Roy C. Page

Case Definitions for Use in Population-Based Surveillance of Periodontitis

Many definitions of periodontitis have been used in the literature for population-based studies, but there is no accepted standard. In early epidemiologic studies, the two major periodontal diseases, gingivitis and periodontitis, were combined and considered to be a continuum. National United States surveys were conducted in 1960 to 1962, 1971 to 1974, 1981, 1985 to 1986, 1988 to 1994, and 1999 to 2000. The case definitions and protocols used in the six national surveys reflect a continuing evolution and improvement over time. Generally, the clinical diagnosis of periodontitis is based on measures of probing depth (PD), clinical attachment level (CAL), the radiographic pattern and extent of alveolar bone loss, gingival inflammation measured as bleeding on probing, or a combination of these measures. Several other patient characteristics are considered, and several factors, such as age, can affect measurements of PD and CAL. Accuracy and reproducibility of measurements of PD and CAL are important because case definitions for periodontitis are based largely on either or both measurements, and relatively small changes in these values can result in large changes in disease prevalence. The classification currently accepted by the American Academy of Periodontology (AAP) was devised by the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. However, in 2003 the Centers for Disease Control and Prevention and the AAP appointed a working group to develop further standardized clinical case definitions for population-based studies of periodontitis. This classification defines severe periodontitis and moderate periodontitis in terms of PD and CAL to enhance case definitions and further demonstrates the importance of thresholds of PD and CAL and the number of affected sites when determining prevalence.

Update on Prevalence of Periodontitis in Adults in the United States: NHANES 2009 to 2012

BACKGROUNDnThis report describes prevalence, severity, and extent of periodontitis in the US adult population using combined data from the 2009 to 2010 and 2011 to 2012 cycles of the National Health and Nutrition Examination Survey (NHANES).nnnMETHODSnEstimates were derived for dentate adults, aged ≥30 years, from the US civilian non-institutionalized population. Periodontitis was defined by combinations of clinical attachment loss (AL) and periodontal probing depth (PD) from six sites per tooth on all teeth, except third molars, using standard surveillance case definitions. For the first time in NHANES history, sufficient numbers of non-Hispanic Asians were sampled in 2011 to 2012 to provide reliable estimates of their periodontitis prevalence.nnnRESULTSnIn 2009 to 2012, 46% of US adults, representing 64.7 million people, had periodontitis, with 8.9% having severe periodontitis. Overall, 3.8% of all periodontal sites (10.6% of all teeth) had PD ≥4 mm, and 19.3% of sites (37.4% teeth) had AL ≥3 mm. Periodontitis prevalence was positively associated with increasing age and was higher among males. Periodontitis prevalence was highest in Hispanics (63.5%) and non-Hispanic blacks (59.1%), followed by non-Hispanic Asian Americans (50.0%), and lowest in non-Hispanic whites (40.8%). Prevalence varied two-fold between the lowest and highest levels of socioeconomic status, whether defined by poverty or education.nnnCONCLUSIONSnThis study confirms a high prevalence of periodontitis in US adults aged ≥30 years, with almost fifty-percent affected. The prevalence was greater in non-Hispanic Asians than non-Hispanic whites, although lower than other minorities. The distribution provides valuable information for population-based action to prevent or manage periodontitis in US adults.

Update of the Case Definitions for Population-Based Surveillance of Periodontitis

BACKGROUNDnThis report adds a new definition for mild periodontitis that allows for better descriptions of the overall prevalence of periodontitis in populations. In 2007, the Centers for Disease Control and Prevention in partnership with the American Academy of Periodontology developed and reported standard case definitions for surveillance of moderate and severe periodontitis based on measurements of probing depth (PD) and clinical attachment loss (AL) at interproximal sites. However, combined cases of moderate and severe periodontitis are insufficient to determine the total prevalence of periodontitis in populations.nnnMETHODSnThe authors proposed a definition for mild periodontitis as ≥ 2 interproximal sites with AL ≥ 3 mm and ≥ 2 interproximal sites with PD ≥ 4 mm (not on the same tooth) or one site with PD ≥ 5 mm . The effect of the proposed definition on the total burden of periodontitis was assessed in a convenience sample of 456 adults ≥ 35 years old and compared with other previously reported definitions for similar categories of periodontitis.nnnRESULTSnAddition of mild periodontitis increases the total prevalence of periodontitis by ≈31% in this sample when compared with the prevalence of severe and moderate disease.nnnCONCLUSIONnTotal periodontitis using the case definitions in this study should be based on the sum of mild, moderate, and severe periodontitis.

Host Response Tests for Diagnosing Periodontal Diseases

Extensive data collected over the past decade demonstrate clearly that diseaseactive and disease-inactive periodontal pockets exist, disease progression is infrequent and episodic, and most progression occurs in a small proportion of highly susceptible individuals. Furthermore, traditionally used diagnostic procedures do not identify susceptible individuals nor distinguish between disease-active and disease-inactive periodontal sites. New diagnostic tests based on host response factors that will aid in resolving these problems appear to be possible. Sources of material for use in such tests include gingival crevicular fluid (GCF), blood cells, and blood serum. Of these, components in GCF are most promising, at least in the immediate future. Although more than 40 GCF components have been studied, efforts that attempt to relate the presence and amount of a given component to an independent measure of active disease are very few in number. As a consequence, we do not yet know the potential for most GCF components as the basis of diagnostic tests. Those components that have been documented to associate with active disease as measured by attachment loss of 2 mm or greater include alkaline Phosphatase, β-glucuronidase, prostaglandin-E2 , aspartate aminotransferase, and IgG4 antibody subclass. Even in these cases, the data base is small and additional clinical studies are needed to document claims. At the present time, tests based on β-glucuronidase, nonspecific neutral proteases, and aspartate aminotransferase are being commercialized. One test has received FDA approval. Tests based on blood cells have limited application for patients with adult periodontitis, but are useful for patients with earlyonset forms of periodontitis. An abnormality in the leukocyte adherence molecules on the surfaces of neutrophils is diagnostic for generalized prepubertal periodontitis, and defects in chemotactic receptor numbers and in a surface molecule designated as GP110 are found on the neutrophils of most but not all localized juvenile periodontitis patients. Recent data indicate that enhanced unstimulated or stimulated release of PGE2 and Interleukin-1 by peripheral blood monocytes may be an indicator of susceptibility to severe periodontitis. Assessment of the humoral immune response as reflected by serum antibodies to antigens of periodontopathic bacteria shows little promise as the basis for tests diagnostic of site-specific disease activity. However, the capacity of an individual to mount an IgG2 subclass response to carbohydrate antigens may have potential as an indicator of disease susceptibility. J Periodontol 1992; 63:356-366.

Tooth Loss in 776 Treated Periodontal Patients

BACKGROUNDnThe most common form of periodontitis is a variably progressive dynamic pathologic process that causes attachment loss, destroys the alveolar bone supporting a tooth, and terminates with tooth loss. We evaluated the loss of teeth of treated periodontal patients categorized by severity and risk.nnnMETHODSnEach of nine periodontists evaluated 100 consecutive periodontal maintenance patients. The disease severity and risk level were determined from data at the initial examination. The number of teeth lost was determined from data at the initial and maintenance visits.nnnRESULTSnA stepwise regression analysis showed that disease (P = 0.0000478) and risk (P = 0.00129) scores predicted the mean tooth loss rate. The adjusted R(2) statistic was 88.56%. The ordinal logistic regression model showed that only the disease score (P <0.0005) was significantly associated with the probability of patients losing a specific number of teeth.nnnCONCLUSIONSnCategorizing a patient by severity may be beneficial in the management of the periodontal patient. The disease score can be used to establish a criterion and target for care. For example, treatment can result in nearly no lost teeth when the severity is low, and this benefit is lost when the severity is high. The disease score provides an objective means to quickly determine severity. An increase in the disease score provides evidence that a new treatment plan is needed. Therefore, the effect of the routine use of the disease score could result in fewer patients with severe disease and reduce the number of teeth lost.

Periodontal Therapy: Prospects for the Future*

Prior to the 1950s, periodontitis was treated mostly by tooth exfoliation or extraction, and that is still the predominant treatment for most of the worlds populations today. Debridement of the root surface by scaling and root planing came into relatively common use in the first half of the present century and has become the central feature held in common by all currently-used forms of periodontal therapy. Until the 1980s, the most commonly-used treatment consisted of scaling and root planing, followed by resective surgery aimed at achieving zero pocket depth. During the 1980s, data were obtained demonstrating that the thoroughness of root debridement and subgingival infection control, not the presence or absence or periodontal pockets, is the major determinant of successful periodontal therapy, and non-surgical therapy became a commonlyused treatment. Neither resective surgery nor non-surgical therapy results in significant regeneration of periodontal attachment. With the realization that periodontitis is an infectious process, the use of antibiotics and other anti-infective agents came into common use as adjuncts to other standard therapies. An understanding of the pathways by which the soft and calcified tissues of the periodontium are destroyed has led to the likelihood of widespread future use of the non-steroidal, anti-inflammatory family of drugs to suppress alveolar bone destruction by blocking prostaglandin production, and to the use of chemically-modified tetracyclines that chelate divalent cations and thereby block tissue destruction by the metalloproteinases. Recent data clearly show that regeneration of the previously-destroyed periodontal attachment tissues is biologically possible, and regeneration has become the goal of therapy for the 1990s. Use of osteoconductive and osteoinductive graft materials can, under favorable conditions, induce roughly 60% to 70% regeneration of bone lesion height or volume with concomitant improvement in the clinical conditions. Regeneration by grafting may be further enhanced by use of barrier membranes that exclude gingival fibroblasts and epithelium from the healing site. Still further enhancement seems to be possible by local application of various growth factors, although studies in this important area are now only in their infancy. The future of periodontal therapy is exceedingly bright. It seems likely that we may be able to achieve nearly complete regeneration of periodontal attachment at many, although not all, sites through the use of root debridement and anti-infective and anti-inflammatory drugs and agents that inhibit metalloproteinases to arrest progress of disease and resolve the inflammatory process, followed by the combined use of graft material, barrier membranes, and growth factors to induce regeneration of periodontal attachment tissues. J Periodontol 1993; 64:744-753.

Periodontitis Vaccine Decreases Local Prostaglandin E2 Levels in a Primate Model

ABSTRACT Interleukin-1β, tumor necrosis factor alpha, prostaglandin E2 (PGE2), and Porphyromonas gingivalis-specific immunoglobulin G levels in gingival crevicular fluid were measured in primates immunized with a P. gingivalis vaccine followed by ligature-induced periodontitis. Only PGE2 levels were dramatically suppressed (P < 0.0001) in immunized animals versus controls. A significant correlation (P < 0.027) was also found between PGE2 levels and decreased bone loss scores. This study presents the first evidence of a potential mechanism involved in periodontitis vaccine-induced suppression of bone loss in a nonhuman primate model and offers insight into the role of PGE2 in periodontal destruction.

Chapter 62 – Mucosal Vaccines for Dental Diseases

The host immune system has significant potential for intervention or interference in periodontal infection. Many periodontitis patients exhibit a humoral immune response during the course of their spontaneous infection. Many of those who are seronegative convert to seropositivity following routine periodontal therapy. The antibodies, however, may have relatively low avidity and capacity to opsonize. Immunization studies demonstrate that immunization can reduce pathogenic subgingival flora, even in the presence of ligatures, and high levels of specific antibody titers can alter the progression of periodontal tissue destruction. It has also been demonstrated that T-cell and B-cell osteoclastogenic functions may contribute to bone resorption and inflammation in experimental periodontal diseases. Systematic evaluation of both mucosal and systemic vaccines is necessary. Inductive sites usually are in close association with antigen-handling cells such as M cells, macrophages, and dendritic cells. Initial stimulation of mucosal Ig-producing B cells occurs in the organized mucosa-associated lymphoreticular tissue (MALT), particularly the Peyers patches. Effector cells migrate from these inductive sites from the peripheral blood to exocrine tissues throughout the body. Studies show that there are preferential pathways for migration of effector cells from MALT as opposed to more distal sites of the mucosal immune system such as the urogenital tract.