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Oral biofilms revisited: A novel host tissue of bacteriological origin
Richard P. Darveau,Michael A. Curtis
doi : 10.1111/prd.12374
Volume 86, Issue 1 p. 8-13
The central theme of this volume of Periodontology 2000 is that the microbial dental plaque biofilm, specifically the subgingival dental plaque biofilm, mimics a human tissue in both structure and function. As a basis for this assertion we use the definition of a tissue as an aggregate of similar cells and cell products forming a defined structure with a specific function, in a multicellular organism. Accordingly, we propose that the dental plaque biofilm represents an acquired human tissue largely of bacterial origin that maintains the health of gingival tissue. Furthermore, we acknowledge that disease can be defined as a deviation from the normal structure or an interruption to the function of any body part, organ, or system, and that is manifested by a characteristic set of symptoms and signs whose etiology, pathology, and prognosis may be known or unknown. Therefore, in this volume we present the concept that periodontitis is a disruption of the normal function of the healthy subgingival plaque biofilm with concomitant disruption to its functional properties in relation to innate defense surveillance and tissue maintenance, leading to excessive, deregulated inflammation and tissue destruction.
Interactions of host-associated multispecies bacterial communities
Heidi Goodrich-Blair
doi : 10.1111/prd.12360
Volume 86, Issue 1 p. 14-31
The oral microbiome comprises microbial communities colonizing biotic (epithelia, mucosa) and abiotic (enamel) surfaces. Different communities are associated with health (eg, immune development, pathogen resistance) and disease (eg, tooth loss and periodontal disease). Like any other host-associated microbiome, colonization and persistence of both beneficial and dysbiotic oral microbiomes are dictated by successful utilization of available nutrients and defense against host and competitor assaults. This chapter will explore these general features of microbe-host interactions through the lens of symbiotic (mutualistic and antagonistic/pathogenic) associations with nonmammalian animals. Investigations in such systems across a broad taxonomic range have revealed conserved mechanisms and processes that underlie the complex associations among microbes and between microbes and hosts.
The dental plaque biofilm matrix
Nicholas S. Jakubovics,Steven D. Goodman,Lauren Mashburn-Warren,Graham P. Stafford,Fabian Cieplik
doi : 10.1111/prd.12361
Volume 86, Issue 1 p. 32-56
The extracellular matrix is a critical component of microbial biofilms, such as dental plaque, maintaining the spatial arrangement of cells and coordinating cellular functions throughout the structure. The extracellular polymeric substances that comprise the matrix include carbohydrates, nucleic acids, proteins, and lipids, which are frequently organized into macromolecular complexes and/or are associated with the surfaces of microbial cells within the biofilm. Cariogenic dental plaque is rich in glucan and fructan polysaccharides derived from extracellular microbial metabolism of dietary sucrose. By contrast, the matrix of subgingival dental plaque is a complex mixture of macromolecules that is still not well understood. Components of the matrix escape from microbial cells during lysis by active secretion or through the shedding of vesicles and serve to anchor microbial cells to the tooth surface. By maintaining the biofilm in close association with host tissues, the matrix facilitates interactions between microorganisms and the host. The outcome of these interactions may be the maintenance of health or the development of dental disease, such as caries or periodontitis. The matrix affords microbial cells protection against chemical and physical insults and hinders the eradication of pathogenic dental plaque. Therefore, strategies to control the matrix are critical to maintain oral health. This review discusses recent advances in our understanding of the composition, origins, and function of the dental plaque matrix, with a focus on subgingival dental plaque. New strategies to control subgingival dental plaque based on targeting the biofilm matrix are also considered.
Microbial signatures of health, gingivitis, and periodontitis
Loreto Abusleme,Anilei Hoare,Bo-Young Hong,Patricia I. Diaz
doi : 10.1111/prd.12362
Volume 86, Issue 1 p. 57-78
The subgingival crevice harbors diverse microbial communities. Shifts in the composition of these communities occur with the development of gingivitis and periodontitis, which are considered as successive stages of periodontal health deterioration. It is not clear, however, to what extent health- and gingivitis-associated microbiota are protective, or whether these communities facilitate the successive growth of periodontitis-associated taxa. To further our understanding of the dynamics of the microbial stimuli that trigger disruptions in periodontal homeostasis, we reviewed the available literature with the aim of defining specific microbial signatures associated with different stages of periodontal dysbiosis. Although several studies have evaluated the subgingival communities present in different periodontal conditions, we found limited evidence for the direct comparison of communities in health, gingivitis, and periodontitis. Therefore, we aimed to better define subgingival microbiome shifts by merging and reanalyzing, using unified bioinformatic processing strategies, publicly available 16S ribosomal RNA gene amplicon datasets of periodontal health, gingivitis, and periodontitis. Despite inherent methodological differences across studies, distinct community structures were found for health, gingivitis, and periodontitis, demonstrating the specific associations between gingival tissue status and the subgingival microbiome. Consistent with the concept that periodontal dysbiosis is the result of a process of microbial succession without replacement, more species were detected in disease than in health. However, gingivitis-associated communities were more diverse than those from subjects with periodontitis, suggesting that certain species ultimately become dominant as dysbiosis progresses. We identified the bacterial species associated with each periodontal condition and prevalent species that do not change in abundance from one state to another (core species), and we also outlined species co-occurrence patterns via network analysis. Most periodontitis-associated species were rarely detected in health but were frequently detected, albeit in low abundance, in gingivitis, which suggests that gingivitis and periodontitis are a continuum. Overall, we provide a framework of subgingival microbiome shifts, which can be used to generate hypotheses with respect to community assembly processes and the emergence of periodontal dysbiosis.
The human oral phageome
Szymon P. Szafra?ski,J?rgen Slots,Meike Stiesch
doi : 10.1111/prd.12363
Volume 86, Issue 1 p. 79-96
Oral bacteriophages (or phages), especially periodontal ones, constitute a growing area of interest, but research on oral phages is still in its infancy. Phages are bacterial viruses that may persist as intracellular parasitic deoxyribonucleic acid (DNA) or use bacterial metabolism to replicate and cause bacterial lysis. The microbiomes of saliva, oral mucosa, and dental plaque contain active phage virions, bacterial lysogens (ie, carrying dormant prophages), and bacterial strains containing short fragments of phage DNA. In excess of 2000 oral phages have been confirmed or predicted to infect species of the phyla Actinobacteria (>300 phages), Bacteroidetes (>300 phages), Firmicutes (>1000 phages), Fusobacteria (>200 phages), and Proteobacteria (>700 phages) and three additional phyla (few phages only). This article assesses the current knowledge of the diversity of the oral phage population and the mechanisms by which phages may impact the ecology of oral biofilms. The potential use of phage-based therapy to control major periodontal pathogens is also discussed.
Spatial scale in analysis of the dental plaque microbiome
Gary G. Borisy,Alex M. Valm
doi : 10.1111/prd.12364
Volume 86, Issue 1 p. 97-112
Ecologists have long recognized the importance of spatial scale in understanding structure-function relationships among communities of organisms within their environment. Here, we review historical and contemporary studies of dental plaque community structure in the context of three distinct scales: the micro (1-10 µm), meso (10-100 µm) and macroscale (100 µm to ?1 cm). Within this framework, we analyze the compositional nature of dental plaque at the macroscale, the molecular interactions of microbes at the microscale, and the emergent properties of dental plaque biofilms at the mesoscale. Throughout our analysis of dental plaque across spatial scales, we draw attention to disease and health-associated structure-function relationships and include a discussion of host immune involvement in the mesoscale structure of periodontal disease–associated biofilms. We end with a discussion of two filamentous organisms, Fusobacterium nucleatum and Corynebacterium matruchotii, and their relevant contributions in structuring dental plaque biofilms.
Resilience of the oral microbiome
William G. Wade
doi : 10.1111/prd.12365
Volume 86, Issue 1 p. 113-122
The human mouth harbors a complex microbiota, the composition of which is potentially influenced by a wide range of factors, including the intake of food and drink, the availability of endogenous nutrients, the host immune system, drug treatments, and systemic diseases. Despite these possible influences, the oral microbiota is remarkably resilient, particularly in comparison with the microbiota of the large intestine. Diet, with the exception of excessive and/or frequent consumption of fermentable carbohydrate or supplementation with nitrate, has minimal impact on the composition of the oral bacterial community. The common oral diseases dental caries and the periodontal diseases is associated with modification of the oral microbiota primarily as a result of the ecological changes induced by excessive acid production and inflammation, respectively. Systemically-administered antimicrobials have only a small effect on the composition of the oral bacterial community, and while locally delivered antimicrobials can have some clinical benefits, the biofilm lifestyle of oral bacteria lends them substantial resistance to the agents used. Saliva plays an important role in oral microbial ecology, by supplying nutrients and providing protection against colonization by nonoral organisms. Dry mouth is one condition that has a major effect on the microbiota, resulting in increased colonization by opportunistic pathogens. Some systemic diseases do affect the oral microbiome, notably diabetes, in which raised levels of glucose in saliva and tissue impact on bacterial nutrition.
Acquisition and establishment of the oral microbiota
A. M. (Marije) Kaan,Dono Kahharova,Egija Zaura
doi : 10.1111/prd.12366
Volume 86, Issue 1 p. 123-141
Acquisition and establishment of the oral microbiota occur in a dynamic process over various stages and involve close and continuous interactions with the host and its environment. In the present review, we discuss the stages of this process in chronological order. We start with the prenatal period and address the following questions: ‘Is the fetus exposed to maternal microbiota during pregnancy?’ and ‘If so, what is the potential role of this exposure?’ We comment on recent reports of finding bacterial DNA in placenta during pregnancies, and provide current views on the potential functions of prenatal microbial encounters. Next, we discuss the physiological adaptations that take place in the newborn during the birth process and the effect of this phase of life on the acquisition of the oral microbiota. Is it really just exposure to maternal vaginal microbes that results in the difference between vaginally and Cesarian section-born infants? Then, we review the postnatal phase, in which we focus on transmission of microbes, the intraoral niche specificity, the effects of the host behavior and environment, as well as the role of genetic background of the host on shaping the oral microbial ecosystem. We discuss the changes in oral microbiota during the transition from deciduous to permanent dentition and during puberty. We also address the finite knowledge on colonization of the oral cavity by microbes other than the bacterial component. Finally, we identify the main outstanding questions that limit our understanding of the acquisition and establishment of a healthy microbiome at an individual level.
Maintaining a protective state for human periodontal tissue
Matsuo Yamamoto,Ryo Aizawa
doi : 10.1111/prd.12367
Volume 86, Issue 1 p. 142-156
Periodontitis, caused by infection with periodontal pathogens, is primarily characterized by inflammatory bone resorption and destruction of connective tissue. Simply describing periodontitis as a specific bacterial infection cannot completely explain the various periodontal tissue destruction patterns observed. Periodontal tissue damage is thought to be caused by various factors. In recent years, research goals for periodontal pathogens have shifted from searching for specific pathogens to investigating mechanisms that damage periodontal tissues. Bacteria interact directly with the host in several ways, influencing expression and activity of molecules that evade host defenses, and destroying local tissues and inhibiting their repair. The host's innate and acquired immune systems are important defense mechanisms that protect periodontal tissues from attack and invasion of periodontal pathogens, thus preventing infection. Innate and acquired immunity have evolved to confront the microbial challenge, forming a seamless defense network in periodontal tissues. In the innate immune response, host cells quickly detect, via specialized receptors, macromolecules and nucleic acids present on bacterial cell walls, and this triggers a protective, inflammatory response. The work of this subsystem of host immunity is performed mainly by phagocytes, beta-defensin, and the complement system. In addition, the first line of defense in oral innate immunity is the junctional epithelium, which acts as a physical barrier to the entry of oral bacteria and other nonself substances. In the presence of a normal flora, junctional epithelial cells differentiate actively and proliferate apically, with concomitant increase in chemotactic factor expression recruiting neutrophils. These immune cells play an important role in maintaining homeostasis and the protective state in periodontal tissue because they eliminate unwanted bacteria over time. Previous studies indicate a mechanism for attracting immune cells to periodontal tissue with the purpose of maintaining a protective state; although this mechanism can function without bacteria, it is enhanced by the normal flora. A better understanding of the relationship between the protective state and its disruption in periodontal disease could lead to the development of new treatment strategies for periodontal disease.
Maintaining homeostatic control of periodontal bone tissue
Jessica D. Hathaway-Schrader,Chad M. Novince
doi : 10.1111/prd.12368
Volume 86, Issue 1 p. 157-187
Alveolar bone is a unique osseous tissue due to the proximity of dental plaque biofilms. Periodontal health and homeostasis are mediated by a balanced host immune response to these polymicrobial biofilms. Dysbiotic shifts within dental plaque biofilms can drive a proinflammatory immune response state in the periodontal epithelial and gingival connective tissues, which leads to paracrine signaling to subjacent bone cells. Sustained chronic periodontal inflammation disrupts “coupled” osteoclast-osteoblast actions, which ultimately result in alveolar bone destruction. This chapter will provide an overview of alveolar bone physiology and will highlight why the oral microbiota is a critical regulator of alveolar bone remodeling. The ecology of dental plaque biofilms will be discussed in the context that periodontitis is a polymicrobial disruption of host homeostasis. The pathogenesis of periodontal bone loss will be explained from both a historical and current perspective, providing the opportunity to revisit the role of fibrosis in alveolar bone destruction. Periodontal immune cell interactions with bone cells will be reviewed based on our current understanding of osteoimmunological mechanisms influencing alveolar bone remodeling. Lastly, probiotic and prebiotic interventions in the oral microbiota will be evaluated as potential noninvasive therapies to support alveolar bone homeostasis and prevent periodontal bone loss.
Maintaining homeostatic control of periodontal epithelial tissue
Ana M. Chang,Nutthapong Kantrong,Richard P. Darveau
doi : 10.1111/prd.12369
Volume 86, Issue 1 p. 188-200
Years of coevolution with resident microbes has made them an essential component of health. Yet, little is known about oral commensal bacteria’s contribution to and role in the maintenance of oral health and homeostasis. Commensal bacteria are speculated to play a host protective role in the maintenance of health. In this review, we describe and provide examples of the coordinate regulation that occurs between oral commensal bacteria and the host innate immune response to modulate and maintain oral homeostasis.
Microbial transitions from health to disease
Susan Joseph,Michael A. Curtis
doi : 10.1111/prd.12377
Volume 86, Issue 1 p. 201-209
Recent advances in our understanding of the microbial populations that colonize the human mouth, their acquisition, interdependency, and coevolution with the host, bring a different perspective to the mechanisms underpinning the maintenance of periodontal health and the development of disease. In this work we suggest that our knowledge map of the etiology of periodontal health and disease can be viewed as a broad, highly connected, and integrated system that spans the entire spectrum of microbe/host/clinical interactions. The overall concept of present Periodontology 2000, that the microbial biofilm can be considered a human tissue of bacteriological origin, is entirely consistent with this integrated system view. The health-associated community structure of microbial biofilms can be considered a system that is normally resilient to perturbation. Equally, there is evidence to suggest that the dysbiotic community structure in disease may share similar resilience properties. In both instances, the resilience may be governed by the precise makeup of the acquired microbiome and by the genetics of the host. Understanding the mechanisms that enable the resistance to change of healthy and dysbiotic microbial populations may be important in the development of approaches to prevent the progression of disease and to restore health in diseased individuals.
Polymicrobial communities in periodontal disease: Their quasi-organismal nature and dialogue with the host
George Hajishengallis,Richard J. Lamont
doi : 10.1111/prd.12371
Volume 86, Issue 1 p. 210-230
In health, indigenous polymicrobial communities at mucosal surfaces maintain an ecological balance via both inter-microbial and host-microbial interactions that promote their own and the host's fitness, while preventing invasion by exogenous pathogens. However, genetic and acquired destabilizing factors (including immune deficiencies, immunoregulatory defects, smoking, diet, obesity, diabetes and other systemic diseases, and aging) may disrupt this homeostatic balance, leading to selective outgrowth of species with the potential for destructive inflammation. This process, known as dysbiosis, underlies the development of periodontitis in susceptible hosts. The pathogenic process is not linear but involves a positive-feedback loop between dysbiosis and the host inflammatory response. The dysbiotic community is essentially a quasi-organismal entity, where constituent organisms communicate via sophisticated physical and chemical signals and display functional specialization (eg, accessory pathogens, keystone pathogens, pathobionts), which enables polymicrobial synergy and dictates the community's pathogenic potential or nososymbiocity. In this review, we discuss early and recent studies in support of the polymicrobial synergy and dysbiosis model of periodontal disease pathogenesis. According to this concept, disease is not caused by individual “causative pathogens” but rather by reciprocally reinforced interactions between physically and metabolically integrated polymicrobial communities and a dysregulated host inflammatory response.
Peri-implantitis is not periodontitis: Scientific discoveries shed light on microbiome-biomaterial interactions that may determine disease phenotype
Georgios A. Kotsakis,Daniel G. Olmedo
doi : 10.1111/prd.12372
Volume 86, Issue 1 p. 231-240
Peri-implantitis is an immune-mediated biological complication that is attributed to bacterial biofilms on the implant surface. As both periodontitis and peri-implantitis have similar inflammatory phenotypes when assessed cross-sectionally, treatment protocols for peri-implantitis were modeled according to those used for periodontitis. However, lack of efficacy of antimicrobial treatments targeting periodontal pathogens coupled with recent discoveries from open-ended microbial investigation studies create a heightened need to revisit the pathogenesis of peri-implantitis compared with that of periodontitis. The tale of biofilm formation on intraoral solid surfaces begins with pellicle formation, which supports initial bacterial adhesion. The differences between implant- and tooth-bound biofilms appear as early as bacterial adhesion commences. The electrostatic forces and ionic bonding that drive initial bacterial adhesion are fundamentally different in the presence of titanium dioxide or other implant alloys vs mineralized organic hydroxyapatite, respectively. Moreover, the interaction between metal surfaces and the oral environment leads to the release of implant degradation products into the peri-implant sulcus, which exposes the microbiota to increased environmental stress and may alter immune responses to bacteria. Clinically, biofilms found in peri-implantitis are resistant to beta-lactam antibiotics, which are effective against periodontal communities even as monotherapies and demonstrate a composition different from that of biofilms found in periodontitis; these facts strongly suggest that a new model of peri-implant infection is required.
