Periodontal disease - Evidence-based best practice

Periodontitis

Periodontitis, also known as Pyorrhoea, is a group of inflammatory diseases which result in destruction of the tissues that surround and support the teeth. Periodontitis results in the sporadic but progressive loss of the bone around the teeth, and if left untreated, will lead to the loosening, migration and subsequent loss of the teeth. Periodontitis is caused by the presence of certain bacteria within the dental plaque of those who develop the disease.

Periodontal Disease Classification

The 2017 classification system for periodontal diseases and conditions listed seven major categories of periodontal diseases and these are as follows:

Gingivitis (plaque associated and non-plaque associated)
Necrotizing Periodontal diseases
Periodontitis as a manifestation of systemic disease
Periodontitis (divided on: 1) Severity; 2) Distribution and 3) rate of progression.

Of these conditions the items listed 2-4 are termed destructive periodontal disease because the damage is essentially irreversible.

Signs and Symptoms

In the early stages, periodontitis has the same symptoms as gingivitis but many people do not seek treatment until the disease has progressed significantly.

Symptoms may include:

Redness or bleeding of gums;
Recurrent swelling of the gum;
Bad breath (Halitosis), and sometimes a persistent metallic taste in the mouth
Recession of the gums, resulting in lengthening of teeth above the gum.
Deep pockets between the teeth and the gums.
Loose or migrated teeth, in the later stages.

Importantly periodontitis is largely painless so the usual warning signs of disease are not present. People may wrongly assume painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing periodontitis in that patient.

Causes and Progression

The aetiological agents that induce periodontitis are certain bacteria found within the dental plaque. However within those people who carry the bacteria the level of oral hygiene has a very large influence upon the disease progression rate. Other factors that may influence the disease progression rates are systemic diseases, such as Diabetes, and the degree of smoking of the patient.

Periodontitis progresses through variable sporadic bursts of activity followed by variable periods of stability. In fact the major thrust of treatment today is to keep the disease in these periods of stability and to prevent the periods of progression. However even with these therapies ~12-15% of subjects will continue to show periods of progression. It is these progressive disease patients who really need to be referred to a periodontist. We will devise different treatment approaches for patients with progressive disease and now offer more comprehensive evaluation to allow us to personalize your treatment. It is important to know the underlying reasons for the progression to allow us to choose the correct treatment options.

Genetics of Disease Susceptibility

Recent research has identified a number of genes that are associated with disease susceptibility, these include anomalies in immune modulating genes such as interleukin 1, 4, 10 and 19. These genes modulate the amount of inflammation that occurs and if the inflammation is increased or reduced they may make the patient more susceptible to periodontal tissue destruction. Also identified are genes such as CDKN2B-AS1 which form a long RNA called ANRIL which modulates the expression of the DNA and in doing so makes patients susceptible to periodontitis as well cardiac disease and other systemic diseases. Also genes related to Vitamin D have been identified and these include the vitamin D receptor, the vitamin D carrier protein, Megalin/Cubulin and genes such as CYP2R1,CYP27B1 and CYP24A1 that regulate vitamin D activation and deactivation. Clearly there are no single gene anomalies that make a patient susceptible. The gene combinations need to be assessed.

Gene tests are now available to assess many of these genes and the cost is now economical for many patients. As we are principle researchers for these types of anomalies at the University of Melbourne our practice has the capability of assessing these anomalies. If we identify any of these genes or the observable combinations we will work with your medical practitioners to get your the best aetiological based treatments.

Periodontitis and Vitamin D

Periodontitis has been linked to variation in vitamin D status and anomalies in gene related to vitamin D regulation. Vitamin D is an important anti-inflammatory hormone and regulates the activity of many white blood cells. It is also important for the regulation of the production the antibacterial proteins, such as Cathelicidin, within the skin and gums. So low levels will be associated with an enhanced inflammatory response and the potential for increased periodontal disease progression. Supplementation of periodontitis patients has been linked to reduction in gingival inflammation but no studies have evaluated the effect upon periodontal maintenance disease status and the rate of intermittent progression seen in patients. However excessive vitamin D, especially the active 1,25 Vitamin D may also result in anomalies so it is important to be monitored by appropriate medically qualified personel.

Vitamin D is made from a metabolite which was is in the cholesterol synthesis pathway and therefore is highly correlated with the levels of cholesterol in the patients blood. The conversion of this cholesterol pathway metabolite is related to ultraviolet light exposure. Exposure at high latitudes comparing summer and winter levels shows a 20% variation in both sexes, with females having lower levels than males. However the variation in southern Australia would be less than that seen in this high latitude study, whilst summer/winter variation in northern Australia would be minimal. The variation in the levels seems less to do with light exposure than currently accepted. Interestingly, many Statin drugs (not all) which inhibit cholesterol synthesis are also associated with reduced vitamin D levels. Drugs such as this may be more important in Vitamin D level variation in Australia.

Genes related to Vitamin D regulation are far more important in determining activated vitamin D status of patients. Studies showing variation in the vitamin D receptor and the Vitamin D carrier protein have both been linked to altered vitamin D responses and Periodontitis. We can assess the known variants of these genes in our patients.

Supplementation with Vitamin D, without a proper assessment of its status and the gene variations and drugs being taken, is not recommended. Some patients have increased CYP27B1 and reduced CYP24A1 activity which results in high active vitamin D levels even with low non-activated vitamin D levels.

Racial Distribution

Periodontitis is very common, and is widely regarded as the second most common dental disease worldwide and has a prevalence of 20–50% of the population with any form of the disease.

Assessment of the world’s population reveals some populations to have higher rates of severe disease than others. The highest rates of severe disease seem to be in the Indian, Pakistani and Sri Lankan populations at around 8%. The next highest populations are the Hispanic and native inhabitants of Mexico, Latin America and South America, the populations of Siberia, Eastern Europe, the Mediterranean countries (Italy, Greece, and Turkey), Africa and the Indonesian archipelago with rates between 4% and 8%. The lowest incidence of severe periodontitis occur in North Western Europeans, North America, the Middle East, China and Australia with rate <3.5% of the population.

The genetics and microbial factors behind these differences are currently being investigated and introduced into the personalization of your treatment.