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D i s c u s s i o n :N a t u ra i h is to ry o fp e r io d o n ta i d is e a s ein m a n

John C. GreeneProfessor and Dean, School of Dentistry,University of California, San Francisco, CUSA

It is a distinct privilege to have the op-portutiity to comment on Dr. HaraldLoe's paper. First, I want to congratu-late him and his co-workers on makingyet another significant contribution toour understanding ofth e natural historyof periodontal disease in man. Theyhave rnade major contributions throughtheir series of publications involving a

longitudinal study of the population inSri Lanka that we've just heard about,and a comparison group in Norway.

The paper today gives us a picture ofthe changes in attachment loss over a15-year period in a very unique popu-lation - one that has had no dental in-tervention, either personal or pro-fessional. There has beeti no brushing,and calculus that formed remained inplace during the study period. Thatthere are sizable variations in the pro-gress of the disease in these circum-stances is particularly significant. Ofspecial interest in today's presentationis the divisioti ofth e population into the3 sub-groups according to the rate ofdisease progression, and the oppor-tunity to make comparisons amongthem. However, as valuable and as in-triguing as these data are - I have twofairly major conerns about our in-terpretation of them:1. Sample size. Unfortunately, attrition

has taken a heavy toll in the initialgroup - only 161 were present atboth the first and last examination,and of these only 88 were present forall of the exams.

When this group is divided into the 3subgroups, the num bers get pretty small especially when the 2 groups of ex-tremes combined comprise less than2 0 % of the total. Additionally, spread-ing this small sample over specific agesfrom 15 to 40 increases the number ofproblems. Great caution should be usedwhen interpreting mean values based on

so few individuals. Detailed analyses ofthese data will present some interestingstatistical challenges as one tries to learn

2 . The unusually high prevalence of at-tachment loss at an early age. 80% ofthose at age 15 and 100% at age 20years were found to have significantattachment loss. One has to wonderwhether this is an unusually suscep-tible population, a different disease,a result of different or more virulentmicro-organisms than are commonly

seen elsewhere, or whether th is reallyis the normal picture one finds whenthe disease is left undisturbed. Inother words, perhaps Dr. Loe haspresented a picture ofth e natural his-tory of periodontal disease and thatwhat is observed in other popu-lations where the process is disturbedby personal and professional inter-vention is theunnatural history of thedisease. Another possibility is thatthe naturai history for Sri Lanka isdifferent from other populations.

Further studies to explore these ques-tions would appear to be of greatvalue.

While I have some other commentsabout the study itself, I would like todo so in the broader context ofth e orig-inal title of this section of the confer-ence, that is the Epidemiology of Peri-odontitis:

On The Epidemiology of Periodonfitis

Reviews of the epidemiology of peri-odontal disease(s) most often deal withgingivitis and periodontitis as a con-tinuum in such a way that data cannotbe disaggregated for examination ofthose that are specific to the deeperstructures. Thus, the dental scientificliterature contains limited informationabout the epidemiology of periodontitisas distinguished from gingivitis or the"periodontal diseases". Investigatorshave failed to agree on a single defi-nition of periodontitis, or on what con-

stitutes clinical evidence of its presenceor suitable gradations of its severity.They have used a variety of indicators

3 mm or more; loss of epithelial atment beyond the CEJ; loss of alvbone visible on radiographs; preseninflammation in the deeper structurdetermined by bleeding on periodprobing, and breaks in the epithelitachment, labeled "obvious periodpockets" in the periodontal index (sell 1956).

As far back as 1918, a report oepidemiological study of periodoappeared in the dental literature (B1918). Using radiographs to detecveolar bone loss among 600 "noradults over 20 years ofage , Black fothe % of persons affected to range f13 % among the youngest to 88%those over 50 years of age. (TablSeveral studies ofth e prevalence ofpodontitis have appeared in the literasince that time. (Among these are Bing and others 1953, Marshall-Daa l. 1955, Bosert & Marks 1956, Set al. 1959, Ormes & Sheridan 1Hughes et al. 1982, Douglass e1983). Examples of some of these fings are shown in Fig. 1.

Although the absolute values forgiven age group vary tremendously,obvious from these data that the prlence of periodontitisis low in the youadult and that it increases with From these data, it appears that prevalence of periodontitis in the

can be estimated conservatively toapproximately 10% at age 20, ab3 5 % at the age 50-55% at the ageThese US prevalence estimates neebe contrasted with the Sri Lankan presented today by Dr. Loe where

Table 1. Alveolarmal adults

Age group

20-24

25-2930-3940-49

bone loss among 600

% affected

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42 Greene

100-.

90 -

80 -

' " -

60-

50 -

1 -30 -

20 -

10 -

Douglolf (1W1.T4)

Fig. 1 Prevalence of periodontitis by age (se-ected US studies).

Das Vorkommen der Parodontitis in den Le-bensaltern (Ausgewahtte Studien aus denUSA).

Prevalence {"/o atteint) de la parod ontite sui-vant l'age (choix d'etudes aux Etats-Unis).

prevalencewas

80% at age15

and 100%at age 20.Several qualifications to the preva-

lence data shown in this figure shouldbe mentioned, however. The onlystudies of this group that were based ona national probability sample were theones from the National Center forHealth Statistics reported by Douglasset al. (1983). These studies relied on theuse of Russell's original periodontal in-dex, which does not m ake use of radio-graphs or a periodontal probe, and thusprobably underestimates periodontitis.The study by Hughes et al. (1982) wasfrom a carefully drawn household sam-ple from the state of North Carolina.However, for simplicity, the data fromthe study shown here include only whitemales. Prevalence data for non-whitemales and females were somewhat high-er and for white females the values wereslightly lower. Finally, these estimatesfor the US are not based on current dataand the situation may have changed bynow. These and other populationstudies also demonstrate increased se-verity with advanced age. More teethare affected and m ore attachm ent is lostas a population ages.

Let us now examine some of the fac-tors that appear to influence the preva-lence of periodontitis. First is age.Whether the association between peri-odontitis and age is a result ofthe agingprocess, or represents the destructionthat takes place in response to increasedlength of exposure to etiologic factors,or a combination of these two can beresolved only by further investigation.However there have been some reports

creased age. For example, Hansen re-ported finding gingivitis and loss of at-tachment to be more associated withbiologic age than chronologic age (Han-sen 1973). Holm-Pedersen et al. studiedexperimental gingivitis in young andold. They found that gingivitis de-veloped more rapidly and became more

severe in the older group (Holm-Peder-sen et al. 1975).Another possible factor is gender.

Just as in the case of gingivitis, reportsin the literature show a pa ttern of slight-ly greater prevalence and severity ofperiodontitis among men than amongwomen of the same age in the same orsimilar populations. Numerous studiesalso report better oral hygiene levels inwomen than in men. Thus, the differ-ences probably are due to differences inthe amount and characteristics ofplaque rather than biologic differences.

Studies by Lindhe et al. (1975) andSaxe etal. (1967) workers using the bea-gle dog have demonstrated that allow-ing plaque to accumulate on the teethfor long periods of time can result in lossof alveolar bone, and that this process isinhibited when the teeth are kept clean.Similarly, studies in humans by Suomiet al. and Loe et al. have demonstratedthat attachment loss takes place morerapidly in individuals whose mouths are

not kept as clean than it does in thosewhose mouths are kept cleaner (Suomiet al. 1971, Loe et al. 1978).

Longitudinal studies conducted inNorway and Sri Lanka by Loe and co-workers provide an example of the as-sociation found between advanced dis-ease and oral hygiene status (Loe et al.1978). The Norwegian population hadunusually good oral hygiene, whereasthe opposite was true for the populationexamined in Sri Lanka. While there

were other differences between the twopopulations, significant differences inperiodontal pocket measurements wereobserved initially and over time. TheNorwegian population fared better inboth respects; attachment loss was near-ly 3 times greater in the Sri Lankangroup. These findings are consistentwith several cross-sectional populationstudies and the longitudinal clinical in-tervention study conducted by Suomiand others (Suomi et al. 1971).

For a number of years it has beenassumed that gingivitis and periodonti-tis are closely associated, that one must

d th th d th t if i i iti

100

90

80

t 20-

TIIr1~"T~T Ir

Age Groups

from: MunholJ Ony er ol. [ 1955;

Fig. 2 Prevalence of periodontal disease.Das Vorkommen der Parodontalkrankheit Erkranktes Zahnfleisch, keine Knoebeteiligung. Chronisch destruktive P arodtalkrankheit.

Prevalence (% du groupe examine) de la ladie parodontale suivant le groupe d'age teinte gingivale sans atteinte osseuse , madie parodontale chroniquc destructrice )

cent years, this model of diseaseitiation and progression has been cainto question (Page & Schroeder 19That it persisted so long is undoubtdue to early reports of the differeages at which the prevalence ratethese 2 conditions reach signifilevels (Fig. 2). The fact that these show gingivitis to be very prevalenchildren by the early teens, while odontitis becomes common sevyears later, suggests that gingivitis precurser of periodontitis.

This study also shows that almosadults examined had both gingivitisperiodontitis. However, not all ofdata from this study are consistent this close association. For examplsome age groups as many as 15% reported to have chronic destruperiodontal disease or periodonwithout gingivitis at the time ofstudy. A study by M orrison et al. (1

reports that the severity of gingiduring periodontal maintenance tpy does not appear to have a sigcant impact on maintenance of thelial attachment levels.

In a recent report of a 3-year ltudinal study, Listgarten et al. (1found no significant progression ofpodontal destruction despite a relathigh prevalence of gingivitis. In arecent report by Reddy et al. (1from a high fluoride area of Southrica (2-3 ppm), little periodontastruction was found among adulspite of large amounts of plaque

hi h l f i

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Discussion

some respects and like the Norwegiansubjects in others. Plaque scores werehigh similar to those in Sri Lanka, whileattachment loss was low as in Norway.The author postulated that fiuoridelevels or genetics may have played a rolein these findings.

The paper presented here today by

Dr. Loe provides yet another im portantpiece of information that helps tocharacterize the association betweengingivitis and periodontitis. In his study,3 subgroups of the Sri Lankan popu-lation were identified based on loss ofattachment in interproximal areas andtoo th mortality rates. The three dispar-ate groups characterized by (1) rapidprogression, (2) moderate progression,and (3) no progression of periodontaldestruction did not differ according tothe ir gingivitis scores. This raises severalquestions. It could be that examinationof data site-by-site over time might yielda different result. Perhaps the tra-ditional method for measuring severityof gingivitis is invalid, or maybe thereis no association between gingivitis se-verity and continued attachment lossonce started.

Nevertheless, epidemiological dataavailable today do not provide a basisfor assuming that gingivitis and peri-odontitis are unrelated. They do sug-gest, however, that (1) gingivitis doesnot always progress to initiate peri-odontitis, (2) gingivitis does precedeperiodontitis and (3) that once peri-odontitis is initiated, gingivitis is notnecessary for the destruction of thedeeper periodontal structures to con-tinue although they are most oftenfound to co-exist.

It has already been pointed out thatperiodontitis is distributed unevenlyhroughout the mouth and that it tends

to be bilaterally symmetrical. The inter-proximals of first molars in both archesare the tetth which most commonlyshow evidence of periodontal destruc-ion , and the premolars and cuspids areeast commonly affected (Loe et al.1978, Page &. Schroeder 1982).

When epidemiological data are exam-ned as group data ranging over time, it

appears that attachment loss occurs ina linear fashion at rates up to about 2.5mm per year (Becker & others 1979).However, as Dr. Listgarten has dis-ussed earlier, when longitudinal datare analyzed by site or by individual,

different picture sometimes emerges

it now appears that there are periods ofacute activity and relative quiescence,whether or not treatment takes place(Hirschfeld & Wasserman 1978, Ax-elsson & Lindhe 1978, Selikowitz 1981,Goodson et al. 1981, Buckley & Crow-ley 1984). These new insights into thenatural history of the disease have en-

gendered new concepts of destructiveperiodontitis which we will hear moreabout later (Socransky et a l. 1984). Theconcept of repeated a ttacks ofacute epi-sodes interspersed with periods of re-mission gradually taking their toll overtime has considerable support in currentdata.

Though their methods vary greatly,the body of published studies bearingon the epidemiology of periodontitisprovide the basis for drawing some con-clusions of significance to the design

and analysis of periodontal ctrials.1. The definition and criteria for

nosis of periodontitis still laccision and uniformity.

2. Periodontitis is uncommon age 15 and becomes more preand severe with advancing age

gingivitis is already very commchildhood and remains at high among adults.

3. The prevalence and severity oodontitis varies from one popugroup to another and tends more pronounced in males thfemales at any given age. Thesferences are associated with ences in plaque levels.

4. The rate of progression of detive periodontal disease appeavary by population, individua

ReferencesAxelsson, P. & Lindhe, J. (1978) Effect of controlled oral hygiene procedures on ca

periodontal disease in adults.Journal of Clinical Periodontology 5, 133-151.Becker, W., Berg, L. & Becker, B. E. (1979) Untreated periodontal disease: a long

study. Journal of Periodontology 50, 234-244.Belting, C. M., Massler, M. & Schour, I. (1953) Prevalence and incidence of alveolar

in man. Journal of American Dental Association 47, 190-197.Black, A. D. (1918) Roentgenographic studies of tissue involved in chronic mouth in

Dental Summary 38, 924-932.Bosert, N. A. & Marks, H. H. (1956) Prevalence and characteristics of periodontal di

12,800 persons under periodic dental observation.Journal of the American Dental Aation 52, 429-442.

Buckley, L. A. & Crowley, M. J. (1984) A long itudinal study of untreated p eriodon tal Journal of Clinical Periodontology 11, 523-534.

Douglass, C. W., Gillings, D., Sollecito, W. & Gammon, M. (1983) National treprevalence and severity of the periodontal diseases.Journal of the American Dental Aation 107, 403^12.

Go od son , J. M., Tanner, A. C. R., Haffajee, A. D. & Socra nsky, S. S. (1981) EvideEpisodic Periodontal Disease Activity.Journal Dental Research 60 (Supp. A), 387.

Hansen, G. C. (1973) An epidemiologic investigation of the effect of biologic aging breakdown of periodontal tissue.Journal of Periodontologv 44, 269-277.

Hirschfeld, L. & Wasserman, B. (1978) A long term survey of tooth loss in 600 periodontal patients.Journal Periodontology 49, 225-237.

Holm-Pedersen, P, Agerbaek, N. & Theilade, E. (1982) Experimental gingivitis in you

elderly individuals. Journal Clinical Periodontology 2, \A~1A.Hughes, J. T, Rozier, G. R. & Ramsey, D. L. (1976-77)Natural history of dental diseasNorth Carolina, pp. 39-50. Durham: Carolina Academic Press.

Lindhe, J., Hamp, S. E. & Loe, H. (1975) Plaque induced periodontal disease in BeaglA 4-year clinical, roentgenographical and histometric study.Journal Periodontal Rese10, 243-255.

Listgarten, M. S., Schifter, C. C. & Laster, L. (1985) Three-year longitudinal study periodontal status of an adult population with gingivitis.Journal of Clinical Periodonto12, 225-238.

Loe, H.; Anerud, A. & Smith M. (1978) The natural history of periodontal disease iJournal of Periodontology 49, 607-620.

Marshall-Day , C . D., Stephens, R. G. & Quigley, L. F.: (1955) Periodontal disease: preand incidence. Journal of Periodontology 26, 185-203.

Morriso n, E. C , RamQ ord, S. P , Burgett, F. G., Missle, R. R. & Schick, R. A. (198

significance of gingivitis during the maintenance phase of periodontal treatment.Jouof Periodontology 53, 26-30.

Ormes, W. M. & R. C. Sheridan (1965) Prevalence of periodontal disease determined

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Greene

and time period. The rate of pro-gression is affected by the presenceand quality of microbial plaque.Variations in host response tosubgingival microbial deposits un-doubtedly influence the destructiveprocess.

The association between gingivitis

and periodontitis remains to be clari-fied. One cannot assume with cer-tainty that all periodontitis is pre-ceded by gingivitis (although it prob-ably is) , or that gingivitis is necessaryfor the destructive processes to con-tinue once initiated.

Reddy, J., Parker, J. R., Africa, C. W. & Stephe, L. X. G. (1985) Prevalence and sevperiodontitis in a high fluoride area in South Africa.Community Dentistry Oral Epology 13, 180-120.

Russell, A. L. (1956) A system for classifying and scoring for prevalence surveys of perdisease. Journal of Dental Research 35, 350-359.

Saxe, S. R., Gre ene, J. C , Boha nnon, H. M . & Vermillion, J. R. (1967) Oral de bris, and periodontal disease in the Beagle dog.Periodontics 5, 217-225.

Schei, O., Waerhaug, ]., Lovdal, A. & Arno, A. (1959) Alveolar bone loss as relatedhygiene and age. Journal of Periodontology 30, 7-16.

Selikowitz, H., Sheiham, A . D. & Williand, G. M.; (1981) Retrospective long itudinaofthe rate of alveolar bone loss in humans using bite-wing radiographs.Journal of CliPeriodontology 8, 431-432.

Socransky, S. S., Haffajee, A. D., Good son, J. M . & Lindhe, J. (1984) New concdestructive periodontal disease.Journal of Clinical Periodontology I I , 21-32 .

Suomi, J. D., Greene, J. C , V ermillion, J. R., Doyle, J., Cha ng, J. J. & Leath erw oo(1971) The effect of controlled oral hygiene procedures on the progression of perdisease in adults; results after third and final year.Journal of Periodontology 42, 152

G e n e r a l d is c u s s io n

DR. LISTGARTEN: I don't think thateriodontitis can progress in the ab-ence of inflammation, although the in-ammation might not be visible in theingivitis when the tissues are examinedlinically. So, if one is going to talkbout gingivitis, one can either talkbout gingivitis as inflammation of theingiva, which may or may not be visualo the naked eye, or one can talk aboutingivitis in the clinical sense as redums. There's a difference between thewo and that difference should be keptn mind when statements are made thateriodontitis may progress in the ab-ence of gingivitis and can, but not inhe absence of inflammation.

DR. MARTHALER: How do teethet lost in Sri Lanka? Dr. Loe has usedhe term exfoliation. I would like to askre they using folklore practices of ex-racting teeth?

DR. LOE: The teeth get to be un-omfortable for the individual patientnd they just remove the teeth with theirwn fingers. Of course some of themre accidentally chewed up, but there is

no other way of taking care of it. Thiss the practice in those tea plantations.

DR. PAGE: Harald, I find your studybsolutely fascinating, and I obviously

want more information - I think all ofus do. I have one particular questiono ask. In this group of people, there's

probably a fair amount of in breeding I

progress and the 8% that have the dis-ease?

DR. L O E :I think this is a fascinatingsituation. We have absolutely no pedi-gree for any of these patients; there is alot of work to be done here. It is aconfined situation. There is a popu-

lation in one square mile. I think thatJohn Green's comment was very fair.His point about the lost follow-upshould be tempered, though, with thedesign of the study, where you clearlysee that they're working in differentgroups, into the same age groups andrunning over, all the time. I think thisstrengthens the study. It is somewhatproblematic in the older end of thestudy and as we go along we'll have tosee to it that we retain these people. But

the major loss occurred in 1974, 1975when there was a relocation programthat we didn't know about. That hascome to a halt and since that time wehaven't really had much. So I have afeeling tha t whatw e have at the momentis what we're going to have in the nextfew years and I think that's probablypromising.

DR. GREENE: Is there a differentdisease in that population from whatwe're seeing in the western world?

DR. L O E : I think we have a naturalprogression of disease here. No, I don'tthink there's a different disease. They

fiuctuations in periodontitis in ociety may have many causes ansons, one of them being the tremehygiene that we have and at thetime a faulty hygiene in some areathat's why you get some attacareas moving and others not. But

population, it is just growing stonto the apical areas of all teeth.are many other reasons, not to ggeneral, on the basis of studyinpopulation only, but this is one Somebody else will have a stusome other populations and whwhole thing comes together, it's poto generalize.

DR . IMR EY: I'd like to congraboth speakers for taking advantthis marvelous experiment in nat

studying this Sri Lanka popu latiodiscussions tended to relate prito differences between populatiohygiene and plaque and gingivhave a two-part question. Part L o e , if you could enlighten us ondifferences between the popuwith respect to diet and envirowhich might be expected to infthe disease and, secondly, particto Dr. Greene, if you could helpterms of understanding the diffe

between the Marchall Day studthe Belting study, both of whichextraordinary studies as I unde

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