plaque hypothesis ppt

The Evolution of Plaque Hypotheses in Periodontal Disease Progression

The Oral Microbiome: A New View of Plaque Biofilm

Course Number: 676

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Course Contents

• Introduction
• Plaque as a Biofilm
• The Sequential Theory of Colonization
• The Relationship Between Plaque Biofil...
• The Evolution of Plaque Hypotheses in ...
• The Polymicrobial Oral Biofilm
• Future Treatment Implications
• Other Novel Approaches
• References / Additional Resources

Figure 10. The Evolution of Plaque Hypothesis

When Anton Von Leeuwenhoek first discovered the existence of microbes in the 17th Century, there was no way of identifying specific bacterial species. In the late 19th Century, with advances in science, several specific pathogens were identified to be associated with a variety of systemic diseases, however none were found for oral diseases despite ongoing searches. Subsequently, dental scientists believed that periodontal disease was linked with some constitutional defect in the individual. 25 That time period is referred to as the ‘Golden Age of Microbiology’ .

The search for specific periodontal bacteria continued beyond the mid-part of the 20th century. However, since no specific bacteria could be identified, all plaque was viewed as bad plaque. Mechanical irritants such as calculus and overhanging restorations were also thought to play a major role in the pathogenesis of periodontal disease. 26 Stringent plaque control thus became the focus of periodontal therapy. This period of time was referred to as the Non-specific Plaque Hypothesis since no specific microorganisms were identified.

Discoveries in the late 1960’s and early 1970’s marked a return to the idea of a Specific Plaque Hypothesis when researchers successfully demonstrated that periodontal disease could be transmitted between hamsters. 27 The specific plaque hypothesis identified a shift from predominantly gram positive aerobes to gram negative anaerobes in oral communities. Research efforts also identified specific groups of bacteria that were significantly associated with periodontitis. Socransky used DNA-DNA hybridization to identify complexes, or groups of bacteria that were thought to be major etiologic contributors to periodontal diseases. Yellow, green, blue and purple complexes were thought to be compatible with gingival health, while orange and red were associated with disease. Once it was identified that some of these bacteria could also be present in the absence of disease, additional refinement was indicated to support the specific plaque and Socransky’s Microbial Complexes concepts. 28 In 1976 scientists proposed that only a few species from the total microflora were actively involved in disease and thus once again the search for a specific microbial periodontal pathogen began and treatment was aimed at the causative agent. 28 That period however did not last long. In 1986 there was a return to the Non-specific Plaque Hypothesis because scientists began to suspect that the overall activity of the microflora could lead to disease by taking into account differences in virulence among the various species of bacteria. 28

In 1994, researchers combined the key concepts of the earlier two hypotheses proposing that the disease was the result of an imbalance in the microflora that could be caused by ecological stress resulting in an enrichment of certain disease-related microorganisms. 28 This became known as the Ecological Plaque Hypothesis and was the beginning of the concept of dysbiosis that is now in the current literature. 29

More advanced bacterial profiling techniques available in the early 2000’s such as 16SrRNA-based bacterial profiling using next generation sequencing, reverse transcription-polymerase chain reaction, microarray and pyrosequencing technology, enabled the launching of the Human Microbiome project by the NIH in 2008. This project resulted in the identification of over 700 species of distinct oral microbial species with suggestions of numbers as high as 1,200-1,500. 1 Of course not all 700+ species have been found to be associated with periodontal disease.

Following these discoveries made during the Human Microbiome project, the ecological plaque hypothesis was taken one step further in 2012 by Hajishengalis and colleagues 30 who proposed that certain low-abundance microbes could integrate with the host immune system and remodel the microbiota thereby causing inflammatory disease. In line with earlier findings, gram negative anaerobic bacteria were most commonly found to be associated with periodontitis such as Porphyromonas gingivalis, Tannerella forsythia , and Treponema denticola (Red complex bacteria); Prevotella intermedia, Fusobacterium nucleatum, Parvimonas micros , Campylobacter recta, multiple species of Eubacterium, and multiple species of Bacteroides (Orange complex); Aggregatibacter actinomycetemcomitans (Green complex); and F. alocis (gram positive rod more recently identified). 15, 35 Of this group of bacteria, only two are considered as “keystone” microbes, P. gingivalis and F. alocis . Keystone microbes are classified as those appearing in lower numbers but who have inherent virulence factors that allow them to interact with the host innate immune system and alter a symbiotic microbiota into one that is dysbiotic. 15 In addition to being keystone microbes, both P. gingivalis and F. alocis are highly virulent microbes that have a possible commensal relationship and also are able to by-pass the host immune response. 15, 37

This became known as the Keystone Pathogen Hypothesis . 30 This hypothesis was in direct contrast to earlier beliefs that dominant species when abundant were what influenced inflammation. This new hypothesis suggested that keystone pathogens such as Porphyromonas gingivalis (P. gingivalis) triggered inflammation when they were present in “low” numbers by interfering with the innate immune system causing a shift in the host response triggering inflammation. Research began to demonstrate that commensal bacteria must be present to trigger other bacteria to cause disease. 30

Although this hypothesis is the most recent and offers a plausible explanation of the significance of the microbial community when compared with patients who have periodontal disease and those who are healthy, there are still some unknowns. The problem is that keystone pathogens can be any species and some that are not necessarily pathogenic. 29 Newer research has surfaced exploring what actually triggers commensal microbes to alter the symbiotic state and suspect that this alteration ultimately leads to localized inflammation, and if not controlled by the host innate immune system, is what leads to the ultimate state of dysbiosis found in periodontitis. 4 This new model, proposed by Van Dyke et al. the “Inflammation-Mediated-Polymicrobial-Emergence and Dysbiotic-Exacerbation” (IMPEDE) model was designed by its authors as a subsequent follow-up to the 2017 World Workshop Classification of Periodontitis. 4 It hypothesizes that initial inflammation initiated by the innate immune system in its attempt to restore symbiosis, is what ultimately leads to the dysbiosis that causes periodontitis. It also suggests that there are multiple factors that are at play such as one’s genetics, environmental factors, and host response to pathogens. 5

Figure 11. SEM of mature human dental plaque demonstrating corn cob formation. Bar = 10 microns at an original magnification of 2,020.

Image courtesy of Dr. Charles Cobb. University of Missouri-Kansas City

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Dental plaque (bacteria biofilm)

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Dental Plaque

Aug 20, 2012

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Dental Plaque. Definitions. According to Bowden, Dental plaque can be defined as the soft tissue deposits that form the biofilm adhering to the tooth surface or on the other hard surfaces in the oral cavity, including removable and fixed restorations.

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• cultural studies
• positive species
• structural characteristics
• bacterial cell surface
• fusobacterium nucleatum

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Definitions • According to Bowden, Dental plaque can be defined as the soft tissue deposits that form the biofilm adhering to the tooth surface or on the other hard surfaces in the oral cavity, including removable and fixed restorations. • According to Marsh, Dental plaque can be defined as the diverse community of microorganisms found on the tooth surface as a biofilm, embedded in an extracellular matrix of polymers of host and microbial origin.

Dental plaque must be differentiated from other tooth deposits, like materia alba and calculus. • Materia Alba refers to soft accumulations of bacteria and tissue cells that lack the organized structure of dental plaque. • Calculus is hard deposits that form by mineralization of dental plaque and is generally covered by a layer of unmineralised plaque.

Plaque • Plaque can be defined as a complex microbial community, with greater than 1010 bacteria per milligram. It has been estimated that as many as 400 distinct bacterial species may be found in plaque. • In addition to the bacterial cells, plaque contains a small number of epithelial cells, leukocytes, and macrophages. The cells are contained within an extracellular matrix, which is formed from bacterial products and saliva. • The extracellular matrix contains protein, polysaccharide, lipids and glycoproteins

Inorganic components are also found in dental plaque; largely calcium and phosphorus which are primarily derived from saliva. • The inorganic content of plaque is greatly increased with the development of calculus. • The process of calculus formation involves the calcification of dental plaque. • The practical consequences of calculus formation are that the deposit is significantly more difficult to remove once calcified, and it leaves a rough surface on the root which is easily colonized by plaque..

Dental plaque can be classified in several different ways. • Plaque is classified as supragingival or subgingival based on its relationship to the gingival margin. Supragingival plaque is evident on the tooth above the gingival margin • Plaque can also be classified by its relationship to the tooth surface, as either attached or unattached plaque. • The unattached subgingival plaque is more closely associated with the wall of the subgingival tissues than is the attached plaque. • Lastly, plaque has been classified by association with disease state as "health-associated" or "disease-associated". The latter classification is related to differences in the microbial composition of dental plaque in health versus disease.

Development of dental plaque • The development of dental plaque has been studied in humans as well as non-human animal model systems. • One of the most commonly used models of plaque development is referred to as the "experimental gingivitis" model (Loe, et al., 1965). • This protocol involves the examination of subjects (usually dental students!) who abstain from any oral hygiene measures for a period of three weeks. • These studies have provided much information on the structural and microbiological characteristics of dental plaque.

The pellicle is evident as lightly stained material on a tooth surface when patients use disclosing solution. • A newly cleaned tooth surface is rapidly covered with a glycoprotein deposit referred to as "pellicle". • The pellicle is derived from salivary constituents which are selectively adsorbed onto the tooth surface. • Components of the dental pellicle include albumin, lysozyme, amylase, immunoglobulin A, proline-rich proteins and mucins. • The formation of pellicle is the first step in plaque formation.

The pellicle-coated tooth surface is colonized by Gram-positive bacteria such as Streptococcus sanguis, Streptococcus mutans, and Actinomyces viscosus. These organisms are examples of the "primary colonizers" of dental plaque. • Bacterial surface molecules interact with components of the dental pellicle to enable the bacteria to attach or adhere to the pellicle-coated tooth surface. • For example, specific protein molecules found as part of the bacterial fimbria (hair-like protein extensions from the bacterial cell surface) on both Streptococcus sanguis and Actinomyces viscosus interact with specific proteins of the pellicle (the proline-rich proteins) with a "lock and key" mechanism that results in the bacteria firmly sticking to the pellicle-coating on the tooth surface (Mergenhagen et al. 1987). • Within a short time after cleaning a tooth, these Gram-positive species may be found on the tooth surface.

After the initial colonization of the tooth surface, plaque increases by two distinct mechanisms: • the multiplication of bacteria already attached to the tooth surface, and • the subsequent attachment and multiplication of new bacterial species to cells of bacteria already present in the plaque mass. The secondary colonizers include Gram-negative species such as Fusobacterium nucleatum, Prevotella intermedia, and Capnocytophaga species. A key property of these microorganisms appears to be the ability to adhere to Gram-positive species already present in the existing plaque mass. These organisms would typically be found in plaque after 1 to 3 days of accumulation.

After one week of plaque accumulation, other Gram-negative species may also be present in plaque. These species represent what is considered to be the "tertiary colonizers", and include Porphyromonas gingivalis, Campylobacter rectus, Eikenella corrodens, Actinobacillus actinomycetemcomitans, and the oral spirochetes (Treponema species). • The structural characteristics of dental plaque in this time period reveal complex patterns of bacterial cells of cocci, rods, fusiform, filaments, and spirochetes. In particular, specific associations of different bacterial forms have been observed.

The structural interactions of the bacteria probably are a reflection of the complex metabolic interactions that are known to occur between different plaque microorganisms. • One example of this is the production of succinic acid from Campylobacter species that is known to be used as a growth factor by Porphyromonas gingivalis. Streptococcus and Actinomyces species produce formate, which may then be used by Campylobacter species. • Fusobacterium species produce both thiamine and isobutyrate that may be used by spirochetes to support their growth. • The metabolic and structural interactions between different plaque microorganisms are a reflection of the incredible complexity of this ecological niche.

Plaque in health and disease • The overall pattern observed in dental plaque development is a very characteristic shift from the early predominance of Gram-positive facultative microorganisms to the later predominance of Gram-negative anaerobic microorganisms, as the plaque mass accumulates and matures. • This developmental progression is also reflected in the shifts in predominant microorganisms that are observed in the transition from health to disease. • Studies of plaque taken from sites of health or disease and examined either microscopically or by culturing have demonstrated distinct differences in health versus disease-associated microbial populations.

Microscopic studies of plaque have examined the presence of different morphological types ("morphotypes") of bacteria. • studies reveal an increase in the presence of motile rods and spirochetal organisms in gingivitis and periodontitis as compared to gingival health. • A major limitation of studies of bacterial morphotypes is that many "health-associated" microorganisms are indistinguishable from "disease-associated" microorganisms (for example, Streptococcus species and Porphyromonas gingivalis, respectively). • However, cultural studies also reveal characteristic distinctions between health- and disease-associated plaque.

The percentage of Gram-positive rods and cocci decrease in gingivitis- and periodontitis-associated plaque as compared to health-associated plaque. • Similarly, the percentage of microbiota comprised of Gram-negative anaerobic species is greatly increased in gingivitis (approximately 25%) and periodontitis (approximately 75%) as compared to health (approximately 13%, Slots, 1979). • Specific microbial species that are important in plaque development and disease development are outlined below based on their categorization by cell wall morphology (Gram-positive, Gram-negative, or spirochetal) and their physiological status (facultative or anaerobic).

SELECTED BACTERIAL SPECIES FOUND IN DENTAL PLAQUE Facultative Anaerobic Gram-Positive • Streptococcus mutans • Streptococcus sanguis • Actinomyces viscosus Gram-negative • Actinobacillus actinomycetemcomitans • Capnocytophypa species • Eikenella corrodens • Porphyromonas gingivalis • Fusobacterium nucleatum • Prevotella intermedia • Bacteroides forsythus • Campylobacter rectus • Spirochetes • Treponema denticola • (Other Treponema species)

Relationship of Specific Microorganisms to Periodontal Diseases • Our understanding of the relationship between the microorganisms found in dental plaque and the common dental disease of periodontitis has undergone numerous phases historically • Early in the 19th century, it was felt that, like the situation with diseases such as tuberculosis, a specific bacterial species was responsible for the disease processes. • The criteria by which a given bacterial species was associated with disease historically has been through the application of Koch's Postulates.

These criteria were developed by Robert Koch in the late 1800's. The criteria are as follows: • A specific organism can always be found in association with a given disease. • The organism can be isolated and grown in pure culture in the laboratory. • The pure culture will produce the disease when inoculated into a susceptible animal. • It is possible to recover the organism in pure culture from the experimentally infected animal.

Non-Specific Plaque Hypothesis (Loesche,1976) • However, the concept that a specific bacterial species was responsible for periodontal diseases fell out of favor for several reasons. First, despite numerous attempts, a specific bacterial agent was not isolated from diseased individuals. Rather, the organisms found associated with disease were also found associated with health. • Good experimental animal model systems of periodontal disease were not available to test the pathogenicity of specific microorganisms (this, in fact, remains problematic today).

Further, in the mid 1900's, epidemiological studies indicated that the older an individual was, the more likely they were to have periodontal disease. This led to the concept that the bacterial plaque itself, irrespective of the specific bacteria found in plaque, was associated with disease. This concept, known as the Non-Specific Plaque Hypothesis (Loesche, 1976), held that all bacteria were equally effective in causing disease.

Specific Plaque Hypothesis (Loesche,1976 • Several important developments caused a change in this thinking. • First, it was realized that organisms that are found as part of the "normal" bacterial flora (i.e., found in health), may function as pathogens under certain conditions. These organisms may be altered, or increase significantly in numbers relative to other non-pathogenic species, to function as pathogens. • This type of bacterial pathogen is referred to as an endogenous pathogen, in contrast to an organism that is not normally found in healthy states which is termed an exogenous pathogen.

Secondly, tremendous advances were made in the 1960's and 1970's in techniques used to culture anaerobic microorganisms (bacterial species that cannot grow in the presence of oxygen). • These advances were related to the anaerobic culturing conditions as well as the nutrients required in media to grow anaerobic species, which are typically very fastidious in their nutrient requirements • The growth of anaerobic microorganisms, and examination of their properties using in vitro and in vivo model systems, has now led us back to the understanding that different microorganisms have varying potential to cause disease.

Thus, the current concept of the processes involved in the development of periodontal diseases fall under the Specific Plaque Hypothesis (Loesche,1976 • The Specific Plaque Hypothesis states that disease results from the action of one or several specific pathogenic species and is often associated with a relative increase in the numbers of these organism found in plaque. • A form of Koch's Postulates specifically oriented to the situation in periodontal diseases has been proposed by a microbiologist by the name of Socransky (Socransky & Haffajee, 1992).

Socransky's criteria for periodontal pathogens are as follows: • ASSOCIATION: A pathogen should be found more frequently and in higher numbers in disease states than in healthy states • ELIMINATION: Elimination of the pathogen should be accompanied by elimination or remission of the disease. • HOST RESPONSE: There should be evidence of a host response to a specific pathogen which is causing tissue damage. • VIRULENCE FACTORS: Properties of a putative pathogen that may function to damage the host tissues should be demonstrated. • ANIMAL STUDIES: The ability of a putative pathogen to function in producing disease should be demonstrated in an animal model system.

The two periodontal pathogens that have most thoroughly fulfilled Socransky's criteria are Actinobacillus actinomycetemcomitans in the form of periodontal disease known as Localized Juvenile periodontitis (LJP), and Porphyromonas gingivalis in the form of periodontal disease known as adult periodontitis. • Selected properties of these microorganisms that have been associated with disease are summarized in the following tables.

Evidence implicating Actinobacillus actinomycetemcomitans as a periodontal pathogen(Adapted from Socransky, 1992) • CRITERION OBSERVATIONS • Association Elevated in lesions of Juvenile Periodontitis, and some lesions of Adult Periodontitis • Elevated in "active" Localized Juvenile Periodontitis (LJP) lesions • Detected in apical region of periodontal pocket or in tissues of LJP lesions • Unusual in health or gingivitis • Elimination Elimination associated with clinical resolution of disease • Species found in recurrent lesions • Host Response Elevated systemic and local antibody levels in Juvenile Periodontitis • Virulence Factors Leukotoxin, collagenase, endotoxin, epitheliotoxin, fibroblast inhibitory factor, bone resorption-inducing factor • Animal Studies Disease induced in gnotobiotic rats

Evidence implicating Porphyromonas gingivalis as a periodontal pathogen (Adapted from Socransky, 1992) CRITERION OBSERVATIONS • Association Microorganism is elevated in periodontitis lesions Unusual in health or gingivitis • Elimination Suppression or elimination results in clinical resolution • Species found in recurrent lesions • Host Response Elevated systemic and local antibody in periodontitis • Virulence Factors Collagenase, trypsin-like enzyme, fibrinolysin, immunoglobulin degrading enzymes, other proteases, phospholipase A, phosphatases, endotoxin, hydrogen sulfate, ammonia, fatty acids and other factors that compromise PMN function • Animal Studies Onset of disease correlated with colonization in monkey model • Key role in mixed infections in animal models

Other species that have been implicated as pathogens, including Fusobacterium nucleatum, Prevotella intermedia, Eikenella corrodens, Campylobacter rectus, Bacteroides forsythus, and the oral spirochetes of the genus Treponema. • It is important to note that the disease processes involve not only pathogenic microorganisms, but also a susceptible host. • Further, many microorganisms function to the benefit of the host, by inhibiting the growth of potential pathogenic species. One example of such an interaction is Streptococcus sanguis, which produces hydrogen peroxide that is lethal for Actinobacillus actinomycetemcomitans.

"Ecological Plaque Hypothesis" • The data from the mixed cultures studies described above, and from other work, provide an argument for plaque mediated diseases being viewed as a consequence of imbalances in the resident microflora resulting from an enrichment within the microbial community of these "oral pathogens.". • Potentially cariogenic bacteria may be found naturally in dental plaque, but these organisms are only weakly competitive at neutral pH, and are present as a small proportion of the total plaque community • In this situation, with a conventional diet, the levels of such potentially cariogenic bacteria are clinically insignificant,and the processes of de- and re-mineralization are in equilibrium.

If the frequency of fermentable carbohydrate intake increases, then plaque spends more time below the critical pH for enamel demineralization (approximately pH 5.5). The effect of this on the microbial ecology of plaque is two-fold. • Conditions of low pH favor the proliferation of acid-tolerating (and acidogenic) bacteria (especially mutans streptococci and lactobacilli), while tipping the balance towards demineralization. Greater numbers of bacteria such as mutans streptococci and lactobacilli in plaque would result in more acid being produced at even faster rates, thereby enhancing demineralization still further. • Other bacteria could also make acid under similar conditions, but at a slower rate. These bacteria could be responsible for some of the initial stages of demineralization or could cause lesions in the absence of other (more overt) cariogenic species in a more susceptible host. • If aciduric species were not present initially, then the repeated conditions of low pH coupled with the inhibition of competing organisms might increase the likelihood of successful colonization by mutans streptococcior lactobacilli.

Key features of this hypothesis are that • (a) the selection of "pathogenic" bacteria is directly coupled to changes in the environment and • (b) diseases need not have a specific etiology; any species with relevant traits can contribute to the disease process. • Thus, mutans streptococci are among the best adapted organisms to the cariogenic environment (high sugar/low pH), but such traits are not unique to these bacteria. Strains of other species, such as members of the S. mitis-group, also share some of these properties and therefore will contribute to enamel demineralization • A key element of the ecological plaque hypothesis is that disease can be prevented not only by targeting the putative pathogens directly, e.g. by antimicrobial or anti-adhesive strategies, but also by interfering with the selection pressures responsible for their enrichment

Strategies that are consistent with the prevention of disease via the principles of the ecological plaque hypothesis include the following: • (a) Inhibition of plaque acid production, e.g. by fluoride containing products or other metabolic inhibitors. Fluoride not only improves enamel chemistry but also inhibits several key enzymes, especially those involved in glycolysis and in maintaining intracellular pH. Fluoride can reduce the pH fall following sugar metabolism in plaque biofilms,prevent the establishment of conditions that favor growth of acid-tolerating cariogenic species. • (b) avoidance between main meals of foods and drinks containing fermentable sugars and/or the consumption of foods/drinks that contain non-fermentable sugar substitutes such as aspartame or polyols, thereby reducing repeated conditions of low pH in plaque. • (c) the stimulation of saliva flow after main meals, e.g. by sugar-free gum. Saliva will introduce components of the host response, increase buffering capacity, remove fermentable substrates, promote re-mineralization, and more quickly return the pH of plaque to resting levels.

Benefits of dental plaque • They play a critical role in the normal development of physiology of the host. Germ free animals have altered mucosal surfaces, poor nutrient absorption, suffer from nutritional deficiencies and have impaired host defenses. • In mineralization of early carious lesions (white spot) • Resident microflora also reduces the risk of infection by acting as a barrier to colonization by exogenous species termed colonization resistance. Reduction of colonization resistance can result in overgrowth of minor components of microflora, establishment of exogenous species which can lead to pathological changes.

Plaque in children • In Children as in adults the cause of gingivitis is plaque, local conditions and poor oral hygiene favor its accumulation • In preschool children the gingival response to bacterial plaque has been found to be markedly less than that in adults. • Dental plaque appears to form more rapidly in children age 8 to 12 years than in adults • Calculus is uncommon in infants; it occurs approx 9%of children 4 to 6 years of age • In 18 % of those 7 to 9 years and in 33% to 43% of those 10 to 15 years

Plaque as a biofilm • Biofilm is a well-organized ,co-operating community of microorganisms. they form under fluid conditions. • bacteria in the biofilms produce compounds that the same bacteria do not produce in cultures. also the matrix surrounding the colonies acts as a protective barrier. • substances produced by bacteria within the biofilm are retained and concentrated which fosters metabolic interactions among the different bacteria

Properties of a biofilm • cooperating community of various types of microorganisms • microrganisms are arranged in microcolonies • microrganisms are surrounded by protective matrix • within the micromolecules are differing environment • microrganisms have a primitive communication system • microrganisms in biofilms are resistant to antibiotics, antimicrobials and host response.

Significance of plaque as a biofilm • Some bacteria alter their pattern of gene expression when cells encounter a surface. Attached cells up-regulate genes associated with expolymer synthesis and can modify upto30% of surface proteins • Increased resistance of biofilms to antimicrobial agents upto 2-1000 fold. • The surface of a biofilm may restrict the penetration of an antimicrobial agent; some charged inhibitors can bind to oppositely charged polymers that make up the biofilm matrix • Environment in the depth may be unfavorable for optimal action of certain drugs • A susceptible pathogen may be rendered resistant if neighboring cells produce a neutralizing or drug degrading enzyme. • In addition biofilms provide an ideal environment for transfer of resistance genes.

CONCLUSION • Despite tremendous increases in our understanding of the pathogenic properties of specific plaque microorganisms and the role of specific microorganisms in the disease process, current therapy in periodontics is largely non-specific. • The treatments that we utilize (e.g., oral hygiene measures, debridement by scaling and root planning, or even the currently available mouthwashes) are oriented towards reducing the accumulation of plaque on the teeth. • Future developments in periodontics will involve the development of therapies which prevent the colonization or growth of specific microorganisms that are known to function as pathogens in this environment.

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• Open access
• Published: 26 August 2020

Current concepts and an alternative perspective on periodontal disease

• Gunnar Dahlen   ORCID: orcid.org/0000-0001-6803-8118 1 ,
• Ole Fejerskov 2 &
• Firoze Manji 3  

BMC Oral Health volume  20 , Article number:  235 ( 2020 ) Cite this article

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Epidemiological data from countries worldwide show a consistent pattern implying that a fraction of around 10% of those over 40–50 years in all populations will exhibit severe periodontitis with the potential risk of losing teeth during their life-time. The subgingival microbiota shows striking similarities between populations irrespective of disease severity and can only marginally explain the clinical pattern. It is also difficult to explain this pattern by genetic and acquired risk factors such as systemic disease (e.g. diabetes) or habits (e.g. smoking) even if they may have a confounding effect on the disease.

Inflammation of the gingiva appears to be a normal and physiological response to the presence of commensal bacteria along the gingival crevice and in the dental biofilm. Over many years of exposure to the dental biofilm, the chronic inflammation in the gingiva gradually results in a loss of attachment and bone loss. Numerous laboratory and clinical studies have provided insight into the potential role of determinants that are associated with periodontitis. However, it has been difficult to relate the findings to the pattern of the distribution of the disease observed in epidemiological studies. We propose a simple and parsimonious model that considers all the multitude of potential determinants as creating effectively random noise within the dental biofilm to which the tissues react by accumulating the effects of this noise.

Conclusions

We suggest that such a model can explain many of the epidemiological features of periodontal breakdown over time, and we discuss its clinical implications.

Peer Review reports

Introduction

One of the most striking, and perhaps enigmatic, features of the epidemiology of periodontitis is the similarity in the patterns of periodontal loss of attachment in different populations across the world, whether or not they exhibit poor oral hygiene, or receive regular oral health care [ 1 , 2 ]. What we find is that gingival inflammation of some degree is ubiquitous from childhood to old age; the progress of periodontitis is slow, with loss of attachment occurring after the age of 30–40 years, with some degree of loss occurring in everyone; advanced loss of attachment occurs in a minority of the population and increases with age to a prevalence of 10–15%; loss of attachment occurs on buccal and lingual surfaces often accompanied by gingival recession, whereas pocket formation predominates in proximal spaces, often bilaterally; and the core oral microbiome (commensals), including putative periodontopathogens, are widespread with a high carriage rate in human adults globally but appear to have a limited relationship with periodontal disease prevalence or severity.

In this paper we review the different theories or hypotheses proposed to explain these epidemiological features and suggest that while the many laboratory and clinical studies have thrown important light on our understanding of the many and complex determinants involved in periodontitis, they do not necessarily explain why the epidemiological features of periodontitis should be so universal. We explore how a simple random effects model that takes into account the effect on the tissues of a multitude of determinants associated with periodontitis and which might provide some understanding of why the features of periodontitis should be expected to occur universally.

Periodontal disease

Periodontal disease is generally considered to be an inflammatory disease induced and maintained by the microbiota of the dental biofilm (dental plaque). The origin of this concept stems from the “experimental gingivitis in man” studies carried out by Löe and co-workers in the mid 60s [ 3 ]. The inflammatory response in the gingiva was thought to be the initial stage of a disease process, which over time was transformed into a destructive phase, periodontitis, characterised by loss of attachment and bone loss. This was the essence of the “non-specific plaque hypothesis” [ 4 ].

The role of microorganisms in periodontitis is, however, unclear although certain “pathogens” alone or in clusters have been proposed to play a major role [ 5 , 6 , 7 ]. This approach termed “the specific plaque hypothesis” dominated the periodontal microbiology for several decades. Antibiotics were proposed as the mode of treatment.

The “ecological plaque hypothesis” was introduced [ 8 , 9 ], together with an expanded list of potential periodontopathogens [ 10 ], suggesting that the key factor in the disease process was the ecological shift to a dysbiosis. Prevention and treatment were focused on ways to prevent dysbiosis occurring [ 11 , 12 , 13 ].

Recently the key-stone hypothesis and the polymicrobial and dysbiosis hypothesis have been described in order to emphasize the interaction between the polymicrobial community and a dysregulated inflammatory response [ 14 , 15 ]. Although detailed knowledge of the microbiome and its function has increased, the specific role of the microorganisms in periodontitis development and progression remains unclear.

Others have focused more on the quality of the inflammatory response and the influence of genetic and/or environmental factors (smoking, systemic diseases) [ 16 , 17 ] to explain why certain individuals seem to be more “susceptible” and the research focus has turned increasingly towards the host response and systemic host effects rather than the role of the microbiota in the disease process [ 18 ]. Further, a gradual immune senescence by age and/or aging itself have been proposed to impact on oral health including periodontal disease [ 19 , 20 ], while others have argued that inflammatory reactions and immune response in general both quantitatively and qualitatively may be genetically determined [ 21 ]. Consequently, gingivitis and periodontitis may be explained along genetic lines, although the evidence so far has limited predictive value and does not account for the apparent universal pattern observed in epidemiological studies.

While there are many hypotheses about the aetiology of periodontitis, the challenge has been to assess the extent to which they explain the epidemiological features of the disease [ 22 ].

A random “disease” model for periodontal destruction was launched as the “burst theory” already by Socransky et al. [ 23 ] based on a previous observation [ 24 ] that periodontal disease was a dynamic condition of disease exacerbation and remission as well as periods of inactivity. This was further dealt with and theoretically explained by Manji and Nagelkerke [ 25 ] how burst and remissions can occur as a direct consequence of the accumulation of random events. Unfortunately, this concept of explaining the periodontal disease has been neglected during the last 30 years in favor of the deterministic approach and search for “risk factors” for disease development. This approach has been questioned recently [ 26 ].

Periodontal disease epidemiology

Pilot [ 27 ] concluded in his review that “from a public health perspective the relative similarities in periodontal conditions around the world are far more striking than the differences.” Subsequently, Kassebaum et al. [ 2 ] reported in a systematic review and meta-regression paper that severe periodontitis affected about 10.8% of the global adult population. The analyses indicated that prevalence increases dramatically between 35 and 44 years of age and with an incidence peak at 38 years of age. Despite the diversity of case-definitions, the diversity in the number of uncontrolled factors, as well as diverse methodologies employed in these studies, the prevalence of severe periodontitis shows a remarkable similarity [ 2 , 28 ] . Similar conclusions were drawn from studies on periodontal epidemiology [ 1 ] indicating that the prevalence and extent of attachment loss increases with age in all populations and that the extent and severity of destruction tends to be skewed to such a degree that a small fraction of the subjects account for most of the destruction. This between population similarity of periodontal breakdown has been emphasized in a number of studies on natural disease development in populations with poor oral health and with little or no access to dental treatment in Sri Lanka [ 29 ], Tanzania [ 30 ], Kenya [ 31 ] China [ 32 , 33 , 34 ], Southern Thailand [ 35 ], and Northern Thailand [ 36 ]. In a comparative evaluation of the profiles of destructive periodontal disease in different populations with close to 100% presence of gingival bleeding, calculus and plaque [ 34 ], it was concluded that while the periodontal loss profiles may differ in severity or extent between populations, these differences do not conform with the traditional generalization that African and Asian populations suffer more severe periodontal breakdown than other populations. Already in the 1980s. Cutress et al. [ 37 ] suggested that the amount of plaque, calculus and gingival bleeding are of limited value for risk assessment of severe periodontal breakdown.

A similar pattern of loss of attachment has also been observed in Western Europe and North America populations where access to dental treatment is more widespread. In USA, a prevalence of severe periodontitis in adults > 30 years of age was found to be 8.9% [ 38 ]. In Sweden, it was reported a frequency of severe periodontitis to be 7% in adults 50 years of age [ 39 ].

The skewed distribution of attachment loss has been interpreted as indicative of the presence of ‘risk groups’ [ 40 , 41 ], but it remains unclear why diverse populations across the world should exhibit similar patterns of breakdown or why there should be similar proportions of people that constitute ‘risk groups’.

Longitudinal studies on periodontal progression in populations with poor oral hygiene and no dental care are rare [ 33 , 42 ]. In a 10-year study of the progression of destructive periodontal disease in adult and elderly Chinese, Baelum et al. [ 42 ] concluded that virtually all individuals will experience some attachment loss, while the distribution of attachment loss over the 10 year period was skewed in all age groups. The longitudinal data provided results not dissimilar to those found in cross-sectional studies. Baelum et al. [ 42 ] interpreted the findings in adult and elderly Chinese as suggesting that the “causes” of destructive periodontal disease are to be found in the host response to years of dental plaque exposure rather than factors related to the biofilm itself.

Epidemiology of oral microbiota

Microbiological assessments in populations world-wide have shown a high prevalence of putative periodontal pathogens without being directly related to a periodontal disease prevalence [ 43 ] . Using culture methodologies, Dahlen et al. recorded a prevalence of Porphyromonas gingivalis in subgingival plaque samples in 70% of adult Kenyans and in more than 50% of adult Chinese [ 44 , 45 ]. Prevotella intermedia was found in close to 100% of people examined in both populations (Table 1 ). Using Checkerboard methodology, a high prevalence (87.2–100%) was recorded for 27 different species among adults in rural Southern Thailand [ 46 ], and 83–100% for seven putative periodontopathogens in an adult Chines population [ 47 ]. Similar prevalences using checkerboard methods were found in adults in a remote population of Northern Thailand [ 36 ]. Further, a prevalence of 87% for P. gingivalis , 100% for P. intermedia and motile rods, 89% for spirochetes using an indirect immunofluorescens assay was found in individuals 15–25 years of age in Indonesia [ 48 ]. Using the same method, Preus et al. [ 49 ] found in young adults (15–25 years of age) in Sri Lanka somewhat lower prevalence of P. gingivalis (40%) and P. intermedia (76%).

The similarities in the periodontal microbiota across populations in diverse geographical locations are striking. Gram-negative anaerobes and motile bacteria appear to predominate in gingival and periodontal pockets, and could be considered normal commensals. The proportions and load of various genera or species may vary between populations as well as between individuals within the population and sites (e.g. in deep pockets) within the same mouth, but the overall pattern of the oral core microbiota (microbiome) appears to be the same. While a dysbiosis may indeed occur [ 11 , 14 ] this may not be a sufficient factor to explain the epidemiological features of periodontitis. It is possible that certain microorganisms have a stronger impact on the disease progression but the precise role of bacteria and “putative pathogens” in periodontitis still remains unclear [ 50 ].

The microbiome and ecology of the gingival pocket (crevice)

The oral microbiome is different from the microbiome found in other body compartments such as skin, intestine and vagina [ 51 ]. The oral microbiome comprises a highly diverse microbial population, involving more than 700 species [ 52 ]. The dental biofilm has its own microbiome characterized by strong tooth-surface adhering streptococci and Actinomyces [ 46 ]. The dental biofilm appears to be in a dynamic state and self-regulating through the constant competition between the microorganisms for space, ecological conditions and nutrition. Since the streptococci and others of the Firmicutes phylum ( Granulicatella, Gemella, Veillonella ) have the capacity to degrade glycoproteins, they constitute the core microbiome of the dental plaque [ 53 , 54 ]. The microenvironment along the gingival crevice is different from other parts of the tooth surface, the primary source of nutrition coming from gingival crevicular fluid (GCF), the quantity of which correlates with the degree of inflammation. Thus, it seems that the main source of nutrition for the microbiota in this niche is proteins and the main metabolic pathway is proteolytic, favouring the proteolytic rather than the saccharolytic microorganisms. In addition, the GCF, which is a serum exudate, also contains a number of growth supporting factors such as vitamins (K-vitamin or menadione), hormones (oestrogen) and specific serum proteins/peptides (hemin) all favouring many of the fastidious Gram-negative anaerobes that adapt and grow concomitantly with gingival inflammation and deepening gingival pockets [ 12 , 54 ].

Gingival inflammation may result in a deepening of the gingival pocket as a result of swelling and oedema, all of which favour an increasing flow of GCF, influencing the type of microorganisms that are able to colonize the space [ 12 , 55 ]. Similarly, the lowering redox potential (Eh) favours the anaerobes. In contrast to the supragingival plaque, adhesion of the microorganisms does not play a crucial role in the gingival pocket and motile bacteria ( Treponema, Campylobacter, Selenomonas species) are able to establish themselves by mechanical retention [ 53 ]. The GCF contains humoral defence factors (antibodies, complement, antimicrobial peptides) as well as inflammatory cells such as neutrophils and monocytes. Bacteria can escape phagocytosis by producing capsules ( P. gingivalis ) or leukotoxins ( Aggregatibacter actinomycetemcomitans ) or simply by being proteolytic, degrading most proteins including humoral antimicrobial factors such as immunoglobulins (IgG), complement factors or antimicrobial host defence peptide [ 56 , 57 ]. The exudate also contains lysozyme, an enzyme directed towards the peptidoglycan of the bacterial cell wall, which is protected by the outer membrane of Gram-negative microorganisms. The Gram-negatives appear to have a higher survival rate in the inflamed gingival pocket. Inevitably, inflamed gingival pockets contain a microbiota dominated by Gram-negative, anaerobic, proteolytic, and motile bacteria. Numerous studies have been performed using various strategies and molecular biology methods such as qPCR and Next Generation Sequencing (NGS) that have associated a number of culturable and unculturable microorganisms with periodontitis and the environment present in the periodontal pocket but their role in the disease process remains unclear [ 14 , 58 ]. The complexity of the many factors involved within the biofilm is shown in Fig.  1 .

The symbiont-the host-parasite relationship in the interaction between the microbial community within the subgingival dental plaque/biofilm and the host tissue response in inflammation. The factors given within the microbial community represent those that have claimed to be of importance for the activities within the biofilm as well as exposing the host tissues [ 14 , 16 , 57 ]. Similarly, the factors given within the host tissue response are those usually claimed to participate in the inflammatory reaction or as host defence factors against infections. The subgingival microbial community (dysbiosis) is under influence of local environmental factors such as saliva, oral hygiene, diet, pocket depth, antiseptics, antibiotics (local) and probiotics. The composition and activity within the dental biofilm are highly dependent on the assay systems used for evaluation e.g. culture, microscopy DNA-probes, quantitative polymerase chain reaction (qPCR) or next generation sequencing (NGS), biochemical methods and sampling techniques and strategies. The host tissue response of each individual is influenced by population, age, gender and genetics [ 16 ]. Environmental host factors such as medicals (cytotoxic drugs, systemic antibiotics) and smoking [ 17 ] as well as internal host factor such as systemic diseases and conditions (e.g. diabetes, obesity) [ 59 ], psychic stress/allostatic load [ 60 ] The two systems are highly dynamic and constantly fluctuating in activity and characterized by temporality. Abbrevations: NH 3 ammonia, H 2 S hydrogen sulphide, LPS lipopolysaccharide, OSCN- hypothiocyanite, H 2 O 2 hydrogen peroxide, AI-2 Autoinducer-2, CSP Competence-stimulating peptide, GCF Gingival crevicular fluid, IL interleukins (IL-1beta, IL-6, IL-8, IL.-18), TNFalfa Tumor necrotic factor alfa, IFNgamma Interferon gamma, MMP’s Matrix Metalloproteinases, ROS reactive oxygen species, CRP C-reactive protein

Host response

The host response to the microbial challenge in periodontal disease is complex and numerous factors are involved [ 16 ]. Figure  1 illustrates the many factors at play. At prolonged exposition of the gingiva for the dental biofilm an immune-response phase involving lymphocytes and plasma cells, is activated. They are more slowly recruited and are activated producing and releasing a cascade of mediators (e.g. interleukins and cytokines) characteristic for a more chronic type of inflammation [ 16 , 57 ]. In reality, the host response to the dental biofilm is balanced against the bacterial challenge and the activity of the bacterial biofilm characterised by the chronic inflammatory phase and due to continuous fluctuations within the bacterial activity in the dental biofilm also includes various degrees of the acute phase. In addition, the host is under constant or changing influence from external and internal factors such as systemic diseases (e.g. diabetes), medications (cytostatic drugs), smoking and psychological factors (stress, allostatic load), which makes the outcome of the inflammatory response at the individual level during many years of bacterial challenge highly unpredictable [ 59 , 60 ].

An alternative perspective on the development of periodontitis

Numerous laboratory and clinical studies have provided valuable insights into many of the necessary and sufficient biological conditions under which periodontitis occurs. However, the results of such studies do not explain the variations in the distribution of the disease nor, indeed, the reason for the apparent universality of the features of periodontal breakdown observed in epidemiological studies [ 33 , 42 ]. This is primarily because the processes involved in periodontitis are highly complex, with spatial and temporal variations in the number and types of determinants, but also in their relative influence over time. The search for a perfect deterministic model — one that relates perfectly all potential determinants — has not been successful because of the complexity of the processes involved in relation to the composition of the biofilm and the capacity of the host to defend itself (Fig. 1 ). Even if such a model existed, it would be useless because most of the determinants can, at best, be measured only as proxy variables. Even if we had such a model, periodontitis would be unpredictable since the inputs (times, lengths, frequency and type of diet, GCF flow rates, quality and quantity and composition of plaque, and host defence factors) are highly variable and noisy (complex, variable, and like a room full of people talking at the same time where it is impossible to tell who is saying what).

But this very noisiness could well play a crucial role in the process. Hitherto poorly understood phenomena can sometimes be trivially explained by random process theories. The critical test about such theories is whether they are able to explain the epidemiological and clinical features of the disease process [ 25 , 61 ].

Amongst the many characteristics of periodontitis are that age-related changes appear to be visible only when pronounced loss of attachment is examined, whereas age related changes are much less apparent when the milder forms of attachment loss are considered since milder forms of attachments loss tend to be ubiquitous in adult populations [ 19 ]. In addition, the change in the risk of loss of attachment occurring following eruption of a tooth into the mouth is very small, but increases with age in adulthood. At the same time, it is apparent that the longer a tooth surface survives without marked loss of attachment, the less likely is it to occur.

These phenomena are consistent with simplest of random process models — Brownian motion, as described by Einstein [ 62 ].

Given how many factors involved, and given how little we know about what may be happening at any given moment, we can reasonably consider the influence of the multitude of determinants involved over a given period as being effectively random and constituting ‘noise’, some enhancing inflammation, some enhancing recovery, and some perhaps having no influence. While there may be noisy events happening within the biofilm, it is necessary to consider how the tissues are affected by this noise: the tissues respond to these stimuli by accumulating the effects of all the different components of noise (that is to say, the effects on the tissues of the positive, negative and neutral events are added together). This can illustrate by generating random numbers of positive and negative values, each with an equal probability of occurring (with an average value of zero). By adding together these numbers, we can observe unpredictable variations, sometimes substantial rise in their values and sometimes substantial decline. If we consider the response of the gingival tissues accumulating the noise within the biofilm with which it is in contact, the tissues would experience unpredictable bursts and remissions, inflammation and recovery, despite the noise within the biofilm being at a steady state or homeostatic. We would thus expect that the gingiva becomes inflamed for an unpredictable period, and then recover for an unpredictable period. That is in fact what we can observe in experimental gingivitis studies – the phenomenon of unpredictable inflammation and recovery of the gingivae [ 63 ]. The tissue reaction would look like the following set of graphs (Fig.  2 a-c). While the underlying noise may be homeostatic (equal probabilities of positive and negative events) the effect of accumulating the noise leads to unexpected bursts and remissions of activity.

a-c. Three examples of a potentially infinite series showing erratic loss and gain of tissues caused by accumulation of (integrating the effects of small random fluctuations of activity (noise) within the dental biofilm. Adopted from Manji et al. [ 26 , 61 ]

If there are conditions that might enhance inflammation, for example, a weakened immune response, reduction in GCF flows, clumsy probing of periodontium, presence of pathogenic microorganisms, then the balance between inflammation and recovery will be altered, and so the probability of inflammation is increased. Similarly, if the biofilm is disturbed regularly by oral hygiene practices, the probability of recovery is increased.

Here we are assuming that we are dealing only with commensal organisms within the biofilm. These bursts and remissions will occur even in the absence of putative pathogens.

If the random activities of the commensal organisms and of the host defence mechanisms are allowed to continue over time, every now and then the cumulative effects will sometimes be unpredictably so severe that a point of no return is reached (which technically in statistical theory is referred to the ‘absorptive barrier’) where the collagen fibres attaching the gingival tissues to the tooth surface are destroyed by the inflammatory process, resulting in loss of attachment. This can happen even if we consider that within the biofilm the probability of inflammation-inducing and recovery-inducing factors are equal. In other words, this behaviour is intrinsic to a process in which the effects of random noise are accumulated. Thus such breakdown resulting in loss of attachment, can occur over time without any change in the composition of the microbiome or in the capacity of the host to exercise recovery. Naturally, any determinants that are likely to increase the probability of inflammation occurring will increase the probability of loss of attachment to occur.

The statistical properties of this simple random effects model with an absorptive barrier are well known [ 25 , 61 , 64 ]. The model’s probability density function has some interesting features: It generates a cumulative probability curve that is similar to the prevalence of loss of attachment at a given site that would be observed in a cross-sectional study of populations with an age range from eruption of the tooth into the mouth to old age. The model predicts that very few surfaces would be affected shortly after eruption, but in the older age groups there would be an almost complete ubiquity of milder forms of attachment loss, and an almost linear relationship with age in severe loss of attachment. In the oldest age-group the rate at which loss of attachment continues may eventually slow down. The rate at which such loss of attachment occurs depends, of course, on the presence of determinants that increase or decrease the probability of inflammatory reactions or capacity of tissue recovery.

Most interesting of all is the model’s hazard function [ 64 ], that is, the instantaneous probability of a loss of attachment occurring at a given site which until then has survived without having developed one. The model predicts that loss of attachment in the early period after eruption is highly unlikely. Thereafter, the hazard function reaches a peak and subsequently the longer a surface survives without exhibiting any loss of attachment, the less likely is it that it will occur thereafter.

The model described here is an idealization of the processes that occur in reality and assumes that each of the determinant variables involved in the development of periodontitis are independent. However, any positive correlations of inputs would only enhance the degree of inflammation and recovery of the tissues, whereas negatively correlated events would tend to dampen them. In essence, however, the model holds true in either case. The assumptions made are, therefore, not unreasonable.

The model predicts that if one includes all degrees of loss of attachment, then the degree of change with age is relatively little, whereas with advanced loss of attachment the linear relationship with age is evident. This is a result of the intrinsic nature of the process that lead to the loss of attachment. And this may explain why in vastly different populations we see similar patterns of loss of attachment with approximately the same proportion of the older people exhibiting advanced loss of attachment. In practice, the phenomenon of periodontitis being age related may also be influenced by the degree to which aging itself may reduce the capacity of the collagen fibres to recover the ever ongoing inflammatory processes [ 65 ].

This simple random effects model predicts many of the features of periodontitis that are observed in epidemiological studies. It does not require one to postulate the role of one or other pathogenic microorganism or any particular determinant in the etiology of the disease, although of course such factors would increase the probability of loss of attachment. On the contrary, one requires only to have commensal microorganisms to result in the pattern of loss of attachment observed in epidemiological studies in many varied populations.

The model gives expression to the concept of periodontitis as a process involving the tissues accumulating the effectively random noise of inflammatory provocations and factors promoting recovery within the biofilm in contact with the tissues that over long periods of time result in breakdown of the tissues and loss of attachment. The model predicts the occurrence of bursts and remissions in the progress of periodontitis [ 25 ]. The model suggests that some degree of loss of attachment is likely to occur after 30–40 years of age, but that simple measures to disturb the biofilm regularly (oral hygiene) may reduce the probability of loss of attachment.

The model described here complements other more deterministic theories. Using existing knowledge and insights about the development of periodontitis, and making few assumptions, it provides parsimonious and simple explanations for a number of phenomena that have hitherto proved difficult, or have required complex arguments, to explain. What this model offers is one way in which the noise itself may be considered the subject of interest for enhancing our understanding of periodontitis.

Availability of data and materials

All data are available through cited references.

Abbreviations

Gingival Crevicular Fluid

Quantitative Polymerase Chain Reaction

Next Generation Sequencing

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Oral Microbiome and Dental Caries Development

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Dental caries remains the most prevalent oral disease worldwide. The development of dental caries is highly associated with the microbiota in the oral cavity. Microbiological research of dental caries has been conducted for over a century, with conventional culture-based methods and targeted molecular methods being used in order to identify the microorganisms related to dental caries. These methods’ major limitation is that they can identify only part of the culturable microorganisms in the oral cavity. Introducing sequencing-based technology and bioinformatics analysis has boosted oral microbiome research and greatly expanded the understanding of complex oral microbiology. With the continuing revolution of molecular technologies and the accumulated sequence data of the oral microbiome, researchers have realized that microbial composition alone may be insufficient to uncover the relationship between caries and the microbiome. Most updated evidence has coupled metagenomics with transcriptomics and metabolomics techniques in order to comprehensively understand the microbial contribution to dental caries. Therefore, the objective of this article is to give an overview of the research of the oral microbiome and the development of dental caries. This article reviews the classical concepts of the microbiological aspect of dental caries and updates the knowledge of caries microbiology with the results of current studies on the oral microbiome. This paper also provides an update on the caries etiological theory, the microorganisms related to caries development, and the shifts in the microbiome in dental caries development.

1. Introduction

Dental caries is the most common oral disease worldwide. Untreated caries affects 2.5 billion adults and 573 million children all over the world [ 1 ], placing a heavy health burden on health care systems and society. Over the past 25 years, the prevalence of dental caries has remained at a similarly high level despite oral health care providers’ efforts [ 2 ]. The high prevalence of dental caries indicates the effect of the research on dental caries. Dental caries is a multifactorial disease that involves microbial, behavioral, genetic, and environmental factors [ 3 ]. Although these factors are important in caries development, the role of microbial factors cannot be ignored. Because the development of dental caries is closely correlated to oral microorganisms, a comprehensive understanding of caries microbiology is essential.

The microbiology of dental caries has been investigated for over a century, with a revolutionized advance in study approaches. Previous studies have used traditional culture-based methods in order to identify the bacteria related to dental caries [ 4 ]. The culture-based method has allowed for a basic understanding of the dental plaque microbiota composition in dental caries to be established. Microorganisms have been isolated from carious lesions or dental plaque samples collected from a cross-sectional or longitudinal study using culture-based techniques [ 5 , 6 ]. However, bacteria can only be successfully cultured when provided with their own special growth requirements. At present, because artificial media cannot exactly mimic the natural environment within which oral bacteria reside, most fastidious bacteria remain uncultivable in vitro [ 7 ].

Targeted molecular methods for identifying and quantifying caries-associated bacteria were introduced in the early 1990s [ 8 , 9 ]. Targeted molecular methods use DNA probes obtained from cultured bacterial species to enumerate the bacteria [ 10 ]. This allows for identifying and quantifying multiple species in dental plaque samples from more individuals compared to culture-based methods. This also facilitates the analysis of species that are difficult to culture [ 4 ]. However, targeted molecular methods can only detect the preselected bacteria that culture-based methods have already confirmed. Unknown bacteria sets in the dental plaque cannot be detected.

The introduction of sequencing-based technology and bioinformatics analysis has greatly expanded the understanding of complex oral microbiology. Unlike the targeted molecular methods, next-generation sequencing (NGS) techniques identify sequences by comparing them to the curated microbiome database, enabling the detection of novel species that have historically been uncultivable [ 11 ]. Since the development of the Sanger sequencing technique in 1977, great efforts have been made to conquer the high cost and low efficiency of “reading” genes. NGS, also known as massively parallel sequencing technology, stands out for allowing ultra-high throughput with a deeper coverage of the microbial community at a lower cost. During the last decade, targeted 16S rRNA amplicon sequencing, which relies on the amplification of one to three selected hypervariable regions of 16S rDNA, has been widely adopted to study the oral microbiome’s compositional changes in dental caries. However, sequencing fragments of the 16S rRNA gene can miss variants that discriminate different species or strains, which compromises this technique’s taxonomic resolution [ 12 ].

The improvement in sequence length in metagenomics overcomes the limitation of 16S rRNA gene sequencing. It is promising in identifying more members of the microbial community [ 13 ]. Studies that are more recent coupled metagenomics with transcriptomics and metabolomics to investigate how the active microbial community collaborates in the initiation and progression of dental caries [ 14 , 15 , 16 ]. They investigated what the microorganisms in the studied niches were, as well as how the microorganisms actively worked together to cause disease. The understanding of caries microbiology has been greatly enriched with the advancement of sequencing-based technology and bioinformatics analysis in recent years. Therefore, this article aims to review the classical concepts on the microbiological aspect of dental caries and to update the knowledge of caries microbiology with the results of studies on the oral microbiome conducted over the past few years.

2. Materials and Methods

We searched the two most relevant electronic databases, PUBMED and EMBASE, for published evidence with the combination of the following key words: (caries OR “dental decay” OR “tooth decay” OR “carious lesion” OR “white spot”) AND (microbiome OR microbiota OR microbial OR biofilm OR microorganism OR mycobiome OR virome). Studies were limited to English publications published on or before 1 August 2022. Duplicate studies were discarded. Studies were included for review if they met the following criteria: (1) a study on human dental caries or (2) a study that assessed the microbiota of caries using culture-based or molecular-based techniques. The study selection process is presented in the flow diagram below ( Figure 1 ).

Flow diagram of literature search and study selection.

3.1. Oral Microbial Communities

The oral cavity is a complex ecology with various niches. Not only bacteria but also archaea, fungi, and viruses reside in these niches [ 17 , 18 ]. Among them, bacteria make up the main proportion of this diverse community. Bacteria are also the most extensively studied subtype of the oral microbiome. According to the expanded Human Oral Microbiome Database (eHOMD) ( https://homd.org/ (accessed on 1 August 2022)), 774 oral bacterial species have been detected and studied. Around 58% of the species have been cultivated and officially named, 16% have been cultivated but remain unnamed, and 26% remain uncultivated. The majority of these species belong to six broad phyla: Firmicutes, Actinobacteria, Proteobacteria, Fusobacteria, Bacteroidetes, and Spirochaetes [ 19 ].

For several decades, cultivation studies have reported fungi to be oral inhabitants [ 20 ]. Their biodiversity and potential role in the oral ecosystem could not be extensively studied until the last decade because of the uncultivable features of most fungi and the relatively low proportion of the biomass [ 21 ]. A collection of studies has found more than 100 genus-level taxa of fungi as significant constituents of the oral mycobiome, of which only Candida and Malassezia have been well demarcated [ 22 , 23 , 24 ]. Moreover, only Candida has been extensively investigated and claimed to be involved in various oral diseases, including caries [ 25 , 26 ]. Although studies have reported hundreds of fungal taxa, only a few of them have been indicated to be true oral colonizers [ 22 ]. The further isolation and characterization of the other fungal taxa with low abundances are desirable for understanding the diversity and functionality of the fungi in the oral microbiome.

The Archaeal microorganism was first isolated from an oral subgingival sample in 1987 [ 27 ]. Later studies found the presence of Archaea at various oral sites, most frequently at periodontal sites [ 28 , 29 , 30 , 31 , 32 , 33 ], followed by endodontic sites [ 34 , 35 ], but rarely from dental caries [ 36 ], saliva [ 37 ], and the tongue [ 38 ]. Currently, Archaea detected in the human oral cavity is confined to a few phylotypes, including the most abundant Methanogenic archaea and Thermoplasmata [ 36 , 39 , 40 ]. The low abundance and the fastidious cultivation process can hamper the identification of Archaea, which can lead to an underestimation of the diversity of oral archaea. Furthermore, the information related to the role of oral archaea in dental caries is sparse.

Viruses have been identified from oral cavities, including a few eukaryotic viruses and various bacteriophages [ 41 ]. Interpreted from the limited evidence, the oral virome is highly individual-specific but temporally stable [ 42 , 43 ]. Bacteriophages, which are viruses targeting bacteria, are primarily lysogenic. In a previous study, the bacteriophages of lytic styles, which were predominant in the dental plaque of periodontitis, could eradicate their susceptible bacteria hosts or convey new functions to their bacteria host [ 44 ]. Thus, viruses may have a considerable capacity in shaping the oral microbial community’s structure and pathogenesis [ 45 ]. Despite the significance of virus–bacteria interactions to the whole oral microbiome, the role of oral viruses is understudied [ 45 ]. The interspecies and inter-kingdom interactions of the oral microorganisms are the key to maintaining oral health. The pathogenic shifts in the oral microbial communities contribute to the pathogenesis of polymicrobial diseases, including caries [ 33 , 44 , 46 , 47 ]. Therefore, the development of caries is highly associated with oral microbiological changes [ 2 , 14 ].

3.2. The Microbiological Hypothesis of Dental Caries Etiology

The continuous development of microbiological research methods has led to a shift in the microbiological theory of dental caries etiology. In the late nineteenth century, bacteria isolation and identification techniques were far from developed. The etiology of caries was postulated to be determined by the quantity of dental plaque, referred to as the “Traditional Non-specific Plaque Hypothesis”, which Miller proposed in 1890 [ 48 ]. With advances in microscopes and microorganism cultivation techniques, specific bacterial species, mainly Streptococcus mutans and Lactobacillus, were frequently found to be associated with initiating caries, characterizing them as cariogenic species [ 49 , 50 , 51 , 52 ]. Antibiotic treatment that targeted these species reduced caries formation [ 53 ]. Based on this evidence, Loesche proposed the “Specific Plaque Hypothesis” in 1976 [ 54 ]. The “Specific Plaque Hypothesis” states that specific cariogenic bacteria in dental plaque, such as Streptococcus mutans and Lactobacillus, are responsible for dental caries. However, the “Specific Plaque Hypothesis” cannot explain the fact that Streptococcus mutans is absent from some carious sites. In addition, Streptococcus mutans is constantly detected on sound tooth surfaces, indicating that the presence of this species is neither sufficient nor necessary for initiating caries [ 55 ].

With other bacteria species isolated from caries, Marsh proposed the “Ecological Plaque Hypothesis” in 1994 [ 56 , 57 ]. In this hypothesis, it is stated that caries develops along with the disruption of microbial homeostasis under ecological stress, in which some pathogenic species outnumber health-related microorganisms. The ecological plaque hypothesis stresses the critical role of the interaction between the environment and bacteria. The development of molecular identification techniques has led to a continuous revision of the etiology of dental caries. Hundreds of not-yet cultivable oral phylotypes have been identified using gene-sequencing methods, suggesting that an increasingly diverse microflora might play a critical role in the ecological changes resulting in caries onset [ 58 ]. Furthermore, a metatranscriptomic analysis revealed a discrete gene expression profile of oral microflora from which genomics are disclosed, directing the focus to the microbes that are actively involved in caries development [ 59 ]. In 2008, Takahashi further extended the “Ecological Plaque Hypothesis” by incorporating the metabolism of plaque microorganisms. In this extended version, it is stated that the neutral microenvironment tilts to an acidic condition when acid production outweighs the base metabolites’ buffering capacity, followed by acid-induced selection and adaptation within the microflora. This process disrupts a healthy microbial community’s stability and leads to dental caries [ 60 ].

3.3. Microorganisms Associated with Caries Development

Table 1 presents the microbial species that are potentially related to caries based on the currently available literature. Streptococcus mutans has been considered a major pathogen of dental caries since 1971 [ 49 , 61 ]. Many other bacteria have been isolated from carious sites or have been found to feature distinctly throughout the process of caries development, and they have been roughly proposed to be related to caries. With the development of culture-independent identification technology, some fastidious fungi have also been identified to be caries-related ( Table 1 ).

Microbial species related to caries.

It is worth noting that, even though various species of Lactobacillus and Bifidobacteria were reported to be strongly correlated with caries progression, other species of these two genera were demonstrated to be effective probiotics in the context of caries prevention [ 90 ]. These probiotics may exert caries prevention effects by regulating the microflora dysbiosis induced by environment stress [ 91 ]. Considering that different species of the same genus may play opposite roles in the caries development process, a species-level resolution analysis is required [ 92 ].

With the evolutional sequencing-based technology and bioinformatics approaches, more unknown bacterial species were identified, and their roles in the acid-producing process were gradually disclosed [ 93 ]. A comprehensive understanding of caries microbiology is under development.

3.4. Shifts in the Oral Microbiome in Dental Caries

Evidence on the association between the oral microbial profile and caries has been surging in recent decades [ 94 ]. Generally, the oral bacterial community was less diverse in caries-affected than in caries-free subjects [ 95 , 96 , 97 ]. Specifically, the relative abundance of caries-related species rather than the taxonomic diversity changed along with caries development [ 83 , 94 , 98 , 99 , 100 , 101 ]. The changes in the fungal microbiome, or the mycobiome, were similar to those of the bacteriome, with the relative abundance of several taxa that mainly belong to candida increasing significantly in the dental plaque on caries surfaces [ 92 ]. The microbiome research of dental caries has not detected any specific microbial species uniquely associated with caries [ 102 ].

Different microbial interaction profiles between caries-affected and caries-free communities were found in an operational taxonomic unit (OTU) network analysis, although the results are discordant among studies. In a study on early childhood caries (ECC), the interconnection between OTUs was reported to be intensified in the caries-affected community compared to the caries-free community, suggesting the contribution of the intensive species interactions to the development of ECC [ 94 ]. In another study, the intercorrelation among predominant genera was increasingly complex and robust in caries-free sites in an adult population [ 101 ]. The research subjects’ different age groups may explain the inconsistency between the studies. Further explorations are required to obtain a valid conclusion on the changes in microbial interactions in patients with caries.

Because microbiome studies on dental caries are carried out separately in children and adults, there is no direct evidence on comparing the difference in the caries-related microbial shift between different age groups. However, evidence has shown that the microbial composition changes with dentition development [ 103 ]. Thus, the microflora that contributes to the caries process may differ from childhood to adulthood. We extracted the bacterial species with a significantly higher abundance in caries-affected and caries-free subjects from previous articles, and they are presented in Figure 2 . Considering repeatability, only species that were reported in at least two studies were included as being caries-related or health-related. As shown in Figure 1 , only Streptococcus mutans from saliva was shown to be significantly associated with caries in adults, while a variety of taxa from both saliva and plaque were reported to be caries-related or health-related in children [ 102 ].

Common bacteria affecting development of dental caries. Bacterial species with significantly higher abundances in caries-affected status or in healthy status from supragingival plaque or saliva samples. Each quadrant presents a different sample type; for example, the top right quadrant denotes plaque samples from caries-affected subjects. Font size is positively proportional to the frequency of detection. Font color is to distinguish age groups: blue for children and red for adults.

Apart from the overall changes in the oral microbiome in patients with dental caries, the shifts in the caries-associated microorganisms at the different statuses of caries progression were also investigated.

3.4.1. Microbiome Shifts in Caries of Different Stages

The organic and mineral components, as well as the micro-environment, are diverse throughout the different parts of the tooth structure, indicating that the destruction of the different tooth parts may involve distinct microbial-related factors. An early metagenome study on caries reported that both the compositions and the functional profiles of the microbial communities differed greatly between enamel caries and dentin caries [ 97 ]. Genes that encode the functions of sugar fermentation, cell surface adhesion, and acid stress responses were overrepresented in enamel caries while presenting the opposite trend in dentine caries [ 97 , 104 ]. Interestingly, genes overexpressed in the deep dentin microflora correlated to the host’s immune response [ 97 ], indicating the potential significance of the interaction between microbes and their host. Additionally, Lactobacillus species were only detected in dentin caries, and a higher abundance of Prevotella was found deep in the dentin [ 97 ]. According to Richards et al., four species ( S. mutans , Scardovia wiggsiae , Parascardovia denticolens , and Lactobacillus salivarius ) exclusively exist in dentine caries [ 90 ]. On the contrary, some species with a higher abundance in enamel caries decreased or disappeared in dentine caries [ 97 ]. A metatranscriptomic study also showed that the active microbial community differed significantly between carious enamel and dentine, with lactobacilli expressing a much higher level in dentine caries [ 104 ]. In this study, a large number of species expressed at an extremely low abundance existed exclusively in either enamel caries or dentine caries, which indicates that minority species might play an essential role in caries occurrence [ 104 ].

3.4.2. Microbiome Shifts in Caries with Different Activities

Recently, the microbial contribution to dental caries activity was investigated. It was concluded from the evidence that existed that the microbial communities residing on active caries saw a reduction in richness compared to those residing on arrested caries [ 105 ], but they shared a similar beta diversity [ 105 , 106 ]. Additionally, the relative abundance of some caries-associated bacteria was increased in resistant active caries after silver diamine fluoride (SDF) treatment but was decreased in arrested caries [ 105 ]. An in vivo study found that Streptococcus and Veillonella were more evenly distributed with other taxa in arrested caries, while they were predominant in induced active caries [ 107 ]. Further evidence is needed to investigate the microbiome’s role in the shift in caries activity.

3.4.3. Microbiome Shifts in Caries in Different Locations

The biofilm composition of the dental root surface may differ from that of the coronal surface because of the influence of gingival crevicular fluid [ 108 ]. Patients with coronal caries may be free from root caries and vice versa. Thus, there arises the question of whether the bacterial community involved in root caries might differ from that involved in coronal caries. An early culture-based study showed that the major bacteria recovered from the plaque of root caries were distinct from those of enamel caries [ 109 ]. However, no molecular study has investigated the dis/similarity of the microbiome involved in coronal caries and root caries. Most of the up-to-date oral microbiome studies targeted the relationship between the microbial community and coronal caries. A recent study focusing on root caries found that Prevotella dominated the microflora of caries lesions that extended to the subgingival margin, while Streptococcus dominated the microbial community from root caries lesions that were confined within supragingival sites [ 110 ]. However, the periodontal microflora probably confounded the results of this study. The lack of evidence on this subject indicates the urgency of exploring this phenomenon.

4. Discussion and Future Perspectives

The recent advancements in oral microbiology studies have expanded our perspectives on caries etiology. Nevertheless, there are limitations in the caries microbiology studies discussed in the present literature review. Due to the high cost of the new-born omics techniques and the infancy of methodological and analytical protocols, most of the recent studies used 16S rRNA gene sequencing to investigate the microbiological contribution to caries development. However, 16S sequencing only provides information regarding bacterial composition at genus- or species-level resolution, failing to characterize the strain-level diversity of the microbial community and its functional capabilities [ 111 ]. Another non-negligible limitation is that current studies rarely study the diversity and the potential roles of nonbacterial microorganisms, regardless of the enormous diversity of the fungi identified in the oral cavity. As any other infectious disease, the host factor plays a vital role in caries development. Saliva, being the first line of defense in the oral cavity, helps shape the microbial profile of pioneer colonizers, which later “trains” the host immune system to defend against pathological invaders [ 112 ]. The dynamic balance between the host immune system and the microbial commensals maintains the oral health status [ 113 ]. Despite the convincing relationship between immunology and microbiology in the context of caries, there is a lack of studies examining how the microbiota interacts with the host immune system in the course of microbial dysbiosis. Lastly, the lack of consistency in the study protocol hampers the comparisons between studies, compromising the reproducibility of the results.

Future work should be directed toward resolving the limitations in the current studies. As demonstrated, the taxa detected with a high abundance in dental caries do not necessarily actively function and vice versa. Therefore, associating the microorganisms with their functional contributions to dental caries is highly desirable in future studies. Complementary methodological approaches are expected to be employed to uncover the diversity and contribution of the relatively unexplored domains of the microorganisms and their interactions with their bacteria counterparts in the oral microbiome community. Furthermore, the interaction between the microbial community and their host’s immune system should also be explored. Regarding the significant heterogeneity among the results of different studies, consistency in the study protocol, including sampling site selection, sampling methods, sample storage condition, sequencing technique, reference database, and bioinformatics pipelines, is required to achieve comparable results across the extensive number of studies.

5. Conclusions

Research using sequencing-based technology and bioinformatics analysis has revolutionized the classical microbiological concept of dental caries, which is based on culture-based methods. Contemporary evidence validates and extends the “Ecological Plaque Hypothesis”. The inter-species and inter-kingdom interactions of diverse microorganisms contribute to the development of dental caries. Both the predominance and the relative abundance of microbiota change along with the caries development stages. Researchers are further exploring the functionalities of caries-contributing species and the interactions between microbiota and their hosts.

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Author Contributions

Conceptualization, O.Y.Y.; writing—original draft preparation, J.S.Z. and O.Y.Y.; visualization, J.S.Z.; analysis, J.S.Z.; writing—review and editing, C.-H.C. and O.Y.Y. All authors have read and agreed to the published version of the manuscript.

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Periodontal Pathogenesis: Definitions and Historical Perspectives

• First Online: 27 September 2017

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• Nagihan Bostanci 3 &
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Periodontal disease, or periodontitis, is a globally widespread pathology of the human oral cavity. Indeed, approximately 10% of the global adult population is highly vulnerable to severe periodontitis. Another 10–15% appears to be completely resistant to it, while the remainder vary between these two extremes [1, 2]. Moreover, the prevalence of periodontitis is peaking at the fourth decade of life and increasing to 70–85% in the age group of 60–65 [3]. Strikingly, despite major improvements in oral hygiene practices today, these proportions are not far from what was reported in possibly the first epidemiological report of periodontitis in humans back in 1918 (then defined as periodontoclasia or pyorrhea alveolaris ). According to that, the prevalence of the disease in the Chicago area was 13% in the age range of 20–24, 68% in 30–39, and 88% over 50. Much recent data from USA showed that there is not a drop but rather an increase in these numbers among the older individuals [4]. That means that periodontitis is an inevitable oral pathology of the human population, and its prevalence increases with age. Taking also under consideration the increasing life expectancy, periodontitis is a growing health problem.

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Bostanci, N., Belibasakis, G.N. (2018). Periodontal Pathogenesis: Definitions and Historical Perspectives. In: Bostanci, N., Belibasakis, G. (eds) Pathogenesis of Periodontal Diseases. Springer, Cham. https://doi.org/10.1007/978-3-319-53737-5_1

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