The Ideal Teeth Access Cavity Preparations for RCT (Root Canal Treatment)

The correct access preparation for RCT is as follows:

Upper Teeth:

central Incisors : triangular

lateral Incisors: ovoid

canines: ovoid

first premolars: ovoid

second premolars: ovoid

first molars: triangle

second molars: triangle

Lower Teeth:

central Incisors: ovoid

lateral Incisors: ovoid

canines: ovoid

first premolars: ovoid

second premolars: ovoid

first molars: triangle or trapezoid

second molars: triangle or trapezoid

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Differences between 3M ESPE (Z350 XT, Z350, Z250 and P60) Composites

The Differences between the 3M EPSE products is about the shading, color and mechanical properties ...
So that the indications for the use of each products differs according to those criteria ... for example:

Z350 XT Indications:
- Direct anterior and posterior restorations (including occlusal surfaces)
- Core build-ups
- Splinting
- Indirect restorations (including inlays, onlays and veneers)

Z350 Indications:
- Direct anterior and posterior restorations
- Sandwich technique with glass ionomer resin material
- Cusp buildup
- Core buildup
- Splinting
- Indirect anterior and posterior restorations including inlays, onlays and veneers

Z250 Indications:
- Direct anterior and posterior restorations
- Sandwich technique with glass ionomer resin material
- Cusp buildup
- Core buildup
- Splinting
- Indirect anterior and posterior restorations including inlays, onlays and veneers

P60 Posterior Composite Indications:
- Direct posterior restorations
- Sandwich technique with glass ionomer resin material
- Cusp buildup
- Core buildup
- Splinting
- Indirect posterior restorations including inlays and onlays.

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Choose the Product you want for the certain case you want to treat ...
It's not about filling with composite, actually it's all about with which composite you fill ... !!!

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Early Childhood Cavities (ECC)

- More commonly known as "baby bottle tooth decay" is a condition that affects children up to the age of three, or as long as they remain using a bottle. 

- Although rare, ECC may indicate the potential risk for severe tooth decay when the child develops his adult teeth.

- Causes:
1- Sugars and carbohydrates in the child's diet Beverages that contain sugar such as milk, infant formula, fruit juice, or any other liquid that contain or is sweetened with sugar.
2- Bacteria transferred from the caregiver to the child.
3- The frequency of feedings
4- Allowing a child to fall asleep with bottle that contains any liquid other than pure water.

- Prevention:
1- Offering a pacifier rather than a bottle during naps and bed time
2- Speak with your dentist for advice on how to expose your child to fluoride,

- NOTES:
1- if it is not available through your water supply.
Fluoride is recommended by the American Dental Association to strengthen teeth, which may prevent tooth decay.
2- If using a bottle during periods of sleep, fill the bottle with only pure water.

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Amelogenesis Imperfecta

Definition:
Amelogenesis imperfecta is a tooth development disorder in which the teeth are covered with thin, abnormally formed enamel.

Amelogenesis imperfecta presents with abnormal formation of the enamel.
Enamel is composed mostly of mineral, that is formed and regulated by the proteins in it.
Amelogenesis imperfecta is due to the malfunction of the proteins in the enamel: ameloblastin, enamelin, tuftelin and amelogenin.
People afflicted with amelogenesis imperfecta have teeth with abnormal color: yellow, brown or grey.
The teeth have a higher risk for dental cavities and are hypersensitive to temperature changes.
This disorder can affect any number of teeth.

Types:
1- Hypoplastic AI:
Inadequate deposition of enamel matrix.
Enamel matrix present is normal.
Enamel may be "Thin or Pitted".
The thin enamel may be "Smooth or Rough".
Generalized small pits scattered across surface of teeth or localized large area of hypoplastic enamel typically on the buccal middle third of the tooth.
Smooth enamel exhibits a smooth surface which is thin, hard and glossy or rough.
The enamel is more dense than that of smooth pattern.
Most commonly is autosomal dominant inheritance.

2- Hypmaturation AI:
Adequate deposition and mineralization of enamel matrix but inadequate maturation of crystal structure (mineral).
Soft enamel with similar radiodensity to underlying dentin .
Pigmented enamel has mottled , brown appearance .
Snow-Capped Teeth: Zone of opaque white enamel on the incisal / occlusal end of the teeth

3- Hypocalcified :
No mineralization occurs.
Enamel is soft and easily lost.
Enamel is dull, lustreless, opaque white, honey or browned colour.
Enamel and dentin appear radiographically indistinct.

4- hypomaturation hypoplastic:

Causes:
Amelogenesis imperfecta is a hereditary Disorder.

Symptoms:
The teeth enamel become soft and thin.
The teeth appear yellow.
The teeth become easily damaged.
Both baby teeth and permanent teeth are affected.

Differential Diagnosis:
The most common differential diagnosis with the Amelogenesis Imperfecta is the Dental Fluorosis.
- The variability of the fluorosis make it very difficult to differentiate.
- It varies from mild white "flecking" of the enamel to profoundly dense white colouration with random, disfiguring areas of staining and hypoplasia.
- Requires careful questioning to distinguish from Amelogenesis Imperfecta.
- Fluorosis may present with areas of horizontal white banding corresponding to periods of more intense fluoride intake and may show the premolars or second permanent molars to be spared (chronological distribution).
- The history will often reveal excessive fluoride intake either in terms of a habit such as eating toothpaste in childhood, or related to a local water supply.

Treatment:
The treatment depends on the severity of the problem.
The treatment starts from simple composite restorations until a Full crown restorations that will improve the appearance of the teeth and protect them from damage.
Treatment is often successful in protecting the teeth.
The teeth may have to be extracted and implants or dentures are required.
Generally, treatment is veneers , full coverage , overdenture, full denture or extraction and implant.

Complications:
The enamel is easily fractured and damaged, which affects the appearance of the teeth, especially if left untreated.

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Diagnostic Tests Of Dental Pain

There are several simple tests that may assist in diagnosis of dental pain.

- Pulp Sensitivity Test:
This test can be done by using cold or hot stimuli.
Cold Stimulus is done by using Dry ice, or an ordinary ice stick that is placed in the cervical region of the tooth to detect posibility of pulpal inflammation.
Hot Stimulus is done by heating an instrument and placing it to one of the tooth surfaces.
In both of them, if pain occured and faded away once removing the stimulus indicating healthy tooth, if pain occured and persisted for a few minutes indicating inflammed pulp that must be treated endodontically and if the pain didnt occure indicating a necrotic pulp.

- Percussion Test:
Using an instrument handle, the tooth is tapped in the longitudinal axis. A painful response suggests possible periapical inflammation. (ex: Apical Periodontitis)

- Probing:
Placing a fine, blunt probe (Periodontal Probe) gently into the gingival sulcus surrounding the tooth to check the health of the gingival tissues. Bleeding and/or sulcus depths greater than 3-4 mm indicate a periodontal disease and a pocket which then should be diagnosed to have periodontal treatment.

- Mobility Test:
Holding a tooth firmly on the buccal and lingual sides between a finger and a solid instrument enables mobility to be assessed.
All teeth have a small amount of mobility (<0.5 mm) (Normal Or Mild Movement),
The teeth with movement of (0.5-2 mm) should be splinted (Moderate Movement),
While the teeth with (Severe Movement) of (2-4 mm) should be treated surgically or to be extracted.

- Palpation:
Careful digital palpation around the area of concern may reveal tenderness and the type and extent of swelling. (Usefull in cases of Tumor or Abscess or Soft Tissue Abnormalities)

- Radiographic Examination:
Sometimes we need a radiographic X-ray to detect some underlying abnormalities and possible pain sources.
We use periapical radiographes to check 3 neighboring teeth together and it's usefull to detect the extent of caries, reccurent caries, periapical lesions, crown root ratio and fructures.
We use orthopantomograph (OPG) to check the upper and lower full teeth set and neighboring important structures for abnormalities and possible causes of pain and it's very usefull in cases of impacted teeth, relation between upper teeth and maxillary sinus and presence of oral lesions in bone.

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Dental Caries

Index:

Part 1 = Introduction - Definition.
Part 2 = Classification Of Caries.
Part 3 = Factors Influencing Caries Etiology.
Part 4 = Histopathology Of Dental Caries.
Part 5 = Clinical Diagnosis Of Dental Caries.
Part 6 = Management of Deep Dental Caries.
Part 7 = Sequence of Dental Caries.

Introduction - Definition

What is Dental Caries:

It is a disease of microbial origin in which the dietary carbohydrates are fermented by the bacteria forming an acid which causes the demineralization of the inorganic part and disintegration of the organic part of the tooth.

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Classification Of Caries:

A. According to number of surfaces involved:

1) simple (1 surface involved)
2) compound (2 surfaces involved)
3) complex (2 surfaces involved)

B. According to anatomic site:
1) occlusal (pit-and-fissure) caries
2) smooth-surface caries (proximal and cervical caries)
3) root caries

C. According to histology:
1) enamel caries
2) dentinal caries
3) cemental caries

D) According to severity:
1) incipient caries
2) occult caries
3) cavitation caries

E) According to onset:
1) primary (virgin) caries
2) secondary (recurrent) caries
3) residual caries

F) According to duration:
1) acute (rampant)
2) chronic

G) According to chronology:
1) early childhood caries
2) adolescent caries
3) senile caries

H) According to progression:
1) arrested caries
2) recurrent caries
3) radiation caries

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Factors Influencing Caries Etiology.

A)Host factors:

1) tooth factors:
a. Composition surface enamel due to dense
mineralization and high F-
content more resistant to caries than
subsurface layers of enamel.

b. Morphology more chances of caries if deep ,
narrow occlusal fissures or buccal or lingual pits present

2) saliva factors:
a. composition
a1) inorganic less chances of caries if higher Ca2+
and PO43- concentration
a2) organic less chances of caries with higher
ammonia and urea content

b. pH decrease in pH of saliva below 5.5 (ka critical
pH) predispose to caries.
The remarkable buffering-capacity of saliva (due to HCO3-H2CO3 and phosphate buffer systems) controls the marked fall in pH, thus preventing caries formation.

c. Position more chances of caries if malaligned , rotated teeth.

d. quantity decreased amount or absence ( xerostomia)
increases the risk of caries.

e. viscosity

f. antibacterial properties: due to the presence of lysozyme (cleaves the N-acetyl glucosamine and N-acetyl muramic acid components of bacterial cell wall) and salivary peroxidase system ( salivary peroxidase and thiocyanateSCN- components of saliva interferes with glycolytic pathway of bacteria)

3) systemic factors:
a) heredity
even though no strong evidence has been found connecting caries-susceptibility with heredity, studies have shown
“high DMF” father and “high DMF” mother produced offspring with a “high DMF” rate
And “low DMF” parents produced offspring with “low DMF” rates.
b) Pregnancy and lactation
despite the popular belief, there is NO evidence suggesting increase in caries in pregnancy (unless the mother has neglected her general oral health care).

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B) Diet factors
a. physical nature of diet
person taking food with more fibre-content less
susceptible to caries than those taking soft, refined
(worse if sticky) food

b. local factors

b1) carbohydrate content
though all forms of fermentable sugar leads to caries , there is always a higher risk of caries with free sucrose than starches.
Because sucrose in addition to its acid- byproduct produced during fermentation also aids in plaque development and adherence of cariogenous microbes to the tooth surface.
However starches due to large molecular structure, shows limited diffusion and hence can not directly enter the plaque .

b2) vitamin content
vitamins like (vit.D, vit.K and vit.B6) have been found to decrease the incidence of caries,
vit. B-complex deficiency has shown decrease in the rate of caries
whereas even though it is well-established that vit C-deficiency causes severe periodonta land pulpal changes , no evidence of decrease in caries by Vit C-supplement has been reported.
however a more extensive study to confirm the link between vitamins and caries is still desireable.
b3) fluorine content
even though there is reduced incidence of caries with F-in drinking water, there is no significant caries reduction with dietary fluoride (because of its metabolic unavailabilty).

C) Cariogenic potential of the microorganism

Available data strongly suggest an active involvement of Streptococcus mutans in caries initiation (especially in pit and fissure caries, and smooth-surface caries; and to some extent the root surface caries)
On the other hand, oral actinomyces like
Actinomyces viscosus, and
Actinomyces neslundii, have a more important role in root surface caries.
Also A. neslundii, Lactobacillus spp. And other filamentous rods have been implicated in dep dentinal caries.

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Histopathology Of Dental Caries

Enamel is composed of tightly packed hydroxyapatite crystals, which are organized in long columnar rods (enamel rods), but during caries progression certain histological changes are seen in enamel .

The following 4 histological zones of an enamel lesion clearly explains the development of enamel caries

zone 1 translucent zone
zone 2 dark zone
zone 3 body zone
zone 4 surface zone

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Zone 1 translucent zone
Deepest zone representing the advancing front of enamel caries.
In this zone , pores or voids form along the enamel prism(rod) boundaries (due to easy H+ ion penetration)
It appears structureless when perfused with quinolone solution (having refractive index comparable to that of enamel) and seen with polarized light (hence translucent)

Zone 2 dark zone
Next deepest zone
Presence of many tiny pores block light transmission. These smaller air or vapor-filled pores make the regiion opaque.
Loss fo crystalline structure suggesting the process of demineralization and remineralization in this zone.

Zone 3 body zone
In demineralization phase, it is the largest portion of the lesion.
(whereas in remineralization phase, zone2dark zone is the largest portion which increases in the expense of the “body zone”)
Largest pores seen (pore volume 5 to 25%)
Presence of bacteria if pores large enough to permit their entry
Striae of Retzius well marked
(striae of Retzius is the primary point of entry of carious lesion into rodprism cores of enamel)

Zone 4 surface zone
Relatively unaffected by caries (only partial demineralization)
Because surface of enamel is relatively immune to caries (due to hypermineralization- because of saliva contact , and
higher surface F-content)
Also pore volume is lower than the body of lesion.

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After the involving the enamel, the carious lesion progresses to the dentinal structure.
Caries advancement in dentin proceeds through 3 stages:

1) demineralization of dentin (by weak organic acids)
2) degeneration and
dissolution of organic material of dentin , mainly collagen
fibers (type I)
3) bacterial invasion after the loss of structural integrity caused
due to 1) and 2).

During the development of dentinal caries, clinically 5 different zones of progression can be seen (ac to Sturdevant )
zone 1 normal dentin
zone 2 subtransparent dentin
zone 3 transparent dentin
zone 4 turbid dentin
zone 5 infected dentin

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Histologically , 5 zones of early dentinal caries progression can be seen (listed pulpally to occlusally)
zone 1 zone of fatty degeneration of Tomes’ fibers
zone 2 zone of dentinal sclerosis
zone 3 zone of decalcification of dentin
zone 4 zone of microbial invasion
zone 5 zone of decomposed dentin

Zone 1 zone of fatty degeneration of Tomes’ fibers
the most advancing front of dentinal caries characterized by the presence of a layer of fat globules ; hence stains red with the stain, sudan red.
significance

1) fat layer leads to impermiability of the dentinal tubules (DT) – trying to prevent further invasion of  carious lesion
2) favors sclerosis of dentin in zone 2.

Zone 2 zone of dentinal sclerosis
layer of sclerotic dentin which appears white in transmitted light
calcification of DT as a rxn of vital pulp and vital dentin to carious invasion , so as to prevent further penetration of microorganisms.
formation of this zone is minimal in rapidly progressing caries, and prominent in slow caries.

Zone 3 zone of decalcification of dentin
this zone lies above the zone of sclerotic dentin
initial decalcification of only the walls of the DT
presence of PIONEER BACTERIA- first of the microorganisms penetrating DT before there is any clinical evidence of caries.
bacteria present in individual DT are in pure form (i.e. either completely cocci or completely bacilli; not in mixed form)

Zone 4 zone of microbial invasion
in a layer above zone 3.
characterized by the presence of microorganisms in early stage of caries- acidogenic microorganisms in deeper layer- proteolytic microorganisms replace acidogenic bacteria supports the hypothesis that initiation (by acidogenic bacteria) and progression ( by proteolytic microorganisms ) are 2 distinct processes in caries development.

During initiation phase- in the early stage when caries is not deep , acidogenic bacteria predominant which utilizes carbohydrate for their metabolism
Later in progression phase – as the caries goes deeper , less and less of carbohydrate substrate available , hence acidogenic bacteria are replaced by proteolytic microorganisms which uses dentinal protein for their metabolism.

Zone 5 zone of decomposed dentin
Most superficial zone of early dentinal caries.
no recognizable structure in decomposed dentin

collagen and minerals seem to be absent
great number bacteria dispersed in this decomposed granular matter.

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Clinical Diagnosis Of Dental Caries

By one or all of the following:
1) Visual changes in tooth surface texture or color
2) Tactile sensation with judicious use of explorer
3) Radiographs
4) Transillumination
Aided by the knowledge of the probability of overall caries risk and patterns of susceptibility.

-------------------

A) Diagnosis of Pit and Fissure Caries:

Any one or more of the following:
1) Softening at the base of pit and fissure
2) Opacity surrounding the pit or fissure, indicating demineralization of enamel
3) Brown-gray discoloration radiating peripherally from the pit or fissure
4) Softened enamel that may be flaked away by explorer radiolucency beneath the occlusal enamel surface

B) Diagnosis of Proximal Surface Caries:

1) Visual – white chalky appearance or shadow under the marginal ridge
2) Tactile- probing with explorer on proximal surface may detect cavitation, which is defined as the break in the surface contour of enamel
3) Radiographic diagnosis- made with bitewing radiographs which show radiolucency beneath the enamel surface in the proximal area (should not be confused with cervical burnout!)

Arrested Lesions on Proximal Surface:
1) Appears as brown spots
2) On probing, surface is intact and hard
3) Radiograph shows decreased radiographic density in the affected region
4) Usually seen in old patients

Proximal Surface in Anterior Teeth:
1) Transillumination- in which light source directed through the tooth from the lingual side. Proximal surface caries, other than incipient caries, appear as a dark area along the marginal ridge
2) Tactile- exploration to detect any cavitation
3) Radiographs – may detect any small incipient lesion as well.

C) Diagnosis of Smooth Surface caries on the Facial and Lingual surfaces (Usually Gingival)

Initial phase :
1) CHALKY-WHITE, OPAQUE AREAS (“WHITE SPOTS”) over the smooth surface of the tooth, that is visually different from adjacent translucent enamel , which is revealed only when the tooth surface is clean and dry and disappears partially or totally when the tooth is wet . This initial phase of caries in enamel is k/a “incipient caries”.
The tooth at this stage appears to have lost its translucency because of extensive subsurface porosity due to demineralization.
2) Undetectable tectilely since surface is hard , intact and smooth.

Advanced Phase:
1) White to dark brown discoloration
2) Demineralized and softness to penetration

Arrested Lesion:
1) Dark, discolored areas mostly due to extrinsic staining
2) Hardening of lesion (due to remineralization)
3) Sclerotic or eburnated dentin

D) Diagnosis of Root Surface Caries:

1) Look for the following features at CEJ or more apically on cementum
early stage-
a) Well-defined discoloration adjacent to gingival margin,
typically near the CEJ
b) Softened cemental tissue compared with adjacent structure
advanced stage- softening on exploration
and cavitation.

2) Usually in older individuals , or in patients who has undergone perio- surgery , with the following predisposing factors
a) Cemental exposure
b) Dietary changes
c) Systemic diseases
d) Medications that affect amount and character of saliva.

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 Management of Deep Dental Caries

A) Chemical Measures For Caries Control:
Use of:

1) Substances which alter the tooth surface or tooth structure

a) Fluoride Exposure Application
Fluoridation of water supply ( with 1 ppm of F-)
Topical application of fluoride

i) Self-application
- Low dosehigh frequency rinses
(0.05% NaF daily)
- High potencylow frequency rinses
(0.2% NaF weekly)
- Fluoridated Dentifrices Toothpastes
(twice daily)
ii) Professional Application
- acidulated phosphate fluoride gel (APF gel)
(1.23% annually or semi-annually)
- NaF solution (2%)
- stannous fluoride (8%)

b) Bis-biguanides ( like chlorhexidine , alexidine)

c) Silver Nitrate

d) Zinc Chloride and Pottasium Ferrocyanide Solution

----------

2) Substances Which Interfere With Carbohydrate Degradation Through Enzymatic Alteration:

a) Vitamin K – Use of Synthetic Vit K (2-methyl-1,4-naphtoquinone)
b) Sarcoside - Na Lauroyl Sarcosinate,
Na Palmitoyl Sarcosinate,
Na Dehydro Acetate

----------

3) Substabces Which Interfere With Bacteria Growth And Metabolism:

a) Urea and Ammonium Compounds
b) Chlorophyll
c) Penicillin
d) Other antibiotics ( erythromycin, kanamycin, spiromycin, tetracycline, tyrothricin, vancomycin)
e) Caries vaccine
f) Nitrofurans – furacin, furadroxyl

B) Mechanical Measures For Caries Control:

1) Dental Prophylaxis (routine scaling and polishing)
2) Toothbrushing
3) Mouth Rinsing
4) Dental Floss
5) Oral Irrigators
6) Chewing Xylitol Gums (for 5 to 30 mints after meal)
7) Detergent Foods in Diet (hard, fibrous foods)
8) Pit and Fisure Sealants

C) Nutrietional Measures For Caries Control:

1) Diet Counselling
2) Restriction of Soft, Sticky Refined Carbohydrate Intake
3) Limiting in Between Meals.

--------------------------------

Sequence of Dental Caries

The Dental Caries can cause DEATH !!!

- First of all, We should know that the caries is the most common infectious disease for the humans.
- The Caries is a bacterial infection, which occurs briefly due to bacteria that ferment the carbohydrates to produce the Lactic acid which causes the demineralization of the enamel surfaces, causing the decay and cavities.
- The Caries may extend deeply into the tooth layers, to reach the dentin layer, which is sensitive, causing the tooth pain.
- Then the bacteria will penetrate the dentinal layers soon if neglected to reach the pulp chamber (or horns), causing the pulpitis, which will start as reversible OR irreversible.
- The Bacteria may drown deeply inside the pulp chamber to reach the orifices of the pulp causing pulp inflammation that would, if neglected, cause partial pulp necrosis that requires partial pulpectomy to manage.
- Then, the bacteria drown inside more deeply that will necrose the rest of the pulp canals causing complete pulp necrosis, then the patient will feel no pain.
- In this stage, the tooth is most commonly ( Badly Decayed ) and black in color, the patient may no seek dental help because he/she suffers of no pain, this neglection will cause the next serious step, which is the periapical abscess.
- The Periapical Abscess may be acute, because of the sudden increase of the pathogens strength or sudden decrease of the host immunity, causing pain specially during biting and percussion.
- And the periapical abscess may become chronic soon or after, if the immunity increased or the pathogens strength decreased, to wall of the infection.
- The chronic abscess may exacerbate to transform the chronic abscess into acute painful one again that leads the patient to seek dental help.
- The infection may then spread to the facial spaces, lower molars may spread infection to the submandibular and sublingual spaces, while the anterior teeth may spread this infection to the submental space.
- The neglected infection may spread to the spaces causing facial cellulitis and subsequent Ludwig's angina that may be fatal.

So, Caries may Lead to DEATH !!!

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Fissure Sealants

- Those materials are used to prevent occlusal pit and fissure caries by filling the deep pits and fissures, and this is very conservative way of tackling of problem of occlusal caries

- Fluoride, systemically, has an effect on reduction of smooth surface caries but it has less effect on occlusal caries.

- Sealants can reduce the overall cariogenic challenge to teeth.

- Few dentists don't recommend using pits and fissure sealants at all, their motto here is that they fear the procedure would induce caries later on because of the preparatory steps , and giving a chance for later caries development.

Note: The earlier the fissure sealing procedure, the better the results.

- Types:
1- Resins
2- GIC
3- Compomers
4- Flouride containing sealants

The choice between resin/composite and glass ionomer Fissure Sealant should be based on adequacy of moisture control.

- Requirement Of Fissure Sealants:
1- Good adhesion to enamel for a long period.
2- Biocompatible.
3- Simple in application and easy in manpulation.
4- High flow capacity to enter narrow pits & fissures
5- Have proper setting and working time
6- Have very low solubility in the oral fluids.
7- Not causing miecroleakage at the enamel sealant interfaces.
8- It not necessary to fill the entire depth of pit & fissures but it should fill and seal the entire length.

- Indications of Fissure Sealant:
1- Newly erupted un maatured teeth with narrow deep pit& fissure
2- Patient with high susceptibility to caries
3- Patient with history of high caries in his primary teeth
4- The presence of incipent caries
5- PRR or normal restoration

- Contraindication of Fissure Sealant:
1- Patients who are not susceptible to caries
2- Tooth with Large occlusal restoration.
3- Presence of open occlusal restoration or carious on an other surface of the same tooth
4- Patient's behavior which may not permit adequate dry field throughout procedures
5- Matured carious free teeth present in oral cavity for more than four years with wide shallow pits & fissures

- Steps of application of Fissure Sealant:
1- Use Rubber Dam or Cotton Roll and Suction, to isolate the tooth.
2- Clean the tooth very well using a non-fluoridated prophylactic paste and low Rubber Cup.
3- Dry the tooth very well.
4- Acid etch the tooth very well by the use of 30%-50% phosphoric acid or citric acid, for 60 seconds for permanent teeth, and 90 seconds for primary teeth.
5- Wash by water and dry by air very well.
6- Fissure sealant is then applied to the propely etched pit and fissure using its brush or applicator.
7- Make sure that the material is filling the etched pits & fissures.
8- Cure the material if it is light cure, OR, Leave it if it's chemically cured.
9- Check for retention and high spots, by asking the patient to bite or by using articulating papper.
10- Apply fluoride gel on the teeth surfaces to remeneralize the demenralized areas wich may not be covered by the fissure sealant.
11- Ask your patient to avoid rinsing or drinking for 30 secounds.

---------------------------

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Pulp Capping (Direct and Indirect)

- Pulp Capping Procedure:

- Pulp capping:It is a term is derived from the name pulp cap which means trying to sterilize the damaged tooth area as well as one can, followed by stopping the bleeding and placing the right filling material on it.

- The precaution being that teeth that are already abscessed should never be pulp-capped – this is done to those teeth where the nerve is irritated but still alive and healthy enough to repair themselves given a chance to do so.

- Pulp capping gives it a chance by getting out the decayed portions and the bacteria then putting a clean dressing on it with the filling.

- After eliminating the wounded dental tissues of a carious tooth, the next step is usually filing the cavity with a suitable restoring material. When pulpal tissue is exposed it gets contaminated by bacteria and mostly these are the conditions that warrant the clinician to perform pulp capping. When performing this procedure, the degree of the pain and the pulpal size exposure are considered.

- Capping Materials:

- Calcium Hydroxide is the best possible capping material known till now.

- Advantages of Calcium Hydroxide:
1-It's alkaline PH (11) ... Giving more chances to healing of inflamed tissues.
2-Amazing bio-compatibility with pulpal tissues.
3-It's antibacterial Abilities (Bacterio-static).
4-It's ease of application.
5-Availability.
6-It's proven Abilities to dentine bridging for regeneration of healing dentinal tubules in the pathosed dentine pulp complex.

- Disadvantages of Calcium Hydroxide:
1- Associated with primary tooth resorption
2- May dissolve after one year with cavo-surface dissolution.
3- May degrade during acid etching
4- Degrades upon tooth flexure
5- Marginal failure with amalgam condensation
6- Does not adhere to dentin or resin restoration.

- NOTE:
Calcium hydroxide was originally introduced to the field of endodontics by Hermannin:: 1920 as a pulp-capping agent.

- Many studies have showed that direct pulp capping with MTA Is as successful ...

- Placing the restoration directly without capping on a pinpoint exposed pulp:
1- Severe sensitivity the patient will suffer.
2- Failure of restoration.
3- Irreversible pulpal tissue damage that will require endodontic treatment.

- The Pulp Capping is two Types: Direct and Indirect Pulp Capping:

- Direct Pulp Capping:

- The exposed pulp is directly covered. This works best when the exposure is not infected - for example a traumatic exposure caused by slipping with the drill.

- If the pulp becomes exposed while removing soft infected dentine, the chances are that the pulp will be infected also, and a direct pulp cap will fail (that is, an irreversible pulpitis will develop).

- Although Calcium Hydoxide has been proven successful for many years, MTA (Mineral Trioxide Aggregate) is fast becoming the material of choice for direct pulp caps. MTA is however very expensive.

- Indirect Pulp Capping:

- The pulp is not exposed - a layer of infected dentine is deliberately left, rather than expose the pulp.

- Indirect pulp caps, when done correctly, are more successful at maintaining long-term vitality than direct ones.

- It is not currently (2010) known whether it is necessary to "go in again" after a couple of months for further caries removal.

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Bonding To Dentine

- The main problems encounter in "Bonding To Dentine" procedure are:
1- High Water Content of Dentinal Tubules.
2- High Organic Content of Dentinal Tubules.
3- Presence of Smear Layer.

- Indications of "Bonding To Dentine"

1- Marginal Seal where preparations margins are on dentine or cementum.
2- Retention and Seal of direct resin composite restorations.
3- Retention and Seal of indirect porcelain and composite inlays.
4- Repairing Teeth.
5- Veneers.
6- Cementing Ceramic Crowns
7- As An Endodontic Sealer.

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Dental Composite Resin :: In Details ...

Definition

Dental composite resins are types of synthetic resins which are used in dentistry as restorative material or adhesives. Synthetic resins evolved as restorative materials since they were insoluble, aesthetic, and insensitive to dehydration and were inexpensive. It is easy to manipulate them as well. Composite resins are most commonly composed of Bis-GMA monomers or some Bis-GMA analog, a filler material such as silica and in most current applications, a photoinitiator. Dimethacrylates are also commonly added to achieve certain physical properties such as flowability. Further tailoring of physical properties is achieved by formulating unique concentrations of each constituent.Unlike Amalgam which essentially just fills a hole, composite cavity restorations when used with dentin and enamel bonding techniques restore the tooth back to near its original physical integrity.

Composition

Dental composite resin.
As with other composite materials, a dental composite typically consists of a resin-based oligomer matrix, such as a bisphenol A-glycidyl methacrylate (BISMA) or urethane dimethacrylate(UDMA), and an inorganic filler such as silicon dioxide (silica). Compositions vary widely, with proprietary mixes of resins forming the matrix, as well as engineered filler glasses and glass ceramics. The filler gives the composite wear resistance and translucency. A coupling agent such as silane is used to enhance the bond between these two components. An initiator package (such as: camphorquinone (CQ), phenylpropanedione (PPD) or lucirin (TPO)) begins the polymerizationreaction of the resins when external energy (light/heat, etc.) is applied. A catalyst package can control its speed.

Advantages

The main advantage of a direct dental composite over traditional materials such as amalgam is improved aesthetics. Composites can be made in a wide range of tooth colours allowing near invisible restoration of teeth. Composites are glued into teeth and this strengthens the tooth's structure. The discovery of acid etching (producing enamel irregularities ranging from 5-30 micrometers in depth) of teeth to allow a micromechanical bond to the tooth allows good adhesion of the restoration to the tooth. This means that unlike silver filling there is no need for the dentist to create retentive features destroying healthy tooth. The acid-etch adhesion prevents microleakage; however, all white fillings will eventually leak slightly. Very high bond strengths to tooth structure, both enamel and dentine, can be achieved with the current generation of dentine bonding agents. The downside[vague] to composite when compared to amalgam is a shorter lifespan of the filling, and the high likelihood of requiring root canal therapy if the failure of the filling is not caught quickly. Amalgam fillings may crack a portion of the tooth off, but otherwise tend to fail at a much slower rate.

Disadvantages

Composite resin restorations have several disadvantages: They are technique-sensitive meaning that without meticulous placement they may fail prematurely. They take up to 50% longer to place than amalgam fillings and are thus more expensive. In addition clinical survival of composite restorations placed in posterior teeth has been shown to be significantly lower than amalgam restorations.[1].
Survival and reasons for failure of amalgam versus composite posterior restorations placed in a randomized clinical trial.

Direct dental composites

Direct dental composites are placed by the dentist in a clinical setting. Polymerization is accomplished typically with a handheld curing lightthat emits specific wavelengths keyed to the initiator and catalyst packages involved. When using a curing light, remember that the light should be held as close to the resin surface as possible, a shield should be placed between the light tip and the operator's eyes, and that curing time should be increased for darker resin shades. Light cured resins provide denser restorations than self-cured resins because no mixing is required that might introduce air bubble porosity.
Direct dental composites can be used for:

• Filling gaps (diastemas) between teeth using a shell-like veneer or
• Minor reshaping of teeth
• Partial crowns on single teeth

Indirect dental composites

This type of composite is cured outside the mouth, in a processing unit that is capable of delivering higher intensities and levels of energy than handheld lights can. Indirect composites can have higher filler levels, and are cured for longer times. As a result, they have higher levels and depths of cure than direct composites. For example, an entire crown can be cured in a single process cycle in an extra-oral curing unit, compared to a millimeter layer of a filling.
As a result, full crowns and even bridges (replacing multiple teeth) can be fabricated with these systems. A stronger, tougher and more durable product is likely.
Indirect dental composites can be used for:

• Filling cavities in teeth, as fillings, inlays and/or onlays
• Filling gaps (diastemas) between teeth using a shell-like veneer or
• Reshaping of teeth
• Full or partial crowns on single teeth
• And even bridges spanning 2-3 teeth

Composite shrinkage

Composite resins have a notorious reputation for shrinking upon curing, however, uses as a dental restorative material focus on low shrinkage composites. Composite shrinkage can be reduced by altering the molecular and bulk composition of the resin. For example, UltraSeal XT Plus uses Bis-GMA without dimethacrylate and was found to have a shrinkage of 5.63%, 30 minutes after curing. On the other hand, this same study found that Heliomolar, which uses Bis-GMA, UDMA and decandiol dimethacrylate, had a shrinkage of 2.00%, 30 minutes after curing.[3] In the field of dental restorative materials, reduction of composite shrinkage is a "hot topic". Soon to be introduced are patent pending, is a safe, non-leaching antimicrobial agent which minimizes recurrent decay of the tooth and reduces the harmful effects of micro-organisms and which some may cause gingivitis and periodonttitis (periodontal disease).

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Enamel lamellae, Tufts & Spindles

Enamel lamellae:

Type of hypomineralized structure in teeth that extend either from the dentinoenamel junction (DEJ) to the surface of the enamel, or vice versa. In essence, they are prominent linear enamel defects, but are of no clinical consequence. These structures contain proteins, proteoglycans, and lipids.

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Enamel tufts:

Small, branching defects that are found only at the DEJ, and so differ from lamellae which can be facing either direction and are strictly linear.

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Enamel spindles:

Linear defects, they can be found only at the DEJ, because they are formed by entrapment of odontoblast processes between ameloblasts prior to and during amelogenesis.


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