Initial assessment

If you’re reading this article, it is sure that you are a dentist with a dental degree of non-Australian origin and you are willing to register yourself in the Dental Board of Australia to practice dentistry in Australia.  To register yourself in the dental Board of Australia, the first step of the three steps is the initial assessment of your documents by Australian Dental Council.
In the initial assessment process the following documents will be assessed by ADC:

  1. Your professional qualification (bachelor degree)
  2. Your work experience
  3. Details of your dental registration or all registrations if you had/have registration in various countries.
  4. Good standing stated by registering authority

You are eligible for initial assessment by Australian Dental Council, if you have a dental degree of your own country or any country which is recognized by the Australian Dental Council.

As a dentist, you can get assessed by ADC at any time of year by submitting an Initial assessment of professional qualification application form.

Once the application form and supporting documents have been received, you will be assigned an ADC candidate reference number. This number should always be used when you contact the ADC.

For initial assessment, we are here to help you.  Write us at

Frequently Asked Questions

Question: I want to immigrate to Australia as dentist. What should I do?

Answer:  If you want to work in Australia as a registered general dentist with Dental Board of Australia, you need to get your non Australian graduate degree assessed by Australian Dental Council.  For this purpose you are required to sit in the examination conducted by Australian Dental Council. Continue reading “Frequently Asked Questions”

How Healthy Teeth Help You to Stay Healthy


How Healthy Teeth Help You to Stay Healthy

By Susan Cruise

The relationship of the teeth to general health and efficiency was appreciated in a general way long before vitamins or focal infections had been heard of. Toothaches used to be as inevitable as colds; and slave buyers and horse traders inspected the teeth of their prospective purchases before buying. Continue reading “How Healthy Teeth Help You to Stay Healthy”

Fluoride Therapy

Fluoride therapy is widely used to prevent dental caries. Evidence have shown that a constantly maintained low level of fluoride in oral environment is most effective in caries prevention against the earlier popular belief of being it most beneficial against caries during pre-eruptive forming enamel.

Keep your teeth free form cavities, Click HERE to by best tooth paste known as TOOTH MOUSSE.

Continue reading “Fluoride Therapy”

IDA Jamshedpur Conducts Dental Camp and Oral Health Awareness Programm

Jamshedpur, 29 April 2018

Amidst the fun filled Jam-street, Indian Dental Association, Jamshedpur Branch took the opportunity to impart crucial knowledge amongst the people of Jamshedpur about oral hygiene and showed how bad oral health and tobacco habits lead to other serious health disorders.

jam-street 1

Dentists of IDA, Jamshedpur branch came up with a healthy cause and educated the people about the proper way to prevent the development of dental problems such as tooth decay, gum diseases and other oral health complications. They spread awareness about the increasing incidence of oral cancer in India and emphasized the importance of regular oral and dental check-up as a better step towards good health.

Risk of oral cancer increases with age. Oral cancers most often occur in people over the age of 40 years and around 80% of oral cancers are directly attributable to the tobacco and related products (smoking, Gutaka, or Pan Masala).

Jam-street 2

The relationship of tooth decay (dental caries) & pyorrhea (periodontitis) to valvular heart disease, diabetes, kidney disease, vision, brain and skin were explained to the public. It was highly advised to get treatment of dental decay and periodontitis in its early stage to prevent the development of other systemic diseases. 167 persons among 516 attendees were found to be suffering from chronic periodontitis, tooth decay, remaining root stumps, sever attrition, temporomandibular joint disorder and malocclusion. These people were advised to get the proper treatment to make their oral cavity free from dental diseases and improvement in the quality of life.

Doctors who immensely contributed in this dental camp cum awareness program were Dr. Ajai Mohan Singh, Dr. Eric Liu, Dr. Warren Liu, Dr. Richa Angik,  Dr. Saba, Dr. Suman Lodha, Dr. Sikander Prasad, Dr. Aron,  Dr. Ankita, Dr. Aditya, Dr. Shweta Jaiswal, Dr. Pankaj, Dr. Aniket, Dr. Aditya and Dr. Soni.


Article written by Dr Sabyasachi Chatterjee

Dr. Sabyasachi

Department of Prosthodontics, KGMU Conducts 1st International workshop on Maxillofacial Prosthodontics

International Conference Maxillofacial prosthodontics

March 18, 2018, Lucknow, India

“We are providing high quality prostheses for poor and underprivileged people in the faculty of Dental Sciences, said Prof. Pooran Chand, Head of the Department of Prosthodontics, King George Medical University, Lucknow, India.

Professor Pooran Chand was addressing the audience in a workshop conducted by department of prosthodontics King George Medical University. He informed the audience that instead of making one prosthesis, now the department can make 15 prostheses in one day. This has become possible by the use of latest technology in Dentistry. The silicon which is used in the fabrication of prostheses, that used to take more than one and half hour for curing earlier,  now takes shorter duration to by using hot air oven.

Delegates attending a seminar on maxillofacial prostheses

It is also possible to make the eye prosthesis that looks exactly as natural eye, spoke  Dr. Tirath Srithiwaz. Dr. Raghubar Dayal explained the audience about the maintenance of maxillofacial prostheses. Dr. Balendra Pratap spoke on the prostheses in children.  He saidd that the eye prostheses of children should be changed after 2 to 3 years.

Speaking at the opening ceremony of the Ist international workshop on maxillofacial prosthodontics in the department of prosthodontics, honorable vice chancellor of the King George Medical University, Prof M.L. B. Bhat, voiced the motto of the institution, ‘we strive to provide world class medical services’. For a better service, in the field of maxillofacial prosthesis, we have collaborated with Mahidol University, Bangkok Thailand. We are committed to provide cheaper maxillofacial prostheses for a price range between Rs. 500 to Rs. 2000 instead of Rs. 1 lakh to Rs. 1.5 lakh rupees that is being charged in private institutions.

On this occasion, the dean of the faculty of dental sciences, Prof. Shadab Mohammad, also conveyed his views on the recent advances in dentistry.

Office bearers of the Indian prosthodontic Society, Dr Kashinath KR, Dr Prafulla Thumati, Dr Ravindra Savadi, Dr V Rangarajan, Dr JR Patel, Dr Rupesh PL, and Dr. N. Gopi Chander were also present on this occasion.


Based on input provided by Dr. Ajai Singh


We invite comments from participants for a better experience. Please use the comment box given below.




Anticipating Pulpal Reaction To Dental Materials:

1] ability of the dental material to stimulate tissue repair;

2] ability of the dental material to seal the interface between the tooth preparation and the restoration;

3] role of microbes in pulpal disease (from caries, oral environment) à maintenance of asepsis;

4] role of tooth preparation procedures in pulpal disease.

 Influence Of Bacteria On Pulpal Healing:

The classic study by Kakehashi et al. (1965) clearly showed the pathologic role of bacteria in pulpal diseases.

Pulpal exposures were made in …
Normal rat Germ-free rat
8 days later Partial necrosis of dental pulp
14 days later Complete necrosis & periradicular abscess
32 days later Complete necrosis & periradicular abscess Intact dentin bridge with normal pulp tissue beneath newly-formed dentin.

This landmark study showed that bacterial infection of dental pulp was a critical etiologic factor for pulp necrosis. Thus, in Vital Pulp Therapy (VPT), the factors that modify healing of the exposed pulp are:

  • Methods to reduce/ eliminate bacteria à pulpal healing must occur in an environment free of microbes.
  • Duration of pulp exposure: Clinical studies by Cvek (1978) and Mejare (1993) showed that in younger patients, the superficial pulp is resistant to bacterial invasion (bacteria invaded only upto 2 mm at the end of 7 days. Partial Pulpotomy with Calcium hydroxide (Ca[OH]2) dressing can give radiographic success of 93% at follow-up of 4.5 yr.
  • Size of pulp exposure: Cvek (1978) performed partial pulpotomies after traumatic crown fractures and pulp exposures of 0.5-4 mm. The success was 96% with an average follow-up of 31 months in both mature and immature teeth. Hence the exposure size may not be a major factor in the success of VPT.
  • Hemostatic control:

Bleeding from an exposed pulp is due to

a] Pulpal inflammation in response to bacteria and toxins from the carious dentin, and;

b] Trauma from the caries removal procedure.

Importance of hemostasis

a] Bleeding leads to compromised seal and is not conducive to the formation of tertiary dentin bridging or maintenance of pulp vitality, and;

b] Open/ cut vessels may carry the pulp capping materials deep into the pulp, and block the blood vessels and reduce blood flow. This causes delayed healing. The caustic nature of Ca[OH]2 may cause perivascular foci of mummification and inflammation (Ca[OH]2 emboli).

  • Method of placement: The pulp capping material must be placed gently over the exposure site. If placed deeply, the deeply impacted particles of the pulp capping material leads to reduced success of VPT. The material (Ca[OH]2) may be phagocytized and may be retained indefinitely by macrophages and giant cells in the area beneath the dentin bridge.
  • Quality of dentin bridge (the use of appropriate dental materials):

a] Ca[OH]2 – The integrity of dentin bridge is suspect due to the porous nature (tunnel defects) at 4 weeks, that may continue to form overtime (90 days). These porous/ incomplete dentin bridges are not a favourable clinical outcome because any breach of the restoration seal leads to bacterial ingress.

b] Dentin bonding agents – It was theorized that etching and bonding will adequately seal the exposure site with a hybrid layer. But this theory is no longer accepted because dentin bonding agents do not express any proteins/ signals that are required for the induction of odontogenesis.

c] Mineral Trioxide Aggregate (MTA) – This Portland cement-based material gives a good seal and dentin bridging due to its ability to dissolve bioactive dentin matrix components, and the activation of transcription factors that act as signaling molecules for pulp repair.

Benefits of Ca[OH]2 in VPT Drawbacks of Ca[OH]2 in VPT
Antibacterial Tunnel defects (porous dentin bridge)
Hard tissue barrier

®    Ca[OH]2 (high alkalinity ) extracts the fossilized (sequestered) growth factors and bioactive dentin matrix components à Induction of dentin regeneration at the site of pulp exposure.

®    Ca++ ions released from Ca[OH]2 stimulate the fibronectin synthesis by pulp stem cells à induction of differentiation of pulp progenitor cells into mineralized tissue-producing cells.

Inadequate mechanical strength
No adhesion to dentin


High solubility à leads to gap formation beneath the base material.


Benefits of MTA in VPT
Hard tissue barrier

MTA is highly alkaline à this enables the extraction of fossilized (sequestered) growth factors and bioactive dentin matrix components à Induction of dentin regeneration at the site of pulp exposure.

Dentin bridge is dense, thicker and continues as compared to Ca[OH]2.
Has currently replaced Ca[OH]2 as the material of choice in VPT.

Molecular Responses To Pulp Exposure:

In response to pulpal injury, there is the upregulation of genes/ markers.

Gene/ Marker Released by Function

Dentin Sialophosphoprotein (DSPP)

Odontoblasts Odontoblast differentiation
Nestin Odontoblasts, other pulp cells


Transforming Growth Factor (TGF)
Bone Morphogenetic Protein – 2 (BMP-2)
Dentin Matrix Protein – 1


Notch Signaling Proteins


Polymorphonuclear (PMN) lymphocytes Differentiation of pulp stem cells into odontoblast-like cells and perivascular cells.
Adrenomedulin Vasodilator peptide hormone (uncertain role).

[From: Seltzer & Bender’s Dental Pulp].



  • Seltzer & Bender’s Dental Pulp. 2nd
  • Ingle’s Endodontics. 6th
  • Cohen’s Pathways of the Pulp. 10th
  • Walton & Torabinejad. Principles & Practice of Endodontics.
  • Grossman’s Endodontic Principles & Practice.
  • Mount GJ, Hume WR. Preservation and restoration of tooth structure. Barcelona, Spain: MOSBY International. 1998.
  • Inoki R, Kudo T, Olgart LM. Dynamic aspects of dental pulp. Cambridge, Great Britain: Chapman and Hall. 1990.
  • Orban’s Oral Histology.

Inflammation in Response to Mechanical, Thermal & Chemical Insults

lnflammation in Response to Mechanical, Thermal & Chemical Insults

(Pulp Protection During & After Tooth Restoration)

Source of Pulp Damage before, during, and after restoration:

  • As caries advances through dentin, bacteria or their metabolic by-products lead to pulp damage and/or death;
  • Immediately after tooth restoration, the trauma directly related to the preparation and placement of a restoration may lead to pulp damage;
  • Subsequent to restoration, months or years later, the pulp may die because of the effects of bacterial microleakage.

Avoidance Of Pulpal Damage Due To Caries:

As the pulp will be involved almost immediately caries penetrates through the enamel and reaches the dentin, early interceptive therapy to arrest and cure lesions will protect the pulp from damage. Those strategies which prevent the initiation of caries lesions are likely to preserve pulp vitality and conserve tooth structure:

  • Dietary control,
  • Fluoride administration (systemic & topical),
  • Modification of bacterial flora,
  • Sealing of pits and fissures,
  • Maintenance of salivary flow,
  • Good oral hygiene.

Rationale of restoration:

  • The placement of a restoration arrests, or at least slows down the progress of caries and will therefore contribute to pulp protection.
  • As a general principle, a small restoration is less likely to damage the pulp than a large one.
  • Early diagnosis and accurate prognosis of active caries followed by conservative restoration placement, when indicated, are therefore in the interest of the survival of the pulp.

Avoidance of Pulp Damage During Cavity Preparation:

(1) Generation of heat:

Heat generation during tooth cutting has considerable potential for damaging pulpal cells.

Measures to prevent heat damage to pulp

  • The use of air/water spray coolant is essential when using high speed rotary cutting instruments to clean, lubricate and cool both the tooth and the cutting instrument;
  • Handpiece and the bur must also be in good condition and running concentrically because vibration can also cause damage to the pulp.

(2) Drying the dentin:

Dentin is traversed by tubules which normally contain both plasma ultrafiltrate (dentinal fluid) and odontoblastic processes. Cut dentin is therefore naturally wet. However, it is necessary for the surface of dentin to be relatively dry for the successful placement of some restorative materials.  But prolonged and excessive drying causes sudden movement of fluid, leading to damage of odontoblast by disruption of their cell membrane.

Methods of safely drying the dentin before restorative procedures

  • It can be dried using either a jet of high pressure air at ambient temperature or warm air at a lesser pressure from a triple syringe;
  • Organic liquids (acetone, ether) can also be used to take surface water into solution as they wash the dentin, then evaporate.

Protective Measures During Restoration Placement:

(1) Bacterial microleakage –

  • Bacteria can grow beneath restorative materials and that either bacterial by-products or bacteria themselves can move through dentin to induce pulpal damage, inflammation, death.
  • For example, the species Prevotella intermedia and Prevotella melaninogenica are known to be able to produce lipopolysaccaride which may then diffuse through dentine causing a chronic inflammatory response in the pulp, possibly leading on to cell death.
  • Solution – All restorations must be well-sealing against micro- leakage.

(2) Placement of a lining –

If it is necessary to place a restorative material which does not develop a union with dentin, a primary barrier should be laid down first using a varnish, a lining or a base, such as glass-ionomer, which adheres fully to the tooth structure.

(3) Chemical toxicity –

  • All chemical substances are potentially toxic. Whether or not they kill cells depends upon the concentration of a substance in relation to a particular tissue.
  • Dentin is an excellent bufferà it limits diffusion of strongest acids, provided that there is a substantial barrier of sound dentin between the two. Numerous restorative materials can be placed with relative safety on intact dentin, even though they are sufficiently toxic to cause moderate (but reversible) pulpal damage if placed directly on exposed pulp tissue. Direct contact with pulp means the protective effect of dentin has been lost, and the concentration will then be too high in the pulp.
  • Dentin is not a universal barrier and some restorative materials release chemicals which can diffuse through and damage the pulp.
  • For example, moderate to severe pulpal inflammation may occur within days following placement of unfilled bonding resin against deeply etched dentine due to release and diffusion through dentin of toxic chemicals from resin.
  • Low viscosity resin luting cements, which are placed under considerable pressure during crown seating, can also bypass the protective barrier effect, particularly if tubules have been opened by acid etching.

Recovery –

  • Healthy pulp tissue is able to tolerate mild or moderate physical or chemical damage to the odontoblast layer as long as bacteria and their toxins are not present over a long period.
  • In the absence of bacteria, the death of a limited number of pulp cells will induce a transient, acute inflammation. New cells differentiate from the adjacent pulp to replace those which have died and the patient may only be aware of mild symptoms of pulpitis for a few days.

Pathways of Diffusion & Fluid Flow Through Dentin:

Permeability of dentin –

Dentin behaves as an impermeable solid traversed by water-filled tubules. Fluids can diffuse through dentin only via the tubules and motile bacteria can grow and move within the tubule fluid.

The term permeability includes all three types of potential movement, i.e. diffusion, fluid flow and bacterial passage through dentin.

The degree of dentine permeability is determined by

  • Tubule diameter – diameter decreases with age;
  • Density – less tubules (per square mm) at DEJ;
  • Length – proximity of cavity floor to pulp;
  • Presence or absence of Smear layer;
  • Coagulated protein or calcific deposits. e.g. secondary dentin;
  • Restorative materials. e.g. cements, resins or varnishes may modify permeability.

Modifying factors –

  • Permeability of cut dentin is substantially increased by a factor of 4-5 times.
  • Smear layer can be removed rapidly with strong acid etchants, such as phosphoric acid, and a little more slowly with weaker acids, such as EDTA or polyalkenoic acids.

Impact of smear layer removal:

  • Complete smear layer removal may increase bond strength of adhesive restorative materials to dentin;
  • Increases the potential for chemical diffusion from restorative materials through dentin to the pulp;
  • Encourages outward fluid flow through dentin à Prevent development of effective seal for the restorative material à Leads to ingress of bacteria or their by-products.
  • This means that the decision whether or not to remove smear layer involves an assessment of risk/benefit ratio.

Relative area of dentin occupied by tubules increases as the cavity floor approaches the pulp.

  • Number of tubules in coronal dentin is approx. 20,000/mm2 at DEJ à 1% of dentin area;
  • Number of tubules close to roof of pulp is 45,000/mm2 à 22% of dentin area.

Dentin permeability increases as remaining dentin thickness (RDT) decreases towards the pulp because:

  • Tubules are tapered and become larger in diameter;
  • They converge and become more densely packed;
  • They become shorter.
  • Dentin is quite dense at DEJ, but becomes markedly more permeable over the pulp horns, where tubule density is highest and dentin is thinnest.
  • It is also more permeable through axial walls of prepared cavities than beneath occlusal floor.

In Summary,

Factors controlling the potential for pulpal damage during preparation and restoration placement are –

1] Depth of cavity; 2] Location of walls and floor relative to pulp horns, and; 3] Surface condition of dentin

These factors influence the operators’ decisions concerning the need for pulp protection.


Risks to the Pulp from Plastic Restorative Materials:

Glass-ionomer cement (GIC)


o Initial low pH;

o Well buffered by dentin;

o Seals dentin tubules;

o Prevents microleakage.

·    Unreacted acid in freshly mixed cement – it is well buffered by hydroxyapatite of tooth following placement into a cavity.

·    Ion exchange union between GIC and underlying tooth structure leads to the development of an ion enriched layer at the interface which effectively seals the tubules against bacterial penetration

·    Any subsequent failure of the union will be cohesive in the cement rather than adhesive at the interface leaving a fine layer of the ion exchange material still attached to the tooth, sealing the tubules and preventing microleakage

Composite resin


o Releases chemical toxins;

o Adheres well to enamel;

o Short-term adhesion to dentin.

·    May release chemical toxins, particularly in the 1st few days after placement. TEGDMA, the small molecular weight diluent in composite resins can traverse through dentin, in biologically significant quantities, in the 1st days after placement.

·    HEMA has been shown to be toxic in tissue culture.

·    They do not reliably adhere to dentin à may be subject to continuing microleakage.


The degree of damage caused by these toxins will depend on:

®    Dentin permeability;

ü Dentin which has just been debrided of active caries is more permeable;

ü Thickness of remaining dentin is very significant;

ü Acid etching of dentin will reduce its buffering effect.

®    Cavity geometry.

ü  In an intra-coronal box-form cavity which is directly filled with a single increment of light-cured composite resin there is a strong likelihood that a gap will form at one or more cavity walls due to the setting contraction of the resin.


®    The polymerization contraction of light-cured composite resin is controlled by careful incremental packing and curing.

®    Dentin will modify the diffusion (by buffering action of hydroxyapatite) to the extent that the pulp response will be mitigated but there should be a degree of caution exercised (hence cavity depth is relevant).

®    In deep cavities, first place a base capable of sealing the dentin tubules. GIC is the most effective material because it develops an ion exchange adhesion which is proof against microleakage. Whole of the dentin should be covered à cement acts as a dentin substitute and protects against chemical toxicity and microleakage.

®    If the lesion is very deep and close to pulp, carry out an indirect pulp cap routine first à will lead to remineralisation of affected dentin. Removal of all affected dentine from the floor of an active caries lesion is strongly discouraged.

Dental amalgam


·    Low potential for chemical toxicity

·    Amalgam seals the interface between restoration and tooth structure through corrosion, which commences shortly after placement. There is a moderate marginal gap in the first weeks after placement, but this decreases due to the formation of corrosion products and to the calcification of surface pellicle and other organic materials.

·    If amalgam is used alone as a restorative material without a primary layer of resin, varnish, liner or base there may be pulpal inflammation in the days following placement due to early microleakage.

·    Copal varnish has been recognised for many years as providing an effective seal from microleakage in the short term and, as it washes out, the amalgam corrodes and develops its own organic seal. A low viscosity resin or a thinly mixed glass-ionomer is much more likely to be effective in maintaining an antibacterial seal over a longer term.

Luted Restorations When indirectly-fabricated rigid restorations (crowns, inlays) are cemented, the luting agent:

(1) may be a potential source of chemical toxicity and;

(2) will determine whether or not bacterial microleakage will occur.


·     Zinc phosphate, polycarboxylate, and glass-ionomer cements are commonly used luting agents. None of these will release chemicals in sufficient concentrations to harm pulpal cells, provided the dentin is intact and the smear layer has not been removed.

·     The liquid for each cement is a low pH acid, but the hydroxyapatite of intact dentin is capable of acting as an effective buffering agent.

·     Undue cleaning or etching of dentin immediately prior to cementation opens up the tubules and, under the high hydraulic pressure which may arise during cementation, may allow some penetration of the liquid through the tubules leading to pulpal irritation.

·     Possibility of eventual cement dissolution poses a long-term risk to pulp. Zinc oxide eugenol cements hydrolyse and convert to zinc-eugenolate and should not be regarded as long term cements. GIC will last much better and has advantage of ion exchange layer that will remain and continue sealing the tubules, even after loss of cement.

·     Teeth which require indirect restorations often have large caries lesions, failing and leaking existing restorations or mechanical trauma during preparation procedures. If there is a pre-existing chronic inflammation, the superimposition of further acute inflammation may precipitate pulp death.

·     Sometimes pulps which appeared to be healthy immediately prior to preparation phase become painful or die shortly thereafter. The cause is not always easy to determine.

Solution – If the smear layer is removed the tubules will be opened, and a low viscosity mix of cement may be forced through the tubules into the pulp space, thus by-passing the buffering effect. The result may then be post-insertion sensitivity.

ü  Rather than remove the smear layer it is better to seal the tubules with a dentin bonding agent, particularly one containing a polyalkenoic acid.

ü  This is best carried out immediately after preparation of the tooth and prior to taking the impression and making a temporary crown.

ü  As long as crown margins are well-adapted, cement dissolution will be slower. However one can expect pulp death to occur, in some cases, many years after the placement of indirectly restorations on vital teeth. The best defense is to protect dentin with an insoluble and impermeable intermediate layer.

Resin Cements ·       Resin cements, & resin modified GI luting cements contain HEMA à potential for toxicity or allergy.

·       Lightly-filled resin cements have very low solubility à durable at margins. However, they do not flow well à ultimate film thickness is greater than desirable.

·       Acid treatment of dentin before crown cementation à opens the tubules à increased chances of resin components being forced down tubules under the hydraulic pressures involved with cementation, thus damaging the pulp.