Community Dent Oral Epidemiol 2012; 40: 385395 All rights reserved

2012 John Wiley & Sons A/S

Commentary

Contesting conventional periodontal wisdom: implications for periodontal classications

pez R, Baelum V. Contesting conventional periodontal wisdom: implications Lo for periodontal classications. Community Dent Oral Epidemiol 2012; 40: 385395. 2012 John Wiley & Sons A/S Abstract This paper examines the common approach used to classify periodontal diseases and how this obstructs our understanding of the disease process. We address the implications of including etiological and pathogenesisrelated considerations in the classications of complex diseases like periodontitis and argue that the number of periodontal entities in a classication system ought to be determined by well-documented differences in the management of each entity. We nally discuss how an ecosocial theory of disease distribution can be helpful to understand the determinants of the distribution of disease in the population.

pez1 and Vibeke Baelum2 Rodrigo Lo

Department of Periodontology, Faculty of Health Sciences, Aarhus University, Aarhus, Denmark, 2Department of Epidemiology and School of Dentistry, Faculty of Health Sciences, Aarhus University, Aarhus, Denmark
1

Key words: clinical decision making; diagnostic research; epidemiology; periodontal diseases; periodontitis pez, Department of Rodrigo Lo Periodontology, School of Dentistry, Faculty of Health Sciences, Aarhus University, Vennelyst Boulevard 9, DK-8000 Aarhus C, Denmark Tel.: +45 8942 4141 Fax: +45 8613 6550 e-mail: rlopez@odont.au.dk Submitted 9 June 2011; accepted 18 January 2012

The past 25 years have witnessed more than 10 different periodontal disease classication systems (110). However, these systems have consistently been introduced in the absence of clear evidence for their advantages over the one(s) used hitherto. The lack of agreement on the operational denition of periodontitis and the categorization of subjects into disease groups constitute a major problem for researchers and policy makers attempting to summarize the scientic evidence on periodontitis. In view of the countless proposals for a periodontal classication system (47, 9, 1129) made since Fauchard and Hunter initiated the classication endeavor, we nd it prudent to examine the driving forces for these many classication system proposals.

The basis for classication systems

Close scrutiny of the ICD-10 system (30), which is the international standard disease classication system, reveals several different approaches to the denition of disease. The more prominent include diseases dened based on symptomatology (e.g.,
doi: 10.1111/j.1600-0528.2012.00677.x

chronic diarrhea), patho-anatomical characteristics (e.g., gastric ulcer), physiological characteristics (e. g., arterial hypertension), metabolic characteristics (e.g., hypercholesterolemia), and etiology (e.g., asbestosis), and nally, some diseases are dened as syndromes (e.g., Basedows disease) (31). In periodontology, the dominant viewpoint has always been that periodontal disease classications should be based on etiology. Only recently, Armitage (32) stated that One of the main problems with any attempt at subclassifying this [CP] or other forms of periodontitis, is that these infections are polymicrobial and polygenic. In addition, the clinical expression of these diseases is altered by important environmental and host-modifying conditions (e.g. oral hygiene, smoking, emotional stress, diabetes). It is conceivable that with much more information and the application of sophisticated multivariate analyses, it may eventually be possible to subclassify the multiple forms of Chronic Periodontitis into discrete microorganism/host genetic polymorphism groups.. Obviously, the practical use of such a complicated classication system would be

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extremely restricted. Periodontal researchers would face problems when attempting to gather reasonably sized homogeneous study groups, and periodontal clinicians would be likely to abandon such systems right away, deeming them useless for clinical purposes. It is therefore necessary to rethink the conceptual basis for periodontal disease classication systems.

leading. The problem is that disease is continuously confused with etiopathogenesis (38). At the end of the day, the purpose of all our activities, whether in research, public health, or clinical practice, is to be able to control disease.

Identication of points of intervention along the pathway to disease

The criteria listed in Table 1 indicate that all members of the population should be classiable. We must therefore use our epidemiological tools and insights to identify the modiable causal factors along the possibly many pathways to periodontitis. The issue is to identify targets for intervention as these can provide us with the tools to control periodontitis, not only for the conspicuous cases, but for the population at large. Such information is also increasingly called for by clinicians who nd themselves more and more engaged in dental screening activities (39). When a disease comes in all grades of severity, it is insufcient only to consider the identication of the obvious cases for treatment (40). A substantial hidden burden of ill health may exist, which is not necessarily amenable to treatment but for which preventive means should be sought: Preventive medicine should be concerned with the whole spectrum of disease and ill health, both because all levels are important to the people concerned and because the mild can be the father of the severe. The visible tip of the iceberg of disease can be neither understood nor properly controlled if it is thought to constitute the entire problem (40). The need for a distinction between therapy and prevention is therefore less clear than one might think, and owing to the routine nature of oral examinations, it may not even be helpful to try to maintain this distinction in the case of periodontal diseases. Routine dental examinations comprise case-fortreatment detection screening activities and thereby corroborate the high-risk preventive strategy (40). While tting well with the philosophies of medicine and clinical dentistry, this strategy only stands a good chance of success when the modiable risks of disease are conned to identiable subgroups of the population who carry the major disease burden. The evidence regarding periodontitis does not point to this being the case. Rather, the epidemiological evidence points to the ubiquitous occurrence of signs of periodontitis, which follows a

Features of a useful disease classication system

The key desirable characteristics of a classication system are shown in Table 1 (33). Naturalness means that the classication should be based on the observable, which for periodontitis precludes the use of disease progression as an element in the system. The requirements of exhaustiveness and disjointness, and the associated constructability dictate that every member can be classied as belonging to one group only. Usefulness dictates that the classication is clinically valuable for diagnostic, therapeutic, and prognostic decisions (34). Based on these requirements, it is hardly surprising that no one of the periodontal classication systems hitherto proposed have survived long enough to become established. In the context of a complex disease such as periodontitis, it is questionable whether the hankering for disease classications that incorporate as much biological knowledge as possible into the system (35, 36) is a fruitful way forward. As succinctly phrased by Murphy (37): It is in trying to understand the etiology and pathogenesis of disease that we eventually realize how hopeless it is to seek an answer at a high resolution when the question is crude, unexamined, perhaps even grossly misTable 1. Desirable characteristics of a classication system Characteristic Naturalness Exhaustiveness Disjointness Usefulness Constructability Classication should Correspond to the nature of the condition being classied Accommodate naturally every member of the group being classied Exclude membership of more than one group Be useful Be seen by its structure to be exhaustive and disjoint

Adapted from Murphy (33).

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continuum of disease severity such that the absence or low severity of periodontitis merges imperceptibly into high severity and extent (41 44). The most conspicuous determinants of the population distribution of signs of periodontitis are age and socioeconomic position. While smoking is a modiable factor that confers a considerable risk, the epidemiological features indicate that on a population basis, it might be more fruitful to understand the signs of periodontitis as resulting from exposure to many smaller risks. Although severe periodontitis has been observed to occur ` vre with rare diseases such as the PapillonLefe syndrome (45), it is clear that neither smoking nor rare syndromes can account for the major burden of periodontitis. Widespread exposure to smaller risks may actually produce many more cases than the conned exposure to a few large risks (40). When disease results from the exposure to many smaller risks, the population strategy for prevention and control, in the form of campaigns or structural prevention, stands a better chance of being fruitful in combating disease occurrence. As dentists, we should acknowledge that some of the interventions that might be relevant for the prevention and control of periodontitis at the population level do not fall within the territories of traditional dentistry. As an example, while many clinicians might engage in chair-side smoking cessation counseling (46), many more would probably see themselves unt for carrying out such activities, over and beyond of advising their patients to quit smoking (47). Although this does not preclude the dental team from engaging in campaigns or advocating structural prevention, they should bear in mind that quarterly chair-side antismoking sessions might have little impact.

paradigm has therefore led to the use of postgenomic molecular technologies (50) to resolve these complex diseases. The idea is that by reducing the problems of disease to problems of molecular science (48), the relevant molecules may be identied and interventions may be devised that stop the effects of these molecules in disease pathogenesis (51). While many continue to emphasize the promising prospects of this approach (51), increasing concern has been voiced over the fading returns in terms of novel disease interventions arising from the huge investments made in bench-to-bedside research (52, 53). While this state of affairs has commonly been attributed to underfunding of clinical research (54), the lack of academic prestige in clinical medicine (55), or the rush to use the new technologies (55, 56), some have also questioned the underpinning reductionist research paradigm (55, 57, 58). In 2004, the journal Perspectives in Biology and Medicine devoted an entire issue to this problem (59) and identied the conventional linear bench-to-bedside model of scientic progress as a key obstacle for therapeutic innovation (59).

Destructive periodontal diseases as complex diseases

The complex disease perspective also encompasses periodontitis (6062). While a number of rare conditions have been identied as being associated with periodontitis (60), these genetic conditions account for only a small fraction of the total number of cases of periodontitis, even among the young. When it comes to the more common categories of periodontitis, the results remain equivocal concerning the determination of the genetic susceptibility inuences (60, 61), although great faith remains placed in the prospect of being able to elucidate the genetic basis for the varying susceptibility to periodontitis (63, 64). While more knowledge has been generated as a result of these efforts, it is equally clear that no master gene responsible for periodontitis has been identied, and the clinical applicability of the knowledge generated for diagnosis and management of periodontal diseases has been quite limited (65). As has also been observed in medicine (49), our limited ability to validly measure and characterize the disease phenotypes is a major obstacle for the anticipated success in determining the genetic inuences for susceptibility (61, 66). Even so, the periodontal research focus remains in the area of dissecting the variability of the host susceptibility

Limitations posed by the dominant research paradigm

Biomedical research is currently dominated by a reductionist approach (48). The most noticeable result of this has been the identication of genes causing a multitude of Mendelian disorders (49), a result that has been greatly facilitated by the strong relationship between genotype and phenotype in such disorders. However, most diseases are genetically complex in the sense that they involve gene environment interactions, genetic heterogeneity, and variable penetrance and expression (50). The dominant biomedical from-bench-to-bedside research

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to infection (61, 67), and mainstream periodontal research is increasingly characterized as a reductionist enterprise attempting to understand the whole by identifying all the constituent components and elucidating their precise role (55, 68). Wondering why this is so, we proposed as responsible a number of factors: (i) the replacement of the single-agent germ theory disease models with host, agent, and environment models; (ii) the political developments favoring individualism over the shared; (iii) the privilege given to the bench sciences at the expense of clinical and population-based studies in the slipstream of the human genome project; and (iv) the unjustied, yet widespread, belief that laboratory methods are less prone to errors and therefore produce results of higher validity and reliability than may be obtained using clinical and epidemiological methods (55). It is thus a common observation across different elds that bench science, a.k.a. molecular medicine, is more prestigious and academically rewarding than are the poor intellectual cousin sciences of clinical medicine and epidemiology (69). A further sign of the belief in the superiority of the bench research is the overwhelming condence that once the pathobiologic truth has been uncovered, the move from bench to clinical application will be straightforward. In the words of Kornman (62): Although even partial information should improve the ability to identify an individuals susceptibility to disease and a likely response to treatment, the complete expression of these networks should be a valuable tool for determining new preventive and therapeutic approaches (62). However, the ability to take a disease to pieces in molecular terms is not the same as being able to plan interventions with the necessary precision (50). Paraphrasing Rees (50), it seems worth bearing in mind that clinical periodontology may have little regard for a complete description of how a myriad of pathways result in any clinical state. Rather, its goal remains pragmatic; it denes cause by how successful intervention might be obtained, how one, of many, rate-limiting pathways may be circumvented. It is far from self-evident that the reductionist approach taken by current mainstream periodontal research will ever provide answers that are useful to clinicians dealing with patients, let alone for public dental health purposes. In this context, it may be worthwhile to draw on the priorities for genomics research in other complex diseases (49). According to this, genomics research should have high priority if (i)

there is a priori evidence for a genetic etiology of the disease (e.g., disease clustering within families), (ii) the ability to modify exposure or risk factors is limited, and (iii) the disease has a high public health impact. One may question whether any form of periodontal disease exists, which fullls these criteria. Ultimately, the verdict on the outcomes of different research approaches will be based on their health problem-solving capacity, and while the -omics technologies might eventually bring us closer to improved treatment modalities for individual patients, they stand little chance of being valuable in bringing about health for populations.

Destructive periodontal diseases as infectious diseases

The perhaps most compelling reason why downstream reductionist research is so appealing in periodontology relates to the perception that the cause of periodontitis has already been identied as an infection initiated and sustained by dental plaque (70, 71). This is clearly illustrated by the systematic description of periodontitis as an infection through decades in the literature (7275). Certainly, the widespread use of the infection/ host-response terminology indicates reluctance to admit a causal role for any factor apart from and beyond the dental plaque, the periodontal pathogens, or the oral microbiota. Factors such as diabetes and smoking are commonly described as modifying factors (76, 77) for the host response to the causal infection. Rather than being considered component causes (78), they are merely perceived as exogenous modulators of the hosts susceptibility to the causal infection (79). This view is maintained even though less than 20% of the variability in periodontal disease expression can be explained by levels of specic microbes (80). However, the periodontitis-is-a-complex-disease view does not go along very well with the view that infection is the causal centerpiece. Rose (81) was very accurate in noting that the hardest cause to identify is the one that is universally present, for then it has no inuence on the distribution of disease. The occurrence of microbial plaque on tooth surfaces is a condition of life, which we may be able to modulate, but never escape. Moreover, human existence is a coexistence with microorganisms residing on all bodily surfaces, and it is a fact that humankind would not survive without this microbial colonization. Most of the time, the microorganisms work with us in a mutual benecial

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relationship, and it is only in response to stress and ecological pressure that the indigenous microora may change as the result of an ecological catastrophe (82). According to this ecological plaque hypothesis, host factors are as important for the development of periodontitis as are microorganisms, because host factors are mediated by inammation that affect the relative competitiveness of the bacteria, thereby favoring bacteria thriving under anaerobic and alkaline conditions (82). These include some of the main putative periodontal pathogens, although not uniquely so. In its most extreme, the insistence that infection plays the key role, while host or other factors are secondary modulating factors for the initiation and sustainment of destructive periodontal diseases, therefore implies that the preventive and treatment goals should aim at sterile mouths at all times. However, it would seem a much more feasible way forward to take on the complex disease view, thereby realizing that complex disorders may have not a single cause but a causal chain, or multiple such causal chains. These chains may involve genetics, environmental, social and biological risk factors. The effect of no one of these risk factors can be fully understood except in the context of all the other (83). It follows that one of the important consequences of the complex disease view is that no special key factor status can be given to any particular risk factor, because no risk factor works in isolation. While the wish may be understandable to maintain the infectious causal paradigm as a tribute to its founding fathers, it has been recognized by others that periodontitis does not exactly t the mould of a classical infectious disease there are multiple organisms associated with periodontitis that are present in the periodontal spaces even in undiseased mouths (79). The periodontal research community should therefore remain cautious that the infectious causal paradigm does not come to stand in the way of scientic progress. It is certainly a fact that exogenous exposures have attracted comparatively little research interest among major sections of the periodontal research community (84). What is called for is a recognition of the heterogeneity of the dening features of diseases, which avoids commitment to any universal theory of disease causation while still retaining what is useful in any theory that has been advanced, without implying its universality (85). Thus, periodontal cases may be identied where it is appropriate to adopt a specied microbial cause as a key element, but this should not be taken to

indicate that we are committed to a universal microbial theory of destructive periodontal disease (85).

Limitations posed by the concept of causation the causal paradigm

Epidemiologic history is full of examples of how observations of the contextual settings of disease occurrences have led to major disease-controlling breakthroughs even in the absence of knowledge about the causal agents and their biological effects in the human body. In 1847, Danish physician P.A. Schleisner was sent to the Vestmanna Islands off the Icelandic coast to investigate an exceptionally high neonatal mortality resulting in about 600740 deaths per 1000 within 2 weeks postpartum. This mortality level was in contrast to the mainland Iceland and Danish mortality levels of 160175 per 1000 newborns (86). Schleisner noted what in todays terminology will be a strong social gradient in the neonatal mortality with poor peasants and farmhands constituting the most affected group. As these were living in crowded and dirty dwellings in very close contact with domestic animals, he suspected poor hygiene to play a causal role. Following the recommendation of a lying-in house (an obstetric hospital) where better hygiene could be maintained and the use of Peruvian balsam to protect the umbilicus, the neonatal mortality dropped within a year to the mortality levels seen in mainland Iceland and Denmark (86). Also in c Semmelweis observed vastly different 1847, Igna rates of mortality from childbed fever in two divisions of a Viennese lying-in hospital and associated this with the practice in one of the divisions of performing autopsies before attending the maternity wards (87). The institution of routine hand washing using chlorinated lime before entering a maternity ward resulted in an almost instantaneous reduction in the mortality rate from over 12% to <2% per month (87). During the 1854 cholera outbreak in London, geographical mapping of the cholera deaths led John Snow to suppose that they were caused by contaminated water from the Broad Street pump (88). None of these important advances in public health resulted from knowledge of the causal agents, only later identied as bacteria. Instead, the progress resulted from the use of a key epidemiologic principle: That the most important information to have about an infectious disease is its mode of infection (88). It was the careful mapping of disease occurrences, their circumstances, and patterns of clustering that led Schleisner,

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Semmelweis, and Snow in the right direction in terms of their causal pathways and hence the control of these public health problems. Clearly, the conditions they studied comprised rather acute contagious diseases, and this undoubtedly made their study much easier than would have been the case had they been more chronic in nature. Even so, the value remains unquestionable also for chronic diseases of careful mapping of the disease occurrences to obtain better clues regarding the factors relevant to their resolution. The task is formidable, not because of the disease problems per se, but because such mapping necessitates data collection across time, space, and level (89), and the healthcare systems are not necessarily organized in a way that allows this approach to be taken for chronic diseases. The much-needed studies based on the ecosocial theory of disease distribution (89) are difcult to set up under the auspices of a dominant disease paradigm that understands causal mechanisms as biological phenomena only. Along this line of thinking, one may indeed speculate whether the predenition of periodontitis as a class of infectious chronic diseases is more a hindrance than a help for their improved prevention and clinical management. As previously alluded to, the infection/host-response periodontal disease paradigm has proven unhelpful from a disease classication point of view (38). More importantly, it seems to be precisely the infection/host-response periodontal disease paradigm that prevents us from looking upstream and paying more attention, as did Snow, Semmelweis, and Schleisner, to the mapping of the destructive periodontal disease occurrences with a view to identify environmental or contextual patterns of distribution that might provide us with clues to their important determinants. It would seem that the infection/hostresponse periodontal disease paradigm instead forces us to conceptualize overtly environmental exposures, such as smoking, and sociocultural constructs, such as race (55), as merely modifying oil to the pathogenic wheels of infection of the human body engine room. This view has rather dire implications in terms of leading to victim-blaming (90), just as the prioritization of only those factors that are amenable to control by the health professionals maintains the disease-controlling power within the realms of these professionals (89). The health of individuals and populations is just as important a part of the social justication for dental research as is the improvement of the clinical care for the individual patient (59). However, the health of

individuals and populations does not necessarily follow from the prioritization of improved care for the sick (40, 81). It is therefore clear that amendments are necessary to the infection/host-response periodontal disease paradigm such that a causal concept is allowed that embraces the biological processes as no more than the biological incorporation into the body of the material and social world in which we live, from in utero to death (89). In other words, it is insufcient to study periodontitis as a decontextualized biological process occurring within sick peoples bodies, because these biological processes cannot be understood without knowledge of history and individual and societal ways of living (48, 91, 92).

Notes on causal imagery and causal strength

While causation in the laypersons understanding means monocausation, disease causation from a scientic perspective is best construed as an exceedingly complex issue that continues to prompt discussions in the interface between philosophy and empirical science (9395). The expression of this complexity has necessitated the invocation of powerful metaphors and imagery (96), including causal pies (78), the web of causation (97), direct and indirect causes (97), proximal and distal, or upstream and downstream causes (89). When Krieger (98) asked whether anyone had seen the spider (of the causal web) or the cook (of the causal pies), she pointed to the critical conceptual problem underpinning the use of these inuential images and metaphors (96) the confusion of proximal and downstream with biological, close, and powerful. The notion is very strong that a hierarchy exists in etiology, such that higher causal potency is linked to shorter distance: The closer the cause, the greater the effect, just as more distal causes are necessarily thought to exert their inuence through successive steps involving more proximal factors (55, 89). This notion provides an explanation why medical research has been transformed into benchfocused biomedicine under the dominating -omics research paradigm, a transformation that has also been observed in periodontal research under the auspices of the periodontal infection/hostresponse variant of the paradigm. However, the most important effect of the confusion of biology with causal power is that it forms a barrier to the study of disease as the embodied biological expression of ways of living and working differentially afforded by each societys political economy and political ecology (89). What is needed is a

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conceptual model of disease causation based on the ecosocial premise of embodiment. The key clues to the population patterns of disease distribution are found in the social, material, and ecological contexts in which we are born, develop, interact, and endeavor to live (99), and not so much in decontextualized lifestyles, behaviors, or exposures that interact with equally decontextualized genes. Lifestyles, behaviors, and exposures do not strike at random but are socially, culturally, materially, and ecologically patterned, and failure to incorporate this knowledge into the conceptual models of causal pathways will prompt us to draw the wrong conclusions and lead us to intervene by blaming everything on the victims (91).

The ecosocial theory of disease distribution

The ecosocial theory of disease distribution proposed by Krieger (98) takes a broader view on disease causation than can be accommodated by the more traditional biomedical geneenvironment interaction or the periodontal infection/host-response causal models. Where these models are entirely dedicated to the dissection of biological mechanisms, the ecosocial causal model corroborates much better the approaches taken by Schleisner, Semmelweis, and Snow of trying to understand the social, material, and behavioral pathways that lead to disease. The traditional reductionist biomedical causal models are chiey concerned with individuals and their microenvironments and personal susceptibilities and seek to identify deranged mechanisms in sick individuals: Their use may therefore provide answers to no more than the question of the causes of cases or sick individuals (81). Application of the much broader ecosocial causal models leads to a search for the causes of incidence or sick populations (81) using an approach that combines space, time, level, and domain in the investigation of the pathways of embodiment, that is, the biological incorporation from conception to death of the material and social circumstances of our lives. Although, as previously pointed out (55), the conceptual causal models and pathways are only infrequently explicitly stated in periodontal research, they are there. Unfortunately, there is a strong notion that the victim-blaming and disembodied reductionist research carried out under the auspices of the infection/host-response variant of the -omics paradigm is apolitical. This is in stark contrast to the general perception of inequalityfocused population-based research as an immensely

value-laden and politicizing enterprise (100). However, the long-standing discussion over the impact of the causal conceptualization of considerable race-related health disparities (101) which is also manifest in dental health (55) only serves to show that the victim-blaming disembodied research approach is just as political as the more public health-oriented inequality-focused research (102). The unfortunate advantage of the victim-blaming research approach to individual risk factor identication focused on the interplay of individual lifestyles, behaviors, exposures, and genes is that it is much easier to conceal its political aspects from the public, thereby reducing its accountability and transparency. As stated by Rose, it is not possible to combat the iceberg of disease by continuing to cut off its tip (81). The iceberg problem must be tackled at the roots of the problem: the base and the contextual circumstances leading to its formation. This calls for application of the ecosocial theory for disease development and distribution in an attempt to integrate social and biological reasoning and a dynamic, historical, and ecological perspective to develop insights into the determinants of population distribution of disease (89, 99).

Concluding remarks
The core of the above argumentation is that there is an urgent need to abandon the prevailing idea that the periodontal disease classication should be based on etiology. We have argued that the signs and symptoms of periodontitis are widespread and universal and that their distributional characteristics point to a complex disease etiology involving many smaller risks in a myriad of combinations. It is therefore not feasible to continue the essentialistic hankering after periodontal disease classications based in etiopathogenetic considerations. Rather, a nominalistic approach should be adopted. In this approach, a disease name is no more than a label issued to a group of individuals that share certain observable dening characteristics. The name chosen to label the group (e.g., periodontitis) is just a brief statement of the common abnormality by which the particular group of patients with periodontitis can be identied. Importantly, the disease periodontitis is not restricted to encompass only those signs and symptoms that are made explicit by the label (the disease name), but encompasses the whole range

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of signs and symptoms that may be observed in periodontitis-affected subjects. The number of disease entities necessary and sufcient for a useful periodontal classication should be determined by documented differences in the management of each entity (38, 103). A classication system involving many different disease entities is not relevant as long as the parameters of their management, that is, their treatment and prognosis, remain the same (38). The diagnostic distinction between two phenotypes makes little sense until it has been demonstrated, beyond reasonable doubt, that these two phenotypes are most successfully treated using different treatment modalities or have different prognoses after the same therapy. It follows that labels (and hence the classication) should be based on this-disease-needs-this-kindmanagement-and-control considerations, as has also been advocated for dental caries (104). Interestingly, some of the previous periodontal classication systems have had nominalistic features. For example, the distinction between prepubertal, juvenile, and adult periodontitis is nominalistic in the sense that age is an observable characteristic. Moreover, the distinction between prepubertal, juvenile, and adult periodontitis was also underpinned by notions of different treatments for these entities. Generalized prepubertal periodontitis was considered largely intractable necessitating the extraction of all erupted teeth followed by an edentulous period to prevent infection of nonerupted teeth (105). Repeated occlusal grinding was considered an element in the treatment of juvenile periodontitis (106), whereas adult periodontitis could be treated by conventional local periodontal therapy. However, the evidence for the different treatment modalities was anecdotal, and the treatment approaches for the different entities have since undergone many changes. In our view, the only new information that warrants a change of the disease classication system is new knowledge regarding the prognosis and the better treatment of identiable patient groups. All other knowledge should be kept out of the classication until new research has unequivocally demonstrated the utility of different treatment modalities or existence of different prognoses for new categories. This viewpoint is consistent with a nominalistic disease concept, but at variance with the essentialistic concept, which unfortunately continues to underpin most activities in the periodontal eld (38, 103, 107).

Periodontal destruction is a condition that comes in all sizes. Clinical attachment level loss forms a continuum in the population ranging from the barely perceptible destruction in a single site of which we need not take any notice to generalized and severe destruction affecting all remaining teeth in the dentition. Age confounds the picture, and what is severe and highly unusual among younger subjects may be mild and common among a senior. These characteristics force us to somehow incorporate age and to acknowledge the continuum of extent and severity of lesions in the classication of periodontitis. This was indeed achieved in the only truly nominalistic periodontal disease classication system so far proposed (8). While this classication system fullls many of the desirable properties of an ideal classication system, it is not supported by evidence for the need from a therapeutic point of view to distinguish the many categories involved. As it is clearly desirable that a classication system rests on evidence rather than personal idiosyncrasies, we encourage research linking clinical phenotypes to the response to specic therapeutic approaches.

Acknowledgements
This study was partially supported by a grant from the Danish Medical Research Council (Copenhagen, Denmark). The authors declare that there are no conicts of interest in this study.

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