Abnormal pocket depth and

gingival recession as distinct

phenotypes
PHI LI PPE P. HUJ OEL, JOANA CUNHA-CRUZ, HERBERT SELI PSKY &
BARRY G. SAVER
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 can be
associated with signs of clinical inammation 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 and often presents without signs of clinical
inammation. 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 classication, 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 of
life 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 dene when pockets are abnormal.
Destructive periodontal disease
and 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). Briey, since the publication of the
rst 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
inammation, 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, and
anthropologic and comparative medicine features.
The treatments and the economics of
periodontal atrophy and destructive
periodontal 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
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 rst 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 of
destructive 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
attachment disease 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 personwithchronic 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)
frompocket-free gingival recession (pictured here) and not
group them together as chronic periodontitis merely be-
cause they both exhibit attachment loss.
23
Abnormal pocket depth and gingival recession
economics and manpower needs for periodontal
needs.
The etiologies of destructive periodontal
disease and periodontal atrophy may be
different
Emerging epidemiologic evidence suggests that
destructive periodontal disease and periodontal
atrophy 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 inammatory disease (i.e. is the term perio-
dontitis appropriate for describing cases of abnormal
periodontal pocketing when no clinical signs of in-
ammation 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 classication 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 comparative
medicine features of destructive
periodontal disease and periodontal
atrophy 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 current
thinking that any attachment loss is pathologic and
the result of an inammatory process caused by
plaque. Similar ndings regarding an age-related
wasting of the alveolar process have been reported by
other investigators (4) and this nding 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 signi-
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 situation
where 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 (dened 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, or
do 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.
Dening disease is a complex issue. Are meno-
pause and baldness diseases as the FDA suggests, or
are they a reection of normal aging? Can mountain
24
Hujoel et al.
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 reect normal human
variability (38)? Answers to these questions are cul-
ture- and era-specic and depend on whose deni-
tion of disease is used. Disease can be dened as the
sum of abnormal phenomena displayed by a group of
living organisms in association with a specied
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 protable
treatments appear.
Within this context, is periodontal atrophy a
disease? If a young individual is at a reproductive
disadvantage because of periodontal atrophy, an
argument 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 depth
in 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 dened using nor-
mative or arbitrary values, risk-based reference val-
ues, or treatment-based reference values.
Normative or arbitrary values to
diagnose abnormal pockets
Diseases are sometimes dened based on normative
reference values. Fever can be dened 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 dened
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 rst percentile or the fth 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 classication 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 inammatory
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
Abnormal pocket depth and gingival recession
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 dene destructive perio-
dontal disease. For instance, any individual with
three pockets 5 mm or deeper could be classied as
having destructive periodontal disease. Currently, all
denitions 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-specic number of pockets deeper
than 5 mm could be used to dene 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 ve 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 dened 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 classied as nondis-
eased has potentially no relationship to the number
of patients with adverse outcomes such as tooth loss,
periodontal abscesses, or difculty in chewing.
Complex chronic diseases such as diabetes, coronary
heart disease, and destructive periodontal disease
have too much natural variability to allow a suc-
cessful denition of disease based on arbitrary or
normative values.
Risk-based reference values to diagnose
abnormal pockets
Disease can be dened based on the presence of an
attribute that substantially increases the risk for an
adverse health outcome. A body-mass index above 28
is reective of a diagnosis of obesity, as it carries an
increased risk of morbidity and mortality (43). A
fasting plasma glucose level greater than 126 mg dl
(7.0 mmol l) 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 140 90 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 gure 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, noninstitutionalized
population (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% condence limit of the 97.5% percentile; the presence of
pockets deeper than 5 mm on lost teeth cannot be determined in this
sample.
26
Hujoel et al.
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
benets (23).
Therapeutic reference values to diagnose
destructive periodontal disease
The most attractive denition of disease is the
therapeutic diagnosis. Under this denition, 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 denition 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 insufcient to recom-
mend for or against routine screening for prostate
cancer using prostate specic antigen testing or
digital rectal examination (22).
The use of therapeutic reference values in clinical
periodontics was rst suggested in one study that
established how deep periodontal pockets needed to
be before the benets 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 denition 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 benets 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.
0
3 4 5 6 7 8 9 10 11 12
10
20
30
40
50
60
70
80
90
100
Pocket depth (mm)
I
n
c
i
d
e
n
c
e

r
a
t
e

o
f

t
o
o
t
h

l
o
s
s
Fig. 3. Rate of tooth loss (per 1000 teeth year) 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.
27
Abnormal pocket depth and gingival recession
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29
Abnormal pocket depth and gingival recession