Bolsa o Recesion de Acuerdo Al Fenotipo.hujoel Cruz Selipsky Saver.2005

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Abnormal pocket depth andgingival recession as distinct

phenotypesP H I L I P P E P. HU J O E L , JO A N A C U N H A -CR U Z , H E R B E R T S E L I P S K Y &BA R R Y G. SA V E R

Abnormal pocket depth and pocket-free gingival re-

cession have been recognized as two separate peri-

odontal phenotypes (albeit under different names) at

least since the 18th century. With abnormal pocket

depth referred to here as destructive periodontal

disease the alveolar bone loss is associated with

abnormally deep periodontal pocketing, which canbe

associated with signs of clinical inflammation and

periodontal abscesses. With pocket-free gingival

recession which we will refer to as periodontal atro-

phy the alveolar bone loss is associated with gingival

recession andoftenpresents without signs of clinical

inflammation. In the 1970s, it was decided to label

these two clinically distinct periodontal phenotypes as

one and the same disease, namely chronic periodon-titis, under the hypothesis that both are caused by

plaque. After 30 years, this speculation, and therefore

the rationale of the diagnostic classification, has re-

mained unsubstantiated. The evidence for plaque

contributing to either has remained surprisingly

sparse and contradictory; indeed, available evidence

suggests that distinctive etiologies are responsible for

eachphenotype. Furthermore, destructive periodontal

disease and periodontal atrophy have different treat-

ments and therefore economic implications, different

anthropological and comparative medicine features,

and possibly different outcomes in terms of quality oflife and tooth loss.

The continued failure to distinguish destructive

periodontal disease from periodontal atrophy may be

a rate-limiting step in understanding the incidence,

etiology, prognosis, and treatment of the different

periodontal phenotypes. We will suggest that both

phenotypes should once again, after a 30-year hiatus,

be recognized as distinct entities and we will also

explore criteria to define when pockets are abnormal.

Destructive periodontal diseaseand periodontal atrophy: two

distinct phenotypes

The recognition of destructive periodontal disease

and periodontal atrophy as two distinct phenotypes

prior to 1970 was recently summarized by Page &

Sturdivant (36). Briefly, since the publication of the

first dental textbooks in the English language in the

18th century (26), two distinct clinical conditions of

alveolar bone loss were recognized:

periodontal atrophy, where the gums retain a very

healthy aspect and are quite free of pain and

inflammation, and yet will gradually recede (18)

; destructive periodontal disease with the presence

of deepened periodontal pockets and underlying

bone loss (17).

The distinct clinical signs and symptoms of these

two periodontal phenotypes have been described in

detail in older clinical textbooks (see (19)), and con-

tinue to be described as diseases with distinctive

etiologies in at least one oral pathology textbook (9).

In addition to striking phenotypic differences,

destructive periodontal disease and periodontal

atrophy differ with respect to treatments and there-

fore economic implications, suspected causes, andanthropologic and comparative medicine features.

The treatments and the economics ofperiodontal atrophy and destructiveperiodontal disease are different

According to one estimate, 90% of the periodontal

procedures performed today would be eliminated

if periodontal pocketing, the cardinal sign of

22

Periodontology 2000, Vol. 39, 2005, 2229

Printed in the UK. All rights reserved

Copyright Blackwell Munksgaard 2005

PERIODONTOLOGY 2000


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destructive periodontal disease, disappeared (39).

The reasons are twofold. Firstly, treatment guidance

plans established by insurance companies typically

require a certain number of teeth with pockets dee-

per than 4 mm prior to approval of the most widely

used periodontal procedures such as scaling and root

planing. Secondly, the raison detre of most perio-

dontal treatments (other than mucogingival or

clinical crown lengthening) is the presence of perio-dontal pockets. Periodontal pocket reduction or

elimination surgery can only be performed if pockets

are present in the first place. Local antimicrobial

therapies are only approved for use if periodontal

pockets are present in which to put the medication.

For instance, the US Food and Drug Administration

(FDA) approved local drugs for the reduction of

pocket depth in patients with adult periodontitis; no

pockets, no FDA-approved local treatments. Simi-

larly, the presence of periodontal pockets remains,

despite the rapid decline in the smoking-associated

epidemic of destructive periodontal disease (24), an

important economic driver of the periodontal speci-

alty. If nothing more, the economic implications of

abnormal pocket depth dictate that its incidence

should be tracked as a distinct clinical entity (see

Fig. 1).

The recent US nationwide drop in the number of

periodontal treatment procedures (5, 39) aimed at

periodontal pockets suggests that the incidence ofdestructive periodontal disease among the high

socioeconomic status group has been dropping dra-

matically. In contrast, the incidence of periodontal

atrophy may be increasing due to an increasingly

aging population and increased tooth retention. Yet,

both entities have been grouped together as a loss of

attachmentdisease and called chronic periodontitis.

Not having the ability to track these two opposing

trends increased incidence of periodontal atrophy

and decreased incidence of destructive periodontal

disease led to an inability to track the pocket-driven

Fig. 1. A 65-year-old dental professional with good plaque

control and no periodontal pocketing present but with

3 mm + palatal and lower buccal recessions. Why diagnose

this person with chronic periodontitis whentreatment plan

guidelines and the Food and Drug Administration indicate

that this patient is not eligible for chronic periodontitis

procedures (e.g. scaling and root planing, local antibiotics,

pocket reduction surgery). To understand the incidence,

etiology, and prognosis of the deepened pocket cases that

drive 90% of periodontal treatment utilization, we need to

distinguish abnormal periodontal pocketing (not pictured)

from pocket-free gingival recession (pictured here) and not

group them together as chronic periodontitis merely be-

cause they both exhibit attachment loss.

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Abnormal pocket depth and gingival recession


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economics and manpower needs for periodontal

needs.

The etiologies of destructive periodontaldisease and periodontal atrophy may bedifferent

Emerging epidemiologic evidence suggests that

destructive periodontal disease and periodontalatrophy differ with respect to their etiologies. Osteo-

porosis (27, 28), aging (14), continuous eruption (4,

14), aggressive oral hygiene procedures (36), and

anatomic periotypes have been suggested as poten-

tial causes of periodontal atrophy. In contrast, studies

in private periodontal practices that focus on the

treatment of periodontal pockets (destructive perio-

dontal disease) indicate that smoking is a primary

driver of destructive periodontal disease (20, 21).

Interestingly, smoking-induced destructive perio-

dontal disease can present with an absence of

bleeding and gingival tissues with an anemic

appearance, bringing into question whether it is

appropriate to label destructive periodontal diseases

as an inflammatory disease (i.e. is the term perio-

dontitis appropriate for describing cases of abnormal

periodontal pocketing when no clinical signs of in-

flammation are present?). Another possible driver of

destructive periodontal disease that should be men-

tioned is diabetes (8).

The biological basis for claiming that both

destructive periodontal disease and periodontal atro-

phy have plaque as the common etiologic factor hin-ges on identifying epidemiologic evidence that plaque

causes both destructive periodontal disease and per-

iodontal atrophy, and refuting existing evidence that

distinct etiologies are responsible for distinct perio-

dontal phenotypes. Since neither type of evidence has

been procured over the past 30 years, the current

plaque-driven diagnostic classification of periodontal

diseases remains mostly supported by a biological

assumption, largely modeled on experimental gingi-

vitis, and not by epidemiologic studies that controlled

for essential factors such as cigarette smoking, dia-

betes, socioeconomic status, and even age.

The anthropologic and comparativemedicine features of destructiveperiodontal disease and periodontalatrophy are different

Clarke & Hirsch (11) have long suggested, based on

anthropologic and comparative medicine evidence,

that destructive periodontal disease and periodontal

atrophy are two distinct periodontal phenotypes and

that the failure to distinguish between these two

phenotypes lies at the root of fundamental misun-

derstandings of the etiology and the historical disease

prevalence estimates of destructive periodontal dis-

ease. Studies of skulls from 23 different population

groups around the world suggest that age-related

alveolar bone loss is a normal physiological process

(12), an observation which is at odds with currentthinking that any attachment loss is pathologic and

the result of an inflammatory process caused by

plaque. Similar findings regarding an age-related

wasting of the alveolar process have been reported by

other investigators (4) and this finding has been

extended to great apes (15). Studies on prehistoric

skeletal remains distinguished alveolar resorption or

alveolar recession from infrabony pockets because of

the distinct phenotypes and suspected etiologies (13).

These different reports indicate that anthropologic

studies, comparative medicine studies, and studies

on prehistoric skulls distinguish between destructive

periodontal disease and periodontal atrophy.

Discriminating between periodontal atrophy and

destructive periodontal disease may have a signifi-

cant impact on the study of the epidemiology of

periodontal diseases. Periodontal atrophy is a com-

mon clinical condition; the majority of individuals

have some gingival recession after the age of 30 years

(for a pronounced example, see Fig. 2). If this pocket-

free recession, which can be labeled as periodontal

atrophy, is referred to as destructive periodontal

disease, we end up with the anomalous situationwhere close to 100% of the individuals in national

surveys are regarded as having signs of chronic

periodontitis.

Is periodontal atrophy a disease?

Currently, periodontal atrophy is labeled as chronic

periodontitis (defined by attachment loss), and is

therefore considered a disease. But is this type of

pocket-free attachment loss really a disease? Do the

individuals shown in Fig. 1 and 2 have a disease, ordo they simply represent two examples of periodon-

tal changes equivalent to hair loss and wrinkles?

These questions are important, since the prevalence

of periodontal atrophy (a nondisease?) currently may

drive to a large extent the considered prevalence of

so-called chronic periodontitis.

Defining disease is a complex issue. Are meno-

pause and baldness diseases as the FDA suggests, or

are they a reflection of normal aging? Can mountain

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Hujoel et al.


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climbing in this genomic era be considered a disease,

or is it normal risk-taking behavior (6)? Are crooked

teeth a disease, or do they reflect normal human

variability (38)? Answers to these questions are cul-

ture- and era-specific and depend on whose defini-

tion of disease is used. Disease can be defined as the

sum of abnormal phenomena displayed by a group of

living organisms in association with a specified

common characteristic or set of characteristics by

which they differ from the norm of their species in

such a way as to place them at a biological disad-vantage(40). In addition, practical factors may come

into play in deciding what disease is, including

whether there is a laboratory test for the condition,

whether there is a treatment available, whether the

diagnosis is billable, and whether there is a major

lobby advocating disease status. For instance, normal

consequences of aging, such as hair loss and wrinkled

skin, can become treatable diseases once profitable

treatments appear.

Within this context, is periodontal atrophy a

disease? If a young individual is at a reproductive

disadvantage because of periodontal atrophy, anargument for disease status could be made. Some

textbooks have considered that recession of the gin-

giva is a normal physiological age-related process (19,

34, 41). Given that national representative samples of

the US population indicate that attachment loss is

almost universal after the age of 30, that attachment

loss increases with aging (1), and that the wear-and-

tear of aging affects every organ system in the human

body (30), it appears logical to consider the possi-

bility that periodontal atrophy is a normal age-related

process. Further investigation needs to determine

whether, if certain conditions do exist, periodontal

atrophy should be considered a disease.

Diagnosing abnormal pocket depthin destructive periodontal disease

Clinical probing depth is the most obvious marker for

diagnosing destructive periodontal disease; it is sim-ple to determine, it is a clinical measure that is in use

worldwide, it is predictive of tooth loss, and dee-

pened pocket depths been considered the cardinal

measure of destructive periodontal disease for cen-

turies in humans and more recently in mammals

(35). Abnormal pockets can de defined using nor-

mative or arbitrary values, risk-based reference val-

ues, or treatment-based reference values.

Normative or arbitrary values todiagnose abnormal pockets

Diseases are sometimes defined based on normative

reference values. Fever can be defined as an oral

temperature greater than 37.7 C, which is the 99th

percentile of the maximum oral temperatures in

healthy persons (32). The normal heart rate is defined

as ranging between 55 and 95 beats per minute,

which corresponds to the range found for 95% of

healthy individuals (42). Children who are in the

bottom first percentile or the fifth percentile of the

Fig. 2. A 20-year follow-up (A: age 23 years, B: age

43 years) in a dental professional with progressive gingival

recession including furcation exposures, but no perio-

dontal pockets and a history of good plaque control.

Diagnostic classification systems for the last 30 years have

been based on the premise that this individual with

pocket-free gingival recession has a disease by the name

of chronic periodontitis, and that both abnormally deep

periodontal pocketing and pronounced gingival recession

have one and the same etiology plaque. This assumption

remains up to this day unsupported by epidemiologic

evidence. We raise the question whether the above con-

dition can be called a disease, let alone an inflammatory

disease, and suggest that epidemiologic and clinical re-

search should determine the etiology, prognosis, and

possible treatments for this distinct clinical phenotype

(which we label periodontal atrophy).

25



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growth chart may be labeled as diseased with short

stature and in need of growth hormone therapy (7).

If the normal periodontium is postulated to have

no pocket depths deeper than 3 mm, then arbitrary

values could be used to define destructive perio-

dontal disease. For instance, any individual with

three pockets 5 mm or deeper could be classified as

having destructive periodontal disease. Currently, all

definitions of periodontal diseases are arbitrary,which should be cause for alarm. Normative values

may be superior to arbitrary values. Normative values

could be based on parametric or nonparametric

percent cut-off values. For instance, the 97.5th per-

centile of the age-specific number of pockets deeper

than 5 mm could be used to define destructive

periodontal disease. Based on the NHANES III data, a

28-year-old individual with two pockets deeper than

5 mm could be diagnosed as having destructive

periodontal disease, whereas five periodontal pockets

deeper than 5 mm would be required for that diag-

nosis in a 58-year-old individual (Table 1).

Diagnoses based on normative or arbitrary cut-

offs result in normative or arbitrary disease pre-

valence levels, regardless of the distribution of

underlying risk factors. It would not matter whether

1% or 95% of the population smoked three packs of

cigarettes a day for 30 years the prevalence of

destructive periodontal disease would remain equal

to the selected cut-off value. If all human diseases

were defined based on a 5th percentile cut-off value,

the prevalence of all diseases would be equal to 5%:

for example, 5%

of the population would be too

short, 5% would have diabetes, and 5% would have

a fever.

Diagnoses based on percentile distributions can

become disconnected from clinical realities. In such

cases, the number of persons classified as nondis-

eased has potentially no relationship to the number

of patients with adverse outcomes such as tooth loss,

periodontal abscesses, or difficulty in chewing.

Complex chronic diseases such as diabetes, coronaryheart disease, and destructive periodontal disease

have too much natural variability to allow a suc-

cessful definition of disease based on arbitrary or

normative values.

Risk-based reference values to diagnoseabnormal pockets

Disease can be defined based on the presence of an

attribute that substantially increases the risk for an

adverse health outcome. A body-mass index above 28

is reflective of a diagnosis of obesity, as it carries an

increased risk of morbidity and mortality (43). A

fasting plasma glucose level greater than 126 mgdl

(7.0 mmoll) was selected as a diagnostic criterion for

diabetes because it was associated with a steep in-

creased risk of retinopathy (2). A blood pressure

above 14090 can be used as a diagnosis of cardio-

vascular disease since it carries an increased risk for

stroke and myocardial infarction (3). The choice of

the reference value for the diagnosis of disease is

typically based on the level of the surrogate marker

where a steep increased risk for adverse health out-comes is present. The cut-off is still somewhat arbi-

trary, but is connected to clinical realities in terms of

the risk of adverse health outcomes.

A risk-based diagnosis of destructive periodontal

disease requires the conduct of longitudinal perio-

dontal studies, where pocket depth is related to the

risk of adverse outcomes such as tooth loss. The risk

for all-cause tooth loss associated with the maximum

probing depth per tooth was plotted for a cohort of

patients under periodontal specialist care (Fig. 3).

The figure suggests that a pocket depth of 6 mm

could be a diagnostic marker for destructive perio-dontal disease because a distinct increased risk for

tooth loss is associated with pocket depth values

6 mm or deeper (25).

Risk-based diagnosis of chronic diseases may,

however, do more harm than good. A diagnosis of

obesity based on a BMI index of 28 may, for example,

be counterproductive, since weight loss treatments

may increase the risk of mortality (29). The diagnosis

and treatment of ventricular ectopy following

Table 1. The 97.5 percentiles of the number of peri-odontal pockets deeper than 5 mm in a representa-tive sample of the US civilian, noninstitutionalizedpopulation (NHANES III, 198894)*

Age Sample size Normal number

of pockets

2029 years 3311 1

3039 years 3047 3

4049 years 2241 3

5059 years 1410 4

6069 years 1530 4

70+ years 1435 3

All ages 12974 3

*Upper 95% confidence limit of the 97.5% percentile; the presence ofpockets deeper than 5 mm on lost teeth cannot be determined in thissample.

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Hujoel et al.


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myocardial infarction with type I antiarrhythmic

agents resulted in higher mortality (16, 44). A diag-

nosis of high blood pressure (37) or diabetes (33) may

be harmful if the prescribed treatment further

increases the mortality risk.

Similarly, a diagnosis of destructive periodontal

disease based on the presence of periodontal pockets

6 mm or deeper may cause more harm than good if

the suggested periodontal treatments increase dental

or periodontal morbidity. Since destructive perio-

dontal disease is by and large a silent disease, and

since the recent publicity about the potential

association between periodontal pockets and sys-temic diseases may have increased the psychological

damage of labeling somebody as having destructive

periodontal disease, there is an additional onus on

the profession to ensure that a diagnosis of this dis-

ease and its treatment are associated with tangible

benefits (23).

Therapeutic reference values to diagnosedestructive periodontal disease

The most attractive definition of disease is the

therapeutic diagnosis. Under this definition, a person

is screened for a disease only if the diagnosis of dis-

ease leads to better outcomes. The Joint National

Committee on the Detection and Treatment of High

Blood Pressure recommends lower target blood

pressures for persons with diabetes and kidney dis-

ease based on evidence that these lower pressures

improve clinical outcomes (10). A therapeutic

diagnosis definition of disease implies that, for

example, no cancer should be screened for in

asymptomatic individuals unless evidence exists that

cancer treatment actually improves survival or qual-

ity of life. For instance, screening for prostate cancer

is controversial, since it is unclear whether life

expectancy is increased by screening, and treatment

frequently has adverse effects on the quality of life. As

a result, the US Preventive Services Task Force con-

cluded that the evidence is insufficient to recom-mend for or against routine screening for prostate

cancer using prostate specific antigen testing or

digital rectal examination (22).

The use of therapeutic reference values in clinical

periodontics was first suggested in one study that

established how deep periodontal pockets needed to

be before the benefits of scaling outweighed its

damages (31). Scaling in periodontal pockets less

than 3 mm was reported to result in attachment loss,

whereas the same treatment in pockets deeper than

4 mm resulted in attachment gain. The shortcoming

of this therapeutic definition of destructive perio-

dontal disease is that no evidence exists that short-

term changes in attachment level relate to clinically

relevant outcomes such as tooth loss (23). Nonethe-

less, it does provide an indication as to how clinical

trials could establish pocket depth levels at which a

given treatment will likely result in more tangible

clinical benefits than harm.

Conclusion

Destructive periodontal disease and periodontal

atrophy are two phenotypes with distinct clinical

features. Not only are they treated quite differently,

but different lines of evidence suggest that the two

phenotypes have distinct etiologies and different

prognoses. The current custom of labeling both

phenotypes as one and the same disease chronic

periodontitis merely because both exhibit attach-

ment loss, needs to be re-evaluated. Part of this

re-evaluation will need to involve a discussion of

whether periodontal atrophy should be labeled as a

disease, and what constitutes an abnormal perio-dontal pocket.

Acknowledgments

This study is supported by NIH: NIDCR R-01

DE13912 and a grant from Capes Coordenacao de

Aperfeicoamento de Pessoal de Nivel Superior.

03 4 5 6 7 8 9 10 11 12

10

20

30

40

50

60

70

80

90

100

Pocket depth (mm)

Incide

nce

rate

oftoothl

oss

Fig. 3. Rate of tooth loss (per 1000 teethyear) as a func-

tion of maximum probing depth per tooth in a cohort of

1021 patients (aged 4065 years) under periodontal spe-

cialist care for destructive periodontal disease.

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Bolsa o Recesion de Acuerdo Al Fenotipo.hujoel Cruz Selipsky Saver.2005