Periodontitis is an infectious disease that affects the tooth-supporting tissues and exhibits a wide range of clinical, microbiological and immunological manifestations. The disease is associated with and is probably caused by a multifaceted dynamic interaction of specific infectious agents, host immune responses, harmful environmental exposure and genetic susceptibility factors. This volume of Periodontology 2000 covers key subdisciplines of periodontology, ranging from etiopathogeny to therapy, with emphasis on diagnosis, classification, epidemiology, risk factors, microbiology, immunology, systemic complications, anti-infective therapy, reparative treatment, self-care and affordability issues. Learned and unlearned concepts of periodontitis over the past 50 years have shaped our current understanding of the etiology of the disease and of clinical practice.

In the past 50 years, conceptual changes in the field of periodontal diagnostics have paralleled those associated with a better scientific understanding of the full spectrum of processes that affect periodontal health and disease. Fifty years ago, concepts regarding the diagnosis of periodontal diseases followed the classical pathology paradigm. It was believed that the two basic forms of destructive periodontal disease were chronic inflammatory periodontitis and ‘periodontosis’– a degenerative condition. In the subsequent 25 years it was shown that periodontosis was an infection. By 1987, major new concepts regarding the diagnosis and pathogenesis of periodontitis included: (i) all cases of untreated gingivitis do not inevitably progress to periodontitis; (ii) progression of untreated periodontitis is often episodic; (iii) some sites with untreated periodontitis do not progress; (iv) a rather small population of specific bacteria (‘periodontal pathogens’) appear to be the main etiologic agents of chronic inflammatory periodontitis; and (v) tissue damage in periodontitis is primarily caused by inflammatory and immunologic host responses to infecting agents. The concepts that were in place by 1987 are still largely intact in 2012. However, in the decades to come, it is likely that new information on the human microbiome will change our current concepts concerning the prevention, diagnosis and treatment of periodontal diseases.

The notion of periodontal disease being the major cause of tooth loss among adults was rooted in the focal infection paradigm that dominated the first half of the 20th century. This paradigm was established largely by personal opinions, and it was not until the development of periodontal indices in the mid-1950s that periodontal epidemiology gained momentum. Unfortunately, the indices used suffered from a number of flaws, whereby the interpretation of the research results took the form of circular reasoning. It was under this paradigm that therapeutic and preventive intervention for periodontal diseases became entirely devoted to oral hygiene, as poor oral hygiene and older age were understood to explain nearly all the variation in disease occurrence. In the early 1980s, studies appeared that contradicted the concepts of poor oral hygiene as the inevitable trigger of periodontitis and of linear and ubiquitous periodontitis progression, whereby periodontal epidemiology was led into a relatively short-lived high-risk era. At this time, it became evident that old scourges continue to haunt periodontology: the inability to agree in operational clinical criteria for a periodontitis diagnosis and the inability to devise both a meaningful and a useful classification of periodontal diseases based on nominalist principles. The meager outcome of the high-risk era led researchers to resurrect the focal infection paradigm, which is now dressed up as periodontal medicine. Unfortunately, these developments have left the core of periodontology somewhat disheveled and deserted.

Risk factors play an important role in an individual’s response to periodontal infection. Identification of these risk factors helps to target patients for prevention and treatment, with modification of risk factors critical to the control of periodontal disease. Shifts in our understanding of periodontal disease prevalence, and advances in scientific methodology and statistical analysis in the last few decades, have allowed identification of several major systemic risk factors for periodontal disease. The first change in our thinking was the understanding that periodontal disease is not universal, but that severe forms are found only in a portion of the adult population who show abnormal susceptibility. Analysis of risk factors and the ability to statistically adjust and stratify populations to eliminate the effects of confounding factors have allowed identification of independent risk factors. These independent but modifiable, risk factors for periodontal disease include lifestyle factors, such as smoking and alcohol consumption. They also include diseases and unhealthy conditions such as diabetes mellitus, obesity, metabolic syndrome, osteoporosis, and low dietary calcium and vitamin D. These risk factors are modifiable and their management is a major component of the contemporary care of many periodontal patients. Genetic factors also play a role in periodontal disease and allow one to target individuals for prevention and early detection. The role of genetic factors in aggressive periodontitis is clear. However, although genetic factors (i.e., specific genes) are strongly suspected to have an association with chronic adult periodontitis, there is as yet no clear evidence for this in the general population. It is important to pursue efforts to identify genetic factors associated with chronic periodontitis because such factors have potential in identifying patients who have a high susceptibility for development of this disease. Many of the systemic risk factors for periodontal disease, such as smoking, diabetes and obesity, and osteoporosis in postmenopausal women, are relatively common and can be expected to affect most patients with periodontal disease seen in clinics and dental practices. Hence, risk factor identification and management has become a key component of care for periodontal patients.

Periodontal diseases are initiated by bacterial species living in polymicrobial biofilms at or below the gingival margin and progress largely as a result of the inflammation elicited by specific subgingival species. In the past few decades, efforts to understand the periodontal microbiota have led to an exponential increase in information about biofilms associated with periodontal health and disease. In fact, the oral microbiota is one of the best-characterized microbiomes that colonize the human body. Despite this increased knowledge, one has to ask if our fundamental concepts of the etiology and pathogenesis of periodontal diseases have really changed. In this article we will review how our comprehension of the structure and function of the subgingival microbiota has evolved over the years in search of lessons learned and unlearned in periodontal microbiology. More specifically, this review focuses on: (i) how the data obtained through molecular techniques have impacted our knowledge of the etiology of periodontal infections; (ii) the potential role of viruses in the etiopathogenesis of periodontal diseases; (iii) how concepts of microbial ecology have expanded our understanding of host–microbe interactions that might lead to periodontal diseases; (iv) the role of inflammation in the pathogenesis of periodontal diseases; and (v) the impact of these evolving concepts on therapeutic and preventive strategies to periodontal infections. We will conclude by reviewing how novel systems-biology approaches promise to unravel new details of the pathogenesis of periodontal diseases and hopefully lead to a better understanding of their mechanisms.

During the last two to three decades our understanding of the immunobiology of periodontal disease has increased exponentially, both with respect to the microbial agents triggering the disease process and the molecular mechanisms of the host engagement maintaining homeostasis or leading to collateral tissue damage. These foundational scientific findings have laid the groundwork for translating cell phenotype, receptor engagement, intracellular signaling pathways and effector functions into a ‘picture’ of the periodontium as the host responds to the ‘danger signals’ of the microbial ecology to maintain homeostasis or succumb to a disease process. These findings implicate the chronicity of the local response in attempting to manage the microbial challenge, creating a ‘Double Indemnity’ in some patients that does not ‘insure’ health for the periodontium. As importantly, in reflecting the title of this volume of Periodontology 2000, this review attempts to inform the community of how the science of periodontal immunology gestated, how continual probing of the biology of the disease has led to an evolution in our knowledge base and how more recent studies in the postgenomic era are revolutionizing our understanding of disease initiation, progression and resolution. Thus, there has been substantial progress in our understanding of the molecular mechanisms of host–bacteria interactions that result in the clinical presentation and outcomes of destructive periodontitis. The science has embarked from observations of variations in responses related to disease expression with a focus for utilization of the responses in diagnosis and therapeutic outcomes, to current investigations using cutting-edge fundamental biological processes to attempt to model the initiation and progression of soft- and hard-tissue destruction of the periodontium. As importantly, the next era in the immunobiology of periodontal disease will need to engage more sophisticated experimental designs for clinical studies to enable robust translation of basic biologic processes that are in action early in the transition from health to disease, those which stimulate microenvironmental changes that select for a more pathogenic microbial ecology and those that represent a rebalancing of the complex host responses and a resolution of inflammatory tissue destruction.

New concepts evolve when existing ones fail to address known factors adequately or are invalidated by new evidence. For decades periodontitis has been considered to be caused by specific bacteria or groups of bacteria and, accordingly, treatment protocols have largely been based on anti-infective therapies. However, close inspection of current data leads one to question whether these bacteria are the cause or the result of periodontitis. Good evidence is emerging to suggest that it is indeed the host response to oral bacteria that leads to the tissue changes noted in gingivitis. These changes lead to an altered subgingival environment that favors the emergence of ‘periodontal pathogens’ and the subsequent development of periodontitis if the genetic and external environmental conditions are favorable for disease development. Thus, it seems that it is indeed the initial early host-inflammatory and immune responses occurring during the development of gingivitis, and not specific bacteria or their so-called virulence factors, which determine whether periodontitis develops and progresses. In this review we consider these concepts and their potential to change the way in which we view and manage the inflammatory periodontal diseases.

This review aims to highlight concepts relating to nonsurgical and surgical periodontal therapy, which have been learned and unlearned over the past few decades. A number of treatment procedures, such as gingival curettage and aggressive removal of contaminated root cementum, have been unlearned. Advances in technology have resulted in the introduction of a range of new methods for use in nonsurgical periodontal therapy, including machine-driven instruments, lasers, antimicrobial photodynamic therapy and local antimicrobial-delivery devices. However, these methods have not been shown to offer significant benefits over and above nonsurgical debridement using hand instruments. The method of debridement is therefore largely dependent on the preferences of the operator and the patient. Recent evidence indicates that specific systemic antimicrobials may be indicated for use as adjuncts to nonsurgical debridement in patients with advanced disease. Full-mouth disinfection protocols have been proven to be a relevant treatment option. We have learned that while nonsurgical and surgical methods result in similar long-term treatment outcomes, surgical therapy results in greater probing-depth reduction and clinical attachment gain in initially deep pockets. The surgical technique chosen seems to have limited influence upon changes in clinical attachment gain. What has not changed is the importance of thorough mechanical debridement and optimal plaque control for successful nonsurgical and surgical periodontal therapy.

In this review, we reflect upon advances and hindrances encountered over the last three decades in the development of strategies for periodontal regeneration. In this soul-searching pursuit we focus on revisiting lessons learned that should guide us in the quest for the reconstruction of the lost periodontium. We also examine beliefs and traditions that should be unlearned so that we can continue to advance the field. This learned/unlearned body of knowledge is consolidated into core principles to help us to develop new therapeutic approaches to benefit our patients and ultimately our society.

The focus of this review on periodontal self-care will be based primarily on the results of systematic reviews and meta-analyses. Based on the evidence gleaned from systematic reviews, it is notable that most authors of these reviews commented on the relatively small number of trials that could pass the quality-assessment inclusion in the systematic review. Interproximal devices, namely interproximal brushes, are more effective for reducing interproximal plaque and gingivitis than are flossing or brushing alone. Some added benefit may be attributed to the use of rotational oscillation powered toothbrushes over manual toothbrushes. Recommendations by the dentist and dental hygienist to add one or more chemotherapeutic agents to the typical oral hygiene regimen has been shown, in systematic reviews and meta-analyses, to reduce the level of plaque and gingival inflammation in patients. Oral irrigation does not seem to reduce visible plaque but does tend to reduce inflammation, determined by the presence of bleeding on probing, the gingival index score and probing depth measurements. To date, high-quality evidence is either lacking or weak in some areas regarding the efficacy of self-care and periodontal disease. Low educational attainment, smoking and socio-economic status are related to adverse periodontal health outcomes. Variation in self-esteem, self-confidence and perfectionism are associated with oral health status and oral health behaviors. Better understanding of the psychological factors associated with oral hygiene would be of benefit in further developing strategies to help patients improve their oral hygiene in addition to helping professionals design better programs on prevention and education.

Implant stability and maintenance of stable crestal bone level are prerequisites for the successful long-term function of oral implants, and continuous crestal bone loss constitutes a threat to the longevity of implant–supported prosthetic constructions. The prevalence/incidence and reasons for crestal bone loss are under debate. Some authors regard infection (i.e. peri-implantitis) as the cause for virtually all bone loss, while others see crestal bone loss as an unavoidable phenomenon following surgery and implant loading. Irrespective of the cause of continuous crestal bone loss, correct usage and scientifically sound interpretation of radiographs are of utmost importance for evaluation of oral implants. The periapical radiographic technique is currently the preferred method for evaluating implant health based on bone loss, and digital radiographs allow easy standardization of the image contrast. It is suggested that baseline radiographs should be taken at the time the transmucosal part pierces the mucosal tissues and annually thereafter. The number of unreadable radiographs should be presented in scientific publications to give insights into the quality of the radiographic examination. It is suggested that not only mean values, but also the range of bone levels, should be presented to describe the proportion of implants that show continuous crestal bone loss. In the absence of other clinical symptoms, bleeding on probing around implants seems to be a weak indicator of ongoing or future loss of crestal bone. According to recent longitudinal studies on modern implant surfaces peri-implantitis defined as ‘infection with suppuration associated with clinically significant progressing crestal bone loss’ occurs with a prevalence of less than 5 % in implants with 10 years in function.

The concept of focal infection or systemic disease arising from infection of the teeth was generally accepted until the mid-20th century when it was dismissed because of lack of evidence. Subsequently, a largely silo approach was taken by the dental and medical professions. Over the past 20 years, however, a plethora of epidemiological, mechanistic and treatment studies have highlighted that this silo approach to oral and systemic diseases can no longer be sustained. While a number of systemic diseases have been linked to oral diseases, the weight of evidence from numerous studies conducted over this period, together with several systematic reviews and meta-analyses, supports an association between periodontitis and cardiovascular disease, and between periodontitis and diabetes. The association has also been supported by a number of biologically plausible mechanisms, including direct infection, systemic inflammation and molecular mimicry. Treatment studies have shown that periodontal treatment may have a small, but significant, systemic effect both on endothelial function and on glycemic control. Despite this, however, there is no direct evidence that periodontal treatment affects either cardiovascular or diabetic events. Nevertheless, over the past 20 years we have learnt that the mouth is an integral part of the body and that the medical and dental professions need to work more closely together in the provision of overall health care for all patients.

The adoption of new technologies for the treatment of periodontitis and the replacement of teeth has changed the delivery of periodontal care. The objective of this review was to conduct an economic analysis of a mature periodontal service market with a well-developed workforce, including general dentists, dental hygienists and periodontists. Publicly available information about the delivery of periodontal care in the USA was used. A strong trend toward increased utilization of nonsurgical therapy and decreased utilization of surgical periodontal therapy was observed. Although periodontal surgery remained the domain of periodontists, general dentists had taken over most of the nonsurgical periodontal care. The decline in surgical periodontal therapy was associated with an increased utilization of implant-supported prosthesis. Approximately equal numbers of implants were surgically placed by periodontists, oral and maxillofacial surgeons, and general dentists. Porter’s framework of the forces driving industry competition was used to analyze the role of patients, dental insurances, general dentists, competitors, entrants, substitutes and suppliers in the periodontal service market. Estimates of out-of-pocket payments of self-pay and insured patients, reimbursement by dental insurances and providers’ earnings for various periodontal procedures and alternative treatments were calculated. Economic incentives for providers may explain some of the observed shifts in the periodontal service market. Given the inherent uncertainty about treatment outcomes in dentistry, which makes clinical judgment critical, providers may yield to economic incentives without jeopardizing their ethical standards and professional norms. Although the economic analysis pertains to the USA, some considerations may also apply to other periodontal service markets.