EDITORIALS
of the authors and JAMA and
Destructive Periodontal Disease and Tobacco
and Cannabis Smoking
Philippe P. Hujoel, PhD
D
ESTRUCTIVE PERIODONTAL DISEASE CONSISTS OF
loss of the supporting tissues of the teeth and
can lead to tooth mobility, tooth migration, and
eventual tooth loss. Enjoyments in life such as
eating; relaxing; going out; and being free of pain, discom-
fort, and self-consciousness are adversely affected by
destructive periodontal disease in 20% of periodontal
patients seeking specialist care.1 In the United States, the
prevalence of destructive periodontal disease decreased
from 7% in 1988 to 4% in 1999 and 2000.2 In 1999, about
$14 billion was spent on treating and preventing destruc-
tive periodontal disease.3
For most of the latter half of the 20th century, destruc-
tive periodontal disease was considered a disease that oc-
curred after the age of 35 years, caused primarily by dental
plaque and largely unrelated to lifestyle choices. These hy-
potheses were mostly based on animal studies, gingivitis stud-
ies, and case series but not controlled epidemiological stud-
ies on destructive periodontal disease.
In this issue of JAMA, Thomson and colleagues4 present
the findings of a cohort study that have the potential to help
eliminate some established beliefs and bring a more evidence-
based approach to an understanding of the etiology of de-
structive periodontal disease, including the role of canna-
bis smoking. The cohort study consisted of 903 participants
with self-reported tobacco and cannabis smoking informa-
tion collected at the ages of 18, 21, 26, and 32 years and
with half- and full-mouth dental examinations at the ages
of 26 and 32 years, respectively. An average frequency mea-
sure of cannabis smoking at each of the 4 examinations was
related to attachment loss (a linear measure of periodontal
support destruction), which is a surrogate measure of de-
structive periodontal disease. Using this surrogate mea-
sure, the authors found that tobacco and cannabis smok-
ing was associated with an increased incidence of destructive
periodontal disease before the age of 32 years, whereas den-
tal plaque was not.
Strengths of this study include the representative birth
cohort, the high proportion of participants with dental fol-
low-up (88%), the dose-response relationships between can-
See also p 525.
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Editorials represent the opinions
not those of the American Medical Association.
nabis use and destructive periodontal disease, and the sig-
nificant association between cannabis smoking and
destructive periodontal disease among those who never
smoked tobacco. Because the lower confidence limit of the
relative risk is close to a null finding, biases due to residual
confounding by lifestyle factors associated with cannabis use
and reverse causality should be considered. Dental plaque
and socioeconomic status were measured after baseline and
after the periodontal destruction occurred, not at baseline
or before incident disease as is usual in cohort studies. Be-
cause periodontal examinations occurred 8 years after base-
line, the cohort at baseline may have been a mixture of in-
dividuals with and without signs of destructive periodontal
disease, rather than a cohort of disease-free individuals at
the start of follow-up.
Dental care and attachment loss were both ascertained
between the ages of 26 and 32 years, making it difficult to
determine which occurred first. Tooth loss at baseline or
during follow-up (the ultimate dental outcome) and its po-
tential relationship to cannabis smoking were not re-
ported. As a result of these factors, the temporal sequence
of cause and effect was difficult to disentangle and may have
contributed to biases. As the authors indicate, it will be im-
portant to replicate the novel findings on cannabis smok-
ing in other populations. If further studies confirm canna-
bis smoking as a potential factor contributing to destructive
periodontal disease, it may offer opportunities to narrow
which common elements of tobacco and cannabis smoke
are related to the periodontal damage.
The study by Thomson et al adds to growing evidence
that destructive periodontal disease occurs at a much
younger age than previously believed. Obesity has been
associated with signs of destructive periodontal disease in
persons as young as 17 to 21 years.5 Impaired glucose
metabolism has been associated with destructive periodon-
tal disease in 12- to 18-year-olds.6 The study by Thomson
et al confirms that tobacco smoking is associated with onset
of destructive periodontal disease before the age of 35
years4,7 and moreover may be “the primary behavioral risk
factor”4 for destructive periodontal disease.8 However, in
Author Affiliation: Department of Dental Public Health Sciences, School of Den-
tistry, University of Washington, Seattle.
Corresponding Author: Philippe P. Hujoel, PhD, Department of Dental Public Health
Sciences, School of Dentistry, University of Washington, Box 357475, Seattle, WA
98195 (hujoel@u.washington.edu).
©2008 American Medical Association. All rights reserved.

the study by Thomson et al, dental plaque was—to para-
phrase Sir Arthur Conan Doyle—the dog that did not bark,
or at least not very loudly. Incident destructive periodontal
disease was unrelated to dental plaque, whereas prevalent
destructive periodontal disease was inconsistently related to
dental plaque (Table 5 in the article). The lack of a strong
association between dental plaque and destructive peri-
odontal disease is consistent with a systematic review on
this topic.9 Although dental plaque may play a role in the
secondary prevention of destructive periodontal disease, it
is becoming increasingly apparent that an evidence-based
approach to the primary prevention of destructive peri-
odontal disease should include smoking prevention and
cessation and the adoption of healthy eating habits.
Destructive periodontal disease may well be the canary
in the coal mine for chronic noncommunicable diseases
(CNCDs), as was suggested 34 years ago.10,11 Smoking and
unhealthy eating habits lead to destructive periodontal dis-
ease as well as to CNCDs such as diabetes, cardiovascular
disease, and certain cancers in late adulthood. The pres-
ence of strong common causal factors suggests the need for
a synergistic approach to preventing a substantial propor-
tion of both destructive periodontal disease and CNCD cases;
primary prevention of destructive periodontal disease should
help reduce CNCDs, and primary prevention of CNCDs
should help reduce destructive periodontal disease. The lat-
ter may already have occurred; successful smoking preven-
tion and cessation programs aimed at reducing cancer and
cardiovascular mortality may have inadvertently reduced the
incidence of destructive periodontal disease, even before to-
bacco use became widely recognized as a cause of destruc-
tive periodontal disease.
Analogously, dental policy and research priorities aimed
at the primary prevention of destructive periodontal dis-
ease can help reduce the occurrence of CNCDs. Profes-
sional dental organizations have been involved in policies
or programs such as raising public awareness about issues
such as sugar-laden junk food and dental health, in pro-
moting smoking cessation programs in dental offices, in
changing health behaviors, in increasing “the availability and
consumption of healthy foods”11 in school programs, and
in providing appropriate physician referral when suspect-
ing dental signs of potential drug abuse such as metham-
©2008 American Medical Association. All rights reserved.
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EDITORIALS
phetamine-associated caries. The findings reported by Thom-
son et al suggest that cannabis smoking could be added to
the list of recreational drugs with potential dental conse-
quences. Primary prevention of destructive periodontal dis-
ease (as well as dental caries) may lead to benefits beyond
dental health and may have greater implications for gen-
eral health than realized so far.
In summary, Thomson and colleagues have reported find-
ings indicating that smoking of tobacco and potentially can-
nabis are associated with evidence of destructive periodon-
tal disease that can be detected in early adulthood, long before
other smoking-related diseases such as diabetes, cardiovas-
cular disease, and certain cancers become apparent. Given
the high prevalence of dental care in the young population
in the United States, the dental profession has an opportu-
nity to detect the early clinical signs of unhealthy lifestyles,
including potential drug abuse, and could play a role with
physicians in addressing the challenges of reducing
CNCDs.11,12
Financial Disclosures: None reported.
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