This volume of Periodontology 2000 represents the 25th anniversary of the Journal, and uses the occasion to assess important advancements in periodontology over the past quarter-century as well as the hurdles that remain. Periodontitis is defined by pathologic loss of the periodontal ligament and alveolar bone. The disease involves complex dynamic interactions among active herpesviruses, specific bacterial pathogens and destructive immune responses. Periodontal diagnostics is currently based on clinical rather than etiologic criteria, and provides limited therapeutic guidance. Periodontal causative treatment consists of scaling, antiseptic rinses and occasionally systemic antibiotics, and surgical intervention has been de-emphasized, except perhaps for the most advanced types of periodontitis. Plastic surgical therapy includes soft-tissue grafting to cover exposed root surfaces and bone grafting to provide support for implants. Dental implants are used to replace severely diseased or missing teeth, but implant overuse is of concern. The utility of laser treatment for periodontitis remains unresolved. Host modulation and risk-factor modification therapies may benefit select patient groups. Patient self-care is a critical part of periodontal health care, and twice-weekly oral rinsing with 0.10-0.25% sodium hypochlorite constitutes a valuable adjunct to conventional anti-plaque and anti-gingivitis treatments. A link between periodontal herpesviruses and systemic diseases is a strong biological plausibility. In summary, research during the past 25 years has significantly changed our concepts of periodontitis pathobiology and has produced more-effective and less-costly therapeutic options.

Periodontitis: facts, fallacies and the future

Background The results from cross sectional and longitudinal studies show that periodontitis is closely associated with cognitive impairment (CI) and Alzhemer’s Disease (AD). Further, studies using animal model of periodontitis and human post-mortem brain tissues from subjects with AD strongly suggest that a gram-negative periodontal pathogen, Porphyromonas gingivalis (Pg) and/or its product gingipain is/are translocated to the brain. However, neuropathology resulting from Pg oral application is not known. In this work, we tested the hypothesis that repeated exposure of wild type C57BL/6 mice to orally administered Pg results in neuroinflammation, neurodegeneration, microgliosis, astrogliosis and formation of intra- and extracellular amyloid plaque and neurofibrillary tangles (NFTs) which are pathognomonic signs of AD. Methods Experimental chronic periodontitis was induced in ten wild type 8-week old C57BL/6 WT mice by repeated oral application (MWF/week) of Pg/gingipain for 22 weeks (experimental group). Another 10 wild type 8-week old C57BL/6 mice received vehicle alone (control group) MWF per week for 22 weeks. Brain tissues were collected and the presence of Pg/gingipain was determined by immunofluorescence (IF) microscopy, confocal microscopy, and quantitative PCR (qPCR). The hippocampi were examined for the signs of neuropathology related to AD: TNFα, IL1β, and IL6 expression (neuroinflammation), NeuN and Fluoro Jade C staining (neurodegeneration) and amyloid beta1-42 (Aβ42) production and phosphorylation of tau protein at Ser396 were assessed by IF and confocal microscopy. Further, gene expression of amyloid precursor protein (APP), beta-site APP cleaving enzyme 1 (BACE1), a disintegrin and metalloproteinase domain-containing protein10 (ADAM10) for α-secretase and presenilin1 (PSEN1) for ɣ-secretase, and NeuN (rbFox3) were determined by RT-qPCR. Microgliosis and astrogliosis were also determined by IF microscopy. Results Pg/gingipain was detected in the hippocampi of mice in the experimental group by immunohistochemistry, confocal microscopy, and qPCR confirming the translocation of orally applied Pg to the brain. Pg/gingipain was localized intra-nuclearly and peri-nuclearly in microglia (Iba1+), astrocytes (GFAP+), neurons (NeuN+) and was evident extracellularly. Significantly greater levels of expression of IL6, TNFα and IL1β were evident in experimental as compared to control group (p<0.01, p<0.00001, p<0.00001 respectively). In addition, microgliosis and astrogliosis were evident in the experimental but not in control group (p <0.01, p<0.0001 respectively). Neurodegeneration was evident in the experimental group based on a fewer number of intact neuronal cells assessed by NeuN positivity and rbFOX3 gene expression, and there was a greater number of degenerating neurons in the hippocampi of experimental mice assessed by Fluoro Jade C positivity. APP and BACE1 gene expression were increased in experimental group compared with control group (p<0.05, p<0.001 respectively). PSEN1 gene expression was higher in experimental than control group but the difference was not statistically significant (p = 0.07). ADAM10 gene expression was significantly decreased in experimental group compared with control group (p<0.01). Extracellular Aβ42 was detected in the parenchyma in the experimental but not in the control group (p< 0.00001). Finally, phospho-Tau (Ser396) protein was detected and NFTs were evident in experimental but not in the control group (p<0.00001). Conclusions This study is the first to show neurodegeneration and the formation of extracellular Aβ42 in young adult WT mice after repeated oral application of Pg. The neuropathological features observed in this study strongly suggest that low grade chronic periodontal pathogen infection can result in the development of neuropathology that is consistent with that of AD.

Chronic oral application of a periodontal pathogen results in brain inflammation, neurodegeneration and amyloid beta production in wild type mice

The most important development in the epidemiology of periodontitis in the USA during the last decade is the result of improvements in survey methodologies and statistical modeling of periodontitis in adults. Most of these advancements have occurred as the direct outcome of work by the joint initiative known as the Periodontal Disease Surveillance Project by the Centers for Disease Control and Prevention and the American Academy of Periodontology that was established in 2006. This report summarizes some of the key findings of this important initiative and its impact on our knowledge of the epidemiology of periodontitis in US adults. This initiative first suggested new periodontitis case definitions for surveillance in 2007 and revised them slightly in 2012. This classification is now regarded as the global standard for periodontitis surveillance and is used worldwide. First, application of such a standard in reporting finally enables results from different researchers in different countries to be meaningfully compared. Second, this initiative tackled the concern that prior national surveys, which used partial-mouth periodontal examination protocols, grossly underestimated the prevalence of periodontitis of potentially more than 50%. Consequently, because previous national surveys significantly underestimated the true prevalence of periodontitis, it is not possible to extrapolate any trend in periodontitis prevalence in the USA over time. Any difference calculated may not represent any actual change in periodontitis prevalence, but rather is a consequence of using different periodontal examination protocols. Finally, the initiative addressed the gap in the need for state and local data on periodontitis prevalence. Through the direct efforts of the Centers for Disease Control and Prevention and the American Academy of Periodontology initiative, full-mouth periodontal probing at six sites around all nonthird molar teeth was included in the 6 years of National Health and Nutrition Examination Surveys from 2009-2014, yielding complete data for 10 683 dentate community-dwelling US adults aged 30 to 79 years. Applying the 2012 periodontitis case definitions to the 2009-2014 National Health and Nutrition Examination Surveys data, the periodontitis prevalence turned out to be much greater than previously estimated, namely affecting 42.2% of the population with 7.8% of people experiencing severe periodontitis. It was also discovered that only the moderate type of periodontitis is driving the increase in periodontitis prevalence with age, not the mild or the severe types whose prevalence do not increase consistently with age, but remain ~ 10%-15% in all age groups of 40 years and older. The greatest risk for having periodontitis of any type was seen in older people, in males, in minority race/ethnic groups, in poorer and less educated groups, and especially in cigarette smokers. The Centers for Disease Control and Prevention and the American Academy of Periodontology initiative reported, for the first time, the periodontitis prevalence estimated at both local and state levels, in addition to the national level. Also, this initiative developed and validated in field studies a set of eight items for self-reported periodontitis for use in direct survey estimates of periodontitis prevalence in existing state-based surveys. These items were also included in the 2009-2014 National Health and Nutrition Examination Surveys for validation against clinically determined cases of periodontitis. Another novel result of this initiative is that, for the first time, the geographic distribution of practicing periodontists in relation to the geographic distribution of people with severe periodontitis is illustrated. In summary, the precise periodontitis prevalence and distribution among subgroups in the dentate US noninstitutionalized population aged 30-79 years is better understood because of application of valid periodontitis case definitions to full-mouth periodontal examination, in combination with reliable information on demographic and health-related measures. We now can monitor the trend of periodontitis prevalence over time as well as guide public health preventive and intervention initiatives for the betterment of the health of the adult US population.

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Recent epidemiologic trends in periodontitis in the USA.

This report provides a comprehensive overview of the adverse effects of hyperglycemia on the periodontium. It combines data from literature reviews of original data from two large, population-based epidemiologic studies with comprehensive periodontal health assessment. Emphasis is placed on the exploration of hitherto sparsely reported effects of prediabetes and poorly controlled (uncontrolled) diabetes, in contrast to the umbrella term "diabetes." This stems from the realization that it is not simply having a diagnosis of diabetes that may adversely affect periodontal health. Rather, it is the level (severity) of hyperglycemia that is the determining factor, not the case definition of the diagnosis of diabetes or the type of diabetes in question. Importantly, based on existing evidence this paper also attempts to estimate the improvements in periodontal probing depth and clinical attachment level that can be expected upon successful nonsurgical periodontal treatment in people with chronic periodontitis, with and without diabetes, respectively. This exploration includes the implentation of new systematic reviews and meta-analyses that allow comparison of such intervention outcomes between hyperglycemic and normoglycemic subjects. Based on both existing literature and original analyses of population-based studies, we try to answer questions such as: Is there a glycated hemoglobin concentration threshold for periodontitis risk? Does short-term periodontal probing depth reduction and clinical attachment level gain after scaling and root planing depend on glycemic control in type 2 diabetes? Are short-term scaling and root planing outcomes in people with hyperglycemia/diabetes inferior to those in people without diabetes? Do periodontitis patients with diabetes benefit more from the use of adjuvant antibiotics with nonsurgical periodontal treatment than people without diabetes? Does hyperglycemia lead to greater tooth loss in patients in long-term post-periodontal treatment maintenance programs? Throughout this review, we compare our new findings with previous data and report whether the results of these new analyses corroborate, or are in discord with, similar scientific reports in the literature. We also explore the potential role of dental health-care professionals in helping patients control the risk factors that are identical for periodontitis and diabetes. Finally, we suggest various topics that still need exploration in future research.

Periodontal complications of hyperglycemia/diabetes mellitus: Epidemiologic complexity and clinical challenge.

Human oral cavity (mouth) hosts a complex microbiome consisting of bacteria, archaea, protozoa, fungi and viruses. These bacteria are responsible for two common diseases of the human mouth including periodontal (gum) and dental caries (tooth decay). Dental caries is caused by plaques, which are a community of microorganisms in biofilm format. Genetic and peripheral factors lead to variations in the oral microbiome. It has known that, in commensalism and coexistence between microorganisms and the host, homeostasis in the oral microbiome is preserved. Nonetheless, under some conditions, a parasitic relationship dominates the existing situation and the rise of cariogenic microorganisms results in dental caries. Utilizing advanced molecular biology techniques, new cariogenic microorganisms species have been discovered. The oral microbiome of each person is quite distinct. Consequently, commonly taken measures for disease prevention cannot be exactly the same for other individuals. The chance for developing tooth decay in individuals is dependent on factors such as immune system and oral microbiome which itself is affected by the environmental and genetic determinants. Early detection of dental caries, assessment of risk factors and designing personalized measure let dentists control the disease and obtain desired results. It is necessary for a dentist to consider dental caries as a result of a biological process to be targeted than treating the consequences of decay cavities. In this research, we critically review the literature and discuss the role of microbial biofilms in dental caries.

Oral microbial biofilms: an update

The older adult population is growing rapidly in the USA and it is expected that by 2040 the number of adults ≥ 65 years of age will have increased by about 50%. With the growth of this subpopulation, oral health status, and periodontal status in particular, becomes important in the quest to maintain an adequate quality of life. Poor oral health can have a major impact, leading to tooth loss, pain and discomfort, and may prevent older adults from chewing food properly, often leading to poor nutrition. Periodontitis is monitored in the USA at the national level as part of the Healthy People 2020 initiative. In this report, we provide estimates of the overall burden of periodontitis among adults ≥ 65 years of age and after stratification according to sociodemographic factors, modifiable risk factors (such as smoking status), the presence of other systemic conditions (such as diabetes) and access to dental care. We also estimated the burden of periodontitis within this age group at the state and local levels. Data from the National Health and Nutrition Examination Survey 2009/2010 and 2011/2012 cycles were analyzed. Periodontal measures from both survey cycles were based on a full-mouth periodontal examination. Nineteen per cent of adults in this subpopulation were edentulous. The mean age was 73 years, 7% were current smokers, 8% lived below the 100% Federal Poverty Level and < 40% had seen a dentist in the past year. Almost two-thirds (62.3%) had one or more sites with ≥ 5 mm of clinical attachment loss and almost half had at least one site with probing pocket depth of ≥ 4 mm. We estimated the lowest prevalence of periodontitis in Utah (62.3%) and New Hampshire (62.6%) and the highest in New Mexico, Hawaii, and the District of Columbia each with a prevalence of higher than 70%. Overall, periodontitis is highly prevalent in this subpopulation, with two-thirds of dentate older adults affected at any geographic level. These findings provide an opportunity to determine how the overall health-care management of older adults should consider the improvement of their oral health conditions. Many older adults do not have dental insurance and are also likely to have some chronic conditions, which can adversely affect their oral health.

Xingyou Zhang

Papers

Periodontitis prevalence in adults ≥ 65 years of age, in the USA.