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Periodontal Microbiology 2 Alexandrina L Periodontal Microbiology 2 Alexandrina L. Dumitrescu and Masaru Ohara There is a wide agreement on the etiological role of bac- gival plaque. Many subgingival bacteria cannot be teria in human periodontal disease. Studies on the micro- placed into recognized species. Some isolates are biota associated with periodontal disease have revealed fastidious and are easily lost during characterization. a wide variety in the composition of the subgingival Others are readily maintained but provide few posi- microfl ora (van Winkelhoff and de Graaff 1991). tive results during routine characterization, and thus The search for the etiological agents for destructive require special procedures for their identifi cation. periodontal disease has been in progress for over 100 4. Mixed infections. Not only single species are respon- years. However, until recently, there were few consen- sible for disease. If disease is caused by a combina- sus periodontal pathogens. Some of the reasons for the tion of two or more microbial species, the complexity uncertainty in defi ning periodontal pathogens were increases enormously. Mixed infections will not be determined by the following circumstances (Haffajee readily discerned unless they attract attention by their and Socransky 1994; Socransky et al. 1987): repeated detection in extreme or problem cases. 5. Opportunistic microbial species. The opportunistic 1. The complexity of the subgingival microbiota. Over species may grow as a result of the disease, taking 300 species may be cultured from the periodontal advantages of the conditions produced by the true pockets of different individuals, and 30–1,000 spe- pathogen. Changes in the environment such as the cies may be recovered from a single site. release of required substrates from damaged tis- 2. Sample taking. The physical constrains of a pocket sues or deepening of the periodontal pocket Could make it diffi cult to obtain a representative sample be selected by certain opportunistic species. Their from that pocket: that is, a sample that contains the levels may increase concomitant with or after those pathogen and low number of contaminating species. of the true pathogens, and they may thus be diffi - If the sample is too large, the pathogen(s) would be cult to distinguish experimentally. diluted by noncontributory “contamining” species. 6. Disease activity. Periodontal disease appears to If the sample were too small or taken from the progress with periods of exacerbation and remission. wrong place, one might miss the pathogen entirely. Ideally, a plaque sample should be taken at the 3. Diffi culties in cultivation, characterization and iden- peak of the disease activity. Failure to detect the tifi cation of micro-organisms of plaque. Many of the peak of activity may lead to an underestimate of species in pockets are diffi cult or impossible to cul- the contribution of a pathogen(s) to a given lesion. ture and diffi cult to identify. No single medium or 7. Multiple periodontal diseases in different subjects. environment is capable of recovering all of the organ- There appear to be multiple destructive periodontal isms, which currently can be isolated from subgin- diseases that, for the most part, cannot be differen- tiated on a clinical basis. Thus, disease types may be misclassifi ed and inappropriately pooled. 8. The possibility of multiple diseases in a subject. A. L. Dumitrescu ( ) Differences observed in clinical symptoms in dif- Institute of Clinical Dentistry, Faculty of Medicine University of Tromsø, 9037 Tromsø, Norway ferent parts of the mouth may be explained by dif- e-mail: [email protected] ferences in levels of the pathogen or the stage of the A. L. Dumitrescu, Etiology and Pathogenesis of Periodontal Disease, 39 DOI: 10.1007/978-3-642-03010-9_2, © Springer-Verlag Berlin Heidelberg 2010 40 2 Periodontal Microbiology destructive process. Disease might have occurred in infection than in individuals without overt disease or shallow lesions due to one species and in deepening with different forms of disease), elimination (elimina- lesions by a succession of other species. Disease tion of a species should be accompanied by a parallel occurring in one site in the mouth could be due to remission of disease), host response (if a species, or its an agent that is different from the one inducing antigens, gains access to underlying periodontal tissues destruction at a second site at the same time. and causes damage, it seems likely that the host will 9. The carrier state. Pathogens may be carried in low produce antibodies or a cellular immune response that is numbers in mouths that are free of destructive peri- directed specifi cally at those species; thus, the host odontal diseases (the so-called carrier state), mak- response could act as a pointer to the pathogens), viru- ing their role in disease more diffi cult to evaluate. lence factors (potentially damaging metabolites pro- 10. Virulent factors. Strains of putative pathogens may duced, or properties possessed by certain species may differ in virulence. A virulent clonal type might be be suggestive that that species could play a role in the detected in periodontally healthy subjects, whereas disease process), animal studies (experimentally induced virulent clonal types might be present in subjects disease in dogs or monkeys, which can be manipulated with periodontal disease. An inability to distin- to favor selection of single or subsets of species that guish virulent from virulent clonal types would may or may not induce pathology), and risk assessment impede understanding. (prospective studies are performed in which the risk of 11. Genetic virulence elements. It has been suggested periodontal disease progression conferred by the pres- that more virulent strains may harbor bacteriophages ence of an organism at given levels may be assessed). or plasmids. Bacterial plasmids are known to code The discrimination of a pathogen from a nonpathogenic for several virulence factors like invasiveness, adher- species is not based on a single criterion but rather on a ence, and antimicrobial resistance as well as the pro- “weight of evidence” evaluation (Haffajee and Socransky duction of toxins and noxious products. Several 1994). strains of A.actionomycetemcomitans isolated from periodontal lesions of a rapidly destructive perio- dontitis patients have been described to have identi- cal profi les consisting of four plasmids (Olsvik and 2.1 Virulence Factors Preus 1989). A.actionomycetemcomitans phages of Periodontal Pathogens were isolated from recently active periodontal sites in a patient suffering from prepubertal periodontitis, The identifi cation of pathogen(s) of an infectious dis- suggesting an association between periodontal ease, including periodontal diseases, leads inevitably breakdown and phage infection of A.actinomycet- to the question “how do these organisms cause the dis- emcomitans (Preus et al. 1987). ease?” Thus, the study of potential virulence factors The task of defi ning the etiological agents of periodon- produced by oral species including periodontal patho- tal disease and subsequently the development of gens is a very active area of research. improved methods of classifi cation, diagnosis, and The term virulence is generally defi ned as the rela- treatment is clearly a cyclical process with continual tive ability of an organism to cause disease or to inter- revaluation and refi nement (Socransky et al. 1987). fere with a metabolic or physiological function of its The criteria for defi ning pathogens in destructive host. The word derives from the Latin, “virulentus” or periodontal diseases were initially based on Koch’s pos- “full of poison.” Thus, virulence refers to the ability of a tulates. These postulates were: (1) the agent must be microbe to express pathogenicity (e.g., virulent), which isolated from every case of the disease (2) it must not be is contrasted with nonpathogenic or avirulent organ- recovered from cases of other forms of disease or non- isms. Thus, virulence is not a separate property of the pathogenically, and (3) after isolation and repeated microbe, but is a complex interaction between the growth in pure culture, the pathogen must induce dis- microbe and its host; this interaction being dependent ease in experimental animals. These postulates have upon many extrinsic factors of the environment. The been amended and extended in recent years, the criteria characteristic endproducts of bacterial metabolism; the including association (the species should be found more chemical composition of bacterial components; the abil- frequently and in higher numbers in cases of an ity of the intact bacterium or its parts to overwhelm host 2.2 Pathogens Suspected Currently in Destructive Periodontal Diseases 41 defense mechanisms, its invasiveness, and of course its decades, it has been shown that Aggregatibacter actino- ability to kill were all used to characterize and distin- mycetemcomitans can be regarded as a major pathogen guish a virulent microbe from an avirulent one (Holt in destructive periodontal diseases (Slots et al. 1990a; and Ebersole 2005). Poulin and Combs (1999) defi ned van der Reijden et al. 2008; Slots and Ting 1999). The the concept of virulence in terms of the type of mole- species is represented by six serotypes (a–f). Serotype b cules being produced by the microbe. As such, they has been found more frequently and detected in higher defi ned virulence in terms of “virulence factors,” that is, numbers in active periodontitis lesions, whereas sero- components of a microbe, which when present harm the types a and c have a stronger association with periodon- host, but when absent (i.e., mutation) impair this ability. tal health (van der Reijden et al. 2008). Serotype b was This mutation does not affect the ability of the microbe signifi cantly found more often in aggressive than in to grow and reproduce. Thus, virulence factors can have chronic periodontitis. They also found serotype b more a multitude of functions (Holt and Ebersole 2005): frequently in periodontitis subjects under the age of 18 years (60.9%) in comparison to subjects older than 35 • The ability to induce microbe–host interactions years (29%).
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