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• W2016835497 abstract "The hygiene hypothesis contends that fewer opportunities for infections and microbial exposures have resulted in more widespread asthma and atopic disease. Consistent with that hypothesis, decreases in infectious oral diseases over the past half century have coincided with increases in the prevalence of asthma and other allergic diseases. This observation has led some researchers to speculate that exposures to oral bacteria, including pathogens associated with periodontal diseases, such as gingivitis and periodontitis, might play a protective role in the development of asthma and allergy. Colonization of the oral cavity with bacteria, including some species of periodontal pathogens, begins shortly after birth, and the detection of serum antibodies to oral pathogens in early childhood provides evidence of an early immune response to these bacteria. Current knowledge of the immune response to oral bacteria and the immunologic pathogenesis of periodontal diseases suggests biologically plausible mechanisms by which oral pathogens could influence the risk of allergic disease. However, studies investigating the association between oral pathogen exposures and allergic disease are few in number and limited by cross-sectional or case-control design, exclusion of young children, and use of surrogate measures of oral bacterial colonization. Additional studies, particularly well-designed case-control studies among very young children and prospective birth cohort studies, are needed. The hygiene hypothesis contends that fewer opportunities for infections and microbial exposures have resulted in more widespread asthma and atopic disease. Consistent with that hypothesis, decreases in infectious oral diseases over the past half century have coincided with increases in the prevalence of asthma and other allergic diseases. This observation has led some researchers to speculate that exposures to oral bacteria, including pathogens associated with periodontal diseases, such as gingivitis and periodontitis, might play a protective role in the development of asthma and allergy. Colonization of the oral cavity with bacteria, including some species of periodontal pathogens, begins shortly after birth, and the detection of serum antibodies to oral pathogens in early childhood provides evidence of an early immune response to these bacteria. Current knowledge of the immune response to oral bacteria and the immunologic pathogenesis of periodontal diseases suggests biologically plausible mechanisms by which oral pathogens could influence the risk of allergic disease. However, studies investigating the association between oral pathogen exposures and allergic disease are few in number and limited by cross-sectional or case-control design, exclusion of young children, and use of surrogate measures of oral bacterial colonization. Additional studies, particularly well-designed case-control studies among very young children and prospective birth cohort studies, are needed. Over the past half century, dental professionals and pharmaceutical companies have waged an increasingly successful war against the oral pathogens that cause tooth decay, gingivitis, and periodontitis, as evidenced by a steady decrease in rates of tooth decay and periodontal disease in the United States and other developed countries.1Petersen P.E. Challenges to improvement of oral health in the 21st century—the approach of the WHO Global Oral Health Programme.Int Dent J. 2004; 54: 329-343Crossref PubMed Scopus (82) Google Scholar, 2Burt B.A. Eklund S.A. Dentistry, dental practice, and the community.6th ed. Elsevier Saunders, St Louis (MO)2005Google Scholar, 3Dye B.A. Tan S. Smith V. Lewis B.G. Barker L.K. Thornton-Evans G. et al.Trends in oral health status: United States, 1988-1994 and 1999-2004.Vital Health Stat 11. 2007; : 1-92PubMed Google Scholar, 4Borrell L.N. Burt B.A. Taylor G.W. Prevalence and trends in periodontitis in the USA: the [corrected] NHANES, 1988 to 2000.J Dent Res. 2005; 84: 924-930Crossref PubMed Scopus (122) Google Scholar However, researchers have recently begun to ask whether achieving “axenic and inflammation-free oral conditions” has had unintended consequences.5Hujoel P.P. Cunha-Cruz J. Maupome G. Saver B. Long-term use of medications and destructive periodontal disease.J Periodontol. 2008; 79: 1330-1338Crossref PubMed Scopus (9) Google Scholar An impetus for raising this question has been the increasing popularity of the hygiene hypothesis, which contends that reduced opportunities for infection in early childhood have resulted in more widespread asthma and atopic disease. Originally proposed in 1989 by D. P. Strachan to explain his observation of an inverse relationship between family size and the prevalence of hay fever,6Strachan D.P. Hay fever, hygiene, and household size.BMJ. 1989; 299: 1259-1260Crossref PubMed Scopus (3792) Google Scholar the hygiene hypothesis has gained widespread attention among scientists and has been extended to examine the effects of a variety of microbial exposures on the development of asthma and other atopic diseases. These exposures include bacterial, viral, and parasitic infections; living on farms; gut microflora; probiotics; vaccinations; and oral pathogens. The purpose of this article is to review the ecology of oral microflora, review published studies examining associations between oral pathogen–related exposures and allergic disease, and make recommendations for future research.Ecology of oral microfloraApproximately 280 bacterial species have been cultured from the oral cavity and formally named, and studies using culture-independent molecular methods suggest the existence of 500 to 700 common oral species.7Dewhirst F.E. Chen T. Izard J. Paster B.J. Tanner A.C. Yu W.H. et al.The human oral microbiome.J Bacteriol. 2010; 192: 5002-5017Crossref PubMed Scopus (1895) Google Scholar These indigenous oral bacteria typically have a commensal relationship with the host; however, under certain circumstances, some oral bacteria overcome host defenses and become pathogenic. Oral bacteria colonize on oral mucosa and teeth and are present in saliva. Colonization begins shortly after birth, and studies of some bacterial species have shown that transmission occurs from parent to child and child to child, most likely through contact with saliva and the sharing of objects, such as cups or spoons.8Carletto-Korber F.P. Gonzalez-Ittig R.E. Jimenez M.G. Cornejo L.S. Initial acquisition and genetic identity of Streptococcus mutans of mother-child Pairs.Pediatr Dent. 2010; 32: 205-211PubMed Google Scholar, 9Domejean S. Zhan L. DenBesten P.K. Stamper J. Boyce W.T. Featherstone J.D. Horizontal transmission of mutans streptococci in children.J Dent Res. 2010; 89: 51-55Crossref PubMed Scopus (26) Google Scholar, 10Van Winkelhoff A.J. Boutaga K. Transmission of periodontal bacteria and models of infection.J Clin Periodontol. 2005; 32: 16-27Crossref PubMed Google Scholar, 11Darby I. Curtis M. Microbiology of periodontal disease in children and young adults.Periodontol 2000. 2001; 26: 33-53Crossref PubMed Scopus (67) Google Scholar Oral pathogens associated with periodontal disease, including 2 of the most studied pathogens, Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, are commonly found in the mouths of healthy infants and children.12Soncini J.A. Kanasi E. Lu S.C. Nunn M.E. Henshaw M.M. Tanner A.C. Oral microbiota of children in a school-based dental clinic.Anaerobe. 2010; 16: 278-282Crossref PubMed Scopus (8) Google Scholar, 13Kanasi E. Johansson I. Lu S.C. Kressin N.R. Nunn M.E. Kent Jr., R. et al.Microbial risk markers for childhood caries in pediatricians’ offices.J Dent Res. 2010; 89: 378-383Crossref PubMed Scopus (84) Google Scholar, 14Tanner A.C. Milgrom P.M. Kent Jr., R. Mokeem S.A. Page R.C. Riedy C.A. et al.The microbiota of young children from tooth and tongue samples.J Dent Res. 2002; 81: 53-57Crossref PubMed Scopus (123) Google Scholar In a study of 222 healthy Ohio children aged 0 to 18 years, A actinomycetemcomitans and P gingivalis were detected in 48% and 36% of the children, respectively, and both species were detected in infants as young as 20 days old.15Lamell C.W. Griffen A.L. McClellan D.L. Leys E.J. Acquisition and colonization stability of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in children.J Clin Microbiol. 2000; 38: 1196-1199PubMed Google Scholar Serum IgM antibodies to P gingivalis (formerly called Bacteroides gingivalis) have been detected in children less than 6 months of age, indicating a very early systemic response to oral pathogens and perhaps an early opportunity for oral pathogens to influence the immune system with respect to allergic disease.16Mouton C. Hammond P.G. Slots J. Genco R.J. Serum antibodies to oral Bacteroides asaccharolyticus (Bacteroides gingivalis): relationship to age and periodontal disease.Infect Immun. 1981; 31: 182-192PubMed Google ScholarThe species present in the oral cavity and their relative proportions differ within subjects over time, between subjects in a population, and between populations.17Haffajee A.D. Japlit M. Bogren A. Kent Jr., R.L. Goodson J.M. Socransky S.S. Differences in the subgingival microbiota of Swedish and USA subjects who were periodontally healthy or exhibited minimal periodontal disease.J Clin Periodontol. 2005; 32: 33-39Crossref PubMed Scopus (45) Google Scholar Reasons for these differences are not fully understood, although a reasonable assumption is that patterns of colonization are influenced by the timing of and opportunities for bacterial exposures, diet, oral hygiene practices, and interactions between the bacteria and host defenses.Oral bacteria on teeth reside in a biofilm known as dental plaque. Supragingival plaque (plaque at or above the gum line) is associated with the development of tooth decay and gingivitis, a reversible inflammatory condition of the gums. Subgingival plaque (plaque below the gum line) is associated with periodontitis, an inflammatory disease characterized by the irreversible destruction of the epithelium, connective tissue, and bone supporting the teeth. Subgingival plaque resides in a gingival crevice surrounding the tooth. In health that crevice is about 3 mm deep; however, with periodontitis, which can affect a single tooth or multiple teeth, the crevice deepens and widens with the destruction of the periodontal tissues. Dental plaque begins to form on cleaned tooth surfaces within a few hours, and in the absence of further oral hygiene measures, the plaque increases in mass and transitions from mostly gram-positive facultative species to mostly gram-negative anaerobic species.18Haake S.K. Newman M.G. Nisengard R.J. Sanz M. Periodontal microbiology.in: Newman M.G. Takei H.H. Carranza F.A. Carranza’s clinical periodontology. W.B. Saunders Co, Philadelphia2002: 96-112Google Scholar Gingivitis is associated with a mixture of gram-positive and gram-negative species, as well as facultative and anaerobic species. In contrast, periodontitis is predominantly associated with gram-negative anaerobes.18Haake S.K. Newman M.G. Nisengard R.J. Sanz M. Periodontal microbiology.in: Newman M.G. Takei H.H. Carranza F.A. Carranza’s clinical periodontology. W.B. Saunders Co, Philadelphia2002: 96-112Google Scholar Dental hygiene practices, such as tooth brushing, flossing, and professional dental cleaning, can remove dental plaque and also influence its bacterial composition. The extensive use of fluorides in developed countries has contributed much to the decrease of tooth decay. Although fluoride makes tooth enamel more resistant to demineralization, fluoride can also inhibit the growth of many plaque microorganisms.18Haake S.K. Newman M.G. Nisengard R.J. Sanz M. Periodontal microbiology.in: Newman M.G. Takei H.H. Carranza F.A. Carranza’s clinical periodontology. W.B. Saunders Co, Philadelphia2002: 96-112Google Scholar Whether the widespread use of fluorides has affected patterns of oral pathogen colonization at a population level is not known.Gingivitis and periodontitis, along with other conditions of the periodontium, are collectively known as periodontal diseases. Gingivitis is more common among children, whereas periodontitis is more common among adults. In a US national survey, the prevalence of gingival bleeding (an objective sign of gingivitis) among children aged 13 to 17 years was 63%,19Beck J.D. Arbes Jr., S.J. Epidemiology of gingival and periodontal diseases.in: Newman M.G. Takei H.H. Carranza F.A. Carranza’s clinical periodontology. W.B. Saunders Co, Philadelphia2002: 74-94Google Scholar and the prevalence of periodontitis among dentate adults aged 30 years or older was estimated to be at least 35%.20Albandar J.M. Brunelle J.A. Kingman A. Destructive periodontal disease in adults 30 years of age and older in the United States, 1988-1994.J Periodontol. 1999; 70: 13-29Crossref PubMed Scopus (567) Google Scholar Risk factors for gingivitis include age, sex, and oral hygiene status; and risk factors for periodontitis include age, sex, cigarette smoking, diabetes, and socioeconomic status.19Beck J.D. Arbes Jr., S.J. Epidemiology of gingival and periodontal diseases.in: Newman M.G. Takei H.H. Carranza F.A. Carranza’s clinical periodontology. W.B. Saunders Co, Philadelphia2002: 74-94Google Scholar When periodontitis occurs in susceptible subjects, it starts at a young age, often in the teenage years.2Burt B.A. Eklund S.A. Dentistry, dental practice, and the community.6th ed. Elsevier Saunders, St Louis (MO)2005Google Scholar The prevalence and severity of periodontitis increase with age, but these increases are thought to reflect more of a cumulative effect of disease progression than an increased susceptibility to disease.19Beck J.D. Arbes Jr., S.J. Epidemiology of gingival and periodontal diseases.in: Newman M.G. Takei H.H. Carranza F.A. Carranza’s clinical periodontology. W.B. Saunders Co, Philadelphia2002: 74-94Google Scholar On the other hand, in most persons gingivitis does not progress to periodontitis.In periodontally healthy and diseased mouths, pathogens in subgingival plaque elicit both local and systemic immune responses. In periodontally healthy mouths, intact gingival epithelium and neutrophils and serum antibodies in the gingival crevicular fluid keep pathogens in check.21Haake S.K. Nisengard R.J. Newman M.G. Miyasaki K.T. Microbial interactions with the host in periodontal diseases.in: Newman M.G. Takei H.H. Carranza F.A. Carranza’s clinical periodontology. W.B. Saunders Co, Philadelphia2002: 132-152Google Scholar However, if conditions in the gingival crevice favor the proliferation of pathogens, the release of proinflammatory cytokines and matrix metalloproteinases by host cells can lead to inflammation and irreversible destruction of periodontal tissues.21Haake S.K. Nisengard R.J. Newman M.G. Miyasaki K.T. Microbial interactions with the host in periodontal diseases.in: Newman M.G. Takei H.H. Carranza F.A. Carranza’s clinical periodontology. W.B. Saunders Co, Philadelphia2002: 132-152Google Scholar Robust antibody responses are mounted against oral pathogens in subjects with periodontitis, as evidenced by high serum IgG titers to specific periodontal pathogens in subjects with periodontitis, although low titers are often seen in periodontally healthy children and adults, indicating past or current exposure to the pathogens.16Mouton C. Hammond P.G. Slots J. Genco R.J. Serum antibodies to oral Bacteroides asaccharolyticus (Bacteroides gingivalis): relationship to age and periodontal disease.Infect Immun. 1981; 31: 182-192PubMed Google Scholar, 21Haake S.K. Nisengard R.J. Newman M.G. Miyasaki K.T. Microbial interactions with the host in periodontal diseases.in: Newman M.G. Takei H.H. Carranza F.A. Carranza’s clinical periodontology. W.B. Saunders Co, Philadelphia2002: 132-152Google Scholar In subjects with periodontitis, the local bacteria, bacterial antigens, and inflammatory cytokines can enter the circulation and trigger systemic inflammation.22Madianos P.N. Bobetsis Y.A. Van Dyke T.E. Infection and Inflammation.in: Genco R.J. Williams R.C. Periodontal disease and overall health: a clinician’s guide. Professional Audience Communications, Inc, Yardley (PA)2010: 24-41Google Scholar Markers of systemic inflammation associated with periodontal disease include increased numbers of peripheral leukocytes and increased levels of serum antibodies to the bacteria, circulating proinflammatory cytokines, and acute-phase proteins, such as C-reactive protein, fibrinogen, soluble CD14, and LPS-binding protein.22Madianos P.N. Bobetsis Y.A. Van Dyke T.E. Infection and Inflammation.in: Genco R.J. Williams R.C. Periodontal disease and overall health: a clinician’s guide. Professional Audience Communications, Inc, Yardley (PA)2010: 24-41Google Scholar Markers of systemic inflammation are associated with cardiovascular disease, adverse pregnancy outcomes, and diabetes mellitus, and increasing evidence suggests that systemic inflammation caused by periodontitis might increase a subject’s risk for these conditions.22Madianos P.N. Bobetsis Y.A. Van Dyke T.E. Infection and Inflammation.in: Genco R.J. Williams R.C. Periodontal disease and overall health: a clinician’s guide. Professional Audience Communications, Inc, Yardley (PA)2010: 24-41Google ScholarWhat is the evidence?Overview of selected studiesHuman clinical studies published since 1990 and investigating the association between oral bacteria or periodontal diseases and allergic disease or asthma were identified in Medline. Because of a purported link between dental caries and asthma medications, the search excluded studies of dental caries unless the study also examined periodontal disease. A large, although inconclusive, literature has investigated the effects of asthma pharmacotherapy on dental caries.23Maupome G. Shulman J.D. Medina-Solis C.E. Ladeinde O. Is there a relationship between asthma and dental caries?: a critical review of the literature.J Am Dent Assoc. 2010; 141: 1061-1074Crossref PubMed Scopus (26) Google Scholar Twelve studies were identified, reviewed, and classified as being either supportive (Table I) or nonsupportive (Table II) of a beneficial association between oral pathogens and allergy-related outcomes.5Hujoel P.P. Cunha-Cruz J. Maupome G. Saver B. Long-term use of medications and destructive periodontal disease.J Periodontol. 2008; 79: 1330-1338Crossref PubMed Scopus (9) Google Scholar, 24Friedrich N. Volzke H. Schwahn C. Kramer A. Junger M. Schafer T. et al.Inverse association between periodontitis and respiratory allergies.Clin Exp Allergy. 2006; 36: 495-502Crossref PubMed Scopus (40) Google Scholar, 25Arbes Jr., S.J. Sever M.L. Vaughn B. Cohen E.A. Zeldin D.C. Oral pathogens and allergic disease: results from the Third National Health and Nutrition Examination Survey.J Allergy Clin Immunol. 2006; 118: 1169-1175Abstract Full Text Full Text PDF PubMed Scopus (24) Google Scholar, 26Friedrich N. Kocher T. Wallaschofski H. Schwahn C. Ludemann J. Kerner W. et al.Inverse association between periodontitis and respiratory allergies in patients with type 1 diabetes mellitus.J Clin Periodontol. 2008; 35: 305-310Crossref PubMed Scopus (13) Google Scholar, 27von Hertzen L.C. Laatikainen T. Makela M.J. Jousilahti P. Kosunen T.U. Petays T. et al.Infectious burden as a determinant of atopy—a comparison between adults in Finnish and Russian Karelia.Int Arch Allergy Immunol. 2006; 140: 89-95Crossref PubMed Scopus (42) Google Scholar, 28Laurikainen K. Kuusisto P. Comparison of the oral health status and salivary flow rate of asthmatic patients with those of nonasthmatic adults—results of a pilot study.Allergy. 1998; 53: 316-319Crossref PubMed Scopus (53) Google Scholar, 29McDerra E.J. Pollard M.A. Curzon M.E. The dental status of asthmatic British school children.Pediatr Dent. 1998; 20: 281-287PubMed Google Scholar, 30Shulman J.D. Nunn M.E. Taylor S.E. Rivera-Hidalgo F. The prevalence of periodontal-related changes in adolescents with asthma: results of the Third Annual National Health and Nutrition Examination Survey.Pediatr Dent. 2003; 25: 279-284PubMed Google Scholar, 31Eloot A.K. Vanobbergen J.N. De Baets F. Martens L.C. Oral health and habits in children with asthma related to severity and duration of condition.Eur J Paediatr Dent. 2004; 5: 210-215PubMed Google Scholar, 32Mehta A. Sequeira P.S. Sahoo R.C. Kaur G. Is bronchial asthma a risk factor for gingival diseases? A control study.N Y State Dent J. 2009; 75: 44-46PubMed Google Scholar, 33Stensson M. Wendt L.K. Koch G. Nilsson M. Oldaeus G. Birkhed D. Oral health in pre-school children with asthma—followed from 3 to 6 years.Int J Paediatr Dent. 2010; 20: 165-172Crossref PubMed Scopus (35) Google Scholar, 34Grossi S.G. Zambon J.J. Ho A.W. Koch G. Dunford R.G. Machtei E.E. et al.Assessment of risk for periodontal disease. I. Risk indicators for attachment loss.J Periodontol. 1994; 65: 260-267Crossref PubMed Scopus (817) Google ScholarTable ISummary of human studies that support a beneficial association between oral pathogens or periodontal disease and allergy-related outcomesStudyDesignParticipantsOral pathogen or periodontal disease variable(s)Allergy or asthma variable(s)CovariablesResultsGrossi et al,34Grossi S.G. Zambon J.J. Ho A.W. Koch G. Dunford R.G. Machtei E.E. et al.Assessment of risk for periodontal disease. I. Risk indicators for attachment loss.J Periodontol. 1994; 65: 260-267Crossref PubMed Scopus (817) Google Scholar 1994Cross-sectional•1426 residents in and around Erie County, New York•25-74 y of agePeriodontal disease severity defined as mean periodontal attachment loss and categorized as healthy, low, moderate, high, and severe∗Dependent (response) variable(s) in statistical analyses.Subject-reported allergy and asthma/hay fever (asthma and hay fever were combined)†Independent (exposure or predictor) variable(s) in statistical analyses.ORs were adjusted for sex, race, education, income, SES, and oral hygiene status.•In a final ordinal logistic regression model of periodontal disease severity, allergy was inversely associated with periodontal disease (OR, 0.77; 95% CI, 0.58-1.00).•Asthma/hay fever did not remain in the final model.Friedrich et al,24Friedrich N. Volzke H. Schwahn C. Kramer A. Junger M. Schafer T. et al.Inverse association between periodontitis and respiratory allergies.Clin Exp Allergy. 2006; 36: 495-502Crossref PubMed Scopus (40) Google Scholar 2006Cross-sectional survey•2837 persons sampled from the adult population of northeast Germany•20-59 y of agePeriodontal disease extent defined as the percentage of periodontal sites with attachment loss >3 mm and categorized as healthy, low, moderate, and severe†Independent (exposure or predictor) variable(s) in statistical analyses.Subject-reported hay fever, house dust mite allergy, and asthma∗Dependent (response) variable(s) in statistical analyses.ORs were adjusted for sex, age, education, smoking, alcohol consumption, family history for allergies or asthma, and number of teeth.•Relative to periodontal health, the odds of hay fever and mite allergy, but not asthma, decreased significantly with increasing periodontitis categories (Ptrend = .01, .02, and .11, respectively).•ORs (95% CIs) comparing severe periodontitis to health were as follows: 0.53 (0.3-0.9) for hay fever, 0.39 (0.2-0.9) for mite allergy, and 0.48 (0.2-1.0) for asthma.Arbes et al,25Arbes Jr., S.J. Sever M.L. Vaughn B. Cohen E.A. Zeldin D.C. Oral pathogens and allergic disease: results from the Third National Health and Nutrition Examination Survey.J Allergy Clin Immunol. 2006; 118: 1169-1175Abstract Full Text Full Text PDF PubMed Scopus (24) Google Scholar 2006Cross-sectional survey•9385 persons surveyed in NHANES III•12-90 y of ageSerum IgG concentrations (continuous, log-transformed) to 2 oral pathogens: P gingivalis and A actinomycetemcomitans†Independent (exposure or predictor) variable(s) in statistical analyses.Subject-reported, doctor-diagnosed asthma, wheeze, and hay fever∗Dependent (response) variable(s) in statistical analyses.ORs were adjusted for age, sex, race-ethnicity, education, census region, urbanization, serum cotinine level, and body mass index.•For a 1-log-unit increase in P gingivalis antibody concentration, ORs (95% CI) were as follows: 0.41 (0.20-0.87) for asthma, 0.43 (0.23-0.78) for wheeze, and 0.45 (0.23-0.93) for hay fever.•For A actinomycetemcomitans, ORs (95% CIs) were as follows: 0.56 (0.19-1.72) for asthma, 0.39 (0.17-0.86) for wheeze, and 0.48 (0.23-1.03) for hay fever.Friedrich et al,26Friedrich N. Kocher T. Wallaschofski H. Schwahn C. Ludemann J. Kerner W. et al.Inverse association between periodontitis and respiratory allergies in patients with type 1 diabetes mellitus.J Clin Periodontol. 2008; 35: 305-310Crossref PubMed Scopus (13) Google Scholar 2008Cross-sectional•170 type 1 diabetics in northeast Germany•17-80 y of agePeriodontal disease extent defined as the percentage of periodontal sites with attachment loss >3 mm and categorized as healthy, low, moderate, and severe†Independent (exposure or predictor) variable(s) in statistical analyses.Subject-reported hay fever, house dust mite allergy, and asthma dichotomized as respiratory allergies, yes or no∗Dependent (response) variable(s) in statistical analyses.ORs were adjusted for sex, age, smoking, and diabetes duration (education, alcohol consumption, family history of allergies, and hemoglobin A1c levels did not remain in the final model).Relative to periodontal health, the odds of respiratory allergies decreased with increasing periodontitis categories (Ptrend < .01). ORs (95% CIs) were as follows: 0.30 (0.08-1.07) for mild, 0.12 (0.02-0.60) for moderate, and 0.05 (0.01-0.35) for severe.Hujoel et al,5Hujoel P.P. Cunha-Cruz J. Maupome G. Saver B. Long-term use of medications and destructive periodontal disease.J Periodontol. 2008; 79: 1330-1338Crossref PubMed Scopus (9) Google Scholar 2008Cross-sectional review of 7 y of HMO data (1996-2002)•12,631 persons with periodontal disease (assessed between 1999 and 2002)•Health care coverage provided by the HMO for all 7 y•45-61 y of agePeriodontal disease severity categorized as early, moderate, and advanced (no periodontally healthy persons were included)†Independent (exposure or predictor) variable(s) in statistical analyses.Number of years during which at least 1 prescription for a therapy group was filled (fill rate); respiratory agents were one of 16 broad therapy groups.∗Dependent (response) variable(s) in statistical analyses.RRs were adjusted for age and sex.Relative to persons with early periodontitis, persons with advanced periodontitis had significantly lower fill rates for respiratory agents. RRs (95% CIs) were as follows: 0.57 (0.41-0.81) for antihistamines, 0.46 (0.34-0.61) for decongestants, 0.67 (0.55-0.81) for cold/cough agents, and 0.68 (0.49-0.96) for antiasthmatics.OR, Odds ratio; RR, relative risk; SES, socioeconomic status.∗ Dependent (response) variable(s) in statistical analyses.† Independent (exposure or predictor) variable(s) in statistical analyses. Open table in a new tab Table IISummary of human studies that do not support a beneficial association between oral pathogens or periodontal disease and allergy-related outcomesStudyDesignParticipantsOral pathogen or periodontal disease variable(s)Allergy or asthma variable(s)CovariablesResultsLaurikainen and Kuusisto,28Laurikainen K. Kuusisto P. Comparison of the oral health status and salivary flow rate of asthmatic patients with those of nonasthmatic adults—results of a pilot study.Allergy. 1998; 53: 316-319Crossref PubMed Scopus (53) Google Scholar 1998Case-control•33 asthmatic and 33 nonasthmatic adults in Finland•25-50 y of agePeriodontal status index (percentage of teeth with gingival bleeding, calculus, or periodontal pockets)†Independent (exposure or predictor) variable(s) in statistical analyses.Diagnosed asthma∗Dependent (response) variable(s) in statistical analyses.•Subjects were matched on age and sex.•Education was a covariate in the analysis.Asthmatic subjects had a higher mean periodontal status index than nonasthmatic subjects (P < .05).McDerra et al,29McDerra E.J. Pollard M.A. Curzon M.E. The dental status of asthmatic British school children.Pediatr Dent. 1998; 20: 281-287PubMed Google Scholar 1998Case-control•100 asthmatic and 149 nonasthmatic children in England•4-16 y of age•Gingivitis score•Dental plaque score†Independent (exposure or predictor) variable(s) in statistical analyses.Asthma (doctor-diagnosed and currently using an inhaler for asthma control)∗Dependent (response) variable(s) in statistical analyses.•Subjects were matched on age, sex, race, and SES.•Analyses were stratified by age (4-10 y and 11-16 y) and by 6 areas of the mouth.•For both age groups, asthmatic subjects had higher gingivitis scores than nonasthmatic subjects (P < .01).•For the younger group only, asthmatic subjects had higher plaque scores than nonasthmatic subjects (P < .05).Shulman et al,30Shulman J.D. Nunn M.E. Taylor S.E. Rivera-Hidalgo F. The prevalence of periodontal-related changes in adolescents with asthma: results of the Third Annual National Health and Nutrition Examination Survey.Pediatr Dent. 2003; 25: 279-284PubMed Google Scholar 2003Cross-sectional survey•1596 adolescents surveyed in NHANES III•13-17 y of age•Gingivitis (bleeding, yes/no)•Periodontitis (2 outcomes): loss of attachment (yes/no) and periodontal pockets (yes/no)∗Dependent (response) variable(s) in statistical analyses.•Parent-reported, doctor-diagnosed asthma categorized as healthy, mild, and moderate or severe•Asthma medication use†Independent (expos" @default.
• W2016835497 created "2016-06-24" @default.
• W2016835497 creator A5002714937 @default.
• W2016835497 creator A5033821656 @default.
• W2016835497 date "2011-05-01" @default.
• W2016835497 modified "2023-10-18" @default.
• W2016835497 title "Can oral pathogens influence allergic disease?" @default.
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