sometimes

we extract.

-Atraumatic restorative technique (ART)-removal of carious

lesions by hand instruments followed by restoring cavities with

F-releasing restorative material.

Here we have an example of a case have ECC , he was 3.5 years

when he first attended to the clinic, typical ECC ; caries on

anterior teeth then D then C then E. Here is post-operative

treatment, Upper: the Dr. extracted the ant. teeth and this is a

prosthesis- its like a parietal denture!! and did pulpotomy for

the E also artificial teeth for Ds. In the Lower : the Ds

pulptherapy and PRR for the Es, so this is a typical case that we

do it in one and a half hour under GA.

Prevention of ECC:

We have to think about caries balance , we have to look at

protective factors and make them more, the other factors such

as bacteria , salivary flow when its abnormal , frequent eating

and drinking of sugar.

The protective factors is when you increase the salivary flow

and its components like by: chewing gum, or by floride

remineralize the tooth and make them stronger or by xylitol ,

or tooth brushing will kill the bacteria all of these in order to

reach the no caries status.


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So 3 approaches that have been used to prevent

caries:

1) Community based :educating mothers about dietary habits& OH role in ECC, eg; substitute water for cariogenic liquid in

bottle and fluoridating the water supply (the most effective

way and can reach every one) will decrease caries by (40-60%).

2) Provision of examination & preventive care in dental clinics:

regular dental visits and the use of F professional therapy.

3)The development of appropriate dietary and self habits at

home : OHI , use of self applied F at home , chlorohixidine

gel\varnish and xylitol chewing gum .

Now we finished the 1st

part.


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PART 2 :

I'm sorry there won't be slides for this part!!

Before the dr. started this part she said that she will not go intodetails y3ne for the exams we have to study what mentioned in

the lecture.

Then started viewing pics and reading some topics. also said

that every thing has been covered and dont have to explain

farther o_o!

We can study it from the internet!!

But I relied on 2007's script to make it more clear.

DEVELPOMENTAL DENTAL ANOMALIES :

so you have to know:

-Abnormalities in teeth number.

-Abnormalities in teeth shape.

-Abnormalities in teeth size.

-Abnormalities in tooth structure (structural defects in

enamel, dentine and bone).

- Abnormalities in teeth eruption.

Hypodontia

Hypodontia is considered as developmental anomaly in teethnumber and it means a reduction in teeth number.

There are many terminologies used in relation to hypodontia so

we can say hypodontia if there are less than 6 teeth missing , but

if there are 6 teeth or more missing we call this condition

oligodontia while if all the teeth are missing we say Anodontia.


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- Hypodontia: less than 6 teeth missing.- Oligodontia: 6 teeth missing or more.

- Anodontia: all the teeth are missing.

# Incidence of hypodontia

- Primary teeth: 0.10.7 %

- Permanent teeth: 29 %

Teeth that are commonly involved with hypodontia are 3rd

molars, maxillary lateral incisors, 2nd premolars and mandibularcentral incisors.

Of course if you look to different studies, you will find differentpercentages regarding teeth with hypodontia

- You have to know the syndromes associated with hypodontialike:

1. Ectodermal dysplasia

2. Gardner syndrome

3. Down syndrome4. cleft lip and palate

5. facial-cranial dysostosis (pt with this syndrome has a hole

covering all the face!!!)

Supernumerary teeth.

We have classification of supernumerary teeth according to siteso they classified as:

_ Mesiodensethe one that happens in the middle._ Paramolarthe one that happens next to a molar.

_ Distomolarthe one that happens at the distal side of a

molar.


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Supernumerary teeth are also classified according to the

shape into:

* Conical: happens in the anterior region

* Tuberculate (barrelshaped): usually happens in theposterior region but it still can be happened anteriorly,

tuberculate means many cusps.

*supplemental (look like adjacent tooth).* inverted conical: it is the same as conical but it is inverted

upside down and starts erupting at the floor of the nose and it

has to be removed surgically.

-Incidence of supernumerary teeth

- Primary teeth: 0.30.8 %

- Permanent teeth: 13.5 %

It happens in 90% of the cases in the maxilla and 75% of themare mesiodense.

Supernumerary teeth are associated with a syndrome called

clediocranial dysplasia.

This is a very common presentation of supernumerary teeth sothe pt. comes complaining from one permanent central incisor

has erupted and the other central incisor next to it has not

erupted and he will find that the one that has erupted iscompletely or fully erupted or sometimes two thirds of it has

been erupted while the one next to it has no sign of eruption (

this scenario is very common) so you should suspect asupernumerary tooth in this case ,because it could be one of the

reasons but of course not all the time.

Sometimes you will even have a primary tooth is still present sowhen you take an x-ray, you will find that there is a tooth

impeding the eruption of the permanent central incisor.

This is another presentation; here the supernumerary tooth is


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actually erupted. The central incisor had erupted and this

supernumerary tooth is called mesiodense according to thelocation and it is conical according to the shape.

This is clediocranial dysplasia with multiple supernumerary

teeth, depressed nasal bridge and the clavicles are either absent

or having dysplasia (very small in size).

Odontomes

1. Complex odontome2. Compound odontome

Dentigerous cyst

thought to-cystodontogenicis anfollicular cystordentigerous cystA

be of developmental origin - associated with the crown of an unerupted

epithelial cells(or partially erupted) tooth. The cyst cavity is lined by

epithelium of the tooth formingenamelderived from the reduced

,it has been suggested that thepathogenesisorgan. Regarding its

pressure exerted by an erupting tooth on the follicle may obstruct

ducedbetween the reexudatevenous flow inducing accumulation of

.tooth crownenamel epithelium and the

In addition to the developmental origin, some authors have suggested

vital deciduous teeth in proximity to-inflammation of nonperiapicalthat

the follicles of unerupted permanent successors may be a factor for

triggering this type of cyst formation. (wiki)

Macrodontia:

It is rarely affect the whole dentition unless there is somethingsystemic like gigantism which results from increase in the

production of the growth hormone before puberty.

Usually we get single tooth which is macrodontic and it isusually due to a local cause which can't be identified in most

cases, in some cases, they say that there is an increase in arterial
http://en.wikipedia.org/wiki/Cysthttp://en.wikipedia.org/wiki/Odontogenichttp://en.wikipedia.org/wiki/Odontogenichttp://en.wikipedia.org/wiki/Epithelial_cellhttp://en.wikipedia.org/wiki/Epithelial_cellhttp://en.wikipedia.org/wiki/Tooth_enamelhttp://en.wikipedia.org/wiki/Tooth_enamelhttp://en.wikipedia.org/wiki/Pathogenesishttp://en.wikipedia.org/wiki/Pathogenesishttp://en.wikipedia.org/wiki/Pathogenesishttp://en.wikipedia.org/wiki/Exudatehttp://en.wikipedia.org/wiki/Exudatehttp://en.wikipedia.org/wiki/Tooth_crownhttp://en.wikipedia.org/wiki/Tooth_crownhttp://en.wikipedia.org/wiki/Tooth_crownhttp://en.wikipedia.org/w/index.php?title=Periapical&action=edit&redlink=1http://en.wikipedia.org/w/index.php?title=Periapical&action=edit&redlink=1http://en.wikipedia.org/w/index.php?title=Periapical&action=edit&redlink=1http://en.wikipedia.org/wiki/Tooth_crownhttp://en.wikipedia.org/wiki/Exudatehttp://en.wikipedia.org/wiki/Pathogenesishttp://en.wikipedia.org/wiki/Tooth_enamelhttp://en.wikipedia.org/wiki/Epithelial_cellhttp://en.wikipedia.org/wiki/Odontogenichttp://en.wikipedia.org/wiki/Cyst


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blood supply to that area or sometimes neural blood supply but

actually we are not sure why it happens.

Microdontia:

The teeth are smaller than usual.

- True microdontia: all the teeth are small and it is usually rareand hormonal condition (hormonal microdontia is the opposite

of gigantism) a result from reduction in growth hormone and it

is usually relative.

(Relative means in relation to the jaws, the jaws are big whilethe teeth are small leads to relative microdontia)

An example of microdontia is peg-shaped lateral incisor.

Fusion and gemination

Double tooth or sometimes called con-joined teeth because it is

usually hard to differentiate between fusion and gemination andalso in some cases it could be a supernumerary tooth so we

dont usuallyattempt to differentiate between them so we say

double tooth or con joined teeth.

- This is an example of a pt attended to my clinic and he had agemination or fusion or con-joined teeth on this side and after

we did a big study on this case (space analysis, study models,

orthodontic consultation and several x-rays), we found that thebest is to extract the tooth and place a RPD at this stage and aim

for a future implant.

- This is the extracted tooth and here we put an appliance to act

as space maintainer to keep this space open for the eruption ofthe impacted canine on this side while on the other side we

notice that the canine was erupted because of enough space.


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Dense invaginatus

_looks like tooth within a tooth

_We should protect them by fissure sealant or composite as

soon as possible after eruption.

Dense evaginatus.

Talon cusp:

- Excessive cusp on the palatal surface that we have to keep onreducing it many times.

Taurodontism:

of humans whereby the body ofmolar teethis a condition found in the

chamber is enlarged vertically at the expense of thepulpthe tooth and

roots. As a result, the floor of the pulp and the furcation of the tooth is

moved apically down the root. The underlying mechanism of

Hertwig's epithelialtaurodontism is the failure or late invagination of

aping causing, which is responsible for root formation and shroot sheath

an apical shift of the root furcation.

The constriction at the amelocemental junction is usually reduced or

absent. Taurodontism is most commonly found in permanent dentition

although the term is traditionally applied to molar teeth. In some cases

taurodontism seems to follow an autosomal dominant type of

inheritance.

,amelogenesis imperfectaTaurodontism is found in association with

ectodermal dysplasia and tricho-dento-osseous syndrome. The term

means "bull like" teeth derived from similarity of these teeth to those of

ungulate or cud-chewing animals (wiki)
http://en.wikipedia.org/wiki/Molar_teethhttp://en.wikipedia.org/wiki/Molar_teethhttp://en.wikipedia.org/wiki/Pulp_(tooth)http://en.wikipedia.org/wiki/Pulp_(tooth)http://en.wikipedia.org/wiki/Hertwig%27s_epithelial_root_sheathhttp://en.wikipedia.org/wiki/Hertwig%27s_epithelial_root_sheathhttp://en.wikipedia.org/wiki/Hertwig%27s_epithelial_root_sheathhttp://en.wikipedia.org/wiki/Hertwig%27s_epithelial_root_sheathhttp://en.wikipedia.org/wiki/Hertwig%27s_epithelial_root_sheathhttp://en.wikipedia.org/wiki/Amelogenesis_imperfectahttp://en.wikipedia.org/wiki/Amelogenesis_imperfectahttp://en.wikipedia.org/wiki/Amelogenesis_imperfectahttp://en.wikipedia.org/wiki/Amelogenesis_imperfectahttp://en.wikipedia.org/wiki/Hertwig%27s_epithelial_root_sheathhttp://en.wikipedia.org/wiki/Hertwig%27s_epithelial_root_sheathhttp://en.wikipedia.org/wiki/Pulp_(tooth)http://en.wikipedia.org/wiki/Molar_teeth


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Enlarged pulp chambers:

- There are some conditions where the pulp chamber is very

large in size (larger than normal) at the expense of dentine as in:

1. Vitamin D resistant rickets2. Vitamin D dependant rickets

3. Hypophasphtasia

4. Dentinogenesis imperfecta5. Regional odontodysplasia

In particular, all these conditions are related to dentine (they aredentine defects)

- This is an example of enlarged pulp chamber with relation to

enamel and dentine, this pt had Vitamin D resistant rickets

therefore he had enlarged pulp chamber affecting all the teeth

but if it is only in one tooth then you should have somethinglocal while in this case it is something systemic.

Developmental defects of enamel:

- We talked a lot about them.

Extrinsic staining: it is a condition caused by chromogenic

bacteria .

enamel hypoplasia and opacities.

amelogenesis imperfecta (AI), dentinogenesisimperfecta(DI)

- I just want from you to review these conditions because these

are the conditions that we usually diagnose at childhood inpediatric dentistry.

- This is DI, we can easily diagnose it because it is usually

associated with obliterated pulp chamber and bulbous crowns.


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- Most cases of DI are associated with obliterated pulp chamber

(The most significant feature).

Pre-eruptive intracoronal resorption of dentine (PEICR)

- It's caries that happens pre-eruptively (before the tooth erupts)

- This tooth has not erupted yet but we have here radiolucencyin

the crown because this tooth inside the follicle had a defect in

the enamel then became invaded by macrophages, osteoclastsand odontoclasts that invaded enamel and dentine caused

cavitation in it.

Now this is happening inside the dental follicle but once the

tooth erupts, this cavity becomes colonized with bacteria so it

looks like dental caries but actually it started pre-eruptively- Some types of occult caries is like PEICRbut not all the types

because some types of occult caries occur post-eruptively by

invasion of M.O to tooth structure through the deep fissures on

the occlusal surface.

- This is an example of a pt who is 9 years old female, she

complained of pain in 36 , which looks normal and healthy but

when we took x-ray, we found an abscess appears in the

periapical radiograph of that tooth (36) therefore this tooth hasPre-eruptive intracoronal radiolucency which means that this

cavitation started pre eruptively while the tooth was forming.

At pre-eruptive stage we never get an abscess because there isno bacteria in the follicle but when the bacteria colonized the

tooth post-eruptively we will get this abscess so finally we had

to do RCT for this tooth!!


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Eruption hematoma (eruption cyst)

Sometimes it will be very big like an abscess and it appears blue

in color so the parents will be scared and they came panic to the

clinic but it is actually an eruption hematoma or eruption cyst.

Ankylosis

- This tooth here is ankylosed and it happens a lot in primary

teeth especially lower Es and Ds.

Erosion- An example on erosion is the effect of gastroesophegael reflex

(GER).

Reference:

Chapter 7, A Handbook of pediatric dentistry byCameron & widmer.

Or u can Google it ..!


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Part 3:

I'm sorry There won't be slides for this part and its included

for the final exam

Chemotheraputic agents

Chlorohexidene : it's actually a salt, it's concentration = 0.2% or 0.12% .

Its positively charged molecule, so it means that it can bind to anything

negative, like what?

Bacterial cell wall.

It's also bactericidal, at high concentration it cause coagulation of the

cytoplasmic material of the bacteria and then cause cell death.

How do we prescribe it?

0.2% CHX10ml for 1 min.

Or 12%CHX15 ml for 1 min.(most commonly in Jordan).

There is a type of CHX, its gel this is what we use for children , it doesn'tcontain alcohol because it can irritate the mucosa, so they put it in their

tooth brush with no irritation and excellent compliance.

We can use it also before we put composite filling with children whose

high risk carries like ECC.

It can be in a form of tube we call it periogard.

There's another type used called chloroflour which is a combination of

CHX and fluoride gel in one tube .

Advantages :*

1) Bactericidal

2) Reduce discomfort of mouth ulcers

3) Excellent compliance


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4) Low cost

But it can cause some staining.

*Characteristics:

The ability to adsorb to anionic substances, ex; hydroxyapatite

,pellicle ,salivary glycoproteins, mucous membranes and

polysaccharide coats of bacteria, all these are negatively charged.

It's also slow release all the time: which means when it adsorb to

these surfaces it cause slow release we call it substantivity .

And this give 80% reduction in plaque when used as adjunct in oral

hygiene.

The documented uses of CHX :*

1) Plaque control

2) Physically and mentally handicapped pts.

3) High risk caries pts.

4) Pts with removable and fixed ortho appliances

5) In periodontal or gingival cases ,before we use CHX we should

do scaling and polishing to be effective.

*Actions:

As we said bactericidal, anti-plaque, but it's not effective against

the lacto bacilli, it works against the Strep. Mutans.

*Side effect:

1) Staining

2) Dulling of taste

3) Increase calculus formation

4) Desquamation of the epithelium because it contains alcohol.

Now we will move to xylitol:

Its a non-cariogenic sugar sweetener; it means its a sugar but

cannot cause caries, it's produced from xylan-beech wood.

Chemically ; its a pentitol which is a 5 carbonring, it differs

from the sucrose which is 6 carbon ring.


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Characteristic of xylitol evidnce based:

1)Not cariogenic

2)Chewing gum is anti cariogenic ; they found that 93% of children

who chew Xylitol gum got a caries reduction.

Chewing process stimulate salivary flow and washes away the

bacteria and the plaque.

Also it inhibit mother-child transmission of bacteria, so if a

pregnant mother or a mother that has a baby will reduce bacterial

count in her mouth which means it will reduce the transmission to

the child.

3) The explanation for this is that maternal use of xylitol had

effected children's probability of being colonized by S.mutans.

4) Its considered more effective in caries reduction than sorbitol

and sucrose.

5) Xylitol maybe used in preventive program to reduce caries.

Xylitol disadvantages :

The biggest dis. of Xylitol is diarrhea if eaten in large amount,

which is 20 gr per day.(threshold levels would be lower for

children.Another side effects: hypoglycemia if taken in high amount

,osmotic diarrhea, hyperic-acidic levels in blood which can cause

kidney stones , allergies to xylitol which is rare cases.

The recommended amount is 6-8 gr per day for dental benefit.


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[26]

*proposed actions of xylitol:

-Plaque: non-fermentable by MO, reduces plaque quantity,

Strep.mutans reduced, and strains with reduced virulence,

participate in futile metabolic cycle.

reduce adhesion of plaque flora, and also reduce transmission of

bacteria from mother to her baby.

-On saliva: it changes the quality and the quantity of it.

- On enamel: aid in remineralization.

Finally CPP:

CCP ACB = casein phosphopeptide amorphous calcium phosphate

, derived from casein part of the protein found in cow's milk, they

found that its caries resistance it can be used in caries prevention

program ; it increases the level of calcium and phosphate in saliva

and concentrate them in ionic form and can adsorb to tooth

structure and cause remineralization.

The Dr. started showing pic for CPP that present in chewing gum

its name is recaldents (43:41) will combine with fluoride so will be

synergistic effect, so its good to combine fluoride.

And this is tooth mousse and its exactly like yogurt it comes in

different flavors (strawberry, vanilla ..) it's used in the teeth like

topical cream or you can use it in a tooth brush.

There are two types of it, the first type doesnt contain fluoride

then they developed a new type which is called MI phase which

contain fluoride.

So the idea is that it will provide the teeth with calcium and

phosphate in its ionic form to get adsorbed to tooth surface, it

works: anti caries, remineralization , for erosion , hyper sensitivity

, and it has been included to GIC restorative material.


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Its only contraindicated in pts. who have allergy to milk should

avoid product contain recaldent, and this allergy comes from casein

and protein found in CCP.

And can be used for any age.

If you want to read about it more there is an article u can Google it

or send me an email (me-Dr. for sure not me :P)

Immunization:

The idea of immunization y3ne we make vaccine for dental caries!

Its a dream that didnt come true cause it make a problem

regarding: safety, effectiveness, specifity, acceptability.

That's all

Finally it's done..

And no it wasn't fun.

Thank you folks

Good luck & I'm sorry for any mistake.

Hadeel Khutaba

3) early caries - developmantal anamolies

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