The causality of periodontitis
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Aims and objectives
The aim of this article is to examine the evidence base regarding the causality of periodontitis.
On completing this CPD session, the reader will:
• Understand that the causes of periodontal disease are considered to be multifactorial
• Understand the causes may arise in different combinations in individual patients
• Understand that 80% of periodontal tissue damage is due to an inappropriate host response to pathogenic bacteria
• Understand that oral plaque biofilm disruption is currently the most effective way to treat and prevent periodontal disease
• Understand that the multifactorial nature of periodontal disease means that understanding of it will continue to evolve.
The causality of periodontitis
This article examines the evidence base regarding the causality of periodontitis.
In the 19th century, Dr John Riggs focused his dental practice on periodontal disease – or, as he called it, Riggs’ disease – and is generally considered to be the first periodontal specialist.1 Some major developments have, of course, taken place in the intervening years and today the causes of periodontal disease are considered to be multifactorial.1,2
Presenting an overview of current understanding of periodontal disease, Chapple and colleagues’ (2017) report on group 2’s findings from the joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases, wrote: ‘Periodontal diseases and dental caries are complex diseases with multiple and diverse exposures that impact upon risk of disease initiation (risk factors) or progression of existing disease (prognostic factors). Exposures include those that are inherited (e.g. genetic variants), those that are acquired, such as social, educational and economic factors, and the local environment (e.g. biofilm load or composition), other diseases (e.g. sub-optimally controlled diabetes) and lifestyle (e.g. smoking, consumption of sugars, carbohydrate intake) factors. These may arise in different combinations in different individuals, and at an individual patient level may also have differentially weighted effects.’2
The role of plaque biofilm
In 1997, Page and Kornman published a paper stating that plaque is a major cause of periodontal disease, writing: ‘Experts agree that human periodontitis is initiated and perpetuated by a small group of predominantly gram-negative, anaerobic or microaerophilic bacteria that colonize the subgingival area.’3
Adding to this concept, in 2016 Scully reported that: ‘It has been estimated that 80% of the periodontal tissue damage is due to an inappropriate host response to pathogenic bacteria.’4
We know, therefore, that plaque is a main cause of periodontal disease,2 and that plaque biofilm is present on all surfaces in the oral cavity.5 Addressing this challenge, Group B’s consensus report of the 5th European Workshop in Periodontology stated: ‘Currently oral plaque biofilm disruption is the most effective way to treat and prevent both conditions [gingivitis and periodontitis]’.6
Building on this picture, it is important to note that gingivitis and periodontitis are a continuum of the same inflammatory disease.6 However, gingivitis will not always progress to periodontitis.7 On this issue, Chapple and colleagues (2015) wrote: ‘[…] while not all patients with gingivitis will progress to periodontitis, management of gingivitis is both a primary prevention strategy for periodontitis and a secondary prevention strategy for recurrent periodontitis.’7
To manage the situation effectively, as elucidated by Chapple and colleagues (2015): ‘The most important risk factor for periodontitis is the accumulation of a plaque biofilm at and below the gingival margin, within which dysbiosis develops and is associated with an inappropriate and destructive host inflammatory immune response. Plaque removal and/or control is therefore fundamentally important in the prevention of periodontal diseases.’7
A dynamic challenge
Studies have suggested that between 5% and 20% of the global population suffers from severe periodontitis, with the majority of adults experiencing mild to moderate periodontitis.8 Closer to home, according to the Adult Dental Health Survey of 2009, just 17% of dentate adults in England, Wales and Northern Ireland had very healthy periodontal tissues (i.e. 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).9 These figures suggest there remains an unmet need when it comes to tackling periodontal disease.
Looking to a healthier future, Murakami and colleagues (2018) wrote: ‘The debate about the fundamental nature of disease continues because of the dynamic and interactive foundation related to social and cultural norms combined with the explosion of new scientific information. As a result of the shifting circumstances represented by the patient, the health care provider, the basic clinical and/or public health scientist, society at large, and the disease itself, it is essential that periodontists continue to refine the classification of periodontal diseases and conditions through evidence from the expanding knowledge base. As a consequence of seeking to enhance periodontal health, dentistry must continually examine the basic nature of periodontal disease by seeking new knowledge; evaluating what we believe is important in our society, in our dental specialty, and in ourselves; acknowledging our limitations; and contemplating the significance of data, definitions, and classifications.’10
Offering an overview of current thinking, Bouchard and colleagues (2017) explained: ‘Periodontal diseases are among the most complex non-communicable diseases. This is the reason why the management of periodontal patients must rely upon careful consideration, not only upon aetiologic factors; it must take into account all actors playing a role in the causal chain. The control of the periodontal risk network is the cornerstone of success in prevention and periodontal therapy. A conceptual framework intended to clarify the relationship between risk and causality may improve the understanding of the underlying mechanisms of chronic diseases.’ 11
Reddy S. Essentials of Clinical Periodontology & Periodontics. Jaypee Brothers Medical Publishers 2017; 5th edition
Chapple ILC et al. Interaction of lifestyle, behaviour or systemic diseases with dental caries and periodontal diseases: consensus report of group 2 of the joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases. J Clin Periodontol 2017; 44 (Suppl. 18): S39-S51
Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontology 2000 1997; 14: 9-11
Scully C. Churchill's Pocketbooks. Clinical Dentistry. Churchill Livingstone, 4th edition, 2016; 465
Sanz M et al. Role of microbial biofilms in the maintenance of oral health and in the development of dental caries and periodontal diseases. Consensus report of group 1 of the Joint EFP/ORCA workshop on the boundaries between caries and periodontal disease. J Clin Periodontol 2017; 44 (Suppl.18): S5-S11
Kinane DF, Attström R. Advances in the pathogenesis of periodontitis. Group B consensus report of the fifth European workshop in periodontology. J Clin Periodontol 2005; 32(Suppl. 6): 130-131
Chapple ILC et al. Primary prevention of periodontitis: managing gingivitis. J Clin Periodontol 2015; 42 (Suppl. 16): S71-S76
Kassebaum NJ et al. Global burden of severe periodontitis in 1990-2010: a systematic review and meta-regression. J Dent Res 2014; 93(11): 1045-1053
Adult Dental Health Survey 2009. The Information Centre for Health and Social Care 2011
Murakami S et al. Dental plaque-induced gingival conditions. J Periodontol 2018; 89(Suppl. 1): S17-S27
Bouchard P et al. Risk factors in periodontology: a conceptual framework. J Clin Periodontol 2017; 44: 125-131