Robert J. Genco

Prevalence of Periodontitis in Adults in the United States: 2009 and 2010

This study estimated the prevalence, severity, and extent of periodontitis in the adult U.S. population, with data from the 2009 and 2010 National Health and Nutrition Examination Survey (NHANES) cycle. Estimates were derived from a sample of 3,742 adults aged 30 years and older, of the civilian non-institutionalized population, having 1 or more natural teeth. Attachment loss (AL) and probing depth (PD) were measured at 6 sites per tooth on all teeth (except the third molars). Over 47% of the sample, representing 64.7 million adults, had periodontitis, distributed as 8.7%, 30.0%, and 8.5% with mild, moderate, and severe periodontitis, respectively. For adults aged 65 years and older, 64% had either moderate or severe periodontitis. Eighty-six and 40.9% had 1 or more teeth with AL ≥ 3 mm and PD ≥ 4 mm, respectively. With respect to extent of disease, 56% and 18% of the adult population had 5% or more periodontal sites with ≥ 3 mm AL and ≥ 4 mm PD, respectively. Periodontitis was highest in men, Mexican Americans, adults with less than a high school education, adults below 100% Federal Poverty Levels (FPL), and current smokers. This survey has provided direct evidence for a high burden of periodontitis in the adult U.S. population.

Microbial Pathogenicity Black-pigmented Bacteroides species, Capnocytophaga species, and Actinobacillus actinomycetemcomitans in Human Periodontal Disease: Virulence Factors in Colonization, Survival, and Tissue Destruction

There have been many advances in the past decade in our knowledge of the microflora associated with periodontal diseases, the potential of specific periodontal bacterial species to destroy periodontal tissues, and the host responses to bacterial infections of the periodontium. It is the purpose of this and an accompanying paper, to present important features of the host-parasite interaction in human periodontal disease. The present communication emphasizes characteristics of periodontopathic bacteria which may enable them initially to colonize the host, to survive in the periodontal pocket, and possibly to invade the gingival tissue despite potentially effective host defense systems, and to destroy the collagenous periodontal ligament, the alveolar bone, and other tissue components surrounding the tooth. It seems reasonable to assume that a bacterial species must possess factors applicable to most if not all of the above aspects of the infectious process of periodontal disease in order to produce periodontitis.

Current View of Risk Factors for Periodontal Diseases

Periodontal diseases are infections, and many forms of the disease are associated with specific pathogenic bacteria which colonize the subgingival area. At least two of these microorganisms, Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, also invade the periodontal tissue and are virulent organisms. Initiation and progression of periodontal infections are clearly modified by local and systemic conditions called risk factors. The local factors include pre-existing disease as evidenced by deep probing depths and plaque retention areas associated with defective restorations. Systemic risk factors recently have been identified by large epidemiologic studies using multifactorial statistical analyses to correct for confounding or associated co-risk factors. Risk factors which we know today as important include diabetes mellitus, especially in individuals in whom metabolic control is poor, and cigarette smoking. These two risk factors markedly affect the initiation and progression of periodontitis, and attempts to manage these factors are now an important component of prevention and treatment of adult periodontitis. Systemic conditions associated with reduced neutrophil numbers or function are also important risk factors in children, juveniles, and young adults. Diseases in which neutrophil dysfunction occurs include the lazy leukocyte syndrome associated with localized juvenile periodontitis, cyclic neutropenia, and congenital neutropenia. Recent studies also point to several potentially important periodontal risk indicators. These include stress and coping behaviors, and osteopenia associated with estrogen deficiency. There are also background determinants associated with periodontal disease including gender (with males having more disease), age (with more disease seen in the elderly), and hereditary factors. The study of risk in periodontal disease is a rapidly emerging field and much is yet to be learned. However, there are at least two significant risk factors-smoking and diabetes-which demand attention in current management of periodontal disease. J Periodontol 1996;67:1041-1049.

Severe Periodontitis and Risk for Poor Glycemic Control in Patients with Non-Insulin-Dependent Diabetes Mellitus

This study tested the hypothesis that severe periodontitis in persons with non-insulin-dependent diabetes mellitus (NIDDM) increases the risk of poor glycemic control. Data from the longitudinal study of residents of the Gila River Indian Community were analyzed for dentate subjects aged 18 to 67, comprising all those: 1) diagnosed at baseline with NIDDM (at least 200 mg/dL plasma glucose after a 2-hour oral glucose tolerance test); 2) with baseline glycosylated hemoglobin (HbA1 ) less than 9%; and 3) who remained dentate during the 2-year follow-up period. Medical and dental examinations were conducted at 2-year intervals. Severe periodontitis was specified two ways for separate analyses: 1) as baseline periodontal attachment loss of 6 mm or more on at least one index tooth; and 2) baseline radiographic bone loss of 50% or more on at least one tooth. Clinical data for loss of periodontal attachment were available for 80 subjects who had at least one follow-up examination, 9 of whom had two follow-up examinations at 2-year intervals after baseline. Radiographic bone loss data were available for 88 subjects who had at least one follow-up examination, 17 of whom had two follow-up examinations. Poor glycemic control was specified as the presence of HbA1 of 9% or more at follow-up. To increase the sample size, observations from baseline to second examination and from second to third examinations were combined. To control for non-independence of observations, generalized estimating equations (GEE) were used for regression modeling. Severe periodontitis at baseline was associated with increased risk of poor glycemic control at follow-up. Other statistically significant covariates in the GEE models were: 1) baseline age; 2) level of glycemic control at baseline; 3) having more severe NIDDM at baseline; 4) duration of NIDDM; and 5) smoking at baseline. These results support considering severe periodontitis as a risk factor for poor glycemic control and suggest that physicians treating patients with NIDDM should be alert to the signs of severe periodontitis in managing NIDDM. J Periodontol 1996;67:1085-1093.

A Proposed Model Linking Inflammation to Obesity, Diabetes, and Periodontal Infections

BACKGROUND Obesity is an important risk factor for diabetes, cardiovascular disease, and periodontal disease. Adipocytes appear to secrete proinflammatory cytokines which may be the molecules linking the pathogenesis of these diseases. We evaluated the relationship between obesity, periodontal disease, and diabetes mellitus insulin resistance as well as the plasma levels of tumor necrosis factor alpha (TNFα) and its soluble receptors (sTNFα) to assess the relationship of inflammation to obesity, diabetes, and periodontal infections. METHODS The relationship between periodontal disease, obesity, and insulin resistance was examined in the Third National Health and Nutrition Examination Survey (NHANES III). In a population of 12,367 non-diabetic subjects, the variable body mass index (BMI) was used as an assessment of obesity and periodontal disease was assessed by mean clinical attachment loss. The plasma levels of TNFα and sTNFα were assessed in subsets of 1,221 adults from Erie County, New York, who represented the highest and lowest quartile of BMI. These subjects had extensive periodontal and medical evaluations. RESULTS In the NHANES III portion of the study, BMI was positively related to severity of periodontal attachment loss (P <0.001). Weighted multiple logistic regressions showed that this relationship is likely mediated by insulin resistance, since overweight individuals (with BMI ≥27 kg/m2 ) with high levels of insulin resistance (IR) exhibited an odds ratio of 1.48 (95% confidence interval 1.13 - 1.93) for severe periodontal disease as compared to overweight subjects with low IR. In the Erie County adult population, the highest levels of TNFα and sTNFα receptors were found in those individuals in the highest quartile of BMI. A positive correlation of TNFα levels with periodontal disease was found only in those in the lowest quartile of BMI. CONCLUSIONS Obesity is a significant predictor of periodontal disease and insulin resistance appears to mediate this relationship. Furthermore, obesity is associated with high plasma levels of TNFα and its soluble receptors, which in turn may lead to a hyperinflammatory state increasing the risk for periodontal disease and also accounting in part for insulin resistance. Further studies of the molecular basis of insulin resistance and its relationship to diabetes, periodontal disease, and obesity are necessary to fully test the hypothesis that adipocyte production of proinflammatory cytokines is a pathogenic factor linking obesity to diabetes and periodontal infections.

Host responses in periodontal diseases: current concepts.

In periodontal diseases, bacteria trigger inflammatory host responses which, along with the direct destructive effects of the bacteria, cause most of the tissue destruction. Periodontal inflammatory responses are, by and large, immunologic, and our understanding of these reactions has been advanced by the explosion of knowledge in immunobiology, some of which is discussed in this review. Understanding the role of immune cells and their regulatory cell surface molecules such as the MHC, CD antigens, and receptors, as well as knowledge of effector systems set into motion such as phagocytes and cytotoxic T-cells, and the effector molecules such as antibodies, complement, and cytokines, have led to better understanding of the complex pathogenesis of periodontal disease. The role of mediators including the matrix metalloproteinases, proteoglycans, the kinins and anaphylatoxins, and low molecular weight mediators including products of arachidonic metabolism is beginning to be elucidated in periodontal disease. Important avenues of research for development of diagnostic tests based upon host response are apparent. For example, tissue products released during periodontal inflammation including the metalloproteinases, elastase, cytokines, prostaglandins, antibodies, and complement components may provide the basis for future diagnostic indicator tests. The recognition that the neutrophil/antibody/complement axis is critical for protection against periodontal bacteria and that abnormalities in this system often lead to increased periodontal susceptibility provide approaches for the development of diagnostic tests assessing risk. A group of factors which are negative regulators of inflammation including TGF-β, gamma-interferon, and IL-1 receptor antagonist provide potential for assessment of periodontal disease in remission or in the healing phase. Finally, factors such as HLA associations and the molecular basis for neutrophil abnormalities may provide genetic markers for periodontal disease susceptibility. Diagnostic factors based upon host response measures offer great potential for predicting host susceptibility and will likely be used in combination with microbial diagnostics which identify specific infecting organisms. J Periodontol 1992;63:338-355.

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

BACKGROUND This 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). METHODS Estimates 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. RESULTS In 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. CONCLUSIONS This 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.

Risk factors for periodontal disease

Risk factors play an important role in an individuals 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.

Defective polymorphonuclear leukocyte function in a human periodontal disease

HUMAN periodontal diseases are the major cause of adult tooth loss. One such disease, localised idiopathic juvenile periodontitis (IJP) affects young people and is unusually severe, with a rapid progression. Previous studies have shed little light on the unusual susceptibility of some patients to this rare condition. Similarly, destructive periodontal syndromes have been described in patients with polymorphonuclear leukocyte (PMNL) dysfunction. We have measured two parameters of neutrophil function, chemotaxis and phagocytosis, and found that patients with IJP have significantly decreased PMNL function compared with healthy control subjects, but monocyte function remains unaffected in IJP. Reduced PMNL functions may contribute to the unusual susceptibility of patients to IJP.

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

BACKGROUND This 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. METHODS The 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. RESULTS Addition of mild periodontitis increases the total prevalence of periodontitis by ≈31% in this sample when compared with the prevalence of severe and moderate disease. CONCLUSION Total periodontitis using the case definitions in this study should be based on the sum of mild, moderate, and severe periodontitis.