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  Periodontology 2000, Vol. 29, 2002, 7–10 Copyright   C  Blackwell Munksgaard 2002 Printed in Denmark. All rights reserved  PERIODONTOLOGY 2000 ISSN 0906-6713  Global epidemiology of periodontal diseases:an overview  J    M. A    & T   E. R   This volume aims to provide a comprehensiveevaluation of the distribution of various types of periodontal diseases from each of the world’s fivemajor geographic regions. Epidemiology is thestudy of the health and disease in populations, ascompared to individuals (20). Study of the distri-bution of human periodontal diseases and theirrisk factors on a global scale offers a unique inves-tigational model that can provide power and gener-alization to observations on the periodontiummade initially among more limited populations. Inassessing causation between periodontal diseasesand their suspected etiologic risk factors, it is use-ful to demonstrate consistency of the relationshipsin multiple, representative population samples. When diverse study approaches in various popula-tions by different investigators produce similar con-clusions on the distribution of periodontal diseasesand/or their associations with putative risk factors,then one can be more confident that real phenom-enon and/or causal relationships exist (29). Indeed,population-based studies provide external validity to observations obtained from more discrete sub- ject groups, and enable generalization of the con-clusions (14). Alternatively, differences in peri-odontal disease patterns among various populationgroups can be exploited to uncover previously un-identified risk factors that may not be expressed inall populations. Available population-based periodontal diseasedata originate from studies encompassing a widerange of objectives, designs and measurement cri-teria (18). The lack of standardized study design,definition of periodontal disease status, methods fordisease detection and measurement, and criteria forsubject selection markedly limit interpretation and 7  analysis of available population-based periodontaldisease data from around the world. However, sev-eral broad trends on the nature of human peri-odontal diseases are apparent across the wide rangeof population-based data.Population studies confirm the close relationshipbetween dental plaque and gingivitis that was ini-tially described by Löe et al. (21) in nonpopulation-based studies. Throughout the globe, dental plaquegrowth and inflammation of gingival tissue areubiquitous and strongly linked, irrespective of age,gender or racial/ethnic identification. More than82% of U.S. adolescents have overt gingivitis andsigns of gingival bleeding (2), with similar or higherprevalences of gingivitis being reported for childrenand adolescents in other parts of the world (4, 12,13, 15, 25). A high prevalence of gingivitis is alsofound in adults, with more than half of the U.S. adultpopulation estimated to exhibit gingival bleeding (1,6, 24), and other populations showing even higherlevels of gingival inflammation (25). While gingivitis parallels the level of oral hygienein a population, it is by itself a poor predictor of sub-sequent periodontitis disease activity (5, 16, 19).However, young subjects with overt gingival in-flammation more frequently exhibit periodontalattachment loss than adolescents without gingivalinflammation (2). Furthermore, gingivitis always ap-pears to precede the development of periodontitis,as no data from around the world indicate that theonset of periodontitis occurs without gingival in-flammation.It is clear from global epidemiology data that a lesspronounced relationship appears to exist betweendental plaque and severe periodontitis. Severe formsof human periodontitis frequently affect only a sub-   Albandar & Rams  set of population groups globally, even thoughplaque-induced gingivitis and slight to moderateforms of periodontitis are widespread within thesame population groups. A relatively small subset of populations in the United States (6), Central andSouth America (15), Europe (27), Africa (7), and Asia/Oceania (10) exhibit severe forms of periodontalattachment loss with deep periodontal pocket for-mation. The relatively lower occurrence of severeperiodontitis in many of the studied populationsmay in part be attributed to the lack of standardizedstudy design and disease measurement criteria used,and the effects of marked tooth loss in persons withsevere periodontitis, which would serve to reducethe prevalence of severe periodontitis as edentulousconditions occur. However, it is likely that ad-ditional, unidentified risk factors beyond dentalplaque and gingivitis alone are important in theonset and pathogenesis of severe forms of peri-odontitis.In this regard, the relative contribution of variousproposed risk factors in severe periodontitis remainto be fully delineated. Most studies fail to assessaspects of study subjects (i.e. genetic, biochemical,microbiologic and/or immunologic markers) be- yond basic demographic characteristics. There is arelative paucity of analytic studies which accountfor a wide range of potential independent risk fac-tors for severe periodontitis. For example, severalgene polymorphisms have been investigated rela-tive to their associations with periodontitis, andsome of these have been shown to be related toincreased risk for aggressive disease (5). The mostsignificant gene aberrations studied so far are thosethought to be associated with altered host immuneresponse to infection, including interleukin-1 (IL-1) gene, vitamin D receptor gene, and fMLP recep-tor gene.However, the effects of various genetic risk factorsare not exclusive, and these effects explain only apart of the variance in the occurrence of aggressiveperiodontitis, and to a lesser degree, chronic peri-odontitis. Studies show that there is a significant in-teraction between genetic factors and other environ-mental and demographic factors, including a poss-ible modifying effect of smoking, and a variability inthe occurrence of certain genotypes in differentrace-ethnicity groups (5). Hence, more analyticstudies encompassing a wider range of potential risk variables are needed to better understand the role of these and other factors in the increased susceptibil-ity to destructive periodontal diseases. Another problem with many population-based 8  periodontal studies has been the reliance uponmeasurement of probing depth as an indicator of disease status. At a population level, probing pocketdepth measurements are of limited value for the ap-praisal of the extent and severity of periodontal dis-eases for the following reasons: O  An increase in the probing depth at a given toothsite may or may not be associated with attach-ment loss at that site. O  The probing pocket depth at a given site is achangeable measure. A reduction of the probing depth with aging due to gingival recession is fre-quently observed (22), and does not necessarily indicate improved periodontal status. O  Probing depth does not provide an accuratemeasure of periodontal tissue destruction ac-cumulated over a person’s lifetime as reliably asassessments of periodontal attachment level.Significant disparities appear to exist in the level of periodontitis among young, adult and senior popu-lations in the world. Subjects of African ethnicity seem to have the highest prevalence of peri-odontitis, followed by Hispanics and Asians. Dis-parities in periodontal status appear to occur large-ly between the poor and the rich. Populations witha lower socioeconomic level cannot afford dentaltreatment. These populations often lack healthy at-titudes and behaviors for oral health, as well as forsystemic health. In addition, periodontal diseasesusceptibility is further aggravated by the apparentoccurrence in these populations of certain biologi-cal and microbiological risk factors that further in-crease their predisposition to periodontal diseases(3, 5).Epidemiologic data can form the basis for selec-tion and implementation of strategies to prevent andtreat periodontal diseases. Three broad strategieshave been advanced (26, 28): O  Population strategy:   uses a community-wide ap-proach in which health education and otherfavorable life practices are introduced in the com-munity, and unfavorable behaviors are attemptedto be changed. O  Secondary prevention strategy  : includes detecting and treating individuals with destructive peri-odontal diseases. Basically, health education is anintegral part of this strategy, although it is morecustomized to the needs of the individual patient.Dental health education approaches to improvethe oral hygiene of the individual patient, al-  Global epidemiology of periodontal diseases  though successful in the short-term, have beenshown to be relatively ineffective in making sus-tained changes in oral hygiene behaviors (27).This may be partly due to the failure to incorpor-ate social contextual factors and other factors,such as loss of function and esthetics, and thegeneral health impact of periodontal diseases, inthese programs. O  Identification of high risk groups for periodontitis  :the early detection of active disease and identifi-cation of subjects and groups who are more likely to develop destructive periodontal diseases in thefuture are important elements of dental care sys-tems planning.The selection of the most appropriate of the abovestrategies for a given population group is dependentupon the disease distribution and nature of risk fac-tors pertinent to periodontal diseases in that par-ticular population.In the future, adoption of better oral hygieneshould have a notable impact on the occurrence of periodontal disease. Awareness of the occurrence of disease, the infectious nature of these diseases, andthe available means of risk assessment and diseaseprevention (11, 23), may be achieved through abetter interaction between oral health providers andcommunity decision makers, and changes in theeducational programs in the population to promotehealthy attitudes. The advent of fluoride and its ef-fect in markedly reducing the incidence of dentalcaries has resulted in a notable increase in tooth re-tention worldwide (9), and a higher number of re-tained teeth may be accompanied by increases in theprevalence and severity of periodontal attachmentloss in the population (17). Finally, as more peopleare living longer, with retention of their teeth, agreater prevalence of destructive periodontal diseasemay be expected to occur (8). Although behavioral changes, including better oralhygiene habits, smoking cessation programs, andother behavioral and promotional programs may po-tentially improve periodontal health, the overallbenefits may be offset and even surpassed by theincreases in the prevalence and severity of peri-odontal attachment loss which will accompany theanticipated increase in tooth retention and longerlife expectancy. In the coming years on a globalbasis, it may be foreseen that a decrease in preva-lence and severity of periodontal attachment loss inpopulations younger than 50years is likely together with an increase in periodontal disease in older agegroups. 9  References 1. Albandar JM, Brunelle JA, Kingman A. Destructive peri-odontal disease in adults 30 years of age and older in theUnited States, 1988-1994.  J Periodontol   1999:  70 : 13–29.2. Albandar JM, Kingman A, Brown LJ, Löe H. Gingival in-flammation and subgingival calculus as determinants of disease progression in early-onset periodontitis.  J Clin Periodontol   1998:  25 : 231–237.3. Albandar JM, Rams TE. Risk factors for periodontitis inchildren and young persons.  Periodontol 2000   2002:  29 :207–222.4. Albandar JM, Tinoco EMB. Global epidemiology of peri-odontal diseases in children and young persons.  Peri-odontol 2000   2002:  29 : 153–176.5. Albandar JM. Global risk factors and risk indicators forperiodontal diseases.  Periodontol 2000   2002:  29 : 177–206.6. Albandar JM. Periodontal diseases in North America.  Peri-odontol 2000   2002:  29 : 31–69.7. Baelum V, Scheutz F. Periodontal diseases in Africa.  Peri-odontol 2000   2002:  29 : 79–103.8. Berkey D, Meckstroth R, Berg R. An ageing world: facing the challenges for dentistry.  Int Dent J   2001:  51  (Suppl.):177–180.9. Clarkson JJ, McLoughlin J. Role of fluoride in oral healthpromotion.  Int Dent J   2000:  50 : 119–128.10. Corbet EF, Zee KY, Lo ECM. Periodontal diseases in Asiaand Oceania.  Periodontol 2000   2002:  29 : 122–152.11. Croxson LJ. Periodontal awareness: the key to periodontalhealth.  Int Dent J   1993:  43  (Suppl.): 167–177.12. Cunha ACP, Chambrone LA. Prevaleˆncia de gengivite emcriancas de um nivel social baixo.  Revista Periodontia  1998:  7 : 6–10.13. Cunha ACP, Chambrone LA. Prevaleˆncia de gengivite emcriancas.  Revista Periodontia   1998:  7 : 1–5.14. Elwood JM.  Causal Relationships in Medicine  .  A Practical System for Critical Appraisal  . Oxford: Oxford University Press, 1988: 172–173.15. Gjermo P, Rösing CK, Susin C, Oppermann R. Periodontaldiseases in South and Central America.  Periodontol 2000  2002:  29 : 70–78.16. Haffajee AD, Socransky SS, Goodson JM. Clinical par-ameters as predictors of destructive periodontal diseaseactivity.  J Clin Periodontol   1983:  10 : 257–265.17. Hugoson A, Laurell L, Lundgren D. Frequency distributionof individuals aged 20–70 years according to severity of periodontal disease experience in 1973 and 1983.  J Clin Periodontol   1992:  19 : 227–232.18. Kingman K, Albandar JM. Methodological aspects of epi-demiological studies of periodontal diseases.  Periodontol 2000   2002:  29 : 11–30.19. Lang NP, Adler R, Joss A, Nyman S. Absence of bleeding on probing. An indicator of periodontal stability.  J Clin Periodontol   1990:  17 : 714–721.20. Last JM, ed.  A Dictionary of Epidemiology  , 4th edn. New  York: Oxford University Press, 2001.21. Löe H, Theilade E, Jensen SB. Experimental gingivitis inman.  J Periodontol   1965:  36 : 177–187.22. Löe H, Anerud A, Boysen H. The natural history of peri-odontal disease in man: prevalence, severity, and extent of gingival recession.  J Periodontol   1992:  63 : 489–495.23. Luhanga C, Ntabaye M. Geriatric oral health issues in Africa: Tanzanian perspective.  Int Dent J   2001:  51  (Suppl.):219–227.   Albandar & Rams  24. Oliver RC, Brown LJ, Löe H. Periodontal diseases in theUnited States population.  J Periodontol   1998:  69 : 269–278.25. Petersen PE, Kaka M. Oral health status of children andadults in the Republic of Niger.  Afr Int Dent J   1999:  49 :159–164.26. Rose G.  The Strategy of Preventive Medicine  . Oxford: Ox-ford University Press, 1992. 10  27. Sheiham A, Netuveli GS. Periodontal diseases in Europe. Periodontol 2000   2002:  29 : 104–121.28. Sheiham A. Public health aspects of periodontal diseasesin Europe.  J Clin Periodontol   1991:  18 : 362–369.29. Susser M.  Causal Thinking in the Health Sciences  .  Concepts and Strategies in Epidemiology  . New York: Oxford Univer-sity Press 1973, 148–149.
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