Scottish Dental

The first two articles in this series examined how dental materials should be handled prior to and during clinical placement to optimise clinical success. While this is obviously very important, failure to select an appropriate material for the situation will not yield the best clinical outcome. This article addresses the factors which the clinician should be mindful of during this decision making process.

Material selection determined by conservation of tooth tissue

Management of the disease

In modern dentistry there has been a huge change in emphasis with respect to how direct restorative materials are selected. A little over a hundred years ago, in the time of the so-called father of dentistry GV Black, the dentist had a choice of only two materials – namely dental amalgam or gold.
Cavities, therefore, had to be prepared to accommodate the properties of the material. This resulted in sound tooth tissue being needlessly sacrificed so rendering the tooth more prone to fracture and a higher incidence of pulpal death.
The modern philosophy is completely opposite to what it was at the turn of the 20th century. Conservation of tooth tissue is now the most important factor and this has been made possible due to the large increase in the number of materials which are now available. The disease should be manage, i.e. the caries removed, the cavity examined and THEN the appropriate material selected (Fig 1).
At this point, some further preparation may be required to optimise the cavity to conform to the properties of the chosen restorative material. Examples would be the removal of unsupported enamel which may fracture due to its friability or sharp internal line angles which would lead to stress concentrations and a plane for failure (Fig 2).

Influence of dental materials’ properties

It is important that the dentist has a working knowledge of the properties of the various materials which may be used for a given situation as these may have an influence on the selection of the chosen material.
For example, a cavity whose depth is less that 2mm is not indicated for dental amalgam. In this case, it is preferable for an alternative material to be selected such as gold alloy or resin composite so that tooth tissue may be conserved (Fig 3).

Material selection determined by clinical situation

Anatomy of the prepared cavity

There are certain prerequisites that may determine the best material for a given situation. For example, resin composite should only be used in cavities which have a complete circumferential enamel margin (Fig 4). This is because the bond gained between enamel and resin composite is the strongest and most durable.
For this reason, the American Dental Association recommends that another material should be selected if a complete enamel margin does not exist ¹.

Achievement of an optimal environment for placement

As discussed in the second article, most dental materials are inherently hydrophobic and require a dry environment when they are placed. The inability of the clinician to achieve excellent moisture control when manipulating and using these materials intra-orally will result in inferior results.
Any direct restorative materials containing resin are most susceptible. If the clinician is unable to achieve and maintain adequate moisture control then an alternative, more forgiving material should be considered.
This is also the case for inherently hydrophobic impression materials such as the silicones (Fig 5). In subgingival areas, adequate moisture control may be very difficult to achieve resulting in the margins of the preparation for a cast restoration not being captured accurately, so compromising the rest of the process.
Classically, this is manifested as a rolled edge in the impression (Fig 6). If the clinician cannot achieve excellent moisture control then they may be well advised to choose an alternative product such as a polyether which is more hydrophilic in nature (Fig 7).
Some materials react with moisture. For example, if a zinc containing dental amalgam alloy is contaminated with water, hydrogen gas is evolved which becomes incorporated into the material resulting in its expansion ². This may have detrimental effects such as extrusion of the material out of the cavity or fracture of the surrounding tooth tissue.

Selecting the appropriate material for mechanical reasons

On occasion, the clinician may be faced with a dilemma of removing more tooth tissue or choosing a material whose mechanical properties are superior. The choice between dental amalgam, gold alloy or resin composite in shallow cavities was discussed earlier. This is also the case for indirect restorations.
If insufficient interocclusal clearance is present, then the clinician may reduce the amount of occlusal reduction done to maintain preparation height and therefore retention for the cast. The use of a non-precious metal alloy in preference to a precious metal alloy will be more successful (Fig 8). Such alloys are stronger, harder and have a reduced ductility than precious metal alloys and may be used in sections of 0.5mm ². Some of the new zirconium based ceramics may now be used in such thin section as they have sufficiently good mechanical properties to be used in this situation.

Biological considerations

Many dental materials are bioactive (the ability to actively promote activity with the tissues) and need be to biocompatible i.e. the ability to support life and having no toxic or injurious effects on the tissues ². Inappropriate selection of materials which are cytotoxic will result in detrimental biological effects.
For example, resin modified glass ionomer cement and zinc oxide eugenol cement are contraindicated to be placed directly on pulpal tissue.
The taking and recording of a thorough and comprehensive medical history is an essential prerequisite prior to embarking on any treatment. Hypersensitivity reactions may occur where individuals can become sensitised to certain components in materials. The commonest allergens are methyl methacrylate and hydroxyethyl methacrylate (HEMA).
This latter chemical is cytotoxic and is a powerful dermatological sensitiser ^{2 3}. Patients and dental staff may become sensitised to this substance if it comes into contact with naked skin. Furthermore as surgical gloves are porous and this molecule small, it may permeate the material of the glove so accessing the skin ^{3 4} (Fig 9).
It is used widely in dentistry in such materials as resin composites, resin modified glass ionomers, compomers and bonding agents to name but a few. Dental staff should therefore be careful when handling these products to avoid hypersensitive reactions. This may be achieved by practising good resin hygiene and by using a no touch technique.

Intermaterial chemical incompatibility

Some materials may interact with each other chemically. There are a number of common examples:

• Zinc oxide eugenol and resin composite. The eugenol acts as a plasticiser (additives that increase the plasticity or fluidity of a material) with the resin resulting in incomplete setting of the composite which will result in inferior mechanical properties and so compromising clinical success (2).
• Self-etch bonding agents may not be used with dual or chemical cured resin composite as they are chemically incompatible. The acidic monomers required for the etching process react with the amine initiator that is needed for the chemical curing mechanism in self- or dual-curing systems (2).
• The catalyst used in silicone impression materials is poisoned by sulphur residues of which are found on latex gloves (2). If the putty presentation of these materials is to be mixed by hand then non latex gloves should be used (Fig 10).
• The astringent Racestyptine (Septodont) and polyether impression materials react chemically resulting in gas being evolved causing porosity in the cast die (2).

The clinician should be mindful of these and other examples and avoid potential chemical reactions when making material selection choices.

Practice management issues

Valid consent

It is important that the advantages and disadvantages of each material are discussed with the patient. This is so that they are involved in the decision and they can make an informed choice as to the care they wish to receive. Sometimes the patient may request the use of a specific type of material at the outset, such as resin composite.
If, at the end of the cavity preparation phase, the clinician feels that the preferred material is not the most appropriate material in the situation then this must be communicated to the patient and the situation discussed. This will involve why this is the case and what the consequences would be if it were to be used.
Furthermore, alternatives should be explained together with their advantages and disadvantages. If there is a deviation from the original agreed treatment plan then an updated one should be issued with it being signed by the patient to confirm their acceptance. At the end of this process, the clinician is safe from a medico-legal perspective with valid consent having been obtained.

Appointment length estimation

Different techniques may result in more time being required to complete the procedure. For example, it has been reported that a posterior resin composite restoration takes three times as long to do as the commensurate amalgam restoration. It is more difficult for the dentist to allocate the correct time to the procedure if there is some uncertainty as to what the final procedure will be.
As mentioned above, a change of material may have increased cost implications as more time may be required to place the restoration.

Surgery set up procedure

The new approach of choosing the dental material to fit the clinical situation is clearly unhelpful for the dental nurse who would prefer to assemble all of the equipment and materials required for the procedure at the beginning of the appointment to facilitate its efficient execution.
They may be well advised to wait until the final decision has been made as to the material selection before getting the chosen materials out of cupboards and drawers.

Conclusions

Each and every dental material has advantages and disadvantages. It is the responsibility of the clinician to carefully consider these together with the intended clinical objectives. Only then can they come to a balanced decision as to the best material to use in the situation which must be underpinned with a thorough knowledge and understanding of all of the materials which are available and their properties. There are so many options that dental material selection is far from Hobson’s choice!

About the author

Steve Bonsor graduated from the University of Edinburgh in 1992 and in 2008 gained an MSc in Postgraduate Dental Studies from the University of Bristol. From 1997 until 2006, Steve was a part-time clinical teacher at Dundee Dental Hospital and School and honorary clinical teacher at the University of Dundee in the sections of operative dentistry, fixed prosthodontics, endodontology and integrated oral care. He currently holds appointments at the University of Edinburgh, as an online tutor on the MSc in Primary Dental Care programme, and at the University of Aberdeen as honorary clinical senior lecturer leading the applied dental materials teaching at Aberdeen Dental School. As well as lecturing throughout the UK, Steve is actively involved in research, having published original research articles in peer-reviewed journals. His main research areas are photo-activated disinfection and the clinical performanceof dental materials.

References

1. Statement on posterior resin-based composites. ADA Council on Scientific Affairs; ADA Council on Dental Benefit Programs. J Am Dent Assoc 1998;129(11):1627-1628.#
2. Bonsor SJ, Pearson GJ. A Clinical Guide to Applied Dental Materials. 1st ed. Edinburgh: Churchill Livingstone Elsevier; 2013.
3. Andreasson H, Boman A, Johnsson S, Karlsson S, Barregard L. On permeability of methyl methacrylate, 2-hydroxyethyl methacrylate and triethyleneglycol dimethacrylate through protective gloves in dentistry. Eur J Oral Sci 2003;111(6):529-535.
4. Tinsley D, Chadwick RG. The permeability of dental gloves following exposure to certain dental materials. J Dent 1997;25(1):65-70.

The early detection of oral cancer has now become a recommended topic by the General Dental Council (GDC) for Continuing Professional Development (CPD).

The importance of raising our suspicions for any lesion was brought home to me as I was writing this paper. The brother of a medical friend had just been diagnosed with mouth cancer at the age of 54. No obvious risk factors were present and yet, despite going to his GP with a persistent ulcer, it was more than two months until he was referred.

My doctor friend called me for advice regarding her brother on the day I received feedback on a lecture I’d given to some medical students doing their cancer prevention module. Despite presaging my lecture with the reasons why medics needed to be as genned up on this as the dentists, one student still felt it was more important for dentists than themselves (presumably a reflection on the numerous other topics competing for their attention within the medical curriculum).

The GDC based their recommendation in part due to an increasing number of patients who are claiming (rightly or wrongly) that their dentist failed to diagnose their mouth cancer and, as such, are suing them for negligence. Other reasons include an increasing number of cancer cases (hence increased likelihood of seeing a patient with oral cancer,) and the life-threatening nature of this disease (the later it is diagnosed, the worse the outcome for the patient).

It used to be an anecdote that a dentist might only see two cases of oral cancer in their entire career. But was or is that actually true? There may be a need to recalculate this because, although there are many more dentists now than, say 30 years ago, the incidence of oral cancer has risen sharply (threefold) over that time period without a marked increase in size of population. We recently recalculated this and arrived at a conservative estimate of one case every 10 years, with two potentially malignant lesions seen every month.1

What can we do to help minimise such an event?

• Reasons why a patient may pursue a case of negligence against a dentist in respect of oral cancer are:
• Failure to identify a lesion in the mouth
• A failure to consider the lesion might be a cancer and thus miss the opportunity to make an early diagnosis
• Failure to refer to a specialist
• Claims for damages following the consequences of a failure to detect the cancer at an early stage
• A perception by the patient that the dentist had not taken their concerns seriously.

Key questions to consider when assessing the malignant potential of an oral lesion:

1. What risk factors are present?

Tobacco

While the number of cigarettes consumed within the UK has dropped profoundly over the last 25 years or so (from a staggering 102 billion in 1990), the reduction in the number of smokers has not been as dramatic. Approximately 20 per cent of the population in Scotland still smoke. Although novel approaches to certain groups have had some success (e.g. “Give it up for baby” – a smoking cessation intervention for pregnant women in Scotland, organised by Paul Ballard and NHS Tayside) – there is still a long way to go.

Clinicians should be actively involved in raising awareness of the potential detrimental effects of smoking on oral health and giving smoking cessation advice. A key question to ask the patient with a clinically suspicious lesion is “Do you smoke?”

At least 75 per cent of oral cancers are associated with tobacco use.

With the increase in cost, many people are turning to hand-rolled cigarettes because they are cheaper but they may lack an effective filter. Key additional questions include recording type of tobacco use, number of years they have smoked and daily quantity consumed.

Don’t forget ecigarettes, although in theory devoid of the usual carcinogens found in tobacco, are still unregulated and hence their exact content is not always known. More than three million ecigarettes were sold in the UK in 2012. However, many patients find Allen Carr’s book Easy Way to Stop Smoking an effective alternative to other techniques such as nicotine replacement therapy.

Alcohol

As with tobacco, it is worth asking about their use of alcohol, as this is an important risk factor for oral cancer, particularly when combined with tobacco use. The Government, and indeed all the Royal Colleges, support the guidance as regard low-risk drinking. For men this is currently considered as no more than four units in a day or 21 units in a week (for women it is no more than three units in a day and 14 units in a week) with at least two days free of alcohol.

Obtaining a reliable alcohol history isn’t always easy, partly because many patients don’t know the alcohol unit content of what they drink, but also because we are often economical with the truth. Studies have shown that in the UK there is a 40 per cent underestimation of what people claim they drink, when compared with actual alcohol sales.

We have gathered data regarding drinking habits and understanding of alcohol guidelines over several years during our annual Mouth Cancer Awareness Week campaigns at the University of Dundee. There is a tendency for students to underestimate the number of units of alcohol in a pint of beer. When this is combined with the frequency that they admit to binge drinking (defined as at least six units in any one session for women, and at least eight units for men), then many students would appear to be drinking at a level that would trigger a brief alcohol intervention.

The development of an appropriate intervention for dental practice is currently being explored2.

Human Papilloma Virus (HPV)

The subtypes ( associated with both cervical cancer and oral cancer) are HPV 16 and HPV 18. It is more often associated with oropharyngeal cancer than oral cancer. The virus interferes with the tumour suppressor gene, P53 that protects us against cancer .The HPV virus disables the protective effect of the P53 gene allowing those mutations which retain the cell’s ability to replicate, to further develop on its journey to potentially becoming a cancer. Infection with HPV can be transitory , with HPV 16 and HPV 18 acquired through oro-genital contact. Perhaps not the easiest question to ask of a patient visiting their dentist! Jaime Winstone’s BBC3 programme “Is oral sex safe?” is well worth viewing.

Don’t forget that a patient doesn’t have to have an obvious risk factor.

2. What is its colour? (‘Red is a mean mean colour’)

While I’m sure Steve Harley didn’t have oral cancer in mind when he wrote that song, it seems peculiarly apposite. Red is a far more significant colour when it comes to early manifestation of oral cancer, yet leukoplakia is often considered the most frequent precancerous lesion. By focusing on the white element, the issue of any surrounding erythema may be lost. Although much is made of the white patch its malignant transformation rate is probably less than five per cent whereas that of the erythroplakia is at least 80 per cent (far more significant).

Having said that, the most significant leukoplakia’s are those that are large and non-homogenous. Far more important and more frequently associated with asymptomatic early oral cancer are the so-called speckled leukoplakia’s (erythroleukoplakia).

3. What does the early oral cancer look like?

The early asymptomatic cancer presents in a far more subtle way than many of the textbooks might suggest. The identification of an oral cancer that has raised, rolled hard edges surrounding an area of ulceration that is oozing blood is an advanced lesion that hopefully no one would miss. Unfortunately, by the time is has that appearance, such an advanced lesion has had plenty of opportunity to either invade surrounding tissues (such as bone) or metastasise to local, regional or distant lymph nodes.

Our attention as clinicians should be to focus on raising our index of suspicion. High-risk sites in the UK are the so-called non-keratinising sites such as ventral tongue and floor of mouth. However, the routine screening and recording in the notes of the entire oral mucosa should be mandatory, not only to help to detect an early lesion, but also to help protect yourself from any claims of negligence that you failed to detect the cancer at an early stage. Such a task that takes minimal time, requires no fancy expensive equipment, but yet could make such a difference to the patient’s prognosis (if a cancer is there), is ignored at our peril. (The use of dyes or techniques based upon fluorescence or cytology are still being evaluated or have not proved to have the sensitivity or specificity to become adopted as routine tests).

Conclusion

The early detection of an oral cancer can quite literally save that patient’s life. In helping to raise your index of suspicion when assessing the malignant potential of an oral lesion we should consider:

• What risk factors are present? (NB tobacco and alcohol, HPV?)
• What is its colour? (NB importance of red)
• How long has it been present? (Review the patient to ensure it has improved/resolved within two weeks or arrange urgent referral when cancer is suspected)
• Is it painful? (Pain is often a relatively late manifestation hence a non-painful ulcer should arouse suspicion)

Remember, the early lesion is often asymptomatic (no pain, no ulceration, no bleeding). Remember too that a patient is never too young to get oral cancer. One in 10 cases now arise in those below the age of 45 years (see the Ben Walton Trust www.benwaltontrust.org).

About the author

Professor Graham R Ogden, is professor of oral surgery and honorary consultant in oral surgery within the Division of Oral and Maxillofacial Clinical Sciences at the University of Dundee Dental Hospital and School.

References

Aspects of this paper were included in the recently published paper, Ogden G Oral cancer: what do we need to know and do? Dental Nursing 2015 11(5) 275–278.

1. G. R. Ogden, C. Scully, S. Warnakulasuriya & P. Speight Oral cancer: Two cancer cases in a career? British Dental Journal 218, 439 (2015) Published online: 24 April 2015 | doi:10.1038/sj.bdj.2015.302
2. Shepherd S, et al Current practices and intention to provide alcohol related health advice in primary dental care British Dental Journal 211:322-3 2011 doi:10.1038/sj.bdj.2011.822

By word of mouth

For those who wish to get involved in raising awareness of oral cancer, for example during Mouth Cancer Awareness Week in November each year, then see the link to “You too can raise awareness of mouth cancer” at http://bit.ly/BWTpdf

The Ben Walton Trust has done much to raise both professional as well as public recognition of the disease. There is also another Scottish-based charity – https://letstalkaboutmouthcancer.wordpress.com – which aims to achieve greater recognition of the disease within the general population.

While we should all maintain our suspicions regarding any lesion within the oral cavity, we can do nothing about the patient that presents to their GP in preference to their GDP. Or can we?

I would suggest that we, as dentists, need to explain to our patients every time they attend that we are screening their mouth for any suspicious changes that they may not even be aware of; that we are trained to examine the whole mouth, not just the teeth and gums.

Establishing links with local GPs should benefit both clinicians and patients. The days when colleagues felt referral for a second opinion implied they were not capable have surely gone. But, to do that, we first have to see the lesion, i.e. examine the whole mouth and then consider that it might be an early cancer. It is for this reason that it is entirely right that oral cancer has become a recommended topic for CPD by the GDC and serves as a reminder that every time a patient attends, there must be a careful clinical examination of the entire oral mucosa.

Where cancer is suspected, the patient should be urgently referred to be seen within two weeks. Furthermore, with an increase in oropharyngeal lesions that may spread to cervical lymph nodes, it is more important than ever that dentists should carefully check for swellings in the neck. This may be particularly important in irregular attenders, as that may be the one chance for early detection, which could quite literally save that person’s life.

Change, socioeconomics and indeed New York are relevant to this update on oral cancer risk. How we define oral cancer is changing. This is important not only for how the disease is managed and its prognosis but also in terms of the changing risk profile and factors associated with oral cancer, which in turn is essential for prevention. Oral cancer is increasingly falling into two distinct diseases: oral cavity cancer (OCC) – “mouth cancer” and oropharyngeal cancer (OPP) – “throat cancer”. Although the tumours do not always recognise such clear-cut boundaries and more often overlap the anatomical sites (particularly in the retromolar trigone – behind the wisdom teeth).

While oral cavity cancer rates are either stable or only marginally increasing, oropharyngeal cancer is the most rapidly increasing cancer in Scotland – with a threefold increase in incidence among men in the last decade, and a 2.5-fold increase among women. Oropharyngeal cancer increases are now greater than malignant melanoma, adeonocarcinoma of the oesophagus and cervical cancer ¹. In 2013 there were 494 cases of oral cavity cancer and 343 cases of oropharyngeal cancer diagnosed in Scotland ². This changing trend of flat-lining oral cavity cancer and increasing in oropharyngeal cancer is a global phenomenon and has been related to changing population risk factors – described as “controlling a tobacco epidemic while a human papillomavirus epidemic emerges” ³.

Risk

When we talk about risk we are talking about probability – the chance that an event/the disease/oral cancer diagnosis will occur. Patients and the public may view risk as completely random chance – the flip of a coin, 50/50, one in two, 50 per cent chance, it will either happen to me or it won’t.

However, risk estimates for cancer can be determined by undertaking studies on large groups of people, which identify the probability that an individual or group will develop the disease over a period of time. These studies also identify risk factors – characteristics or behaviours that are associated with increased risk. We generally define risk in two ways: absolute risk and relative risk.

Absolute risk

This is the numeric chance or probability of developing oral cancer during a specified period of time. The Scottish Cancer Registry computes this over a whole lifetime. The absolute risk of developing oral cavity cancer in Scotland in a lifetime is estimated at 1.7 per cent, or to put it another way – about 1 in 59 persons will develop oral cavity cancer at some time in their lives. For comparison, about one in 12 persons in Scotland will develop lung cancer in their whole lives, while about one in 2.5 persons will develop any type of cancer. These lifetime risks have a lot to do with other factors such as gender and age. A man’s lifetime risk of developing oral cavity cancer in Scotland is higher – 2.4 per cent, or about one in 42 men – but his risk of developing oral cavity cancer (at a younger age) by the age of 64 is 0.7 per cent, or about one in 135 men ².

Relative risk

This is a comparison or ratio rather than an absolute value. It provides an estimate of the relationship between a risk factor and outcome by comparing the number of cases in a group of people with a particular trait or behaviour with the number of cases in a (otherwise similar) group of people who don’t have that trait or behaviour. The risk of oral cavity cancer for people who smoke has been estimated at around 5.8 times higher than for those who don’t smoke – the relative risk is 5.8. Relative risk is also presented as a percentage. In the same example the risk of oral cavity cancer is 580 per cent higher than in those who don’t smoke ⁴.This percentage over 100 per cent and lack of an upper limit in relative risk estimates is counter-intuitive. Most people would think 100 per cent is the highest possible risk. But 100 per cent equates to a doubling of risk associated with a risk factor, while 200 per cent to a tripling of risk estimate.

Population attributable risk

This is another way of expressing relative risk at the population level. It is the difference in the rate of disease between a population exposed to a risk factor and a population not exposed to the risk factor. It is more commonly used in public health policy decisions, where the burden of the disease reduction can be calculated by “hypothetically” removing the risk factor in question.

INHANCE

The most comprehensive and up-to-date data on oral cancer risk can be found from research by the INHANCE (International Head And Neck Cancer Epidemiology) Consortium (www.inhance.utah.edu). It was established in 2004 as a collaboration of researchers from around the world-leading large epidemiology studies of head and neck cancer to improve the understanding of the causes, risks and mechanisms of head and neck cancer.

The consortium includes data on 25,500 patients with head and neck cancer (including oral cavity cancer, oropharyngeal cancer, and larynx cancers), and 37,100 controls who did not have these cancers, from 35 studies from across the world. Overview papers have been published which detail INHANCE methods ⁵ and research findings ₆.

It was a privilege to be invited to participate in the 12th Annual INHANCE consortium meeting in May this year. We convened at the Icahn School of Medicine at Mount Sinai New York City, on the weekend the new Freedom Tower was opened. During our meeting, we reflected on over 10 years of INHANCE research, while at the same time looking forward to taking on the ongoing challenges of the increasing and changing burden of head and neck cancer.

Oral Cancer Risk

It is well recognised that smoking tobacco and heavy alcohol consumption are the main risk factors for oral cancer. INHANCE provides us with an opportunity to understand this risk better, including providing precise estimates of risk, understanding the joint tobacco-alcohol effects and the dose-response, as well as investigating the risk associated with smokeless tobacco and the benefits of quitting both smoking and alcohol.

INHANCE provides sufficient numbers of people who never smoked or drank alcohol – thereby avoiding the problems of confounding – to identify true and precise risk estimates. Among “never” alcohol drinkers, cigarette smoking was associated with a two-fold increased risk of oral cavity and oropharnx cancers ⁷. And heavy alcohol drinking (three or more drinks per day vs never drinkers) among those who never used tobacco was also linked to increased risk but only among heavy alcohol consumers. However, it should be noted that those who reported never smoking and never drinking alcohol may differ in other ways from the wider population. The complexity of the relationship with smoking and alcohol was also unpicked in the estimates of the population attributable risk (PAR) for tobacco and alcohol of 64 per cent, made up of 0 per cent for alcohol alone, 24 per cent for tobacco alone, and 40 per cent for tobacco and alcohol combined ⁸ – but remember this risk description is mainly relevant at the population rather than individual risk level.

In terms of the dose-response relationship, risk for oral cancer increases with increased frequency and duration of both smoking and alcohol. However, fewer cigarettes per day over a longer period of time was worse (gave a greater risk for oral cancer) than more cigarettes per day over a shorter period of time. This contrasts with alcohol consumption which found that higher intake over a shorter period of time was worse (gave a higher risk for oral cancer) than a lower intake for a longer time ⁹. Moreover, there are no safe low-intake levels associated with negligible risk – so, the old sayings: “everything in moderation including moderation itself” or “a wee bit of what you fancy does you good” unfortunately do not hold up here.

Smokeless tobacco in the form of snuff (powdered tobacco) and tobacco chewing are not safe harm reduction alternatives some might want you to believe, with both associated with slight increased risk for oral cavity cancer. But good news does exist in the form of the benefits of quitting – with benefits appearing immediately (one to four years) after stopping smoking, and equating with those who never smoked after 20 years of quitting. The risk effects associated with heavy alcohol consumption last a bit longer with benefits of quitting taking 20 years to emerge ¹⁰.

The promise of the breakthrough in identifying genetic variants as strong markers of increased oral cancer risk has yet to fully materialise. Considerable research effort has found slight increased risks for oral cancer associated with the presence of genetic variants involved with alcohol metabolism, DNA repair pathways, and genes involved in the metabolism of nicotine ⁶. Similarly, there is limited evidence of dietary risk factors for oral cancer beyond confirming the protective effects associated with diets high in fresh fruit and vegetables (with approximately five or more fresh fruit and vegetable portions per day conferring a 50 per cent lower risk than those consuming low levels ¹¹.

The INHANCE work which our team in Glasgow have led on is in relation to socioeconomic inequalities and determinants of oral cancer risk ¹². You can see from the reference list with 75 co-authors the extent of the international collaborative effort involved. In our analysis we identified increased risks for oral cancer associated with low education and income relative to those in higher socioeconomic positions which were not explained by smoking or alcohol consumption, i.e. there were socioeconomic effects operating in two ways both in influencing risk behaviours (the causes of the causes) and also more direct or explained effects from low socioeconomic circumstances to oral cancer risk. Moreover these socioeconomic effects are of a similar magnitude (twofold increase) to risks associated with smoking and alcohol, and are strongest in countries where income inequalities are widest.

Finally, no discussion about oral cancer, and certainly not oropharyngeal cancer, can be complete without talking about sex and oral HPV (human papillomavirus) infection. Oral HPV is mainly associated with oropharyngeal cancer risk, with up to 80 per cent of cases having HPV identified. There are over 200 HPV types, but as for cervical cancer, HPV16 and 18 subtypes are the main high-risk oncogenic types. Increased risk for oropharyngeal cancer has been estimated as high as 15 times greater in those with oral HPV16 infection in the ground breaking New England Journal of Medicine paper ¹³. However, the natural history of oral HPV infection is not well understood (in terms of prevalence, persistence, and determinants). The only large epidemiological study of oral HPV prevalence has been undertaken in US ¹⁴. They found a prevalence of 7 per cent, with slightly greater peaks (around 10 per cent) among 25-30 and 50-55-year-olds, and among men. Risk factors identified included smoking and alcohol, number of sexual partners/oral sex partners, but also open mouth kissing. We are currently completing a feasibility study to undertake a similar study in dental practices in Scotland – HOPSCOTCH (HPV Oral Prevalence in Scotland) study ( http://www.sohrc.org/projects/hopscotch/ ). We are grateful for the outstanding support that we have received from dental practices and teams across Scotland in stepping up to this important research area, and we look forward to disseminating our feasibility study findings and taking forward a full population study in dental practices in due course.

INHANCE studies also point to a slight increased risk for oral cancer associated with six or more lifetime sexual partners, four or more lifetime oral sex partners, and early age (≤18) of sexual debut ¹⁵. However, it is worth noting again that this research and our understanding is at a far earlier stage, perhaps several decades behind our knowledge of the role of HPV in cervical cancer.

Communicating risks for oral cancer is not straightforward. I had a go at trying to explain the oral cancer risks associated with alcohol drinking on the BBC Radio 4 statistics programme More or Less [ http://www.bbc.co.uk/programmes/b03qfzgx ]. I am not convinced I helped communicate this complex risk issue particularly well. This reflection is not helped by my students who let me know I sounded drunk on the interview!

Communicating risk

This is a key challenge for clinicians and public health practitioners. Effective risk communication can stimulate health behaviour/belief change and reduce risk levels ¹⁶. One of the major barriers to communicating risk effectively is the difficulty both patients and clinicians have in understanding statistics and numbers, e.g. even among highly educated adults in a US survey only 21 per cent correctly identified that one in 1,000 was the same as 0.1 per cent ¹⁷.

Communicating risk more generally, in relation to treatment options and associated risks, has similar and perhaps even greater complexity for clinicians and patients, and is beyond the scope of this article.

INHANCE researchers are currently developing and validating a risk-prediction model that could be used to identify those at highest risk of oral cavity and oropharyngeal cancer which could potentially guide opportunistic screening, and risk factor counselling interventions. Such personalised risk information can be presented to individuals based on their characteristics and behaviours and can improve decision making in relation to screening ¹⁸. Such risk tools already exist for presenting breast cancer risk [ http://www.cancer.gov/bcrisktool/ ] and are widely available for cardiovascular risk [ http://www.qrisk.org/ ]. The major risk factors identified (above) and going forward in this model for oral cancer risk profiling are smoking, alcohol, and socioeconomic status, alongside age and gender determinants.

Prevention strategies

To paraphrase Johannes Clemmesen (the founder of the Danish Cancer Registry), the purpose of all cancer epidemiology studies is to prevent it.

Understanding risk is the key first step in the pathway to prevention. Prevention approaches therefore depend on whether the cancer is HPV-driven or non-HPV driven.

The primary prevention for HPV-driven oral cancer is likely to be via the HPV vaccination. There is one proof of principle study which demonstrates that the HPV vaccine (designed for cervical cancer prevention) prevents oral HPV infection. However, more evidence is needed to fully inform policy in relation to extending the vaccination to males. Although the case could be (and has been in other countries) argued on equity grounds, where men who have sex with men or men who have sex with women outside of the vaccinated population will not benefit from the hypothetical and assumed “herd immunity” to the population now that girls have been widely vaccinated (~90 per cent of 12 year olds from 2008 in Scotland). In addition to HPV vaccination, in theory HPV-driven oral cancer could be prevented via behavioural modification/safer sexual practices (i.e. condom use or dental (rubber) dam use for oral sex – for more information see http://www.nhs.uk/chq/Pages/970.aspx ).

Secondary prevention – whereby we interrupt disease progression via early detection (i.e. “screening”) and early treatment – does have potential to prevent oral cancer. It will remain necessary for oropharyngeal cancer for decades to come (even with the prevention prospects of the HPV vaccine) as there will be a substantial unvaccinated cohort who will suffer the future oropharyngeal cancers. Unfortunately, there is no validated “screening” method for oropharyngeal cancer (although HPV16 E6 antibody serology blood test could be promising). Problems and research evidence gaps remain in relation to oropharyngeal cancer screening include: there is no identifiable precancerous lesion (like the Pap smear detected cervical intraepithelial neoplasm (CIN)), uncertainty about effectiveness of early intervention and treatment, and demonstrable reductions in cancer mortality.

The same difficulties for direct visual inspection of the oropharynx do not exist for comprehensive visual inspection of the oral cavity, and there is some limited evidence of effectiveness and cost-effectiveness of opportunistic screening ^19 20. Research questions remain (and we have three PhD students working on some of them) including: what constitutes best practice for oral examination/screening? Can risk assessment and profiling assist in focusing on groups or on recall interval? Given low volume of disease is early detection a realistic proposition? Are there inequalities in access and uptake of the opportunity to screening? And what are the barriers and facilitators to delivering screening?

Non-HPV driven (oral cavity cancer) prevention in or via dental practice is important. Again we have research in our group ongoing in this area. The principles of prevention for oral cancer should reflect the evidence from our understanding of risk. These principles include: i) age is not an issue in terms of risk factors – work led by Tatiana Macfarlane, Aberdeen Dental School has shown that even among young adults with oral cancer the same risk factors smoking and alcohol dominate ²¹; ii) risk can reduce when behaviours stop; iii) oral health assessment is an important first step in any prevention intervention (we must ask the questions); iv) signposting and/or referring for more intensive preventive intervention services; and v) the role of tailoring advice and support to individual patients needs – recognising the dominant role of socioeconomic circumstances.

Public health and policy response needs to focus on the upstream structural causes of the causes; on what has been defined as the “common risk factor” approach ²² (Sheiham and Watt 2000) – risk factors for oral cancer overlap with periodontal disease, with other cancers, with cardiovascular disease and so on…; and on multiple risk factors – our research has shown that risk factors do not exist in isolation – they cluster: people who smoke also drink heavily and have poor diets, this clustering is even more socioeconomically determined ²³. Policy developments also need to extend to the increasing preventive focus and wider healthcare role of dental practitioners and teams.

And as the times they are a changin’ – we would do well as a profession to more proactively contribute to the political and policy discourse; to advocate for societal change for tackling health inequalities; to prioritise research and development to tackle the burden of oral cancer – a burden on health services and society, but an even greater burden of suffering on communities, families, and patients.

About the Author

David Conway, Clinical Senior Lecturer /Honorary Consultant in Dental Public Health, Community Oral Health Group. University of Glasgow Dental School / NHS National Services Scotland. Tel. 0141 211 9750

Email. david.conway@glasgow.ac.uk

Twitter. @davidiconway

References

1. Junor EJ et al (2010) Oropharyngeal cancer. Fastest increasing cancer in Scotland, especially in men. BMJ 340:c2512.
2. Scottish Cancer Registry (2015) Cancer Statistics. NHS National Services Scotland. Information Services Division. http://www.isdscotland.org/Health-Topics/Cancer/Cancer-Statistics/
3. Hashibe M, Sturgis EM (2013) Epidemiology of oral-cavity and oropharyngeal carcinomas: controlling a tobacco epidemic while a human papilloma virus epidemic emerges. Otolaryngol Clin North Am 46(4):507-20.
4. Lee YC, et al. (2009) Active and involuntary tobacco smoking and upper aerodigestive tract cancer risks in a multicenter case-control study. Cancer Epidemiol Biomarkers Prev 12: 3353-61.
5. Conway DI, et al. (2009) Enhancing epidemiologic research on head and neck cancer: INHANCE – The INternational Head And Neck Cancer Epidemiology consortium. Oral Oncol 45(9):743-6.
6. Winn DM, et al. (2015) The INHANCE consortium: Towards a better understanding of the causes and mechanisms of head and neck cancer. Oral Dis doi: 10.1111/odi.12342
7. Hashibe M, et al. (2007) Alcohol drinking in never users of tobacco, cigarette smoking in never drinkers, and the risk of head and neck cancer: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. J Natl Cancer Inst 99(10): 777-89.
8. Hashibe M, et al. (2009) Interaction between tobacco and alcohol use and the risk of head and neck cancer: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. Cancer Epidemiol Biomarkers Prev 18(2):541-50.
9. Lubin JH, et al. (2009) Total exposure and exposure rate effects for alcohol and smoking and risk of head and neck cancer: a pooled analysis of case-control studies. Am J Epidemiol 170(8):937-47.
10. Marron M, et al. (2010) Cessation of alcohol drinking, tobacco smoking and the reversal of head and neck cancer risk. Int J Epidemiol 39(1):182-96.
11. Chuang SC, et al. (2012) Diet and the risk of head and neck cancer: a pooled analysis in the INHANCE consortium. Cancer Causes Control 23(1):69-88
12. Conway DI, Brenner DR, McMahon AD, Macpherson LM, Agudo A, Ahrens W, Bosetti C, Brenner H, Castellsague X, Chen C, Curado MP, Curioni OA, Dal Maso L, Daudt AW, de Gois Filho JF, D’Souza G, Edefonti V, Fabianova E, Fernandez L, Franceschi S, Gillison M, Hayes RB, Healy CM, Herrero R, Holcatova I, Jayaprakash V, Kelsey K, Kjaerheim K, Koifman S, La Vecchia C, Lagiou P, Lazarus P, Levi F, Lissowska J, Luce D, Macfarlane TV, Mates D, Matos E, McClean M, Menezes AM, Menvielle G, Merletti F, Morgenstern H, Moysich K, Müller H, Muscat J, Olshan AF, Purdue MP, Ramroth H, Richiardi L, Rudnai P, Schantz S, Schwartz SM, Shangina O, Simonato L, Smith E, Stucker I, Sturgis EM, Szeszenia-Dabrowska N, Talamini R, Thomson P, Vaughan TL, Wei Q, Winn DM, Wunsch-Filho V, Yu GP, Zhang ZF, Zheng T, Znaor A, Boffetta P, Chuang SC, Ghodrat M, Amy Lee YC, Hashibe M, Brennan P (2015). Estimating and explaining the effect of education and income on head and neck cancer risk: INHANCE consortium pooled analysis of 31 case-control studies from 27 countries. Int J Cancer 136(5):1125-39.
13. D’Souza G, et al. (2007) Case-control study of human papillomavirus and oropharyngeal cancer. N Engl J Med 356(19):1944-56
14. Gillison ML, et al. (2012) Prevalence of oral HPV infection in the United States, 2009-2010. JAMA 307(7):693-703.
15. Heck JE, et al. (2010) Sexual behaviours and the risk of head and neck cancers: a pooled analysis in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Int J Epidemiol 39(1):166-81.
16. Ahmed H, et al. (2012) Communicating risk. BMJ 344.
17. Gigerenzer G (2002) Reckoning with risk – learning to live with uncertainty. 1st ed. Penguin Press. London.
18. Edwards AG, et al. (2006) Personalised risk communication for informed decision making about taking screening tests. Cochrane Database Syst Rev 4:CD001865.
19. SIGN (2006) Diagnosis and management of head and neck cancer. NHS Quality Improvement Scotland.

20 Speight PM et al. (2006) The cost-effectiveness of screening for oral cancer in primary care. Health Technol Assess 10(14):1-144, iii-iv. Review.

21. Macfarlane TV, et al (2010) The aetiology of upper aerodigestive tract cancers among young adults in Europe: the ARCAGE study. Cancer Causes Control;21(12):2213-21.
22. Sheiham A, Watt RG(2000) The common risk factor approach: a rational basis for promoting oral health. Community Dent Oral Epidemiol 28: 399-406
23. Lawder R, Harding O, Stockton D, Fischbacher C, Brewster DH, Chalmers J, Finlayson A, Conway DI. BMC Public Health. 2010 Jun 11;10:330.

The first part of this article described how to arrive at a pulpal diagnosis of a clinically healthy or diseased pulp. Part two will describe the up-to-date terminologies for periradicular health and disease and the clinical findings usually associated with each of these diagnoses.

How to identify clinically normal periradicular tissues

Clinically ‘normal’ periradicular tissues are those which have no swellings or sinuses visible or palpable, the tissues are not tender to palpation and the tooth is not tender to percussion.Radiographically, the periodontal ligament space is uniform around the root and the lamina dura intact.

Teeth with normal and reversibly inflamed pulps would be expected to exhibit ‘normal’ periradicular tissues.

Some teeth with symptoms of symptomatic irreversible pulpitis can be difficult to localise because in the early stages, the periradicular tissues are often not yet affected. At this point, the tooth will not be tender to percussion or palpation and no swelling or sinuses will be present. Conventional radiographs are frequently insufficiently sensitive to show the initial periradicular changes which can hamper localisation and diagnosis of the source of the pain. Thus, teeth diagnosed with symptomatic and asymptomatic irreversible pulpitis will often appear to have normal periradicular tissues radiographically until pulpal necrosis ensues.

Previously initiated and previously treated teeth may also exhibit normal periradicular tissues if treatment hasbeen successful.

What are the clinical signs and symptoms of symptomatic periradicular periodontitis?

Teeth exhibiting signs and symptoms of symptomatic periradicular periodontitis are most likely to have a pulpal diagnosis of pulpal necrosis; previously initiated endodontics or previous endodontic treatment. Table 1 reviews the range of clinical findings which can be associated with this diagnosis.

When the pulpal diagnosis associated is ‘pulpal necrosis’, the periradicular changes are caused by microbes gaining access to the root canal system mainly through cracks, caries, dentinal tubules and micro-leakage. This results in an inflammatory reaction in the periradicular tissues because of the egress of toxins through the apical foramina. The source of these toxins is the polymicrobial infection within the root canal system.

Where the pulpal diagnosis associated is ‘previously treated’ (i.e. a failed previous non-surgical or surgical endodontic treatment), the cause of the periradicular disease in the majority of cases is persistent or new (secondary) microbial infection of the root canal system. For example, where a dental/rubber dam is not used for isolation of the tooth during a root canal treatment, it is extremely likely that microbes will persist within the root canal system throughout and following treatment.

In a case where a previously successful root canal treatment (i.e. no clinical signs or symptoms of pathosis and no periradicular radiolucency is seen associated with the tooth radiographically) manifests with clinical and/or radiographic signs and/or symptoms of treatment failure, the most likely explanation is that either previously surviving microbes have now flourished within the root canal system to a pathogenic level or that new microbes have gained access, e.g. because of the loss of the coronal seal ¹.

In the minority of cases where a failed root canal treatment is identified, the reason may also be attributable to a foreign body reaction, extra-radicular infection or the presence of a true cyst.

Each of these can also present with the signs and symptoms of symptomatic periradicular periodontitis. Figures 1a and 1b illustrate a case of a radicular cyst.

What are the clinical signs and symptoms of an asymptomatic periradicular periodontitis?

This particular periradicular diagnosis is often an incidental finding, for example when taking a routine periapical radiograph prior to replacing a failing crown. This finding potentially poses a management dilemma for the patient and clinician alike.

Should we embark on root canal treatment or re-treatment on a tooth which has presented the patient with no problems and risk iatrogenic errors occurring and the monetary costs associated with the endodontic procedures undertaken²? Table 2 outlines the range of clinical findings usually associated with this diagnosis.

It has long been recognised in Scotland that a large proportion of the population who have had extensive coronal restorations on vital teeth or teeth with previous endodontic treatment, will have asymptomatic periradicular periodontitis present (identified by radiographic periradicular radiolucencies) ³⁴⁵.

This is a disappointing finding and raises questions as to the understanding and management of endodontic pathosis by clinicians, as well as to the techniques used to monitor the endodontic status of teeth.

The literature is relatively sparse in ascertaining the risk of monitoring such asymptomatic lesions rather than embarking on active treatment (root canal re-treatment, surgical endodontic procedures or tooth extraction).

It has, however, been reported that those teeth which already have a root canal treatment in situ and are maintained with a good quality coronal seal, are at little risk of either becoming symptomatic or demonstrating an increase in size of the periradicular radiolucency on radiographs⁶.

What are the clinical signs and symptoms of a chronic periradicular abscess?

The clinical scenarios frequently encountered with this periradicular diagnosis are outlined in Table 3.

When a chronic periradicular abscess is present, drainage can occur through the periodontal ligament space (Figs 2a and b), forming a narrow, deep periodontal pocket over time or it may drain through the alveolar bone forming a sinus/fistula.

When present, a sinus can fluctuate between discharging and non-discharging. Once identified as present, two factors should be noted: First, the location of the sinus as those located close to the gingival margin can be associated with vertical root fractures⁷. Testori et al., identified coronally located sinuses in 42 per cent of vertically root fractured teeth⁸.

Sinus tracts closer to the apical area are more commonly associated with periradicular pathosis. Secondly, the sinus should be palpated to see if it is discharging. If so, a gutta percha cone can be threaded into the sinus tract until it stops and a periapical radiograph taken of the cone in situ, thus tracking the source of the infection.

Sinuses can occur both intra-orally or extra-orally and can be some distance from the source of the infection and so where possible it is advisable to radiograph with a gutta percha cone in situ to localise the source with some accuracy.

When a sinus is identified as associated with a previously endodontically treated tooth, this is a clear indication that further intervention is required (tooth extraction or further endodontic treatment).

Table 1 – The Clinical Signs and Symptoms of Symptomatic Periradicular Periodontitis

What are the clinical signs and symptoms of an acute periradicular abscess?

Table 4 summarises the probable clinical findings associated with a periradicular diagnosis of acute periradicular abscess.

When diagnosing the source of an acute abscess it is important to discern between a possible periodontal abscess and a dental abscess. Both periodontal abscesses and blocked periodontal pockets can present a similar clinical picture to that of a dental abscess (e.g. the tooth and associated tissues can exhibit tenderness to percussion and palpation, swelling and the patient reporting pain).

To aid diagnosis, thorough clinical examination in conjunction with a number of tests (cold, hot, electrical pulp tests, test cavities and periapical radiographs) can be useful to deduce which teeth are vital (and therefore likely to have a periodontal abscess) and those which are non-vital (with a pulpal necrosis and likely dental abscess). It is of note however that multi-rooted teeth can present with false positive and negatives to pulpal tests and hence the need for several pulpal investigations and/or tests to increase reliability of the findings.

Figures 3, 4a and b illustrate two cases where pulp testing was invaluable in coming to a diagnosis and for treatment planning. The case in Figure 3 is that of a deep non-healing periodontal pocket in the 13, 12 region. All sensibility tests undertaken revealed 13 and 12 to respond normally and both 13 and 12 were diagnosed with a clinically normal pulp. Excisional biopsy was undertaken and histological processing revealed a lateral periodontal cyst to have been present.

In Figure 4a, a radiograph of tooth 12 is shown. Clinically, 12 had deep periodontal pockets and mobility. If the diagnosis was made based on the radiographic findings alone, tooth 12 may have been thought to have a pulpal necrosis and evidence of an asymptomatic periradicular periodontitis. However, this tooth responded normally to all sensibility tests and was diagnosed with a clinically normal pulp. The history sheds light on this unusual appearance. Figure 4b shows an earlier radiograph which was taken prior to the recent surgical removal of an impacted canine. Figures 5a and b show an example of a tooth diagnosed as ‘previously treated and acute periradicular abscess’ and its management.

What are the clinical signs and symptoms of a condensing osteitis?

Condensing osteitis is a relatively commonly occurring radio-opaque lesion in the jaws, seen in 4-7 per cent of the population. Its cause reported as due to pulpal degeneration/inflammation or necrosis which results in the replacement of cancellous bone by dense, compact bone in some individuals⁹. It is frequently found as an incidental discovery associated with an often asymptomatic tooth (Fig 6) and hence it can be identified as associated with asymptomatic irreversible pulpitis cases amongst other diagnoses.

As illustrated in Figures 6 and 7, its identification is usually radiographically because clinical signs and symptoms (described in Table 5) rarely show that periradicular changes are present. Condensing osteitis indicates pulpal inflammation is present and thus sensibility testing of the tooth in question is warranted. Where the pulp is found to be necrotic, root canal treatment or extraction is the treatment of choice.

Alternatively, in cases where the tooth is still vital, a plan of watchful waiting or root canal treatment can be considered.

If further invasive treatment is intended, such as a crown preparation, it may be advisable to consider an elective root canal treatment as evidence of a stressed, irreversibly inflamed pulp is present (Fig 7). Condensing osteitis will usually resolve following appropriate treatment (removal of the irreversibly inflamed or necrotic pulp through root canal treatment or tooth extraction).

Table 4 – The Clinical Signs and Symptoms of an Acute Periradicular Abscess

Conclusions

Suggested up-to-date diagnostic terminologies for pulpal and periradicular health and disease are conveniently based on describing the clinical, rather than histological findings. This aims to simplify the diagnosis and aid communication between colleagues and patients alike. It is recommended that both a pulpal and periradicular diagnosis be made for every endodontically-involved tooth and that this be recorded in the dental notes.

Clinicians should be mindful of the dynamic nature of endodontic disease and use a range of investigations and special tests to try to ascertain as accurate information as possible on the status of the pulp and periradicular tissues to allow precise diagnosis and appropriate treatment planning. Following any treatment to the pulp and periradicular tissues (such as pulp cap, pulpotomy, root canal treatment, re-treatment and surgery), reviewing the pulpal and periradicular status on an annual basis, or more frequently, is recommended.

It is noteworthy that, in cases of odontogenic pain (where the treatment plan involves a root canal treatment or re-treatment), following pulpal extirpation and biomechanical preparation of all root canals to full working length (under a rubber dam and using sodium hypochlorite irrigation in the apical third), but for a transient inflammatory reaction to the endodontic procedure itself, the odontogenic pain experienced should decrease rapidly. Where this does not occur, the original diagnosis should be reviewed.

A small number of patients who have had good quality endodontic management will continue to experience post-treatment pain. Nixdorf and colleagues¹⁰ reported ongoing persistent pain in 5.3 per cent of cases following endodontic treatment, concluding that around 3.4 per cent of these cases were in fact due to pain of non-odontogenic origin which had been misdiagnosed as odontogenic pain at the outset. Accurate diagnosis of pulpal and periradicular tissues will help avoid inappropriate treatment.

References

1. Abbot PV. Diagnosis and management planning for root-filled teeth with persisting or new apical pathosis. Endodontic Topics. 2011; 19: 1–21
2. Wesselink PR. The incidental discovery of apical periodontitis. Endodontic Topics. 2014; 30: 23-8
3. Saunders WP, Saunders EM. Prevalence of periradicular periodontitis associated with crowned teeth in an adult Scottish subpopulation. British Dental Journal 1998;
185: 137–40.
4. Saunders WP, Saunders EM, Sadiq J, Cruickshank E. Technical standard of root canal treatment in an adult Scottish sub-population. British Dental Journal. 1997; 182:382–6.
5. Dutta A, Smith-Jack F, Saunders WP.Prevalence of periradicular periodontitis in a Scottish subpopulation found on CBCT images. International Endodontic Journal. 2014; 47(9): 854-63.
6. Van Nieuwenhuysen JP1, Aouar M, D’Hoore W Retreatment or radiographic monitoring in endodontics. International Endodontic Journal. 1994; 27(2): 75-81.
7. Tsesis I, Rosen E, Tamse A, Taschieri S, Kfir A. Diagnosis of Vertical Root Fractures in Endodontically Treated Teeth Based on Clinical and Radiographic Indices: A Systematic Review. Journal of Endodontics. 2010; 36: 1455–1458
8. Testori T, Badino M, Castagnola M. Vertical root fractures in endodontically treated teeth: a clinical survey of 36 cases. Journal of Endodontics 1993; 19: 87–91.
9. T.L. Green TL, Walton RE, Clark JM, Maixner D. Histologic Examination of Condensing Osteitis in Cadaver Specimens. Journal of Endodontics. 2013; 39(8): 977-9.
10. Nixdorf DR, Moana-Filho EJ, Law AS, McGuire LA, Hodges JS, John MT. Frequency of non-odontogenic pain after endodontic therapy: a systematic review and meta-analysis. Journal of Endodontics. 2010; 36(9): 1494-8

The first article in this series discussed the potential problems that can arise even before the dental material has been placed in the mouth by inappropriate handling of the product. It stressed that materials must be used in line with the manufacturers’ directions to yield predictable clinical results.

This article discusses how materials should and, equally should not, be handled in the mouth to achieve the best
clinical outcome.

Moisture control

Once the material has been mixed by the dental nurse and handed to the dentist, there are various factors with respect to clinical placement that will have a bearing on the success or otherwise of the restoration. The most obvious is the control of moisture.

Placing a material into an inherently wet environment and expecting it to bond must be regarded as something of a tall order. Most dental materials are hydrophobic at worst or are adversely affected by water at best. Suboptimal performance will inevitably result if water contamination occurs during placement and before final setting. Indeed, poor moisture control is a major cause of adhesive failure and leads to inferior mechanical properties¹ so it is critical that a dry environment is gained during material placement.

The ability to achieve and maintain an adequately dry field may well influence material selection, as will be discussed in the next article in this series. Although many aids are available to achieve this (Fig 1), the most predictable and effective method is the placement of rubber dam (Fig 2)².

Moisture contamination may occur in the fluid form and also by water vapour in exhaled air. Intra-oral humidity can adversely affect the quality of the bond gained, particularly with resin-based composite materials. However, this potential problem may be easily overcome by the use of rubber dam². With its application, the operator can control the environment much more precisely, so facilitating technically demanding procedures such as bonding³.

To underline this, the American Dental Association does not support the placement of resin composite restorations without rubber dam placement⁴. Rubber dam also has other merits and these have been widely reported.

Timeous placement and assessment of set

As soon as the two constituents of a two-paste system are bought together, the setting reaction starts. There is, therefore, a finite amount of time during the mixing and working phases in which placement of the material to the site of use must be completed prior to the commencement of the setting phase. Good teamwork and understanding is essential between operator and dental nurse to achieve this.

With many auto-mixed products, the first dispensed material should not be used clinically as it may not have fully mixed3. Figure 3 illustrates that this initial (in this case impression) material should be expressed onto the bracket table.

However, this material may be used to help the operator by gauging the completion of set of the rest of the mix. The ambient temperature in the surgery is lower than the intra-oral temperature, so when the expressed material has set on the bracket table, then the product in the mouth will have definitely completed its set.

Correct intra-oral handling

The operator must pay particular attention when manipulating the material in the mouth, as failure to do this correctly will result in failure.

As mentioned earlier, the material should be placed into the intended site prior to the commencement of the setting phase. Irrespective of an impression or direct restorative material, once in situ, it should not be disturbed during this phase.

Failure to allow dental cements to go to full set without being disturbed leads to damage to the bulk of the material, leading to a stressed and weakened material³. Similarly the operator should provide even support for the impression tray to prevent inadvertent movement of the tray until the impression material has achieved full set (Fig 4).

Movement of the tray during this phase may lead to drags and stresses and strains in the impression material, leading to inaccuracies.

Once placed in the cavity, resin composite should not be excessively manipulated, as this leads to the introduction of air, leading to porosity, areas of stress concentrations and sites of failure⁵.

Furthermore, resin composite shrinks on polymerisation and so it is imperative to use a sectional matrix system when restoring a Class II cavity, as this helps to compensate for the shrinkage (Fig 5)⁶.

When the retaining ring is placed, the teeth are forced apart due to a luxation force. When the resin composite has been cured, the matrix system is removed, allowing the teeth to return to their original position. The creation of a good broad contact area with the approximal surface of the adjacent tooth is considered to be the most challenging aspect of doing a Class II restoration in resin composite.

This cannot be adequately achieved with the use of a matrix band intended for use with dental amalgam such as a Siqveland. This type of matrix band may also bend weakened cusps into the cavity, causing the resin composite restoration to be bonded in the cavity under stress. This may result in fracture of the tooth or manifest as pain, especially on chewing as the tooth flexes during function.

It goes without saying that the matrix should be correctly applied so that the material is properly contained and with the correct contour.

Dental materials should never be mixed with other materials unless expressly stated by the manufacturer. This is because they may be chemical incompatible. For example, it may be that materials are made of the same generic resins e.g. Bis GMA, but the synthesis of this molecule can vary from manufacturer to manufacturer.

It is, therefore, essential that different products used in one restoration are sourced from the same manufacturer, otherwise a substandard material with inferior mechanical properties will result. This also holds true for the combination of bonding agent and the resin composite restorative material. Consistency is a very important consideration³.

Light Curing

Advantages

The problem of disturbing partially set material has been largely overcome by light curing. This permits the operator to cure the material in a matter of seconds by the application of light energy. This is very convenient, as this “command set” provides an extended working time without the commensurate protracted setting time seen with chemical-cured materials.

Compatibility of systems

Light curing has some hidden pitfalls, however. In recent years, there has been a move away from resin composites that use camphorquinone as its photo-initiator. Examples of these materials are lighter shade resin composites, flowable composites, bulk fills, orthodontic bonding cements and temporary inlay materials.

There are a couple of reasons for this. Firstly, camphorquinone is yellow in colour and this precludes its use in bleaching and lighter shades of resin composite as it adversely influences the shade. To overcome this problem, another photo-initiator must be used which is white in colour. Phenylpropanedion (PPD) or Lucirin TPO are commonly used (Fig 6).

Secondly, these latter photo-initiators are more efficient than camphorquinone and so require less energy to effect the setting reaction. For this reason, they have been used in the bulk fill materials that boast a curing depth of up to 4mm.

The recent scientific work shows great promise for these materials⁷. These chemicals have a peak absorption wavelength of 380 and 430nm opposed to 470nm for camphorquinone. Their increasing use will have significant consequences, as many clinicians will have to purchase curing lights able to effect cure at these lower wavelengths. It is strongly advised that the dentist ensures that each new material introduced into the clinic is compatible with the surgery curing light able to deliver sufficient energy at the photo-initiator’s peak absorption wavelength, otherwise the material will not fully cure.

Choice of curing light

The clinician broadly has a choice of a halogen or light emitting diode (LED) curing lamp. The former has a good track record, but its broader spectral range means that it is less efficient (Fig 7).

With time, the filament in the halogen bulb ages by thinning, with the result that the wavelength of light emitted changes. This reduces the amount of energy emitted at the peak absorption wavelength.

This may result in insufficient energy being emitted at this critical wavelength leading to incomplete cure. This is impossible to detect with the naked eye, as the light remains blue. The output of the lamp should therefore be checked regularly, with a radiometer included in the base unit of many models. Halogen bulbs should be changed every three to six months or sooner if the bulb has become darkened.

LED curing lights have, in recent years, become much more commonplace. They are very powerful, emitting in excess of 1W of energy, and produce very effective polymerisation of resin composites, provided their narrow spectral band corresponds to the peak wavelength of the photo-initiator.

Their long-term performance is good, as the wavelength of light delivered does not change unlike halogen lights.

Some manufacturers have overcome the problem of insufficient energy at the optimum wavelength by incorporating a number of LEDs in the lamp head to encompass all the desired peak absorption wavelengths.

Curing factors

There are many factors which influence the rate of cure. As the intensity varies as the inverse square of the distance, it is imperative that the tip of the curing light is held close to the restoration and perpendicular to ensure an even amount of energy dispensed to the material (Fig 8).

Clearly, this light must transmit through the material to reach the photo-initiator in all of the unset material. Light penetration is affected by a number of factors, namely the particle size of the filler, with material consisting of small particles taken longer for the light to transmit through as it is attenuated by the particles.

More opaque and darker shades will need more time for the light to transmit through. Furthermore, if there is a mismatch between the optical properties of the glass and resin, then this will have a detrimental effect, as will variables in the diketone/amine chemistry that is necessary for set.

Curing light care and maintenance

In 2001, Mitton and Wilson⁸ looked at curing lights in general dental practice that showed some alarming results. They found that 28 per cent of the lights had inadequate light output, 47 per cent were damaged or had been repaired and 35 per cent had varying amounts of material adhering to the light exit portal, which would have the effect of decreasing the amount of light which could be emitted from the light.

They made some useful and practical suggestions that could be easily introduced into surgery protocols. For example, all components of the light should be regularly inspected for damage and the light guide checked for conductance by viewing daylight through the distal end. Black spots or speckling indicates damaged fibres in the fibre bundle (Fig 9).

The light guide should be replaced if more than 10 per cent of the fibres are damaged. There is a useful addendum in the paper and readers would be well advised to incorporate the recommendations into surgery protocols.

During use, the dental team should avoid contamination of the light guide with unset resin composite material or bonding agents during curing. This would lead to set material compromising the light being emitted.

The light guide should be cleaned immediately after each use and decontaminated between patients. Sheaths are available for use over the light guide, but there is some evidence that this affects the quality of light emitted.

A universal shade composite is packed into the cavity and cured. The wedge is then inverted and if soft material remains on the base the light is not functioning adequately.

Thermal trauma

Many dental materials undergo an exothermic reaction during setting and the clinician should be aware of the potential problems associated with any temperature changes. These can be marked particularly with any resin systems.

Light guides emit much heat with the higher the intensity, the more energy and therefore the more heat. This may have detrimental effects on the dental pulp with a rise of 12˚C, causing irreversible damage leading to pulpal death.

Finishing

Careless finishing and polishing can also transmit heat to the tooth and the dentist is advised, where possible, to carry out any rotary finishing under water spray to dissipate any heat generated. This prevents localised heating of the resin leading to hot spots in the material above the glass transition temperature leading to melting alterations in resin form.

The correct instruments should be used to finish and polish restorations and this should be done at the appropriate time. For example, glass ionomer cements should be left to fully set before they are polished, a process which can take 24 hours.

The appropriate post-operative instructions should then be given to the patient.

Conclusions

Placement factors and well as pre-placement factors have a significant bearing on the success or otherwise of the restoration. Attention to detail at each stage is essential.

The next article in this series examines appropriate material selection and its relationship with tooth preparation.

About the author

Steve Bonsor graduated from the University of Edinburgh in 1992 and in 2008 gained an MSc in Postgraduate Dental Studies from the University of Bristol. From 1997 until 2006, Steve was a part-time clinical teacher at Dundee Dental Hospital and School and honorary clinical teacher at the University of Dundee in the sections of operative dentistry, fixed prosthodontics, endodontology and integrated oral care. He currently holds appointments at the University of Edinburgh, as an online tutor on the MSc in Primary Dental Care programme and at the University of Aberdeen as honorary clinical senior lecturer leading the applied dental materials teaching at Aberdeen Dental School. As well as lecturing throughout the UK, Steve is actively involved in research, having published original research articles in peer-reviewed journals. His main research areas are photo-activated disinfection and the clinical performance of dental materials.

References

1. Smales RJ. Rubber dam usage related to restoration quality and survival. Br Dent J 1993 May 8;174(9):330-333.

2. Haruyama A, Kameyama A, Tatsuta C, Ishii K, Sugiyama T, Sugiyama S, et al. Influence of different rubber dam application on intraoral temperature and relative humidity. Bull Tokyo Dent Coll 2014;55(1):11-17.

3. Bonsor SJ, Pearson GJ. A Clinical Guide to Applied Dental Materials. 1st ed. Edinburgh: Churchill Livingstone Elsevier; 2013.

4. Statement on posterior resin-based composites. ADA Council on Scientific Affairs; ADA Council on Dental Benefit Programs. J Am Dent Assoc 1998 Nov;129(11):1627-1628.

5. Chadwick RG, McCabe JF, Walls AW, Storer R. The effect of placement technique upon the compressive strength and porosity of a composite resin. J Dent 1989 Oct;17(5):230-233.

6. Burke FJ, Shortall AC. Successful restoration of load-bearing cavities

in posterior teeth with direct-replacement resin-based composite. Dent Update 2001 Oct;28(8):388-94, 396, 398.

7. Moorthy A, Hogg CH, Dowling AH, Grufferty BF, Benetti AR, Fleming GJ. Cuspal deflection and microleakage in premolar teeth restored with bulk-fill flowable resin-based composite base materials. J Dent 2012 Jun;40(6):500-505.

8. Mitton BA, Wilson NH. The use and maintenance of visible light activating units in general practice. Br Dent J 2001 Jul 28;191(2):82-86.

Oral mucosal conditions are common and can be worrying and troublesome for patients. With demands on waiting lists in secondary care and the desire of some dental practitioners in primary care to take on “special interests”, now is the time to challenge the need to refer so many patients with oral mucosal disease into a secondary care setting?

Perhaps also now is the time to augment the relationship between doctor and dentist in the primary care setting to ensure that patients receive a first-class, joined-up service with a reduced need for onward referral? With this construct in mind, we offer management regimes for patients with oral mucosal disease in a primary care setting and invite referral of patients with more serious or sinister disease into secondary care, along with those who do not respond promptly to the regimes proposed in this paper.

We hope that this paper will serve as an aide-memoire in your practice or clinic.

Recurrent aphthous stomatitis (RAS)

RAS is the commonest inflammatory oral mucosal disease, said to affect 20 per cent of the adult population. It comes in three main forms: Minor (85 per cent), Major (10 per cent) and Herpetiform (5 per cent) and may be indicative of underlying systemic disease.

RAS is primarily a disease of exacerbation and remission, commonly occurring in late childhood or adolescence and remaining into adulthood. It is an easy diagnosis to make from the history alone – essentially any recurring ulcers of the oral mucosa are likely to be aphthous in type. Appearance may clinch the diagnosis – ulcers are round or oval in shape, with a red, inflammatory border and a yellow fibrinous base.

We are seeing less cases of RAS due to deficiencies of iron, folate and vitamin B12, but more due to the Koebner effect of mucosal damage due to trauma from tooth clenching/grinding and tongue thrusting. These habits are thought to be part of a person’s outworking of stress and seem to be ever more common in our stressful world.

Clinical tip

Patients who develop RAS in adulthood should be viewed with some concern as there is almost always an important underlying cause such as deficiency or hypersensitivity.

Case

A 54-year-old man developed RAS with no background of the condition. He was referred promptly by his dentist and blood tests revealed a picture of iron deficiency. Further investigations revealed an early bowel tumour which was readily resected. His iron deficiency resolved and his mouth ulcers settled.

What to ask

Patients with RAS should be asked about the following:

• What sites are involved?
• Frequency of episodes?
• Number of ulcers in each episode?
• Size of ulcer(s)?
• How long do the ulcer episodes last?Other systems involved? (e.g. eyes, genitalia, skin)
• Other symptoms? (e.g. swelling of joints or upset lower gut)
• Related to stress/stressful events?
• Aware of tooth clenching/grinding or tongue thrusting?
• Use of toothpaste containing Sodium Lauryl Sulphate (SLS)?
• Dietary consumption of fizzy drinks (benzoates)?
• Use of prescribed drugs? (e.g. Nicorandil, NSAIDs).

Examination

• Presence (confirmatory appearance) of ulcer(s)
• Size of ulcer
• Type of ulcer: minor, major, herpetiform
• Any evidence of trauma, cheek biting/chewing, tongue-thrusting?

Investigations

• Liaise with patient’s medical practitioner to request the following blood tests:
• FBC (with the inflammatory markers PV or CRP if systemic disease suspected)
• Levels of folate, ferritin, vitamin B12
• Coeliac antibody screen (TTG)
• ANA antibody if any history or suggestion of autoimmune disease.

RAS has both person-specific and environmental factors involved in its aetiology (see below).

Factors that cause RAS

PERSON SPECIFIC

• Genetic
• Nutritional (e.g. deficiencies in folate, iron or vitamin B12)
• Hormonal (e.g. menstrually related)
• Associated systemic diseases

ENVIRONMENTAL

• Dietary factors causing hypersensitivity reactions (e.g. benzoates in fizzy drinks)
• Trauma (Koebner phenomenon)
• Possibly others, yet to be identified (e.g. viral/bacterial)

A relatively “new” syndrome associated with RAS is PFAPA which particularly occurs in children, adolescents and young adults. PFAPA is an acronym for: Periodic Fever, Aphthous stomatitis, Pharyngitis and cervical Adenitis.

It is said to respond promptly to high dose oral corticosteroids but also, interestingly, to tonsillectomy. Patients suspected of this condition should be referred to secondary care (oral medicine, paediatrics or ENT) for assessment.

Clinical tip: remember all the ‘20s’

• RAS affects up to 20 per cent of the UK population
• Up to 20 per cent of sufferers have an underlying haematinic deficiency (e.g. iron, folate, vitamin B12)
• A further 20 per cent may have an “allergic” (hypersensitivity) basis (e.g. benzoates in fizzy drinks or colophony in chewing gum).

Management of patients with recurrent aphthous stomatitis

1. Identify and eliminate sources of trauma (consider soft occlusal splint if bruxist or tongue thrusting)
2. Review with blood results
3. If deficiency identified, discuss with GP regarding possible cause and onward referral
4. If coeliac antibody positive, or any possibility of Crohn’s disease or OFG, refer to consultant gastroenterologist
5. Once cause of deficiency established, consider replacement therapy via GP: review three months
6. If consumer of fizzy drinks, consider diet advice regarding empirical benzoate avoidance
7. Change to an SLS-free toothpaste
8. If Behcet’s Syndrome is possible (in view of skin, eye or genital lesions), or you are concerned about another systemic disease, liaise with GP and refer to appropriate specialist for opinion (e.g. oral medicine, dermatology, ophthalmology or gynaecology)
9. Consider referral for patch testing if you practice in an area where this service is routinely provided
10. Topical therapies:
    a. Chlorhexidine gluconate (0.2 per cent) mouthwash twice daily for 28 days initially
    b. Benzydamine hydrochloride mouthwash up to three times daily as required
    c. Gengigel
    d. Gelclair or Aloclair
    e. Topical steroid therapy (see Appendix 1).
11. Should the patient fail to respond to the above regime, then refer to secondary care (oral medicine).

Lichen planus and lichenoid tissue reactions

Lichen planus (LP) is another common oral mucosal disease, affecting approximately 1-2 per cent of the population. Increasingly, LP is considered to be an autoimmune disease.

Autoimmune diseases arise in part from our genetic make-up and in part from an environmental factor – most of which are yet to be identified. Interestingly, LP is increasingly seen in conjunction with other autoimmune disorders, such as hypothyroidism.

There is often confusion in the literature about terminology – is it lichen planus or a lichenoid tissue reaction? For avoidance of doubt, we suggest that where the condition is deemed to have no obvious cause (and therefore likely to be autoimmune in origin), the term oral lichen planus (OLP) is used.

Where a causative or contributory factor is identified, we suggest that the term lichenoid tissue reaction (LTR) is used. Such factors may be stress, drug reactions and dental materials, such as amalgam and even gold.

Clinical varieties of OLP and LTRs

• Reticular (striated)
• Erosive
• Plaque
• Atrophic
• Papular
• Bullous
• Desquamative gingivitis.

Clinical tip

Many drugs have been identified as contributing to LTRs, including: beta-blockers, diuretics, NSAIDs, oral hypoglycaemics, anti-epileptics, lithium, ACE-inhibitors, chloroquine and certain vaccines.

Case

A 48-year-old woman complained bitterly of discomfort when eating her favourite dish of Indian origin. Her GDP identified striated lesions on a red background on the buccal mucosae bilaterally and on the left ventro-lateral surface of her tongue. She had been started on a beta-blocker for anxiety several months previously.

The GDP discussed with the GP the possible role of this drug and the patient was happy to stop the medication. Her symptoms lessened over the subsequent weeks and the lesions disappeared completely within three months. The patient was delighted to be able to visit her local curry house again.

Patients with OLP/LTR should be asked:

Do you have any itchy skin lesions (purple papules, red spots or white, lacey lesions) – particularly at the wrists, on the shins; or do you have any white or red areas on the genitals?

Examination

• Presence (confirmatory appearance) of OLP/LTR?
• Extent of condition – localised or more generalised?
• Relation to old amalgam (or other) restorations?
• Any evidence of trauma, cheek biting/chewing, tongue thrusting (Koebner effect)?
• Record clinical type of OLP/LTR.

Lichen planus is a mucocutaneous disorder which can affect the oral mucosa, genital mucosa and skin. Patients should be asked specifically about the possibility of lesions at sites outside the mouth. This is particularly important with regard to identifying those patients who might have vulvo-vaginal-gingival syndrome or peno-gingival syndrome, as both appear to have increased risk of genital, and possibly oral, malignancy.

The presence of extra-oral LP will also influence management options and may move the patient more quickly to a secondary care environment for combined oral medicine/dermatology management.

Once again, the Koebner phenomenon is important in OLP (and in LTRs) and mucosal trauma should be reduced by careful assessment of the dentition, restorations and prosthesis. Mucosal trauma due to tooth clenching or grinding should also be sought and eliminated.

SLS-containing toothpastes and mouthwashes tend to irritate the oral mucosa of patients with OLP and LTRs and should be changed to SLS-free variants. Indeed, the question should be asked: are proprietary mouthwashes required at all for anyone?

Smoking is considered to increase the risk of the patient’s OLP or LTR transforming to oral squamous cell carcinoma and so patients with OLP/LTR must be encouraged to stop smoking and understand fully the risks in maintaining the habit.

Clinical tip

What to do?

• Asymptomatic, reticular: review
• Symptomatic, reticular: biopsy, treat and review
• Other types: biopsy, treat and review
• Smokers: biopsy all types
• Local lesion: remove amalgam
• Widespread lesions: consider patch testing.

Investigations

• If the patient’s OLP/LTR is causing symptoms and is of a non-reticular variant, liaise with the GP to exclude contributory systemic factors by way of blood tests: check FBC, folate, ferritin, vitamin B12.
• If the patient also has hypertension (from history), liaise with the GP to check random blood glucose to exclude Grinspan’s Syndrome – a triad of OLP, hypertension and Type 2 diabetes mellitus.
• In a secondary care setting if the patient is of mainland European, Middle Eastern or Far Eastern origin, it may also be worth considering checking liver function tests and Hepatitis C serology as there is an apparent link in certain ethnic groups between OLP and Hepatitis C viral infection.
• In a secondary care setting if the patient has the bullous variant, check indirect immunofluorescence serology to exclude other bullous disorders.
• Also, a biopsy should be taken from a representative area (or areas) for routine histopathology, especially if a smoker. Where different variants of the condition co-exist, biopsies should be taken from different sites. Where bullous lesions are evident or reported, peri-lesional biopsy tissue should be sent for direct immunofluorescence.

If a patient has asymptomatic, reticular OLP/LTR and is a non-smoker, then no referral to secondary care is required. Instead, such patients should be advised of the diagnosis, the possibility of skin or genital lesions and the small risk of subsequent oral squamous cell carcinoma. The importance of maintaining a smoke-free status should be emphasised, alongside the advice to ensure that alcohol consumption is within recommended limits. Such patients should be placed on regular six monthly review, but also advised to return for further assessment/advice if any changes within the mouth occur in the interim period.

If a patient has symptomatic OLP/LTR of any variant (including reticular), then referral to secondary care is advised – with a biopsy likely to exclude any super-added fungal infection or dysplasia. Similarly, a smoker with any variant of OLP/LTR (including reticular) should be referred to secondary care for assessment and consideration of biopsy.

Management

1. Identify and eliminate sources of trauma
2. Change to an SLS-free toothpaste
3. Maximise oral hygiene to eliminate irritation from plaque
4. Advise to stop smoking, if required. Support quit attempt, via GP or local smoking cessation services
5. If chronology of drug use fits with onset of symptoms/signs, consider liaising with prescribing GMP or hospital specialist to request changing to structurally unrelated drug. This should be pursued where a patient has symptoms
6. If lesions are localised and related to an obvious cause (e.g. old amalgam restoration), consider the replacement of the restoration with a non-mercury containing restoration (e.g. composite, porcelain or gold) or cover the tooth/restoration with an appropriate crown. This should be pursued where a patient has symptoms
7. If the lesions of OLP/LTR are extensive and the patient has symptoms, a trial of a systemic anti-fungal drug (e.g. fluconazole or itraconazole) at conventional dose for two weeks or so may be worthwhile
8. If other systems are involved or, from symptoms, potentially involved, a referral to the appropriate hospital specialist should be instituted (e.g. dermatology, gynaecology)
9. Topical therapies:a. Chlorhexidine gluconate 0.2 per cent mouthwash twice daily for 28 days initially
   b. Benzydamine hydrochloride mouthwash up to three times daily
   c. Gingigel
   d. Gelclair or Aloclair
   e. Aloe vera mouthwash
   f. Topical steroid therapy (see Appendix 1).
10. Should the patient fail to respond to the above regime, then refer to secondary care (oral medicine).

Helpful references and resources:

The British Society for Oral Medicine www.bsom.org.uk/clinical-care-chooser/soft-tissue-conditions/
The Scottish Dental Clinical Effectiveness Programme (SDCEP) www.sdcep.org.uk/published-guidance drug-prescribing/
Oral and Maxillofacial Medicine: the basis of diagnosis and treatment (Third Edition) Scully, C. Churchill Livingstone, 2013

APPENDIX 1

Topical corticosteroid therapies:

Hydrocortisone mucoadhesive buccal tablets: 2.5mg (as sodium succinate) Dissolve one tablet slowly in the mouth up to four times daily.
Beclometasone dipropionate puffer: 50g: apply two puffs two to three times daily directly to the oral mucosa. NB: Advise patient to shake inhaler prior to use to mix steroid and propellant. Useful for one or two lesions.
Betamethasone sodium phosphate: 500g (0.5mg) tablet. One tablet to be dissolved in water and used as a mouthwash for two minutes, and expectorated, two to three times daily for seven to 10 days initially, and then intermittently as required. NB: Advise patient not to swallow solution. Useful for multiple/widespread lesions.

Notes

Use therapies as soon as lesions appear
Use therapy for as little time as possible and make steroid-free episodes regular occurrences
Where therapy is likely (or confirmed) to be long-term and/or involving systemic steroids too, discuss with GP about when to arrange bone density scan and consider osteoporosis prophylaxis.

ABOUT THE AUTHORS

John Gibson is professor of medicine in relation to dentistry and honorary consultant in oral medicine at Glasgow Dental Hospital and School

Alexander Crighton is consultant in oral medicine and honorary senior lecturer in medicine in relation to dentistry at Glasgow Dental Hospital and School

Most routine dental treatment provided to patients is aimed at preventing pulpal and periradicular inflammation and infection. However, it is known that numerous patients seeking emergency dental care have pain of either pulpal and/or periradicular origin ¹². Thus it is essential that clinicians are conversant in up-to-date recommended pulpal and periradicular diagnostic terminologies for identifying both healthy and diseased tissues and the associated appropriate management options.

In 2009, The American Association of Endodontists (AAE) ³ released a consensus statement generated from the recommendations of the invitation-only Consensus Conference held in the USA in 2008. This document suggested the adoption of consistent, standardised pulpal and periradicular descriptive terminologies pragmatically based on typical clinical presentations (rather than histological findings).

The aims were to aid accurate endodontic diagnosis and hence treatment, and to enhance communication to patients and colleagues and to heighten understanding of the often degenerative sequence of endodontic disease. Descriptions of the clinical findings for each of the suggested diagnostic terminologies have been produced, however, there is a spectrum of presenting signs and symptoms for odontogenic pain and those patients who fall out with the ‘central tendency’ of the usual clinical presenting features are much more challenging to diagnose.

Furthermore, every clinician should be mindful of the dynamic nature of pulpal and periradicular disease which can manifest in both asymptomatic and symptomatic presentations and it is not uncommon for symptomatic conditions to undergo asymptomatic periods and vice versa.

The diagnosis is made following systematic and detailed exploration of the patients’ pain, dental and medical history, clinical and radiological examination, and appropriate special tests and investigations likely to help identify pulpal and periradicular changes. Medico-legal advice ⁴ recommends documenting details of presenting history, examination, investigations/special tests, diagnoses made and decisions taken/treatment plan made etc. These endorsements are further reinforced within the 2013 guidance from the General Dental Council ⁵.

It is recommended that a pulpal and periradicular diagnosis should be made for every endodontically involved tooth. This means that, if evidence of a previously pulp-capped, pulpotomised or root-filled tooth is seen, for example on a bitewing radiograph, or a patient gives a history of such treatment, it would be advisable to then examine that tooth clinically for signs and/or symptoms of pulpal and/or periradicular inflammation and infection, and document the results of these findings (both positive and negative) within the patient records.

Depending on the clinical findings related to such a tooth, a periapical radiograph may be considered, particularly if signs or symptoms of possible pulpal and/or periradicular inflammation or infection are identified, or where further restorative intervention is planned for the tooth ⁶.

The diagnostic terminology presented in this article aims to update clinicians with current terminologies and the most likely clinical scenario encountered with each. Familiarity with this information can facilitate more accurate diagnosis, communication and management of the health or disease of the pulp and /or periradicular tissues. Early diagnosis in endodontics can not only impact favourably on the treatment outcome, but can also involve less expensive, more cost-effective treatment for patients.

Figures 1a and 1b show an example of a late diagnosis which, if made earlier, may have delayed or prevented the loss of a strategic tooth in an elderly, periodontally compromised patient. Figures 2a and 2b show a tooth with a reduced periodontal support which could potentially have been successfully managed had a horizontal root fracture been identified earlier.

Table 1 (below) lists the terminologies suggested by the AAE and it is advised that both a pulpal and periradicular diagnosis is made and documented for each endodontically involved tooth. For example: symptomatic irreversible pulpitis and normal apical tissues.

In formulating an endodontic diagnosis, it is accepted that patient responses to investigations and special tests can be notoriously variable. Clinicians are limited by many of the tests available which often deduce indirect rather than direct information regarding the status of the pulp and/or periradicular tissues ⁷. Furthermore, no commonly available tests are 100 per cent accurate 100 per cent of the time. And, consequently, the more information clinicians gather regarding the likely status of the pulp and/or periradicular tissues (through using a variety of tests and investigations), the more probable that the diagnosis made will reflect the true status of the pulp and/or periradicular tissues, including identification of when there is no pulpal and/or periradicular disease.

In all cases, it is recommended that a normally funct-ioning tooth with a normal pulp is first tested to generate baseline information against which the test results of potentially problematic teeth can be compared. Discussion of these investigations and tests and their accuracy is outwith the scope of this article and the reader is directed to two excellent papers for more information – Mejàre and colleagues ⁷ and Pretty and Maupomé ⁸.

How to identify a clinically healthy/normal pulp

Table 2 illustrates the findings usually associated with a clinically normal pulp. A clinically normal pulp would be expected to respond and function within normal parameters although, histologically, evidence of previous inflammation (fibrosis) may be seen.

Where a tooth is identified, for example on a bitewing radiograph as appearing to have had a previous pulpotomy or pulp cap, further investigation of the pulpal status of that tooth is warranted to confirm whether the tooth is functioning with an apparently clinically normal pulp or not. This is because such teeth are recognised to be susceptible to loosing pulpal vitality in a protracted, asymptomatic fashion that can go undetected⁹. Diagnosis and treatment of pulpal degeneration at a stage which precedes pulpal necrosis and periradicular changes seen radiographically, is well known to be associated with a more favourable endodontic treatment outcome¹⁰.

What are the clinical signs and symptoms of a reversible pulpitis?

Table 3 summarises the clinical signs and symptoms of a reversible pulpitis. In contrast to an irreversible pulpitis, the discomfort experienced from a reversible pulpitis is always caused by a stimulus and never spontaneously occurring.

Dentine sensitivity or hypersensitivity is included under the umbrella of a reversible pulpitis and is an unusual situation in that a chronic pulpal problem can develop and persist although it is not normally associated with degenerating to an irreversible pulpitis.

Reversible pulpitis can be successfully treated by removing any irritant present (such as caries) and protecting exposed dentine (as in the case of a dentine hypersensitivity). This should allow the pulp to return to normal function. However, it is prudent to follow-up and pulp test any teeth which are thought to be at risk of developing an irreversible pulpitis as it is currently impossible to ascertain clinically an individual tooth’s ability to recover from a reversible pulpitis.

The capacity for pulpal recovery will be influenced by previous pulpal insults and inflammation, the degree of pulpal fibrosis and the true histological status of the pulp. Using a minimum of two assessment methods to assess the pulpal status should generate a more reliable assessment of the pulp at the time of symptoms. These can be repeated two to four weeks later for teeth identified as being at risk of undergoing an asymptomatic degeneration of the pulp or an irreversible pulpitis and then necrosis (e.g. heavily restored teeth in older individuals).

What are the clinical signs and symptoms of a symptomatic irreversible pulpitis?

The clinical signs and symptoms demonstrated within this diagnosis are notoriously variable in both intensity of symptoms and the signs/symptoms themselves. Table 4 outlines the varying clinical scenarios which can present to the clinician for this pulpal diagnosis.

Referred, unlocalised pain is regarded as common in symptomatic irreversible pulpitis and so tests which help localise pain can be very useful. For example, selective anaesthesia can aid in localising between mandibular and maxillary pain. Electric pulp testing and other thermal tests can often help highlight the tooth which is the source of the pain.

In contrast to a reversible pulpitis, the discomfort experienced with a symptomatic irreversible pulpitis often arises spontaneously, in the absence of any stimulus and the pain may be worsened by postural changes. Analgesics and systemic antimicrobials are notoriously ineffective in relieving the pain felt with a symptomatic irreversible pulpitis.

What are the clinical signs and symptoms of an asymptomatic irreversible pulpitis?

Teeth which have had pulp caps or pulpotomies performed due to carious pulp exposures are known to be at risk of losing vitality in a slow, asymptomatic fashion because of the extent of the pre-existing inflammation in the pulp at the time of the pulpal exposure. In time, an asymptomatic pulpitis will degenerate further to pulpal necrosis.

Teeth which have a history of what appears to be a symptomatic irreversible pulpitis for which there has been no active treatment, perhaps symptoms spontaneously resolved, are also likely to have either an asymptomatic irreversible pulpitis or pulpal necrosis.

Investigation into the pulpal status of such teeth is advisable. Root canal treatment performed prior to the development of either pulpal necrosis or an identifiable pre-operative radiographic periradicular pathology has a more favourable treatment outcome. It is not unusual for dynamic changes to occur within the root canal system leading to periods of quiescence where symptomatic irreversible pulpitis is asymptomatic.

Older individuals (53 years of age or more) are reportedly at more risk of developing asymptomatic irreversible pulpitis than younger individuals, the latter more frequently presenting with symptomatic irreversible pulpitis. This finding may be because of the reduced innervation of the pulp with ageing and potentially the difficulties that this poses in achieving reliable findings from pulp tests in such teeth9.

Multi-rooted teeth are of note because each canal/pulp may be at a different stage in the degenerative process and thus teeth which are becoming non-vital may still be stimulated to give a positive response to a pulpal test, complicating the diagnostic process.

What are the clinical signs and symptoms of a pulpal necrosis?

Pulpal necrosis is the end result of an irreversible inflammation of the pulp and almost always indicates an infected root canal system is present. This is often evidenced by the development of a periradicular radiolucency seen on a periapical radiograph of the affected tooth +/- the development of other signs and/or symptoms outlined in Figure 3. This is a clear indication to undertake either a root canal treatment or extraction of the tooth in question.

‘Previously Initiated’ and ‘Previously Treated’ pulpal diagnoses

The two remaining pulpal diagnostic terminologies suggested by the AAE are ‘Previously Initiated’ and ‘Previously Treated’. These fairly self-explanatory descriptors allude to either a tooth which has had partial endodontic treatment previously, such as a pulpotomy, pulp cap, pulp extirpation (i.e. ‘Previously Initiated’ endodontic treatment). The latter category describes those teeth which have had a previous root canal treatment completed or surgical endodontics performed (‘Previously Treated’).

Having made a pulpal diagnosis, a periradicular diagnosis can be made and the clinical scenarios and terminology associated with each will be discussed in part two of this article.

About the author

Julie K Kilgariff, BDS MFDS RCS MRD RCS, works as a locum consultant in endodontics at Glasgow Dental Hospital and as a specialist in endodontics at Blackhills Specialist Dental Referral Clinic, Aberuthven.

References

• Dailey YM, Martin MV. Are antibiotics being used appropriately for emergency dental treatment? British Dental Journal. 2001; 191(7): 391-3
• Tulip DE, Palmer NO. A retrospective investigation of the clinical management of patients attending an out of hours dental clinic in Merseyside under the new NHS dental contract. British Dental Journal. 2008; 205(12): 659-64
• The American Association of Endodontists. Consensus Conference Recommended Diagnostic Terminology.  aaeconsensusconferencerecommendeddiagnosticterminology.pdf  (Accessed 22 January 2015)
• The Medical and Dental Defence Union of Scotland. Essential Guide to Medical & Dental Records. essential guide to medical and dental records12-09.pdf (Accessed 22 January 2015)
• General Dental Council. Standards for the Dental Team. Standards for the Dental Team.pdf (Accessed 22 January 2015)
• European Commission. Radiation Protection 136. European Guidelines on Radiation Protection in Dental Radiology. Luxembourg Office for Official Publications of the European Communities, 2004
• Mejàre IA, Axelsson S, Davidson T, Frisk F, Hakeberg M, Kvist T, Norlund A, Petersson A, Portenier I, Sandberg H, Tranaeus S, Bergenholtz G. Diagnosis of the condition of the dental pulp: a systematic review. International Endodontic Journal. 2012; 45(7): 597-613
• Pretty IA, Maupomé G. A closer look at diagnosis in clinical dental practice: part 1. Reliability, validity, specificity and sensitivity of diagnostic procedures. Journal of the Canadian Dental Association. 2004; 70(4): 251-5
• Michaelson PL, Holland GR. Is pulpitis painful? International Endodontic Journal. 2002; 35(10): 829-32
• Ng YL, Mann V, Gulabivala K. A prospective study of the factors affecting outcomes of nonsurgical root canal treatment: part 1: periapical health. International Endodontic Journal. 2011; 44(7): 583-609

Table 1

Table 2

Table 3

Table 4

For many years dental practices have been working with X-ray film and the associated processing chemicals. Quality Assurance was well documented and was taught to undergraduate dental students and Dental Care Professionals (DCPs) in training. Ongoing Continuing Professional Development (CPD) of the dental team clarified how to deal with processing problems and so, over many years, the quality assurance of film images has improved with education.

Digital imaging, with technology advancing in dental practices, has become more and more popular and a growing number of practices now work with digital systems. Quality Assurance in relation to monitors, to view images, and how to recognise and correct errors in the digital image production should now be part of a practice’s Quality Assurance programme. A Quality Assurance programme aims to produce consistently high quality images while keeping doses as low as reasonably practicable (ALARP). Practice Quality Assurance should be documented and audited.

Many dental practices have made the move to digital imaging but not all dentists are happy with the resulting images. The two parts of this article seek to assist understanding of the issues concerned. In the first part, by looking at some of the problems dental practices experience in recognising the problems with the resulting image and at possible ways to rectify them and, in the second part, by looking at the role computer systems can have in relation to the optimisation of digital images

There are two types of digital image receptor both of which capture a two dimensional image of the three dimensional patient. These are computed radiography (CR) photostimulable phosphor plates (PSPs) and direct digital radiography (DR) solid-state detectors (SSDs). There are approximately 256 shades of grey pixels which together make up the finished digital image. The sensors are very sensitive to X-rays and so the exposure to the patient can sometimes be dramatically reduced in relation to that which was used with conventional radiographic emulsion film.

Photostimulable phosphor plates (PSPs)

Under a protection layer is a photosensitive phosphor plate. This layer absorbs and stores the X-ray energy. After exposure, the plate is placed in a processor where it is scanned and the energy is released as light. The light is detected by a photomultiplier and the image is divided into pixels. A photomultiplier gives them a numerical value in relation to the intensity of the light released and the digital information is stored in the computer. The image can then be manipulated and displayed. PSPs are comparable in size to a conventional X-ray film and are compatible with most film holders. They are patient friendly and are suitable for use on most individuals including children and elderly patients. The more radiation that hits the sensor the darker the image will be. The capturing of the image is not instant but it takes only a matter of seconds rather than the few minutes it takes to process an emulsion film. After the plate has been scanned, the latent (invisible) image is then cleared by being exposed to light, either in the scanner or, less often nowadays, manually on a light box.

Quality Assurance for PSPs

1. Surface marking

The phosphor layer is delicate and very easily marked by any form of rough handling. All staff that handle PSPs should be aware that they must not bend or scratch them, since even normal handling can damage the surface. This marking can degrade the image significantly and is irreversible for any future image production.

If the scanning system does not have an integral white light clearer then the plates should be placed on an X-ray viewing box to erase the latent image. Problems can occur when the plate is lifted off after clearing. If the plate is slid across the surface of the box, the plate can be scratched (Fig 1). To minimise the possibility of this occurring, the box can be covered with cling film or see through bubble wrap allowing the plate to be lifted off rather than slid across the surface.

Custom-made mats are available that resemble a rubber bubble wrap on which the plate can be placed prior to and after scanning allowing the plate to be lifted off any work surface without scratching.

To ensure that PSPs are not marked beyond what is acceptable for image reading, the serial number should be taken and regular checks should be done to monitor for marks. To do this, the plate should be placed on a surface in its protective packet. No step wedge should be used. Next, the spacer cone should be lined up with the plate at a distance of 20 cm (the usual focal skin distance used in paralleling technique). The exposure given is very small (tiny flash exposure) and, when scanned, any marks will be visible. Each surgery should be responsible for its own plates. The time frame between these checks will vary in relation to the number of images captured and the quality of sensor handling by the staff.

 2. Fogging limitation

As the PSPs are very sensitive to radiation, even background radiation can base fog them. To limit this, the plate should be cleared every day by placing on a light box for a few minutes before use. If this is done in the morning the plate should be fine until the end of the working day. Once again, to avoid marking, cling film can be stretched over the viewing box or see through bubble wrap placed on the box before placing the sensors, blue side down, on the surface to clear. Alternatively, if the scanner has an integral light clearer, the sensors can be cleared first thing every morning in the scanner.

3. Sensor positioning

Problems can occur in relation to the image receptor not being firmly held by the bite blocks in paralleling technique holders, if the same bite blocks are used with the phosphor plates that were being used with X-ray film. An X-ray film packet is much thicker than a phosphor plate. Whereas an X-ray film has black paper around it, lead foil behind it and a thick waterproof cover, the phosphor plate is usually the only item in the waterproof packet and is consequently much thinner. The difference in thickness of the sensor in the bite block compared to a film packet makes accurate positioning in the mouth very difficult, as the plate tends to slip off the holder. To avoid this happening, thicken the phosphor cover with a white cardboard bitewing tab (Fig 2). This tab also doubles as a “target” when checking the position of the sensor in the mouth before aligning with the spacer cone (Fig 3). The sensor now stays securely in the holder. This cardboard tab also protects the plate at the point where it is placed in the bite block and where it can easily be damaged.

4. Endodontic X-ray holders

Due to the lack of back support on the endodontic holder, many image receptors bend in the roof of the mouth and the apex of the root is missed or elongated. Also, the image receptor also often moves in the holder making accurate imaging difficult. Use two bitewing tabs to stiffen the waterproof packet and ensure that the image receptor is held securely during positioning (Figure 4).

5. Bitewing images

When using a black waterproof cover in a dark mouth with a heat seal round the edge, it becomes very difficult to see the mesial edge of the image receptor. This was not such a problem with emulsion film because the waterproof cover was white. To overcome this difficulty, use bite tabs around the front edge of the waterproof cover to allow exact positioning of the bitewing sensor (Fig 5). It should be possible to image two premolars and two molars on one phosphor plate (size 2).

6. Ambient light image removal ensuring the image stays captured. Are your right and left bite wings the same shades of grey?

After image acquisition, the plates should be protected from ambient light image removal (Figs 6a and b). The exposed plates should not be left, even for a few minutes, unprotected from light even when in a waterproof packet. Ideally, when taking the images, the room blinds should be closed and the lights dimmed and light boxes switched off. As the image is cleared in the scanner by light, the plate should be kept as dark as possible when image capturing and when being transferred to the scanner.

To ensure this, the exposed plate should be kept in a light tight box prior to scanning and the scanner should be positioned in a dim room away from bright lights to enable plates to be loaded without losing image quality.

Special black boxes can be purchased that allow the plate to be posted in the top like a money box. Light cannot get in and the latent image will be safe until it is transported to the scanner. Alternatively, a dental appliance box or similar could be used. These are small, light tight, easy to clean, non-expensive and possibly already in the practice.

7. Exposure settings

PSPs have wide exposure latitude, which means they can give similar results when using a number of different exposures, unlike emulsion films which will be light or dark in relation to the exposure. A number of test images can be taken using step wedges or extracted teeth to ascertain the lowest exposure that gives an acceptable enhanced image. This becomes the maximum exposure. Guidance should be sought from a medical physicist to ensure that exposure settings are adjusted when a practice moves to a digital system.

Other problems that can be encountered are with images that lack contrast and have an overall grey appearance (“greying out”) (Fig 7). These are not images that can be enhanced by the computer to give more contrast. It is possible that the exposure is too low. If changes of exposure are being considered to give better quality images then guidance once again should be sought from your medical physicist.

8. Artefacts that mimic pathology. Unsharp Mask Subtraction (UMS)

Many of the image acquisition processes on digital systems are outwith the control of the user. These are intended to improve the image but sometimes artefacts that mimic pathology can result.

Areas where there are high intensities, like the base of a restoration or around dense bone, can result in a dark halo effect which can look like pathology. This is called “rebound artefact”. During processing and prior to viewing on the monitor, part of the acquisition process takes a blurred version of the image and subtracts it from the original. The blurred image is wider than the original and so when subtracted it can cause a shadow effect (Fig 8).

Image processing artefacts are becoming more subtle with more sophisticated systems. To minimise potential misdiagnosis, it might be prudent to consider other areas unrelated to the area in question and consider if the halo effect is present.

9. Viewing conditions

Many dental surgeries are bright, well-lit rooms. This can cause problems when reading images on computer monitors. It is important to ensure that optimum viewing conditions are obtained to allow accurate assessment of the computerised image. The monitor should be placed in a dimly lit area where the light levels are approximately equal to that which would be normal in an overcast day or darker. A light level of about 50 to 100 lux, the SI unit of luminescence, would be acceptable. Many surgeries are lit to a level of 300 to 500 lux which is too bright for optimum viewing conditions. The solution is to move the monitor or place a hood around it to cut down on light pollution.

10. Monitors

Test patterns that can be used to check monitor condition can be downloaded from the web: Society of Motion Pictures and Television Engineers (SMPTE) (Fig 9) and Technical Group 18 QC (TG18-QC).

These images should be captured and archived to be displayed at regular intervals, possibly monthly. These test the overall operation of the system and should be viewed in the same light conditions used in the surgery when viewing digital images. These images should be viewed full-screen for all tests. Whichever test pattern is used, the monitor should be checked for brightness, contrast, resolution and geometric distortion.

There are two squares on the test pattern, one black and one white, which are marked 5 per cent detail on the 0 per cent square (black) and 95 per cent detail on the 100 per cent square (white). Both of these should be distinctly visible and if not the monitor settings should be adjusted until they become so. Most monitors cope better with the 95/100 per cent than the 0/5 per cent but if the ambient light is kept low then both should be clearly visible. (Figure 9)

SSDs contain solid state materials such as amorphous silicon or amorphous selenium in their construction. There are two types of detectors containing either a charge coupled device (CCD) or complementary metal oxide semiconductor (CMOS). The intra-oral systems generally have a flexible cable connecting the detector directly to the PC. Images are collected in real time and can be viewed on the monitor.

The sensors are bulky and rigid and compromised patients, children and elderly, will probably not deal well with SSDs. In comparison to conventional film or PSPs the imaging area is smaller and, as a result, approximately three less points of interest will be captured by the Direct Digital Sensor (Fig 10). Consequently, accurate positioning is essential to cover the area of interest. The presence of the cable will not allow the teeth to be in occlusion during the taking of bite wing radiographs (Fig 11).

A consequence of overexposure could be pixel overload “blooming” which can result in black banding on the image.

ABOUT THE AUTHOR

Barbara Lamb qualified as a general radiographer in 1974 and, since then, has worked exclusively as a specialised radiographer in the dental field.

Further reading

• Brettle D, Carmichael F. The impact of digital image processing artefacts mimicking pathological features associated with restorations. Br Dent J 2011; 211: 167-170.
• Rout J, Brown J. Ionizing Radiation Regulations and the Dental Practitioner: 3. Quality Assurance in Dental Radiography. Dent Update 2012;39: 334-339.
• Greenall C, Drage N, Ager M. Quality Assurance Tests for Digital Radiography in General Dental Practice. Dent Update 2014; 41: 126-134
• Thomas B L, Davies J, Whaites E. Shall I Go Digital? Dent Update 2014;41: 314-326.

Dental material manufacturing companies go to great lengths and spend large amounts of money developing dental materials which, if used correctly, will yield predictable clinical results. Unfortunately, there are many factors outwith the control of the manufacturer which may subsequently contribute to failure of the material, thereby decreasing its longevity.

This article, the first of two on the use and abuse of dental materials, explores the potential problems which can arise even before the dental material has been placed in the mouth and offers practical advice on how these factors may be circumvented to optimise clinical success.

Cause of failure

In 1990, Mjör et al. published a paper examining the cause of failure when working with dental materials clinically. He found that 88 per cent of all failures were technique related, with the balance being material failures. Operator (or more correctly, dental team) variability is one of the commonest causes of failures.

During the manufacturing process, the manufacturer ensures that each product is supplied in perfect condition. However, when the product arrives in the clinic, there is much potential for the material to be compromised by incorrect handling.

Importance of following instructions

Long before the material is manipulated at the chairside, there are various factors which could compromise its clinical success. Very often, the first thing that happens when a new product arrives in the clinic is that the Directions For Use (DFU) supplied with each product is often discarded (Fig 1).

In dentistry, and not dissimilar to the assembly of flat pack furniture, there is a popular misconception that the DFU should only be referred to when there is a problem which the operator cannot solve. It is critically important that the DFU is read carefully prior to use and followed fastidiously.

Dental materials do evolve with time and the manufacturer may make slight modifications to products. Therefore, the DFU will consequently change. The dental team should be cognisant of this and adapt accordingly, otherwise the material may be used inappropriately, resulting in decreased clinical performance.

The member of staff responsible for ordering and stock control could be delegated to check every new pack of material for changes in the DFU upon arrival in the clinic and disseminate these to the rest of the team if necessary. Many clinics collate the DFUs in a materials file for easy reference (Fig 2). Only one set of instructions per product need be kept and this file can be kept centrally where all staff can readily access. The file is also useful for COSHH (Control of Substances Hazardous to Health) purposes.

Effect of temperature and humidity on materials

It is important that the stock room environment is carefully controlled so that materials are stored in optimum conditions and do not degrade prematurely. Unfortunately, this is very often overlooked. It is desirable for the material store to have an ambient temperature and humidity. This may be monitored easily by purchasing an inexpensive gauge from a hardware store (Fig 3).

Temperature has a major influence on materials during storage with extremes having detrimental effects. In a hot environment, materials may prematurely age even before they reach their ‘use by’ date. Furthermore, increased temperature accelerates the setting reaction of the material leading to premature set. As the temperature tends to be higher in the dental surgery itself, it is therefore sensible to keep a minimum amount of material in this room.

At the other extreme, too cold conditions decrease setting time and increase working time. The viscosity of some materials (such as some elastomeric impression materials) may also increase at lower temperature, making them more difficult to mix. Many impression materials are now mixed in a machine and, if the product is not at the correct temperature, its increased viscosity may place undue stresses on the pistons of the machine, potentially inflicting damage.

When mixing cements, if the temperature of the glass slab is reduced to below the dew point (that is the temperature that air must be cooled for water vapour to condense into liquid) then beads of moisture will form on the surface of the slab (Fig 4). This water will then become incorporated into the cement mix, so reducing the powder to liquid ratio and producing a weakened cement.

However, a lower temperature may be beneficial as some materials such as silane coupling agents and whitening agents should be kept in the refrigerator to prolong their shelf life.

Humidity also has an effect on setting time with increased humidity causing premature set. Furthermore, moisture inclusion into the material may be detrimental and is most significant during the mixing phase. An air conditioning unit may be installed in the surgery to maintain a constant temperature and humidity. Rubber dam is an invaluable tool to provide an environment with a lower humidity compared to exhaled air. This is most critical when a bonding procedure is being carried out using hydrophobic materials such as resin composite (Fig 5).

Importance of product packaging

To ensure that each product arrives in an optimal condition, its packaging is carefully designed and presented. The packaging may serve to protect against light and prevents contamination by moisture in the case of photolytic and hydrophobic materials respectively (Fig 6).

For example, as water is required to complete their setting reaction, any uptake of moisture will cause compomers to set prematurely. It is therefore strongly advised that materials are left in their original packaging until ready for use. The manufacturer’s instructions should also be followed with respect to storage, e.g. keep in the refrigerator, dark etc.

Each dental material has an expiry date and this should be checked prior to use. If this date has passed then the material should be discarded as the catalyst may have degraded and undesirably retarding the set of the product.

Factors affecting mixing

Powders should always be shaken prior to use as settling and compaction occurs over time, so more powder will be dispensed, increasing the powder to liquid ratio. The constituents of the powder may also separate during storage and shaking the bottle will mix the contents thoroughly. Similarly, bottles of liquid should be shaken to ensure a homogeneous solution.

Mixing by hand involves a mixing slab or pad made of glass, silicone or paper and the correct spatula which is compatible with the material being mixed. They must then be used together in the correct manner. The choice of mixing pad will depend on the material being mixed. It is recommended that zinc phosphate is mixed on a chilled glass slab to dissipate the heat produced during its exothermic setting reaction as well as increasing its working time. There are advantages and disadvantages to the other pads.

A spatula appropriate for the material being mixed should be selected. For example, a metal spatula should not be used to mix glass ionomer cement as the abrasive glass may abrade the metal of the instrument during mixing and incorporating it into the mixed material, instead an agate spatula should be used (Fig 7).

Finally, the material should be mixed as per the manufacturer’s instructions. Some resin modified glass ionomer cements presented in powder and liquid form rely on micro-capsular technology. This is similar to the ‘scratch and sniff’ panels used in lifestyle magazines to demonstrate perfumes and aftershave scents. During mixing, the shell of the microcapsule must be broken down to allow the active ingredients to be released from the microcapsule to react with the liquid and this will only occur with proper spatulation.

On occasion, when the clinic is running low of a powder, there may be a temptation to use another similar product to compensate, for example using zinc oxide powders interchangeably. This is a very dangerous strategy as often the chemicals contained in powders vary and, therefore, the material at best will not function as intended and at worse may not set. It is, therefore, good advice never to mix dissimilar or unrelated materials.

Encapsulated cements and mechanical mixing

The presentation of the product has a significant effect on the way the material may be mistreated. While hand mixed materials affords the operator more control to vary proportions, materials that are provided as components which the user must mix are most at risk as the potential for error is very high.

Furthermore, it can be difficult to dispense components in the correct proportion of each and difficult to mix a much smaller volume of one with a large volume of the second and ensure even distribution of the two components. To overcome some of the problems with hand mixed materials, manufacturers offer some powder and liquid products in the form of capsules (Fig 8).

These containers hold the active ingredients in separate compartments until activation (Fig 9). The capsule then becomes the mixing chamber and delivery vehicle. As with hand mixed powders, it is important that the capsule is shaken prior to use to ensure that all of the constituents of the powder are thoroughly mixed.

Pressure must also be applied to the capsule for two seconds so that all of the liquid can be expressed from the pillow to yield the correct powder to liquid ratio. While the desired mix may be more consistently produced, there are some limitations with capsules. It is difficult for manufacturers to provide a precise dose of powder and metering of small volumes of liquid to fill the pillow produces some variation.

Additionally, a small nozzle, which may be the most appropriate size for precise delivery into the cavity, may not be able to physically extrude (more viscous) material with a higher powder to liquid ratio.

The dental team should be aware that different mechanical mixing machines may exhibit different types of movement, such as a figure of eight oscillation or a rotatory movement. The amount of energy imparted to the material contained within the capsule differs due to the throw of the mixing arm and the speed of oscillation. The machine should be set to the correct speed and movement applicable to the product being mixed.

The correct mixing time should also be carefully adhered to. For example, too short a mixing time will realise an incoherent mass with the powder and liquid inadequately mixed. Too long a mixing time will produce a reduced working time and accelerated set. There may also be a reduction in the mechanical properties of the material in some cases. It sounds obvious but the correct time will produce the correct mix and this information may be gleaned from the DFU.

Light-cured product evolution

Although mechanical mixing may eliminate many potential errors, it is not a panacea and not without shortcomings. For this reason, compules (also known as Tips or Cavifils depending on the manufacturer) have evolved. These are small cylindrical containers with a delivery tip and plunger and contain all the active ingredients already mixed together by the manufacturer into an injectable paste (Fig 10).

This is advantageous for many reasons. Firstly, the proportioning of the ingredients and the mixing of the materials are optimised. Secondly, the risk of incorrect mixing is reduced as the components are already blended together, and, thirdly, the product should be (almost) free of air voids. These materials require an external energy source (such as visible light) to initiate the setting reaction.

Cartridges

The other modern method for the mixing and delivery of (impression and bite registration) products are paste-paste systems supplied in cartridges. A spiral tube with a varying number of helical turns (the number depending on the viscosity of the material) which both mixes and delivers the paste is attached to the cartridge containing the base and catalyst (Fig 11).

The material may be conveniently extruded at the site of use. Partly used cartridges should be stored with the previous mixing tip in situ (Fig 12). The original cap should be discarded after the product has been opened and never replaced, as base and catalyst retained at the orifices of the tubes may come into contact, so setting and occluding the exit ports. The set material will also form a seal preventing contamination from the environment.

Some impression materials are incompatible with certain mixing machines. This is a clever marketing ploy employed by some manufacturers to ensure that only their own products can be used in the machine to protect their commercial interests. Without stating the obvious, the dental team should ensure that any new product is compatible with the machine in the clinic.

Conclusions

As has been illustrated in this article, there are many pitfalls into which the dental team may fall when handling dental materials, even before they have been placed intra-orally. The most significant is operator variability which accounts for the commonest causes of failures.

This is despite the efforts of dental manufacturers who have attempted to produce materials which are as foolproof as possible. It is therefore imperative that the dental team reads and follows the DFU to ensure optimum performance and treatment outcome.

The author

Mr Steve Bonsor graduated from the University of Edinburgh in 1992 and in 2008 gained a MSc in Postgraduate Dental Studies from the University of Bristol. From 1997 until 2006 Steve was a part-time clinical teacher at Dundee Dental Hospital and School and honorary clinical teacher at the University of Dundee in the sections of operative dentistry, fixed prosthodontics, endodontology and integrated oral care.

He currently holds appointments at the University of Edinburgh, as an online tutor on the MSc in Primary Dental Care programme and at the University of Aberdeen as honorary clinical senior lecturer leading the applied dental materials teaching at Aberdeen Dental School.

As well as lecturing throughout the UK, Steve is actively involved in research, having published original research articles in peer-reviewed journals. His main research areas are photo-activated disinfection and the clinical performance of dental materials.

Literature on the management of dental trauma in general practice suggests that difficulties may be encountered due to gaps in knowledge and a lack of training on the subject.

Barriers to providing this care include lack of time, lack of confidence in diagnosis and inadequate remuneration (Hamilton et al 1997, Stewart and Mackie 2004, Jackson et al. 2005, Hu et al. 2006). Coupled with this is the fact that these patients may present relatively rarely in practice, adding to the stresses associated with management.

The keys to managing traumatic injuries involve correct technical management underpinned by a sound knowledge of the biological processes at play. This incorporates detailed history-taking, prompt emergency management and structured long-term follow-up to deal with the delayed complications often encountered.

How, what, when, where?

Initial interview of the patient must focus on any potential head injury, with emphasis on whether there has been a loss of consciousness. Often, many patients may have attended a local emergency department for immediate management prior to presentation at a dental practice.

One of the primary goals of immediate patient management is reassurance. History taking should begin with questioning of the patient in relation to how the injury occurred. The patient should be allowed to give their version of events with minimal interruption from the clinician. This component of the history may be especially important if there are any criminal or civil proceedings which may follow.

Interview in relation to the type of injury the patient has suffered may begin to shed light on the severity of the injury and the tissues involved. It is important to ask the patient what they feel has happened to their teeth i.e. whether the teeth are broken or not and whether there have been any alterations to the occlusion. History-taking should encourage the patient to use their own words to describe the injuries. Examination of previous photographs may shed light on the pre-operative situation. Interestingly, Dental Trauma UK, a new charity recently founded in the UK, has recommended that clinicians encourage the general public to join the “selfie” craze, taking a photograph of their smile, thereby providing invaluable information for the clinician managing a dental trauma.

The time elapsed since the injury may have an effect on pulpal and periodontal ligament survival and influence our decision-making in relation to the treatment we choose. Re-implantation of an avulsed tooth may not be possible if an extended time has passed since the injury due to clot formation and remodelling of the socket.

The site of the injury may influence our decision on whether the patient will need tetanus prophylaxis although, as aforementioned, this may often have been dealt with in a hospital setting. The site of the injury may also need to be searched for any missing tooth fragments, while cleaning of avulsed teeth contaminated with any gross debris will need to be completed before an attempt at re-implantation.

Immediate management

A traumatic injury to the dentoalveolar complex is an upsetting and worrying injury to any patient. It can also be a stressful occurrence for the dentist which, thankfully, may present relatively rarely in general practice.

Patients often present with multiple soft and hard tissue injuries and, in the first instance, it can be difficult to identify and diagnose the injuries. A calm approach is essential at this early stage, both to reassure the patient and to avoid missing any important detail during this initial examination (Fig 1).

The emergency management should commence with cleaning of the injured site. This can readily be accomplished using some sterile gauze soaked in chlorhexidine. It is wise to avoid using compressed air and water from the “3 in 1” syringe in the first instance to avoid startling an already nervous patient and to avoid disruption of the injured soft tissues. Although rare, this may lead to introduction of air into the soft tissues leading to a surgical emphysema.

Initial assessment of the injured site should be done by visual inspection, noting any malposed and fractured teeth, with attention paid to any previous treatment which may have been carried out. This should be followed by careful digital palpation of the site, taking care to identify any step deformities or mobility of the alveolar bone. This may be indicative of luxated teeth or fracture of the alveolar bone. Priority should always be given to treatment to encourage bony union during healing as the consequences of poor healing can be catastrophic.

Imaging

Radiographs are an essential tool in the diagnosis of dental trauma and a decision on which types and angles must be taken at the initial assessment appointment. As a rule of thumb, periapical radiographs of the maxillary anterior teeth (3-3) should be taken following a moderate injury to the maxillary anterior teeth. A decision on whether to take radiographs of the corresponding mandibular teeth can be taken depending on the results of the clinical examination and the perceived severity of the injury. Location of tooth fragments within the soft tissues is best done using a combination of digital palpation along with reduced exposure of a large periapical film. More recently, cone beam CT has been used in the diagnosis of traumatic injuries, offering the advantage of three dimensional assessment of displaced and injured teeth (Patel et al. 2007). This can offer great benefit in the case of dentoalveolar fractures and luxated teeth, often difficult to identify on standard periapical radiographs.

Classification of injuries

Classification of dental trauma is often complicated by the concomitant injury of multiple tissues. A thorough understanding of the tissues at risk of injury is critical to facilitate correct diagnosis and management of these injuries. As aforementioned, priority should be given to the treatment of any bony injury in order to minimise the risk of more severe complications later. A proposed classification of traumatic injuries in increasing order of severity is shown in Table 1.

Table 1

Repositioning and splinting

Adequate anaesthesia must always be achieved prior to any clinical intervention post trauma. This is essential to allow for adequate manipulation of injured tissues and to avoid adding to the patient’s stress. Repositioning of luxated teeth should begin with an understanding of how the injury has occurred and how this may have altered the position of the root within the alveolar housing. Frequently, the apices of luxated teeth may be “locked” into the alveolar bone.

Re-positioning, therefore, requires a firm but controlled force on the alveolar bone in order to manipulate the tooth into position. A clicking sound is often heard when this is done correctly. Palpation of the overlying soft tissues afterwards to assess labial contour helps to confirm this.

It is imperative in the case of avulsed teeth that they are first gently cleaned under running water while holding the tooth by the clinical crown. This ensures removal of any gross debris prior to an attempt at re-implantation. Storage medium and extra-oral dry time are two critical prognostic factors in the outcome following avulsion injuries, with literature suggesting the risk of replacement resorption being much higher in those teeth with a dry time of greater than 60 minutes (Andreasen 1981, Andersson et al. 1989). Patients should also be advised to store avulsed teeth in either milk or saliva (possibly even intra-orally) as opposed to in water. Ideally, an attempt at re-implantation should be made immediately although this may prove difficult in terms of positioning and angulation for those not familiar with the situation. Other storage media (Khademi et al. 2008) have also been proposed. However, they may not be readily available at the time of injury (Figs 2 and 3).

A variety of splinting protocols have been proposed for the stabilisation of injured tissues (Table 2).

Basic biological principles should be adhered to when fabricating a chairside splint. Wire-composite splinting is most commonly used and adheres to these principles if placed correctly. Guidelines previously recommended utilisation of rigid and non-rigid splints for different injuries but this has now been replaced by a protocol of non-rigid splinting for all injuries, of varying duration. This usually takes the form of an 0.16 Ni-Ti orthodontic archwire, although newer products on the market may supersede this (Fig 4).

Care should be taken initially to pre-bend the wire where possible to adapt it well to the labial surfaces of the injured and supporting teeth. This avoids application of an orthodontic force to the region. Teeth should be spot etched at the mid-labial aspect and a small amount of bonding agent added with the tip of a probe. Over zealous application of bonding agent results in difficulties in the removal of excess composite at the splint debond appointment. This may have obvious implications for direct physical trauma and potential heat transfer to an already injured pulp.

Composite should be placed at the mid-labial aspect of the teeth, well clear of the gingival margin and should be polished to avoid any overhangs, which may act as a plaque trap and a source of irritation to the patient. Splinting of teeth by direct composite union should be avoided due to its rigid nature, difficulties in maintaining oral hygiene and in removal.

Table 2

Review protocol

A robust review protocol is essential in the management of these cases. Various timings have been suggested and a common sense approach should prevail. The necessity for regular review is dependent on the severity of the initial injury and the likelihood of healing complications later. In general, review should be arranged one week, two weeks, four weeks, three months and six months following the date of the injury although slight variations have been proposed to this.

The key to review of traumatic injuries lies in establishment of baseline readings at the initial appointment and subsequent repetition of the examination and recording of results. This can be aided by the development of a custom trauma screen for in-office dental software or a simple stamp for written records. This ensures that nothing is missed at review.

Care must be taken in the interpretation of the results of sensibility tests in the aftermath of these injuries. Literature has suggested that teeth presenting giving positive responses at the initial appointment have a better pulpal prognosis but a period of monitoring is essential before committing any tooth to root canal treatment. The only exception to this appears to be avulsed permanent teeth, in which treatment can be initiated immediately.

A common sense approach should be adopted towards repeat radiographic examination. Over-exposure of the patient by taking excessive numbers of radiographs is ill-advised both in terms of the ALARA (as low as reasonably achievable) principle and also in terms of diagnostic yield.

Splint removal based on the timings outlined above is best carried out by removing the composite from the injured tooth/teeth first. This allows for their assessment in terms of mobility prior to deciding on whether to debond the whole splint or not. This saves time and avoids subsequent manipulation of injured teeth (Fig 5).

Definitive endodontic treatment

A decision on the necessity and timing of endodontic treatment on traumatised teeth must be taken following comparison between the clinical and radiographic findings at the initial appointment and subsequent review.

Various literature proposes the strategy of waiting for a period of three months, during which pulp sensibility tests give negative responses prior to initiating root canal treatment on injured teeth. The obvious exception to this is in the case of an avulsed tooth with a closed apex. Root canal treatment is advised immediately in this situation although practically, clinicians may often delay this by one week. This allows the focus of the initial appointment to be on patient reassurance and emergency management. Additionally, healing of soft tissue injuries will have progressed well during that initial period.

Caution must be exercised in interpreting the results of pulp sensibility tests following a traumatic injury. The injured pulp may be in a state of ‘shock’ and may not respond positively to the stimulus applied. Equally, it is well documented that immature teeth may give erroneous results due to the lack of development of the pulpal neural network. A prolonged delay leading to necrosis of the pulp, however, may affect the outcome of root canal treatment and put the tooth at risk of catastrophic resorption.

Where possible, endodontic treatment should be commenced with the splint in place as this confers extra stability on the injured teeth during the procedure. This is usually limited to teeth which have suffered an avulsion injury due to the recommended splinting times (Table 2) and the timing of definitive treatment. It may also lead to difficulties in rubber dam placement, with the split dam technique in the isolation of multiple teeth being necessary.

Timely management of complicated enamel dentine fractures is essential to optimise the outcome. Depending on the duration of pulpal exposure, the goal must be maintenance of pulpal vitality in these cases. Any direct exposures should be capped using a slurry of non-setting calcium hydroxide and restored with a glass ionomer cement base followed by a composite restoration. While mineral trioxide aggregate (MTA) remains the gold standard material for pulp capping of posterior teeth, caution must be exercised in the use of both grey and white MTA in these cases as subsequent discolouration of the tooth may provide an aesthetic challenge in the future. Biodentine may provide a suitable alternative in non-load-bearing areas.

Endodontic access to injured teeth is often straightforward due to their anterior location and lack of complex anatomy. Care must be taken to design and position the access cavity correctly, ensuring that the pulp horns are included to allow for removal of necrotic debris and access for irrigant. This prevents subsequent discolouration of these teeth post-treatment. Access may prove much more difficult in the case of traumatised incisors which have undergone pulp canal obliteration (PCO). Several groups have reported that 4-24 per cent of teeth undergo these changes in response to traumatic injuries, while McCabe and Dummer (2012) highlighted a useful series of steps to follow clinically in the management of this clinical scenario.

Instrumentation and irrigation of the root canal system should be carried out adhering to the biological principles of endodontic treatment. Difficulty may be encountered in determination of working length (WL) in teeth with open apices or in those with crowns and should be confirmed radiographically where doubt exists over the accuracy of the electronic apex locator (EAL) reading. Teeth suffering from horizontal root fractures should only be instrumented to the level of the fracture line and not beyond (Fig 6). The apical fragment of these teeth is almost always vital and unnecessarily instrumenting and obturating it poses difficulties for the clinician. Care must also be taken in the placement of the irrigation needle in close proximity to an open apex or root fractured tooth to avoid extrusion of sodium hypochlorite, the gold standard irrigant in such cases where dissolution of pulpal tissue is essential.

Various inter-appointment medicaments have been proposed for traumatised teeth with Ledermix showing promising results in the case of avulsed teeth (Bryson et al. 2002). This may not now be readily available in the UK and Odontopaste is proving to be a reliable alternative. In the case of other traumatic injuries, non-setting calcium hydroxide is advised.

Prior to the advent of MTA for the apexification (physical apical barrier formation) of immature teeth, long term dressing with calcium hydroxide was common. This proved to be a time consuming and unreliable method of barrier formation and potentially pre-disposed teeth to cervical fracture (Andreasen et al. 2002). MTA placement in these cases is best achieved using an apical placement system such as a Dovgan carrier or the Micro Apical Placement System by Dentsply.

Such devices simplify the technique and ensure placement of an adequate thickness of the material, while avoiding extrusion (Fig 6). The remaining canal is often best obturated using a thermoplasticised technique thereby minimising voids in the root filling.

More recently, case reports have emerged of revascularisation of teeth with open apices using combinations of antibiotics (Banchs and Trope 2004), combinations of irrigants (Shin et al. 2009) or simply sodium hypochlorite and EDTA, along with MTA. Results of these are promising, although doubts remain regarding the structure and origin of such regenerated tissue as it appears to be more similar to bone than pulpal tissue.

Discolouration of traumatised teeth may also pose problems in management. As aforementioned, care must be exercised to remove remnants of pulpal tissue from the pulp horns in access cavity design and the root filling material should always be compacted to a level 1mm below the cervical level of the tooth. This avoids subsequent discolouration from residues of root canal sealer and allows for correct placement of composite. The current protocol for non-vital bleaching of root-filled teeth dictates that bleaching agents containing a maximum of 6 per cent hydrogen peroxide are allowed. The “walking bleach” technique often results in acceptable aesthetic results for patients and clinicians alike.

Complications and prognosis

The biological complications following a traumatic injury to the dento-alveolar complex most frequently involve the pulp and the periodontal ligament (PDL). These healing complications are primarily a result of the extent of the injury (often the physical displacement of the tooth/teeth) and the efficiency with which we manage the injury.

Pulpal necrosis

While the severity of the initial injury is a prognostic factor for pulpal survival following trauma, the stage of development of the tooth is also important. Intuitively, we would assume that teeth with immature apices have a greater repair capability and this is borne out in the literature. Reports on pulpal revascularisation appeared in the literature as early as 1978 (Skoglund et al. 1978) and more recently, various protocols have been proposed in order to potentially regenerate injured and even partially necrotic pulps.

Literature suggests that the incidence of pulpal necrosis in permanent incisors is high in teeth suffering severe lateral luxation, intrusive and obviously avulsion injuries. In the case of horizontal root fractures, the degree of separation between the coronal and apical fragments often dictates whether the coronal pulp survives. In the case of an avulsed tooth,necrosis is almost certainly inevitable and endodontic treatment should be initiated within 10 days to limit the potential for associated complications.

Resorption

Dental resorption involves the removal of mineralised dental tissues and, according to Fuss et al. (2003), involves two distinct phases, injury and stimulation. In dental trauma cases, there are a number of categories of resorption which concern us and these are specifically related to certain injury types. In essence, resorption involves the loss of hard tissue while the unmineralised predentine and precementum remain protected. This protection of the predentine layer has been attributed to an unknown “protection factor” (Wedenberg 1987). While a detailed description of resorption is beyond the remit of this article, an outline of the types is given below.

Internal inflammatory resorption (IIR) may arise following a traumatic injury in the presence of a partially necrotic pulp. Bacterial contamination in the root canal system may act to stimulate an inflammatory response in the remaining pulpal tissues, with the subsequent loss of dental hard tissues. This presents as a ballooning radiolucency of the anatomy from the internal aspect of the root canal.

Infection may also act as a stimulus for external inflammatory resorption (EIR), with the dentinal tubules acting as a pathway for exit of bacteria and their associated by-products to the periodontium. These lesions present as radiolucencies at the lateral aspects of the root or in the apical region (Fig 7). Radiographically, the radiolucency is often superimposed over the root canal, with the lines of the root canal anatomy visible.

As the aetiology suggests, our management of these cases should focus on the removal of the infective stimulus which will halt the resorptive process. It is critical that we do not misdiagnose such cases or delay commencement of root canal treatment in traumatised teeth for too long, as the effects of the process can lead to devastating loss of hard tissues.

Often, our dilemma as clinicians is between allowing an injured pulp every chance to exhibit signs of recovery, while not delaying our treatment for too long. Importantly, not all types of resorption are as damaging and this often depends on the extent of the initial injury. In some trauma cases, we may see subtle signs of an EIR process which seems to self limit and cease over time.

Replacement resorption arises due to damage to the external surface of the root and is common after avulsion injuries, especially those teeth with a long extra-alveolar dry time or those that are mishandled (both in terms of manual handling and storage medium). This process essentially involves loss of dental hard tissue and subsequent replacement with bone. With injured teeth losing their aforementioned protective layer, bone resorbing osteoclasts begin this process of replacement resorption. Unfortunately, our knowledge of this disease process is limited and it may continue gradually until an entire root has been resorbed.

Various figures have been proposed to define the extent of replacement resorption needed to cause ankylosis of an injured tooth, with 20 per cent being suggested. Such teeth will, of course, lose their physiological mobility and have a high or metallic percussive tone. It is best to continue to monitor these cases and inform the patient of the likely complications which may arise in the future.

Conclusion

Management of injuries to the dentoalveolar complex involves strict adherence to biological principles and a common sense approach to the technical aspects of the treatment. Our approach at all times should be targeted at facilitating efficient healing of the tissues and allowing adequate time for this to occur. A regular and structured review protocol should be implemented with strict attention being paid to the possible healing complications, their appearance and the effect on prognosis.

About the author

Dr Robert Philpott, BDS MFDS MClinDent MRD (RCSEd), qualified from Cork Dental School in 2003 and completed his endodontic training at the Eastman in London in 2009. He has worked as a specialist in endodontics in Ireland, London and Australia. He currently divides his time working as a consultant in endodontics at Edinburgh Dental Institute and in private practice at Edinburgh Dental Specialists.

Further reading

Readers are directed to the following websites:
www.dentaltraumaguide.org
www.dentaltrauma.co.uk

References

• Andersson L, Bodin I, and Sorensen S. ‘Progression Of Root Resorption Following Replantation Of Human Teeth After Extended Extraoral Storage’. Dental Traumatology 5.1 (1989): 38-47. Web.
• Andreasen JO ‘Effect Of Extra-Alveolar Period And Storage Media Upon Periodontal And Pulpal Healing After Replantation Of Mature Permanent Incisors In Monkeys’. International Journal of Oral Surgery 10.1 (1981): 43-53. Web.
• Andreasen JO, Farik B, and Munksgaard EC. ‘Long-Term Calcium Hydroxide As A Root Canal Dressing May Increase Risk Of Root Fracture’. Dental Traumatology 18.3 (2002): 134-137. Web.
• Banchs F, and Trope M.‘Revascularisation Of Immature Permanent Teeth With Apical Periodontitis: New Treatment Protocol?’. Journal of Endodontics 30.4 (2004): 196-200. Web.
• Bryson EC, et al. ‘Effect Of Immediate Intracanal Placement Of Ledermix Paste On Healing Of Replanted Dog Teeth After Extended Dry Times’. Dental Traumatology 18.6 (2002): 316-321. Web.
• Fuss Z, Tsesis I, and Lin S. ‘Root Resorption – Diagnosis, Classification And Treatment Choices Based On Stimulation Factors’. Dental Traumatology 19.4 (2003): 175-182. Web.
• Hamilton FA, Hill FJ, and Holloway PJ. ‘An Investigation Of Dento-Alveolar Trauma And Its Treatment In An Adolescent Population. Part 2: Dentists’ Knowledge Of Management Methods And Their Perceptions Of Barriers To Providing Care’. Br Dent J 182.4 (1997): 129-133. Web.
• Hu LW, Prisco CRD, and Bombana AC. ‘Knowledge Of Brazilian General Dentists And Endodontists About The Emergency Management Of Dento-Alveolar Trauma’. Dental Traumatology 22.3 (2006): 113-117. Web.
• Jackson NG, Waterhouse PJ, and Maguire A. ‘Management Of Dental Trauma In Primary Care: A Postal Survey Of General Dental Practitioners’. Br Dent J 198.5 (2005): 293-297. Web.
• Jafarzadeh H and Abbott PV. ‘Review Of Pulp Sensibility Tests. Part I: General Information And Thermal Tests’. International Endodontic Journal 43.9 (2010): 738-762. Web.
• McCabe PS and Dummer PMH. ‘Pulp Canal Obliteration: An Endodontic Diagnosis And Treatment Challenge’. International Endodontic Journal 45.2 (2011): 177-197. Web.
• Mousav B et al. ‘Standard Oral Rehydration Solution As A New Storage Medium For Avulsed Teeth’. International Dental Journal 60.6 (2010): 379-382. Web.
• Patel S, et al. ‘The Potential Applications Of Cone Beam Computed Tomography In The Management Of Endodontic Problems’. International Endodontic Journal 40.10 (2007): 818-830. Web.
• Shin SY, Albert JS, and Mortman RE. ‘One Step Pulp Revascularisation Treatment Of An Immature Permanent Tooth With Chronic Apical Abscess: A Case Report’. International Endodontic Journal 42.12 (2009): 1118-1126. Web.
• Skoglund A, Tronstad L, and Wallenius K. ‘A Microangiographic Study Of Vascular Changes In Replanted And Autotransplanted Teeth Of Young Dogs’. Oral Surgery, Oral Medicine, Oral Pathology 45.1 (1978): 17-28. Web.
• Stewart SM, and Mackie IC. ‘Establishment And Evaluation Of A Trauma Clinic Based In A Primary Care Setting’. International Journal of Paediatric Dentistry 14.6 (2004): 409-416. Web.

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