Journal of Periodontology

A classification scheme for periodontal and peri‐implant diseases and conditions is necessary for clinicians to properly diagnose and treat patients as well as for scientists to investigate etiology, pathogenesis, natural history, and treatment of the diseases and conditions. This paper summarizes the proceedings of the World Workshop on the Classification of Periodontal and Peri‐implant Diseases and Conditions. The workshop was co‐sponsored by the American Academy of Periodontology (AAP) and the European Federation of Periodontology (EFP) and included expert participants from all over the world. Planning for the conference, which was held in Chicago on November 9 to 11, 2017, began in early 2015.

An organizing committee from the AAP and EFP commissioned 19 review papers and four consensus reports covering relevant areas in periodontology and implant dentistry. The authors were charged with updating the 1999 classification of periodontal diseases and conditions and developing a similar scheme for peri‐implant diseases and conditions. Reviewers and workgroups were also asked to establish pertinent case definitions and to provide diagnostic criteria to aid clinicians in the use of the new classification. All findings and recommendations of the workshop were agreed to by consensus.

This introductory paper presents an overview for the new classification of periodontal and peri‐implant diseases and conditions, along with a condensed scheme for each of four workgroup sections, but readers are directed to the pertinent consensus reports and review papers for a thorough discussion of the rationale, criteria, and interpretation of the proposed classification. Changes to the 1999 classification are highlighted and discussed. Although the intent of the workshop was to base classification on the strongest available scientific evidence, lower level evidence and expert opinion were inevitably used whenever sufficient research data were unavailable.

The scope of this workshop was to align and update the classification scheme to the current understanding of periodontal and peri‐implant diseases and conditions. This introductory overview presents the schematic tables for the new classification of periodontal and peri‐implant diseases and conditions and briefly highlights changes made to the 1999 classification. It cannot present the wealth of information included in the reviews, case definition papers, and consensus reports that has guided the development of the new classification, and reference to the consensus and case definition papers is necessary to provide a thorough understanding of its use for either case management or scientific investigation. Therefore, it is strongly recommended that the reader use this overview as an introduction to these subjects. Accessing this publication online will allow the reader to use the links in this overview and the tables to view the source papers (Table 1).

Background: The principal objectives of this study were to examine the relationship between cigarette smoking and periodontitis and to estimate the proportion of periodontitis in the United States adult population that is attributable to cigarette smoking.

Methods: Data were derived from the Third National Health and Nutrition Examination Survey, a nationally representative multipurpose health survey conducted in 1988 to 1994. Participants were interviewed about tobacco use and examined by dentists trained to use standardized clinical criteria. Analysis was limited to dentate persons aged ≥18 years with complete clinical periodontal data and information on tobacco use and important covariates (n = 12,329). Data were weighted to provide U.S. national estimates, and analyses accounted for the complex sample design. We defined periodontitis as the presence of ≥1 site with clinical periodontal attachment level ≥4 mm apical to the cemento‐enamel junction and probing depth ≥4 mm. Current cigarette smokers were those who had smoked ≥100 cigarettes over their lifetime and smoked at the time of the interview; former smokers had smoked ≥100 cigarettes but did not currently smoke; and never smokers had not smoked ≥100 cigarettes in their lifetime.

Results: We found that 27.9% (95% confidence interval [CI]: ±1.8%) of dentate adults were current smokers and 23.3% (95% CI: ±1.2%) were former smokers. Overall, 9.2% (95% CI: ±1.4%) of dentate adults met our case definition for periodontitis, which projects to about 15 million cases of periodontitis among U.S. adults. Modeling with multiple logistic regression revealed that current smokers were about 4 times as likely as persons who had never smoked to have periodontitis (prevalence odds ratio [OR_P] = 3.97; 95% CI, 3.20‐4.93), after adjusting for age, gender, race/ethnicity, education, and income:poverty ratio. Former smokers were more likely than persons who had never smoked to have periodontitis (OR_P = 1.68; 95% CI, 1.31‐2.17). Among current smokers, there was a dose‐response relationship between cigarettes smoked per day and the odds of periodontitis (P <0.000001), ranging from OR_P = 2.79 (95% CI, 1.90‐4.10) for ≤9 cigarettes per day to OR_P = 5.88 (95% CI, 4.03‐8.58) for ≥31 cigarettes per day. Among former smokers, the odds of periodontitis declined with the number of years since quitting, from OR_P = 3.22 (95% CI, 2.18‐4.76) for 0 to 2 years to OR_P = 1.15 (95% CI, 0.83‐1.60) for ≥11 years. Applying standard epidemiologic formulas for the attributable fraction for the population, we calculated that 41.9% of periodontitis cases (6.4 million cases) in the U.S. adult population were attributable to current cigarette smoking and 10.9% (1.7 million cases) to former smoking. Among current smokers, 74.8% of their periodontitis was attributable to smoking.

Conclusions: Based on findings from this study and numerous other reports, we conclude that smoking is a major risk factor for periodontitis and may be responsible for more than half of periodontitis cases among adults in the United States. A large proportion of adult periodontitis may be preventable through prevention and cessation of cigarette smoking. J Periodontol 2000;71:743‐751.

This study examined the risk indicators for alveolar bone loss associated with periodontal infection. A cross‐section of 1,361 subjects aged 25 to 74 years, from Erie County, NY were evaluated for interproximal alveolar bone loss and potential explanatory variables including age, gender, history of systemic diseases, smoking, and presence of 8 subgingival bacteria. Interproximal alveolar bone loss was measured from the alveolar crest to the CEJ and a mean computed for each subject. The mean bone loss per subject (BL) ranged from 0.4 to 8.8 mm, and this outcome variable was grouped into 4 ordered categories. The degree of association between the explanatory variables and BL was examined utilizing an ordinal stepwise logistic regression model. Factors which were positively associated with more severe bone loss included subgingival colonization with B. forsythus (O.R. 2.52; 95% CI: 1.98 to 3.17) or P. gingivalis (O.R. 1.73; 95% CI: 1.27 to 2.37), race (Native American, Asian, or Pacific Islanders) with an O.R. 2.40 (95% CI: 1.21 to 4.79), and gender with males having higher odds than females. Smokers had greater odds for more severe bone loss compared to non‐smokers ranging from 3.25 (95% CI: 2.33 to 4.54) to 7.28 (95% CI: 5.09 to 10.31) for light and heavy smokers, respectively. Individuals at older ages also showed more severe levels of bone loss. History of kidney disease (O.R. 0.55; 95% CI: 0.35 to 0.89) and history of allergies (O.R. 0.76; 95% CI: 0.59 to 0.98) were inversely associated with severity of bone loss. Severity of alveolar bone loss is associated with increasing age, smoking, race, and colonization with subgingival B. forsythus or P. gingivalis. This and other studies directed to identifying true risk factors associated with periodontal disease may lead to preventive measures directed to reducing the deleterious effects of modifiable risk factors. J Periodonol 1995;66:23–29.

Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non‐periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored.

Two broad categories of gingival diseases include non‐dental plaque biofilm–induced gingival diseases and dental plaque‐induced gingivitis. Non‐dental plaque biofilm‐induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque‐induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque‐induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non‐periodontitis patient or in a currently stable “periodontitis patient” i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced). A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1), and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis.

Precision dental medicine defines a patient‐centered approach to care, and therefore, creates differences in the way in which a “case” of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations.

Although periodontal diseases are initiated by bacteria that colonize the tooth surface and gingival sulcus, the host response is believed to play an essential role in the breakdown of connective tissue and bone, key features of the disease process. An intermediate mechanism that lies between bacterial stimulation and tissue destruction is the production of cytokines, which stimulates inflammatory events that activate effector mechanisms. These cytokines can be organized as chemokines, innate immune cytokines, and acquired immune cytokines. Although they were historically identified as leukocyte products, many are also produced by a number of cell types, including keratinocytes, resident mesenchymal cells (such as fibroblasts and osteoblasts) or their precursors, dendritic cells, and endothelial cells. Chemokines are chemotactic cytokines that play an important role in leukocyte recruitment and may directly or indirectly modulate osteoclast formation. This article focuses on aspects of osteoimmunology that affect periodontal diseases by examining the role of cytokines, chemokines, and immune cell mediators. It summarizes some of the key findings that attempt to delineate the mechanisms by which immune factors can lead to the loss of connective tissue attachment and alveolar bone. In addition, a discussion is presented on the importance of clarifying the process of uncoupling, a process whereby insufficient bone formation occurs following resorption, which is likely to contribute to net bone loss in periodontal disease.

Background: Recent studies have suggested that periodontal disease is a risk factor for preterm low birth weight (PLBW). A randomized controlled trial was undertaken to help further evaluate the proposed association between periodontal disease and PLBW.

Methods: Four hundred pregnant women with periodontal disease, aged 18 to 35, were enrolled while receiving prenatal care in Santiago, Chile. Women were randomly assigned to either an experimental group (n = 200), which received periodontal treatment before 28 weeks of gestation or to a control group (n = 200) which received periodontal treatment after delivery. Previous and current pregnancies and known risk factors were obtained from patient medical records and interviews. The primary outcome assessed was the delivery at less than 37 weeks of gestation or an infant weighing less than 2,500 g.

Results: Of the 400 women enrolled, 49 were excluded from the analyses for different reasons. The incidence of PLBW in the treatment group was 1.84% (3/163) and in the control group was 10.11% (19/188), (odds ratio [OR] 5.49, 95% confidence interval [CI] 1.65 to 18.22, P = 0.001). Multivariate logistic regression analysis showed that periodontal disease was the strongest factor related to PLBW (OR 4.70, 95% CI 1.29 to 17.13). Other factors significantly associated with such deliveries were: previous PLBW (OR 3.98, 95% CI 1.11 to 14.21), less than 6 prenatal visits (OR 3.70, 95% CI 1.46 to 9.38), and maternal low weight gain (OR 3.42, 95% CI 1.16 to 10.03).

Conclusions: Periodontal disease appears to be an independent risk factor for PLBW. Periodontal therapy significantly reduces the rates of PLBW in this population of women with periodontal disease. J Periodontol 2002;73:911‐924.

The success of dental implants is highly dependent on integration between the implant and intraoral hard/soft tissue. Initial breakdown of the implant‐tissue interface generally begins at the crestal region in successfully osseointegrated endosteal implants, regardless of surgical approaches (submerged or nonsubmerged). Early crestal bone loss is often observed after the first year of function, followed by minimal bone loss (≤0.2 mm) annually thereafter. Six plausible etiologic factors are hypothesized, including surgical trauma, occlusal overload, peri‐implantitis, microgap, biologic width, and implant crest module. It is the purpose of this article to review and discuss each factor. Based upon currently available literature, the reformation of biologic width around dental implants, microgap if placed at or below the bone crest, occlusal overload, and implant crest module may be the most likely causes of early implant bone loss. Furthermore, it is important to note that other contributing factors, such as surgical trauma and periimplantitis, may also play a role in the process of early implant bone loss. Future randomized, well‐controlled clinical trials comparing the effect of each plausible factor are needed to clarify the causes of early implant bone loss. J Peridontol 2002;73:322‐333.

Background: The aim of this study was to assess the prevalence and extent of gingival recession, gingival bleeding, and dental calculus in United States adults, using data collected in the third National Health and Nutrition Examination Survey (NHANES III).

Methods: The study group consisted of 9,689 persons 30 to 90 years of age obtained by a stratified, multi‐stage probability sampling method in 1988 to 1994. The weighted sample is representative of U.S. adults 30 years or older and represents approximately 105.8 million civilian, non‐institutionalized Americans. Gingival recession, gingival bleeding, and dental calculus were assessed at the mesio‐buccal and mid‐buccal surfaces in 2 randomly selected quadrants, one maxillary and one mandibular. Data analysis accounted for the complex sampling design used.

Results: We estimate that 23.8 million persons have one or more tooth surfaces with ≥3 mm gingival recession; 53.2 million have gingival bleeding; 97.1 million have calculus; and 58.3 million have subgingival calculus; and the corresponding percentages are 22.5%, 50.3%, 91.8%, and 55.1% of persons, respectively. The prevalence, extent, and severity of gingival recession increased with age, as did the prevalence of subgingival calculus and the extent of teeth with calculus and gingival bleeding. Males had significantly more gingival recession, gingival bleeding, subgingival calculus, and more teeth with total calculus than females. Of the 3 race/ethnic groups studied, non‐Hispanic blacks had the highest prevalence and extent of gingival recession and dental calculus, whereas Mexican Americans had the highest prevalence and extent of gingival bleeding. Mexican Americans had similar prevalence and extent of gingival recession compared with non‐Hispanic whites. Gingival recession was much more prevalent and also more severe at the buccal than the mesial surfaces of teeth. Gingival bleeding also was more prevalent at the buccal than mesial surfaces, whereas calculus was most often present at the mesial than buccal surfaces.

Conclusions: Dental calculus, gingival bleeding, and gingival recession are common in the U.S. adult population. In addition to their unfavorable effect on esthetics and self‐esteem, these conditions also are associated with destructive periodontal diseases and root caries. Appropriate measures to prevent or control these conditions are desirable, and this may also be effective in improving the oral health of the U.S. adult population. J Periodontol 1999; 70: 30‐43.

Oral malodor was measured using a portable sulphide monitor in 2,672 individuals aged 18 to 64 years. In addition, dental (DMFT) and periodontal conditions (CPITN and attachment loss), dental plaque, and tongue coating status were assessed. Before clinical examination, subjects were interviewed about their oral health habits, smoking habits, and medical history. Data on volatile sulphur compounds (VSC) were analyzed by gender, age group, and time of measurement. There were no significant differences observed in the VSC between males and females in any age group. In each age group, the measured values of oral malodor were highest in the late morning group (58.6 ppb in average), followed by the late afternoon group (52.1 ppb), while lowest values were shown in the early afternoon group (39.4 ppb). Significant correlation was observed only between the VSC value and periodontal conditions and tongue coating status. The results also suggest that oral malodor might be caused mainly by tongue coating in the younger generation and by periodontal diseases together with tongue coating in older cohorts in the general population. Age was not a risk factor for increasing VSC. J Periodontol 1995;66:679–684.