摘要:Objectives. We investigated the relationship between Helicobacter pylori infection and abnormal periodontal conditions. Methods. Data from the first phase of the third National Health and Nutrition Examination Survey were used. A total of 4504 participants aged 20 to 59 years who completed a periodontal examination and tested positive for H. pylori antibodies were examined. Results. Periodontal pockets with a depth of 5 mm or more were associated with increased odds of H. pylori seropositivity (odds ratio [OR] = 1.47; 95% confidence interval [CI] = 1.12, 1.94) after adjustment for sociodemographic factors. This association is comparable to the independent effects of poverty on H. pylori (OR = 1.54; 95% CI = 1.10, 2.16). Conclusions. Poor periodontal health, characterized by advanced periodontal pockets, may be associated with H. pylori infection in adults, independent of poverty status. Helicobacter pylori is a gram-negative, spiral-shaped bacterium that infects nearly a third of the total population of the United States and is associated with a variety of socioeconomic indicators. 1 In the developing world, researchers have proposed that the age distribution of H. pylori infection resembles a cohort effect, reflecting reduced transmission in younger age groups as sanitary conditions improve. 2 H. pylori causes duodenal ulcer disease and has been implicated in the development of gastric ulcers. Moreover, it has been associated with an increased risk for gastric cancer. 3– 6 Recently, researchers have suggested that the primary extragastric reservoir for H. pylori is the oral cavity. 7 Because human infection by this pathogen appears to involve an oral route, it seems biologically plausible that oral health status directly or indirectly influences the process of H. pylori infection or reinfection. Although H. pylori was first isolated nearly 20 years ago, the process of infection or human transmission remains unclear. Because most gastrointestinal microbes have been commonly believed to be transmitted by either oral–oral or fecal–oral pathways, numerous H. pylori carriage sources, including dental plaque, saliva, vomit, and feces, have been postulated and explored. 8– 25 Some studies have examined plaque and saliva and have produced positive findings of an association with H. pylori , 8, 10, 13– 17 whereas others have not. 18– 25 Findings of a positive association between poor oral health (undefined periodontal disease) and H. pylori have been reported as well. 26 The suggestion has also been made that either H. pylori may promote the development of oral mucosal lesions—specifically, recurrent aphthous ulcers—or oral mucosal lesions may function as an intermediary in the route of oral–gastric infection. 27, 28 Again, study results have been contradictory. 29– 31 Most of the prior studies that examined an oral condition as a factor in the promotion of extra gastric H. pylori activity examined dental plaque as a vehicle for H. pylori carriage. Dental plaque is primarily a collection of microorganisms embedded in an intracellular matrix composed of organic compounds (e.g., glycoproteins) and inorganic compounds (e.g., calcium and other minerals) that forms a biofilm. The biofilm matrix promotes and protects bacterial ecology, but not all of the bacteria residing within the biofilm are capable of becoming pathogenic. Dental plaque typically adheres to supragingival and subgingival tooth surfaces, and it will quickly form in the absence of good oral hygiene measures. Over time, undisturbed plaque progresses into calculus, which consists of a mineralized core that is superficially covered by the soft biofilm. Plaque biofilm can enhance the survivability of some bacteria by providing access to urea, which then can be reduced by ureaseproducing microorganisms to neutralize the effects of acidification. 32 The suggestion has recently been made that bacterial biofilms not only are commonly associated with many chronic infections but also are much more resistant to antibiotics than freely circulating bacteria. 33 Many previous H. pylori studies have randomly acquired plaque samples from unspecified periodontal areas, mucosa, and saliva. Most studies collected plaque with a curette by upwardly scraping along the tooth surface. 13, 15, 16, 20, 21, 23, 24 Some studies used a paper point, a cytology brush, or a toothpick to remove the plaque specimen from periodontal sites. 19, 25, 29 Although some studies attempted to isolate supragingival plaque from subgingival plaque for separate analyses, others did not. 15, 18, 20, 24, 29, 34 Moreover, among studies that collected isolates from pocket sites, many failed to describe the depth of the periodontal pocket from which the isolates were obtained. 15, 18, 19, 20, 25 Some studies even used periodontal index measures as an indicator of overall oral health status. 15, 18, 25 Methods used in testing isolates for H. pylori also have varied among studies. Cultures, urease activity tests, enzyme-linked immunosorbent assay (ELISA) tests, and polymerase chain reaction amplification tests have all been used. However, these tests are not uniformly sensitive or specific in their ability to identify H. pylori activity. Finally, many of these studies failed to account for sociodemographic factors within the study population, and only 1 study concluded that future investigations should account for race/ethnicity characteristics. 16 Periodontitis promotes deep-pocket formation and increased loss of clinical attachment of the tooth. More than 300 bacterial species may be associated with periodontal pockets alone, but only half of these have been cultivable. 35 Numerous microorganisms, mostly spirochetes and gramnegative rods, are associated with advanced periodontitis, and about 75% of the subgingival microorganisms that are found in advanced periodontitis are gram-negative anaerobic rods. 36, 37 In individuals with a healthy periodontium, gram-negative rods constitute less than 13% of the microflora. The most current epidemiological findings indicate that 53% of Americans aged 30 to 90 years have at least 1 dental site with moderate to severe (≥ 3 mm) loss of attachment, compared with 9% who have moderate to severe (≥ 5 mm) pocket depth. 38 We know that periodontal disease increases with age, is consistently more prevalent in males, and is associated with certain socioeconomic indicators. In this study, we attempted to examine the relationship between H. pylori seropositivity and abnormal oral conditions (e.g., recurrent aphthous ulcers) or clinical dental parameters suggestive of poor periodontal health. Our hypothesis was that some attributes indicative of poor periodontal health are associated with H. pylori infection. It has been suggested that “well designed, population-based studies that adequately consider confounding” would clarify the process of H. pylori transmission. 2 By using a nationally representative sample, we hoped to shed light on the epidemiological relationship between specific abnormal oral conditions and H. pylori infection.