Gingivitis is one of those words that can make you seem like an instant expert (which actually you are) when someone asks what it means. “Gum disease,” you reply “‘itis’ meaning inflammation and ‘gingiv’ referring to the gums or gingival tissues. Inflammation of the gums; bleeding gums!” The enquirer thinks you’re wonderful.
Dinner parties and pub quizzes aside, the knowledge that we have built up in the last half century on gingivitis and periodontitis is immense, and we are still learning. It still seems surprising that the initial work on plaque and the establishment of the link between it and soft tissue inflammation was completed in the 1960s and 1970s with the pioneering work notably in Sweden of Löe and co-workers.
With the benefit of hindsight, what then followed was logical but we now think not entirely correct. In the excitement of watching plaque grow on the teeth and gum margins of Nordic volunteers, the subsequent measurement of bleeding and then the resolution back to healthy pink tissue with the control of plaque, the logic of the process guided us to believe that the inevitable continuation of gingivitis was periodontitis; a linear progression. It is easy now to scoff but this was the teaching and accepted wisdom for many years (and probably still lingers in some backwaters).
We now acknowledge that such a simplistic route does not explain the observations of gingivitis and periodontitis through any of the established hierarchies of evidence, from randomised clinical trials, through epidemiology to individual case reports. Instead, a far more complex aetiology has emerged in which the host, the environment and the disease process itself have all come to influence our understanding. In some cases the linear process does apply but certainly not in all.
Adult Dental Health Surveys in the UK have continued to show that a high percentage of the population do not have very healthy periodontal tissues (83 per cent of dentate adults in the 2009 survey) and no periodontal disease, that is no bleeding, no calculus, no periodontal pocketing of 4mm or more, and in the case of adults aged 55 or above, no loss of periodontal attachment of 4mm or more anywhere in their mouth. However, overall 45 per cent of adults had periodontal pocketing exceeding 4mm, although for the majority (37 per cent) disease was moderate with pocketing not exceeding 6mm. In other words, the progression is not linear and not inevitable.
Strangely, perhaps, I am not going to pursue the reasons in this article for the apparent contradictions, these you can research elsewhere in huge and elaborate detail – and it is worth doing as it reveals remarkable science and serious detailed and dedicated research. What I am going to do is to argue instead that whatever gingivitis does or doesn’t lead on to, without question it is better not to have it at all, since we can then assure optimum oral health.
Returning not to the 1960s but to their observations the truth still remains that accumulation of dental plaque causes gingival inflammation and that effective removal of the plaque either prevents it or helps in repair and regeneration of the tissues. In the same way that our knowledge of the disease processes has advanced so too has our understanding developed in the field of plaque prevention and removal. Back in the ‘swinging’ decade who could have foreseen the remarkable technology that has brought us oscillating-rotating power toothbrushes with the ability to exceed the effects of manual toothbrushes. There has also been a revolution in toothpastes with such sophisticated formulae that they can be applied to individual clinical problems as well as those like the recent launched Oral-B ProExpert which has no less than eight beneficial effects.
Here again, the application of linear thinking has been diverted. Not only is effective plaque control about the brush and the paste (important as these are) it is also about the ‘host’, the motivation and dexterity of the user. This is where adjuncts such as self-timing devices, for example, can add a significant boost to plaque removal by helping the user to brush for longer and where pressure sensitive brush-heads can ensure that no damage is done by the additional enthusiasm.
But the prevention of gingivitis is not only about the possible progression to periodontal disease. With more of us keeping more teeth for longer, we want our gum health to be life-long and this also means that we wish for less gingival recession. This reduces the possibilities of cervical sensitivity and it aids in lessening the likelihood of tooth surface loss, a substantial new problem in the brave new world of increased tooth retention.
But a final word of caution; beware of egoitis - ‘itis’ meaning inflammation and ‘ego’ meaning we think we know it all. In another 50 years it will almost certainly all have changed again.
References available on request.