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DENT2022 Course Summary

MODULE 0 PREVENTIVE DENTISTRY (Prof. Lawrence Walsh) 2 (BLOCK TEACHING WEEK)

MODULE I CARIOLOGY (Dr Sowmya Shetty) 6

MODULE II RADIOLOGY (Various) 26

MODULE III TOOTH PREPARATION (Dr Sowmya Shetty) 63

MODULE IV DEEP CARIOUS LESIONS (Various) 75

MODULE V COMPOSITE RESIN (Dr Sowmya Shetty) 79

MODULE VI MISCELLANEOUS TOPICS (Various) 89

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Module 0 – Preventive Dentistry

CARIES DIAGNOSTICS

New diagnostics for dental caries are classified into two separate tests:

o Sensitivity is the ability to detect diseased tissue (a high sensitivity diagnostic test is accurate at

detecting the presence of caries)

o Specificity is the ability to detect healthy tissue (a low specificity diagnostic test gives false-

positive readings for the presence of caries when the tooth is actually healthy)

Sensitivity and specificity varies according to the particular diagnostic approach:

o In a visual exam with a mirror and probe, there will be a high specificity (0.81 − 0.98) but a

lower sensitivity (0.20 − 0.54), as our ability to detect healthy tissue is in general better than

our ability to detect diseased tissue. Being able to notice a carious lesion with just a visual exam

is almost like tossing a coin (50/50 chance).

o On a dental X-ray, the sensitivity increases (0.40 − 0.67), while the specificity mainly stays the

same (0.81 − 0.95). It is easier to detect carious lesions on a radiograph than with a visual exam,

but the lesion must still have lost a substantial amount of mineral before it can readily be seen on

a radiograph – this is a problem.

Fissure caries is difficult to detect by visual means alone, as the fissure may contain stain and protein

debris rather than caries.

There are many diagnostic tests which focus on the disease process:

o SALIVA TEST – Testing the patient’s resting and stimulated salivary parameters

o IMMUNO-ASSAY – Looking for specific indicator (disease-associated) species such as S. mutans

and S. sobrinus, as well as antibodies to these indicator species.

o BIOFILM DIAGNOSTICS – Assessing the thickness and age of dental plaque deposits.

o PLAQUE FERMENTATION – Measuring plaque fermentation at a single site via culture-based

tests or ATP bioluminescence.

o PLAQUE DISCLOSING – 3-tone disclosing of plaque on teeth to show fermentation across the

mouth on exposure to sugar.

All these tests can be used to monitor the impacts of lifestyle changes on the ecology of dental plaque.

The ICDAS-II system recognises the existence of the pre-white spot lesion, which can only be seen

when the tooth surface is clean and dry.

Methods for detecting caries:

o Using a sharp probe with pressure can damage fissure enamel and is unreliable for caries

detection. Only use some pressure, and if a very slight pull is required to remove it, the pit should

be marked for restoration even if there are no signs of decay.

o Caries detector dyes stain areas of the enamel with greater porosity (selective penetration of

the solvent). They can cause false positive staining of dentine when caries is removed with

methods that do not leave a smear layer (e.g. Carisolv or laser).

o Bitewing radiographs show areas of mineral loss greater than 1/3 of the buccolingual width of

the tooth. There is an imperfect correlation between the appearance on a bitewing radiograph

and the depth of the carious lesion on the approximal surface, and whether or not it is cavitated.

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Module I – Cariology

PRESENTATION

Dental caries is a multifactorial, transmissible, infectious oral

disease caused by the complex interaction of cariogenic oral

flora (biofilm) with fermentable dietary carbohydrates on the

tooth surface over time. The earliest clinical sign of caries is

the appearance of a white spot lesion. Repeated

demineralisation events may result in varying degrees of

cavitation and discolouration, and radiographically this can be seen as radiolucent (see-through) areas.

There are many different types of caries lesions:

Tooth habitats favourable for harbouring cariogenic biofilm include:

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1. Pits and fissures – these are particularly susceptible areas for caries initiation, as they provide

excellent mechanical shelter for microorganisms.

2. Smooth enamel surfaces immediately gingival to proximal contacts, and in the gingival third of

the facial and lingual surfaces of the crown – these areas are relatively protected from the effects

of mastication, tongue movement and salivary flow.

3. Root surfaces (particularly near the cervical line) – these areas are unaffected by flossing

because it may have concave surface contours and occasional roughness.

4. Subgingival areas – these areas are usually neglected in oral hygiene procedures.

The following diagrams illustrate plaque biofilm formation on posterior teeth.

A. Teeth No. 19 and No. 20 are in a

contacting relationship

interproximally.

B. The crown of No. 20 has been

removed, showing plaque

biofilm on No. 19 both at the

proximal contact and

underneath it (sub-contact).

Facial plaque can also be seen.

C. During periods of unrestricted

growth, the mesial and facial

plaques merge and form a

continuous biofilm around the

tooth periphery.

D. In a horizontal cross-

section, the

interproximal space

below the contact area

is filled with gelatinous

plaque. This

concentrates the effects

of plaque metabolism on the adjacent tooth smooth surfaces. All interproximal surfaces are

subject to plaque

accumulation and acid

demineralisation.

Frequent ingestion of fermentable

carbohydrates promotes the growth

of highly acidogenic bacteria (such

as streptoccus mutans). If they are

not neutralised, the pH will drop and

once below the critical pH (5.2 – 5.5

enamel, 6.5 dentin), the

demineralisation process begins. In

time, saliva will bring the pH back to

normal resting levels,

remineralising the tooth.

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DIAGNOSIS

There are many methods available to diagnose caries:

o VISUAL-TACTILE – The traditional, most-used method is the visual-tactile method – this entails

simply looking for visual changes in the tooth surface texture/colour, or detecting surface

roughness with a dental explorer/probe. Good lighting and a clean, dry tooth surface is

required. However, the probe MUST NOT BE USED TO DETERMINE A ‘STICK’ (a resistance to

withdrawal from a fissure or pit), as this irreversibly turns a sound, remineralisable surface into a

possible cavitation prone to progression. Instead, a blunt probe should be judiciously used by

gently stroking across the tooth surface.

o RADIOGRAPHS – Smooth-surface caries in proximal regions are usually diagnosed

radiographically. Bitewing radiographs can show mineral loss greater than 1 3⁄ of the

buccolingual width of the tooth, or 2 3⁄ – 3 4⁄ of the enamel thickness. By this stage, the tooth

requires operative treatment/restoration.

o DIGITAL FIBRE OPTICAL TRANSILLUMINATION (FOTI) – Fibre Optic Transillumination (FOTI)

works on the principle of light scattering forward to create a dark area where there is caries

present or a crack in the tooth. FOTI is a useful adjunct to the diagnosis of approximal lesions.

o LASER FLUORESCENCE (DIAGNODENT) – Laser fluorescence technology can be used to detect

and measure bacterial products and changes in the tooth structure. Positive fluorescence occurs

when light is given off by carious tissue. This principle is used by DiagnoDENT.

o ELECTRONIC CARIES DETECTION – When a carious lesion is present, the porosity increases, and

this changes the way that alternating electrical current flows across the tooth. A device called

the CarieScan can measure this change in the flow of current through a tooth.

o OPTICAL COHERENCE TOMOGRAPHY (OCT) – Optical coherence tomography (OCT) provides

high resolution three-dimensional data sets using non-ionising infrared laser radiation, which

could in future replace some applications of conventional dental X-rays.

Radiographs are essential in

the diagnosis of approximal

lesions, where a contact point

is present. A film-holder and

beam-aiming device should

always be used to ensure the

correct angulation of the

beam, and as an aid in

reproducing the same

geometry in any subsequent

radiograph if the lesion is to be

monitored.

There are two types of

radiographs:

o INTRAORAL (item code

022) – The two most

commonly used are bitewing (crown and

supporting interdental bone) and periapical

(apex of tooth including the root and PDL).

o EXTRAORAL (item code 037) – This commonly

refers to an orthopantomograph (OPG).

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Module II – Radiology

RADIATION PHYSICS

X-rays are invisible, have high energy and short wavelengths. They have no mass or charge, as they

are composed of photons. All X-rays travel in a straight line at the speed of light, but they also diverge

from their point of origin. They can either penetrate matter, or be absorbed by it to varying degrees

(depending on the density). X-rays can also cause some substances to fluoresce, and affect photographic

film. Most importantly, X-rays can cause BIOLOGICAL DAMAGE.

An X-ray is a form of high energy electromagnetic (EM) radiation (the movement of energy through

space as a combination of electrical and magnetic fields). Some properties are best described by

quantum physics, whereas others by wave theory:

o QUANTUM THEORY – Quantum physics considers EM radiation as small bundles (quanta) of

energy called photons. Each photon travels at the speed of light and contains a specific amount

of energy. The unit of photon energy is the electron volt (eV) – this is the amount of energy

acquired by one electron accelerating through a potential difference of one volt. Photon energy

and wavelength are related by the following equation:

𝐸 = ℎ ×𝑐

𝜆 where

𝐸 = energy in keV, ℎ = Planck′s constant (4.3 × 10−18 keV)

𝑐 = speed of light, 𝜆 = wavelength in nanometres (nm)

o WAVE THEORY – The wave theory states that EM radiation is propagated in forms of waves.

These waves consist of electrical and magnetic fields oriented in perpendicular planes, oscillating

perpendicular to the direction of travel. All EM waves travel at the speed of light (𝑐) in a vacuum.

Waves also exhibit properties of wavelength

(𝜆) and frequency (𝑣).

𝜆 × 𝑣 = 𝑐 = 3 × 108 m/sec

In comparing the two equations, photon

energy is directly proportional to frequency.

Electromagnetic radiation can be visualised on a

spectrum from high energy to low energy:

o High energy photons (e.g. X-rays) are

typically characterised by energy (eV).

o Medium energy photons (e.g. visible

light) are typically characterised by

wavelength (nm).

o Low energy photons (e.g. AM and FM

radio) are characterised by frequency

(KHz, MHz).

A single atom is composed of protons,

neutrons and electrons. The atomic number

(𝑍) denotes the number of protons in the nucleus. Electrons however move in predetermined shells or

orbits around the nucleus, labelled K, L, M, N and O. Each shell represents a different energy level, and

electrons can move from shell to shell but cannot exist between shells. To remove an electron from the

atom, additional energy is required to overcome the binding energy of attraction. This electron binding

energy decreases as the distance from the shell to the nucleus increases.

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The binding energy refers to the energy required to completely remove an electron from an atom. If a

free, unbound electron is assumed to have a total energy of zero, the total energy of a bound electron is

zero minus its binding energy.

o EXAMPLE: A K shell electron of

tungsten (𝑍 = 74) (−69,500 eV) is

much more tightly bound than the

K shell electron of hydrogen (𝑍 = 1)

(−13.5 eV), because the energies

increase with 𝑍 (atomic number) and

decrease with distance from the

nucleus.

o The energy required to move an

electron from the innermost

electron orbit (K shell) to the next orbit (L shell) is the difference between the binding energies

of the two orbits.

In a neutral atom, the number of orbiting electrons in shells equals the number of protons in the nucleus.

o If an electron is removed, the atom becomes positively charged (ionised).

o If an electron is displaced from an inner to an outer shell, the atom remains neutral, but is in a

state of excitation.

PRODUCTION OF X-RAYS

X-rays are wave packets (photons) of energy of EM radiation that originate at an atomic level. They are

produced when highly energetic electrons interact with matter, and convert their kinetic energy into

EM radiation. An X-ray beam is made up of millions of photons of different energies.

An X-ray tubehead is composed of a cathode and an anode in an evacuated glass envelope. A filament

in the cathode streams electrons out, and these electrons are caught by a target in the anode and then

converted into X-rays.

o CATHODE (−) – The cathode is

composed two parts:

FILAMENT – A heated

filament of tungsten

provides the source of the

electrons. The tungsten is

coiled and mounted on two

stiff wires which carry

electric current.

FOCUSING CUP – The

filament sits in a focusing cup – a negatively

charged, concave reflector made of molybdenum.

The heated tungsten coil creates a cloud of

electrons¸ and these are focused by the cup into a

narrow beam to be directed at the focal spot of the

anode.

o The entire structure is set in a vacuum – this prolongs the

life of the filament and prevents the collision of electrons in

their passage to the focal spot.

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o ANODE (+) – The anode is composed of two parts:

TARGET – A small rectangular piece of

tungsten (1mm x 3mm) set into an angled

face of a large copper block acts as the

target. Its role is to convert the kinetic

energy of the colliding electrons into X-

rays. The point at which the electrons

collide is called the focal spot. The target

is typically angled at 20˚ to the electron

beam to allow for dissipation of heat over

a larger surface area, while still producing

a small focal spot.

Note however that the projected

effective focal spot (1mm x 1mm) is

smaller than the actual focal spot

size (3mm x 1mm). The smaller the

effective focal spot, the higher the

resolution of the radiographic image.

COPPER BLOCK – The copper block is

a good thermal conductor,

removing the heat generated by the

tungsten target.

o The tubehead (along with the glass

envelope) is surrounded by a lead casing to

absorb any unwanted X-rays (as X-rays are emitted in all directions), such that X-rays can only

travel through the window in the lead casing, creating a single effective X-ray beam.

Aluminium filters also remove some of the low energy X-ray photons from the X-ray beam

before it emerges from the X-ray tube.

At the atomic level, there are two types of interactions:

o HEAT-PRODUCING

COLLISIONS – About 99%

of collisions will result in

the production of heat.

The incoming electron

from the cathode collides

with an outer-shell

tungsten electron in the

anode, displacing it to an even outer shell (excitation) or from the atom completely (ionisation),

with a small loss of energy in the form of heat.

o X-RAY-PRODUCING

COLLISIONS –

Sometimes, the

incoming electron

penetrates the

outer electron shell

and passes close to

the nucleus of the tungsten atom. This produces two different types of X-ray spectra:

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X-RAY FILMS

An intraoral dental film is a direct

exposure film that is sensitive to X-ray

photons, while extraoral films are only

sensitive to light photons, and so require

an intensifying screen which converts X-

ray photons into visible light. Each film

packet is wrapped in an outer

packet/wrapper that is moisture and

light-proof. Inside the packet is a sheet of

lead foil and a black, light-proof interleaf

paper wrapper that is folded around the

actual film.

Structure of an intraoral film:

o The plastic film base is made of clear transparent

cellulose acetate which acts only to support the

emulsion.

o A thin layer of adhesive affixes the base to the emulsion.

o The base is sandwiched on both sides by the

film emulsion – this is composed of silver

halide (usually silver bromide) crystals

embedded in a gelatin matrix. The X-ray

photons sensitise the silver halide crystals

that they strike, and these sensitised crystals

are later reduced to visible black metallic

silver in the developer.

o A protective layer of gelatin shields the emulsion from mechanical damage.

Within the film emulsion, as well as Ag-Br crystals, there are also free Ag+ ions in the crystal lattice, and trace amounts of sulfur at the sensitivity site.

Exposing the Ag-Br crystals to X-ray photons results in the release of electrons (recoil electrons) from Br atoms, and these electrons move to the sensitivity site to give it a negative charge.

The free Ag+ ions are also attracted to the sensitivity site, neutralising the negative charge and forming neutral Ag atoms.

The sensitivity site now becomes the latent image site as the neutral Ag atoms hold a latent image. The collection of these latent image sites in crystals across the entire film eventually forms the final radiographic image.

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Module III – Tooth Preparation and Restoration

CLASS II PREPARATION

When is a restoration needed?

o For aiding plaque control on occlusal, approximal, free smooth enamel and root surfaces.

o Sensitivity to hot, cold and sweet

o Danger to the pulp

o Progression of the lesion (previous attempts to control through various preservative techniques

has not worked)

o Impaired function

o Drifting is likely due to loss of contact point (maybe fracture)

o The carious lesion is a visual eyesore (i.e. aesthetics)

An amalgam restoration is successful and lasts for years if:

o Tooth preparation is correct

o Matrix is suitable (and a correctly fitting wedge is used)

o The operating field is isolated properly using a rubber dam

o The restorative material is manipulated properly.

Initial clinical procedures:

1. Local anaesthetic is applied.

2. Occlusal contacts should be marked with articulating paper before tooth preparation is

undertaken. A mental note of the contacts should be made for future reference when restoring.

3. Check the interproximal contacts with dental floss and mark the contact points. Measure the

contact point with a periodontal probe on the radiograph, and also in the patient’s mouth. A

mental note is also made of this to give an idea of gingival extension.

4. Placement of a rubber dam is generally recommended.

Preparation:

1. OCCLUSAL LOCK/STEP – Enter the pit nearest the involved proximal

surface, with the long-axis of the bur and long-axis of the tooth crown

remaining parallel during the cutting procedure. The goal of the initial

cut is to reach the DEJ – in posterior it is approximately 1.5 – 2.0mm

from the occlusal surface. The bur should extend 0.1 – 0.2mm into the

dentine.

While maintaining the same depth and bur orientation, the bur is

moved to extend the outline to include the central fissure and

the other pit (if necessary). The isthmus width should be as

narrow as possible (no wider than ¼ the intercuspal distance).

Maintaining the bur parallel to the long-axis creates occlusally converging walls which is

favourable. A dovetail outline form may be

placed only if there is a diverging fissure

pattern.

Before extending into the involved proximal

marginal ridge, the final locations of the

facial and lingual walls of the proximal box

are visualised (the dotted lines in the

adjacent diagram).

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From the occlusal

aspect, a reverse

curve in the

occlusal outline of

a Class I

preparation often

results when

developing the

mesiofacial wall

perpendicular to the enamel rod

direction, while at the same time

conserving as much of the facial cusp

structure as possible. Lingually, the reverse curve is minimal.

Extend the preparation towards the involved proximal surface, stopping 0.8mm short of

the proximal surface.

Figure E shows the completed occlusal lock.

2. PROXIMAL BOX – There are three objectives when

extending the proximal margins: include all

caries/defects, create 90˚ (butt-joint) cavosurface

margins, and establish not more than 0.5mm

clearance with the adjacent proximal surface

facially, lingually and gingivally.

The bur is positioned over the DEJ in the

pulpal floor next to the remaining mesial

marginal ridge (figure A).

The end of the bur is allowed to

cut a ditch gingivally along the

exposed DEJ – this is the proximal

ditch (figure B).

The axial wall should follow the

faciolingual contour of the

proximal surface and the DEJ

(figure D).

The position of the proximal walls should not be

overextended, as additional extension will occur when the

remaining spurs of enamel

are removed (figure E).

When a small lesion is

prepared, the gingival

margin should clear the

adjacent tooth by only

0.5mm (figure F).

The faciolingual dimension

of the proximal ditch is

greater at the gingival level

than at the occlusal level

(figure G).

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Module IV – Deep Carious Lesions

PULPAL INJURY

Pulp cannot generally not be differentiated from dentine anatomically or functionally, and the two are

usually considered as a dentin-pulp complex. This means that any insult to the dentine will affect the

pulp. It is considered to have three layers:

o Odontoblast zone (peripheral layer) – the outer

layer of the pulp, forming a junction with dentine.

Odontoblasts are found here, extending their

processes into the surrounding dentine.

o Cell-free zone of Weil – beneath the

odontoblastic cells; contains the nerve plexus of

Raschkow.

o Cell-rich zone (containing many fibroblasts) – actual cells of the pulp proper

Pulp injury can be caused by interferences to blood supply, damage through the dentin-pulp complex

(cracks/dentin exposure), or direct exposure and damage to the pulp. Insults the pulp include:

o Dental caries – bacteria / toxins

o Microleakage in restored teeth

o Mechanical, thermal, or chemical trauma (odontoblasts will be killed) – this can be caused by

direct trauma, heat generated during tooth cutting, chemicals applied to dentine, or exposure of

the pulp during cavity preparation.

Note that the pulp is surrounded by unyielding walls of dentine, meaning it cannot expand as a result

of inflammation. The vasculature is terminal arteriolar, meaning it reduces the ability to heal itself easily

after injury. Its innervation lacks proprioceptive sensory mechanisms.

Natural protective mechanisms for pulp protection:

1. SCLEROTIC DENTINE – This is caused by the narrowing of dentinal tubules due to the formation

of peri-tubular dentine. The sclerosis may progress rapidly in the dentine beneath the advancing

carious lesion, but it also occurs slowly as a natural part of ageing.

2. CALCIUM PHOSPHATE DEPOSITION – Crystals of calcium phosphate may be deposited deep

within the dentinal tubules as a normal response to slowly advancing caries. The mechanism is

not understood (presumably mediated by odontoblasts).

3. SALIVARY PRECIPITATION – Precipitation of calcium and phosphate from the saliva can occlude

any dentinal tubules exposed to the saliva and effectively desensitise hyper-sensitive dentine.

Remineralisation will not occur in the presence of actively advancing caries or in acid erosion

(because of the low pH). Precipitation is unlikely in the presence of active abrasion or attrition.

4. REPARATIVE DENTINE –

In a mild injury (e.g. attrition, or preparation of a shallow cavity), most odontoblasts

beneath will survive, and regular reparative dentine (with relatively normal tubules) will

be laid down at the pulp-dentine interface as a continuation of the main body of the

dentine.

In a moderate injury however, odontoblasts may die – this means that the pulpal cells

(undifferentiated mesenchymal cells) produce irregular reparative dentine (may be

poorly mineralised or have defects).

In chronic injury, diffuse calcification may occur (due to secretion of calcific matrix by

mesenchymally-derived cells).

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Module V – Composite Resin

COMPOSITE RESIN

A composite material is a product which consists of at least two distinct

phases, formed by blending together components with different

structures and properties – the aim is to maximise the desirable properties

while minimising the undesirable properties.

A composite resin is typically composed of two distinct phases – an

organic resin and an inorganic filler. It also contains a coupling agent, a stabiliser, pigments and a

photoinitiator. Each component plays a vital role:

o RESIN – The resin or matrix consists of Bis-GMA

(bisphenol-glycidylmethacrylate) or UDMA

(urethane dimethacrylate), as well as TEGDMA

(triethylene glycol dimethacrylate). As

Bis-GMA/UDMA by itself will be too thick to

work with, TEGDMA acts as a diluent monomer,

diluting the resin to make it easier to work with.

The result is a polymer matrix that allows the

composite to be moulded and shaped easily, as

well as be quickly polymerised (set quickly). The

matrix phase is generally the phase that is

transiently fluid during the manipulation or placement of materials. By itself however, the

matrix tends to have the least desirable properties in the mixture:

If polymerisation is incomplete, any residual monomer left behind is cytotoxic and will

gradually affect the pulp. A GIC liner is commonly placed to protect the pulp due to this.

The reaction is exothermic and releases heat, causing thermal damage to the pulp.

While setting, it also contracts by a large amount, moving away from the walls. This

may lead to fluid percolation or microleakage around the cavosurface margins.

It has a low modulus of elasticity, and so is relatively weak and flexible.

o FILLER – The filler consists of quartz, glasses, ceramics,

and graded fillings. The dispersed fillers add strength,

rigidity, optical properties and reduce the CTE. It

tends to counteract many of the resin’s disadvantages:

It enhances the rigidity and hardness of the

composite, counteracting the resin’s low

modulus of elasticity and flexibility.

It has a lower coefficient of thermal expansion (CTE), counteracting the resin’s large

setting contraction and fluid percolation. It also has less setting contraction overall.

o COUPLING AGENT – The coupling agent typically consists of organosilanes, and its main role is

to bind the filler and resin together.

o STABILISER – The stabiliser prevents the composite from going off in storage.

o PIGMENTS – The pigments allow the composite to be tooth-coloured and aesthetic. A wide

range of shades (at least 10) is preferable.

o PHOTOINITIATOR – The photoinitiator allows the composite to be light-cured, making it set

when exposed to a specific wavelength of light.

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Module VI – Miscellaneous Topics

TREATMENT PLANNING

A treatment plan differs from a patient management plan and a patient care plan.

o ‘Treatment’ implies intervention, invasive or otherwise. It may encompass:

Advice entails getting the patient to change habits and modify risk factors, in order to

prevent disease progression and restore health and function

Restorative intervention involves the dentist intervening via an actual procedure (e.g.

minimal intervention procedures or complex procedures such as endodontics).

o ‘Management’ implies an ability to direct, coordinate and lead a team (patient + associated

dental personnel).

o ‘Care’ implies a responsibility of the health professional to attend to the welfare and autonomy

of the patient as a priority (a patient-centric relationship).

Three questions are of importance when treatment planning:

o Why plan?

To ensure nothing is overlooked (no surprises later on in the treatment stage)

To demonstrate a high level of care (benefits both patient & dentist)

To save time and expense (via prior consideration of how each step impacts on future

stages of the treatment)

To track progress (for both the patient & dentist)

For legal reasons (written plan is part of the legal record.

o When to plan?

At the beginning of the patient-dentist relationship

N.B. Do not rush the plan (consideration of all alternatives & gathering the necessary

information can take time).

o How to plan?

Gather the information (as well as the patient’s wishes & expectations)

Analyse the gathered information & consider the evidence

Consider any variables in the situation (risk/predisposing/modifying factors)

Consider any alternatives & select the most appropriate alternative.

Convey findings to patient & gain patient’s acceptance of that alternative (i.e. informed

consent).

Arrange for this alternative to be undertaken.

Document the plan and the patient’s agreement.

Gathering the information:

o INTERVIEW – The interview allows insight into the

patient’s past and current state of oral health, and

any risk factors relating to the oral disease & effect

on lifestyle (e.g. caries, periodontal disease, non-

carious tooth structure loss)

Medical history

Dental history (+ history of current

complaint, if any)

Social history

Oral hygiene regiment

A risk factor refers to a behaviour or

patient characteristic associated with the

occurrence of the disease.

A risk assessment is the prediction of the

occurrence of the event (the disease).

Awareness of the risk factors associated

with the patient allows effective planning

either to modify the factors, or accept

them and work around them.