Diabetes Mellitus & Dentistry
If recent predictions in the popular press are to be believed, then one in seven of the British population and perhaps a similar percentage in other Western societies are suffering from diabetes mellitus and one in three have incipient and undiagnosed pre-diabetes. At first sight this will be a major problem for both our medical colleagues, politicians and the healthcare fund holders, but it may have little effect on our professional lives in dentistry. Unfortunately such dental optimism is as far from the truth as we can get, and as of now, dentists are, or should be, very involved with this group of patients.
There are two main groups of diabetics;
Type I – In this group there is an absolute deficiency of insulin. They are usually, but not necessarily in a younger rather than older age group.
Type II – This group is associated with both insulin resistance and a deficiency. It is usually found in older age groups and is associated with obesity, although this is by no means the only association.
Gestational Diabetes, during pregnancy
Other, associated with other diseases or drug use
Traditionally diabetes has been diagnosed following a fasting blood glucose or a glucose tolerance test. A more simple test for diabetes by measuring HbA1C in blood is now available. This method counts the number of glucose molecules attached to red blood cells during their three month life span. If the blood sugar is between 6.0 and 6.4, this is prediabetes, if above 6.5 mmol/L it is officially diabetes. The target of treatment is to maintain this glycolysated haemoglobin at below 6.5 per cent as this has been shown to lead to fewer diabetic complications.
Risk factors for diabetes include age, obesity and genetics especially for Indian and African peoples.
Both types of diabetes mellitus have serious complications including
- retinopathy leading to blindness,
- both micro and macro arterial disease, often leading to amputations of limbs.
- The sixth, dental, complications, and ones which has received much less publicity, are periodontopathy and xerostomia, and this, of course is of direct relevance to us dentists. Other dental symptoms, caused by neurological changes, include burning mouth and tongue and altered taste sensations.
These risks increase in smokers and with any concomitant condition affecting immunity and the immune response.
We can define periodontal disease as the loss of bony support to the teeth, increased pocket depth and inflammation of the surrounding tissues caused by the body’s reaction to plaque, whilst xerostomia is reduced salivary output with its risk of developing caries. High blood glucose levels are also associated with an increased incidence of oral thrush in its various forms.
Periodontal disease is a reaction to toxins produced by dental plaque and whilst often described as an ‘infection’ it is not, but an abnormal immune response with reduced levels of tissue healing, the severity and progression of which depend on the host response to biofilm. Periodontal disease does not follow the pattern of a classical infection because it does not follow Koch’s Postulates which require:-
- There must be a specific infective agent that can be collected.
- That agent must be capable of being grown in a pure culture.
- If that agent is reintroduced into a host it must give rise to the same disease.
- The agent must be collectable again and be regrown in a pure culture.
Diabetic periodontopathy was first recognised by Williams in 1928, but his findings seem to have fallen by the wayside for many years. However, more recent research has shown as close inter-relation between diabetes and periodontal disease, the one affecting the other and vice versa.
It is now quite clear that diabetes and periodontal disease provide an example of systemic disease predisposing to oral ‘infection’, and once oral ‘infection’ is established, this exacerbates systemic infection. More recent research has shown that:
- Diabetics and non-diabetics have a similar oral flora.
- Diabetics have an increased susceptibility to infection and delayed wound healing.
- There is a common pathogenesis between diabetes and periodontal disease involving an enhanced inflammatory response at both local and systemic level. This is caused by the chronic effects of hyperglycaemia and formation of glycated proteins and lipids that promote the inflammatory response.
- This interrelationship between diabetes and periodontal disease provides an example of systemic diseases predisposing to oral ‘infection’, and once that ‘infection’ is established there is an exacerbation of systemic disease.
- Diabetics have significantly higher levels of local inflammatory mediators, especially cytokines, when compared with systemically healthy people with periodontal disease.
- The severity and progression of periodontal disease and diabetes often does not correlate with the presentation in non-systemically challenged patients.
- The severity of periodontal disease in diabetics may not correspond to levels of bacterial plaque observed clinically.
- C reactive protein levels are raised in both diabetes and periodontal disease.
Various mechanisms for this altered immune response in the periodontal tissues of diabetics have been suggested, including:
- Microvascular disease
- Changes in crevicular fluid
- Changes in collagen metabolism
- Altered host response
- Altered subgingival flora
- Genetic predisposition
- Non-enzymatic glycation
In summary, periodontal disease and diabetes mellitus affect each other. There is some early evidence to suggest that individuals with periodontal disease may be at higher risk of developing Type II diabetes, that is to say, there is a two-way street between these diseases. The one affects the other to the extent that, when periodontal disease is brought under control, the HbA1C level falls, and there can be a reduced requirement for insulin dosage. It also follows that diabetics who smoke have a significantly higher, ten times, risk of developing periodontal disease than non-smokers.
Individual Preventive Strategy
The emphasis for individuals is to improve their personal plaque control, to reduce the numbers of bacteria and biofilm both supra- and sub-gingivally using toothbrushes, floss and interspace brushes.
These patients will also require frequent professional interactions, in depth education, and consistent educational reinforcement.
This means that all diabetic patients should be advised by their General Medical Practitioners that they are at increased risk of developing periodontal disease and need to seek regular dental care. However, unless there is other publicity, I have serious doubts that this will happen. I have offered my own teaching practice doctors a short talk on this, without response. If this is the national pattern then the long term implications for dentistry are huge.
We know that approximately 15 per cent of the present population have major periodontal problems requiring care from either specialists or GDP’s with a special interest in the treatment of periodontal disease. How will they cope with an influx of 5, 10, 15 or 20 per cent increase in workload? If this potential explosion in numbers of patients requiring an enhanced level of care is not met, then more teeth will be lost, and consequently more people will require dentures. Alveolar bone loss can be extensive in these cases leading to very flat ridges and greater clinical difficulty in providing satisfactory prostheses. This will create other problems, as the numbers of both dentists and dental technicians with extensive experience in denture making has fallen. This is a direct result of professional achievement in helping patients keep their natural dentitions for longer (see the Salisbury/Darlington comparisons). There is thus a significant risk that these achievements will be reversed in future.
Secondly, implants can often help patients with alveolar bone loss achieve retentive and stable dentures. Where will the appropriately trained and experienced clinicians to treat these cases come from and who will bear the cost given the severe constraints on NHS budgets that are expected to be a constant feature for the foreseeable future?
Periodontal disease progression.
The evidence is overwhelming that the alveolar bone loss associated with periodontal disease is the result of a complex inflammatory response to plaque antigens. It follows that, if individual patients can be educated and persuaded to fully control their plaque on a daily basis, then the inflammatory reaction will subside. This has been considered in more detail in the series about periodontal disease in Dental Practice earlier this year by Dr Matt Perkins.
However, the question remains why does periodontal disease and bone loss commence interproximally? The answer is quite simple, because that is where patients routinely and persistently leave plaque with their usual brushing technique with conventional brushes. You have only to watch TV toothpaste advertisements, your patients or TV presenters brushing their teeth in a backwards and forwards motion to understand that this is the most manually confortable method of use. However, this will always miss removing plaque in the dental interspace (Fig 1).
Up and down brushing methods are not much better. Electric toothbrushes may help but only if sufficient time is allowed when brushing. Again, observing how patients use their toothbrushes is very instructive as so few can demonstrate a systematic approach to cleaning. The usual finding, rather like a certain insurance company advertisement is ‘a little bit here and a little bit there’ with some sites frequently missed. It is no wonder then that periodontal disease progresses, often in an irregular pattern.
Teaching patients to floss where appropriate is another tool in plaque control whose effectiveness will depend on individual manual dexterity.
As interproximal bone is progressively lost then interproximal spaces will develop for which interspace brushing is the obvious method of plaque control. I make no apology for covering this topic again and drawing colleagues attention to my computerised charting method accessed at www.spacemark-d.com. This programme will allow for recording the correct brush diameter prescription suitable for both dentists and patients use. In this regard I take serious issue with dentists or hygienists who tell patients to use interspace brushes without proper professional guidance, or prescribe just one or two sizes in the mistaken belief that their patients cannot remember. Prescribing a small brush in a large space results in neither effective or efficient plaque control.
For the avoidance of doubt, diabetics have to learn to manage their blood sugar levels following suitable education and guidance. That being the case, the vast majority are perfectly capable of managing and controlling their plaque, providing that the dental profession gives them similar individually targeted, detailed, appropriate and written advice.
Public Health Preventive Strategy
In the section on individual preventive strategy I emphasised the need for in depth education and consistent educational reinforcement. In practice this means that Public and Professional Bodies need to get their act together with front line clinicians. There is no sign that this is happening yet. I strongly suspect that there will be the usual amateurish fudge so typical to British responses to issues of this kind.
The matter is made more complicated because health care in the UK is devolved to the Welsh and Northern Irish Assemblies, the Scottish Parliament as well as the Westminster Government for England. The likelihood is then that each will invent its own wheel in the short term, but in the long term there may just be the possibility of adopting best practice from each jurisdiction.
Here are my suggestions to start this process.
National Health Departments
The main general educational focus has to be yours. You could start with a simple poster campaign placed in every hospital diabetic clinic (and GP practice ?) to advise diabetics to seek regular dental care because diabetes and periodontal disease are interrelated. When all these extra patients require extensive dental treatment in the future you will be picking up that bill. Remember an ounce of prevention is better than a pound of cure. Will this happen? I doubt it, but challenge the four Chief Dental Officers to prove me wrong.
The new NHS dental contract is claimed to promote the prevention of dental disease. With the above risk factors, diabetics will need special, extra consideration.
The Diabetes Now website does mention periodontal disease as a complication of diabetes without explaining in detail what it is or what the consequences can be. I found no mention of the other dental complication xerostomia with that disease’s potential for significantly increasing the risk of rapidly developing and extensive caries.
British Dental Association
Where is your voice on this matter? You seem to me to be just a reactive organisation answering specific questions from journalists, as reported in the popular press, from time to time. You obviously have good contacts with the Press. I suggest you need to become proactive and start to publish articles on a regular basis to inform the public of the medical problems associated with periodontal disease, diabetes, heart disease, miscarriages, rheumatoid arthritis, possibly some forms of nephropathy and Alzheimer’s and urge attendance for preventive care.
Have you considered the manpower implications for all the extra dental treatment that could be required in future? Do you have an information and guidance leaflet for your Members on this important issue? When will you publish a comprehensive examination, advice and treatment schedule for UK dentists to follow for this group of patients rather than leaving matters to individual choice, which are likely to range from, on a normal distribution curve, from excellent to inadequate?
British Dental Health Foundation
You have done a great job to increase the awareness of oral cancer and promote early attendance for professional assessment. However, the numbers though important are relatively small when compared with the potential number of patients with diabetic periodontopathy. Can I urge you to start a new campaign for this group too.
General Medical Practitioners
Advise each diabetic patient to attend for dental examination and care and record who is the GDP. This may be a ‘tick box’ exercise, but hopefully it will start an interprofessional dialogue between doctors and dentists, something I have found consistently lacking during my career. Provide the GDP with details of your care including HbA1C blood test results.
General Dental Practitioners
You will already have taken a comprehensive medical history for each patient and updated it regularly at recall appointments. You should record the name of your patient’s GP and their phone number and be prepared to discuss individual patients especially if their periodontal status is continuing to deteriorate and be prepared to share your dental findings whilst requesting medical results. It also follows that, if you have a patient with developing periodontal disease that has an atypical pattern you must consider diabetes or prediabetes as a contributing factor and refer your patient to his/her GP for blood sugar investigations, especially Hba1C levels.
Accurate, ongoing dental records are essential and here I think the Basic Periodontal Examination is insufficient as it is avery crude measurement of periodontal disease originally devised for epidemiological studies. The scle of 0 to 4* is confusing for patients as it implies a gradual worsening rather than the real apples and pears distinctions with each number dentist know to be the case. I urge full 6 point pocket depth measurements, a bleeding index, record of gingival recession, plaque control and full mouth radiographs to establish bone levels against which comparisons can be made at future appointments, and intra-oral photographs. The move away from chemically processed to digital radiographs is a welcome development, as they can be rapidly viewed. However, if you have more traditional films then the worst thing you can do is put them into one, or more, of those white film packets, simply because they will rarely be viewed again. The human eye is better able to see change on a series of radiographs, so at the very least, all such films should be mounted and dated for this purpose. This also raises the question about the timing of repeat radiographs to avoid unnecessary radiation. This will have to be determined by clinical presentation and the rapidity or otherwise of periodontal deterioration. For apparently well controlled cases, perhaps further radiographs at 3 yearly intervals is indicated.
The Access to Medical Records Acts of 1991 and 1998 gives every patient the legal right to obtain their notes from you. In my experience you will obtain a better patient response if you show your patients what is happening from your examination and special investigations. Even better give your patient a copy of their pocket measurement chart, and Spacemark interspace brushing chart if you have prepared one, and further copies at yearly intervals. In this way patients can see for themselves where there is any deterioration, and this could well be a powerful motivator to improve plaque control.
Stage one of treatment is to remove supra and subgingival calculus and biofilm, the latter of which can only be removed by ultrasonic scaling, teaching OHI and interproximal plaque control.
In the first instance recalls are likely to be at three monthly intervals, depending on patient response, this interval may be increased. The classic signs of periodontal improvement are:
- Reduction in the number of bleeding points
- Reduction in pocket depth
- Reduction in plaque score
- No further bone loss radiographically.
In my experience prescribing a Spacemark chart for correct interproximal brush sizes for each, individual space, patients would regularly report that they could use a larger diameter brush in some spaces. The reason, better plaque control had allowed for further reduction at a microscopic level of the inflammatory response. The fifth sign of periodontal improvement is therefore
- Increase in interspace brush diameter in some interproximal spaces with time. This can be quantified for both clinical improvement and research records.
Dentists also need to be aware that another dental complication of diabetes is xerostomia, and burning mouth or tongue and altered taste, which may be an early sign of diabetic neuropathy.
This is a dental public health disaster about to happen.
The bottom line is clear; control the plaque and control periodontal disease and reduce the effects of systemic diseases. Whilst daily plaque control must remain the responsibility of the patient, as dentists our responsibility is to show patients how to control their plaque effectively and to monitor and record progress (or regress) at regular intervals.
In summary we need:
- Doctors and dentists to work together as never before.
- An education campaign to encourage diabetics to attend for dental care.
- Better dental record keeping and sharing this information with patients
- To develop ways to help patients control their plaque on a daily basis
- Better information about periodontal disease on the internet
- Publicity at national and local level.
The preparation of this article has required much research. Key references are shown below:
American Academy of Periodontology website, 2014.
Bulman JS et al. Demand and need for dental care: a sociodental study.
London, the Nuffield trust, 1962.
Diabetes Now website, 2014.
Matthews DC. The relationship between diabetes and periodontal disease
- Can. Dent. Assoc. 68:161, 2002.
Mealy BL. Periodontal disease and diabetes – a two way street
- Amer. Dent. Assoc. 137: 265, 2006.
Moore PA et al. Type I diabetes mellitus and oral health
- Periodont. 70: 409, 1999.
National Diabetic Information Clearinghouse (NDIC) website (US).
Preshaw B et al. Periodontitis and diabetes – a two way relationship
Diabetologia. 55: 21, 2012.
Salvi G et al. The association between diabetes and inflammatory periodontal disease
- Periodontol. 68: 127, 1997.
Southerland JH et al. Diabetes and periodontal infection – making the connection
Clinical Diabetes 23: 171, 2005.
Steele JS. The dental status, needs and demands of the elderly in three communities.
PhD Thesis, University of Newcastle upon Tyne, 1994.
Turner CH. Implant maintenance
The Dentist pp62, 2011.
Williams, J. Diabetic periodontoclasia
- Amer. Dent. Assoc. 15: 523, 1928