Periodontal Diagnosis and Treatment in the Coming Decades

Gary C. Armitage, DDS, MS

A review of the dominant paradigms and thinking behind periodontal diagnosis and treatment over the past 150 years sets the groundwork for predicting what changes may occur in the next 50 years.

Clinical Characteristics PARADIGM (1870-1920)

From about 1870 to 1920, the classification, diagnosis, and treatment of periodontal diseases were based almost entirely on their clinical features, supplemented by unsubstantiated theories about their causes.1 Arguments raged about local versus systemic etiologies. Favored treatments often included removal of irritating “lime” deposits and gingival massage to increase circulation because poor blood supply was believed to be an important part of the problem. During this period, destructive forms of periodontal disease went by many names, including Rigg’s disease, phagadenic pericementitis, and pyorrhea alveolaris (the most widely used term).

Classical Pathology Paradigm (1920-1970)

By 1920, general pathology had emerged as a major scientific discipline in medicine. In the early days of this medical specialty, it was thought that diseases of all organ systems could be grouped into three major tissue reactions: inflammatory, dystrophic (degenerative), and neoplastic.1 This concept was promoted by influential oral pathologists (periodontists) such as Bernhard Gottlieb and Balint Orban. The most common inflammatory form of destructive periodontal disease was called periodontitis (with simplex and complex types). Putative causes included dental calculus, bacteria, and food debris. It was recognized that the clinical course of periodontitis could be significantly modified by debilitating systemic diseases such as diabetes mellitus and tuberculosis. Treatment of periodontitis was primarily directed at the elimination, or reduction in depth, of periodontal pockets.

A much rarer form of periodontal disease, primarily affecting teenagers and young adults, was called periodontosis. Periodontosis was believed to be a noninflammatory and degenerative condition due to poorly understood developmental disturbances. Severe periodontal destruction was usually confined to permanent incisors and first molars. Because of the presumed degenerative nature of the disease, local treatment was deemed ineffective. Bacteria were not believed to be part of the primary etiology. However, secondary bacterial infection was considered important after the degenerative process destroyed periodontal tissue, leading to the formation of deep periodontal pockets. Therefore, pocket reduction therapy was often recommended to slow down the additional damage caused by bacteria and other irritants.

Infection/Host Response Paradigm (1970-Present)

By 1970, the entrenched beliefs of the classical pathology paradigm were being challenged by the work of many scientists throughout the international periodontal community. Noteworthy among this group were influential Scandinavians (eg, Jens Waerhaug, Harald Löe, Jan Lindhe, Sture Nyman, and Sigurd Ramfjord), who proved that most periodontal infections could be prevented and effectively treated by periodically removing or disrupting dental plaque biofilms.2 These and other investigators showed that most forms of conventional nonsurgical and surgical periodontal therapy were effective as long as treatment emphasized oral hygiene instructions and adherence to a patient-specific program of maintenance care.2

In the late 1970s, Sigmund Socransky and Michael Newman, working together, and Jorgen Slots, working alone, demonstrated that periodontosis had a significant microbial component and was clearly an infection.1,2 Because the disease affected young people, it was given the new name of juvenile periodontitis.1 The much more common form of destructive periodontal disease became known as adult periodontitis. For a variety of reasons, this terminology was changed again in 1999; adult periodontitis became chronic periodontitis and juvenile periodontitis became localized aggressive periodontitis.1 Throughout the 1980s and 1990s, culture-based microbial analyses demonstrated that there are qualitative differences in the subgingival microbiota between healthy and diseased sites. The seminal work of Socransky and Anne Haffajee established that some subgingival bacteria were strongly associated with diseased sites.2 By 1996 the consensus was that, in susceptible hosts, the list of putative periodontal pathogens in many cases of chronic periodontitis should include Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Parvimonas micra, Eubacterium nodatum, Campylobacter rectus, Prevotella intermedia, and Streptococcus intermedius. At the time, Aggregatibacter actinomycetemcomitans appeared to be more associated with cases of localized aggressive than chronic forms of periodontitis.2

As the etiology of most forms of periodontitis became firmly established, it was shown that most of the tissue damage is due to the host inflammatory responses to the microbial irritants.3 Host responses to the entire microbial community appear to be more important than the presence or absence of a single periodontal pathogen.2,3 All forms of periodontitis have a polymicrobial etiology.4 Culture-independent analyses of the subgingival microbiota in different cases of chronic periodontitis have shown disease associations with at least 65 different species of bacteria and 5 species of archaea.4 It appears these infections are caused by a consortium of commensal opportunistic pathogens that flourish when the health-associated homeostasis between the host and the normal (resident) oral microbiota is disrupted. Disruption of this homeostasis is usually linked to perturbations in innate and/or adaptive immune responses of the host. Examples of these perturbations include poorly controlled diabetes mellitus and cigarette smoking. The overwhelming microbial burden associated with poor oral hygiene is perhaps the most common cause for disruption of the host-microbe homeostasis.

The classification and diagnosis of different forms of periodontitis are still based on careful evaluation of medical-dental histories, the combined presence of clinical signs of inflammation, and documentation of periodontal damage (eg, clinical attachment loss, radiographic loss of bone). Treatment of periodontitis includes oral hygiene instructions, supra- and subgingival debridement, probing depth reduction, and maintenance care. In some cases, partial regeneration of soft and hard periodontal tissues is possible.

Relevant to future developments in the classification, diagnosis, and treatment of periodontal diseases are the findings from the National Institutes of Health-sponsored Human Microbiome Project.5 This study used culture-independent analyses of the microbiome, which includes all microbes that live on and in us. One of the surprising findings was extensive inter-individual diversity in the types of bacteria that healthy people carry, whereas the metabolic pathways of the health-associated microbial communities were remarkably similar from individual to individual.5 This suggests that stable metabolic pathways are a fundamental feature of a health-associated homeostasis between a host and the resident microbiome. This feature is shown in Figure 1, where taxonomically different microbial communities exhibit similar functional or metabolic output profiles of complex host-microbe and microbe-microbe interactions.

It is widely known that the development of periodontitis is accompanied by major qualitative changes in subgingival microbial communities.2,4 Quantitative and qualitative changes in the microbiota, including their metabolic activities, is known as dysbiosis.6 It is highly likely that dysbiotic changes associated with periodontitis are accompanied by functional disruptions in the metabolic output of host-microbe interactions. Because of the variable polymicrobial nature of periodontitis, it appears that altered metabolic pathways associated with subgingival dysbiosis are more important than the specific types of bacteria present. Figure 2 suggests that disease is accompanied by dysbiosis-altered metabolic pathways; the main effect of treatment is restoration of metabolic pathways characteristic of a health-associated host-microbe homeostasis.

Molecular Ecology Paradigm (2020-Coming Decades)

The groundwork has been initiated for a revolution in the diagnosis and treatment of periodontal diseases. We are on the verge of entering the next paradigm or stage of understanding. Future developments in this area will emphasize the ecology of host-microbe interactions in health and disease at a molecular level. In the next 50 years, tests will be developed for assessment of disease-associated perturbations in the periodontal ecosystem. The tests will capture the following relevant information:

• host variables (especially those linked to inflammation)
     innate immunity (combined genetics of host + microbiome; gene-environment effects)
     • adaptive immunity (combined genetics of host + microbiome; gene-environment effects)
     • host epigenetics
• microbial variables (especially dysbiosis linked to inflammation)
     • microbe-microbe interactions
     • microbe-host interactions
     • microbe-environment interactions
• environmental variables (those affecting the periodontal ecosystem)

In 50 years, the classification and diagnosis of periodontal diseases will be based on results of clinically validated tests that will detect and analyze molecular perturbations in the healthy host-microbe homeostasis. A range of specific interventions will be guided by the test results. Novel treatments added to current time-tested conventional interventions will include:

• biofilm-disrupting mouth rinses
• evidence-based probiotic procedures
• local application of modulators of inflammation

The above predictions may seem overly optimistic, but 50 years is a long time. As the field of personalized medicine continues to develop, some of these predictions will certainly come to pass. Molecular and ecological analyses of a variety of human diseases are quickly becoming part of mainstream medical care. In periodontology, similar analyses are already in the early stages of development. In the future, they will become essential components of periodontal diagnosis and treatment.

References

1. Armitage GC. Classifying periodontal diseases – a long-standing dilemma. Periodontol 2000. 2002;30:9-23.

2. Armitage GC. Learned and unlearned concepts in periodontal diagnostics: a 50-year perspective. Periodontol 2000. 2013;62(1):20-36.

3. Hasturk H, Kantarci A. Activation and resolution of periodontal inflammation and its systemic impact. Periodontol 2000. 2015;69(1):255-273.

4. Armitage GC. Comparison of the microbiological features of chronic and aggressive periodontitis. Periodontol 2000. 2010;53:70-88.

5. Huttenhower C, Gevers D, Knight R, et al; Human Microbiome Project Consortium. Structure, function and diversity of the healthy human microbiome. Nature. 2012;486(7402):207-214.

6. Stecher B, Maier L, Hardt WD. ‘Blooming’ in the gut: how dysbiosis might contribute to pathogen evolution. Nat Rev Microbiol. 2013;11(4):277-284.

About the Author

Gary C. Armitage, DDS, MS
Professor of Periodontology
University of California School of Dentistry

The author reported no conflicts of interest related to this article.