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Review of obesity and periodontitis:
an epidemiological view
Silie Arboleda,*1 Miguel Vargas,1 Sergio Losada1 and Andres Pinto2
Introduction
Obesity and periodontitis are among the most
common chronic disorders aecting the world
population.1 Obesity is a complex, multifactorial
chronic disease that is strongly associated
with multiple comorbidities.2 Epidemiological
studies suggest that obesity is also associated
with periodontitis.3,4 Multiple authors report
that increased body mass index (BMI), waist
circumference (WC), percentage of subcutaneous
body fat, and serum lipid levels are associated
with increased risk of developing periodontitis
compared with normal-weight individuals.5,6,7
While there is preliminary evidence for these
relationships, a causal relationship remains
elusive. e mechanisms that link obesity and
periodontitis are not completely understood.
However, obesity has several harmful biological
eects that might be related to the pathogenesis
of periodontitis.8 Tumour necrosis factor-α
(TNF-α), and interleukin-6 (IL-6) form part
of the pathophysiology of both diseases.8 e
literature about the effect of obesity on the
outcome of non-surgical periodontal therapy
remains controversial.9
e association of obesity and periodontitis
constitutes an important topic due to the
inammatory component they share and their
high prevalence in the adult population.3 is
narrative review aims to describe the reported
association between these two conditions.
Relevant literature was extracted from PubMed
in the Medline electronic database, using the
following keywords in dierent combinations:
periodontal diseases OR periodontitis OR
alveolar bone loss AND obesity OR body
mass index OR waist circumference. e lters
used in this search were studies conducted in
humans and publications in English.
Obesity
Obesity is dened as abnormal or excessive fat
accumulation that may impair health.10 e
World Health Organisation (WHO) denes
overweight as a BMI≥25kg/m2 and obesity as
a BMI≥30 kg/m2 (Ta b l e 1).10 BMI is dened
as the weight in kilograms divided by the
square of the height in meters (kg/m2).10 is
traditional BMI classication underestimates
risk in Asian and South Asian people.11 A
separate guideline for this population classies
overweight as a BMI between 23 and 24.9kg/
m2 and obesity as a BMI≥25kg/m2.11
BMI is the most frequently used indicator
by WHO because it is inexpensive and easy to
use in clinical and epidemiological studies.12
However, this measure has some limitations.
BMI does not assess body fat distribution,
because it is a measure of excess weight rather
than excess body fat. Factors such as age, sex,
ethnicity, and muscle mass can inuence the
relationship between BMI and body fat.13
Alternative measures that reect abdominal
obesity such as WC have been suggested.13
WC is strongly correlated with cardiovascular
Explains the current knowledge regarding the links
between obesity and periodontitis.
Examines the literature that evaluates the as sociation
between these two diseases.
Describes the effec ts of obesity on the outcome of
non-surgical periodontal therapy.
Key points
Abstract
Obesity and periodontitis are among the most common non-communicable diseases, and epidemiological studies report
the influence of obesity in the onset and progression of periodontitis. Data indicate that increased body mass index, waist
circumference, percentage of subcutaneous body fat, and serum lipid levels are associated with increased risk to develop
periodontitis. The underlying biological mechanisms of this association involve adipose tissue-derived cytokines, such as
tumour necrosis factor-α and interleukin-6, which affect whole-body metabolism and contribute to the development of a
low-grade systemic inflammation. Multiple studies report a positive association between these two diseases across diverse
populations. Obesity does not appear to impair the success of periodontal therapy. However, currently available evidence
is variable and therefore inconclusive. Despite the limited evidence about recommendations on treatment planning, oral
healthcare professionals need to be aware of the complexity of obesity to counsel their patients about the importance of
maintaining healthy body weight and performing good oral hygiene procedures.
1Unit of Clinical Oral Epidemiology (UNIECLO)
Investigations, School of Dentistr y, El Bosque University,
Bogotá, Colombia; 2Department of Oral and Maxillofacial
Medicine and Diagnostic Sciences, Cas e Western Reserve
University, School of Dental Medicine and University
Hospitals Cleveland Medical Centre, Cleveland, Ohio,
United States.
*Correspondence to: Silie Arboleda
Email: siliesoad@gmail.com
Refereed Paper.
Accepted 18 April 2019
DOI : 10.103 8/s41415- 019-0 611-1
BRITISH DENTAL JOURNAL | VOLUME 227 NO. 3 | AUGUST 9 2019 235
GENERAL
© The Author(s), under exclusive licence to British Dental Association 2019
disease (CVD) because abdominal adipose
tissue secretes a greater number of cytokines
and hormones in comparison to the
subcutaneous adipose tissue.13 The WHO
suggests when WC is≥102cm (40 inches) in
men and ≥88cm (35 inches) in women, it is
considered a risk factor for CVD. e biologic
rationale for relating measures of central
adiposity to CVD risk is that abdominal
adipose tissue is related to decreased glucose
tolerance, reduced insulin sensitivity, and
adverse lipid proles.13,14
Obesity is responsible for 3.4 million deaths,
3.9% of years of life lost and 3.8% of disability-
adjusted life years globally.15 Multiple factors,
including genetics, socioeconomic status,
environment and individual decisions play
a significant role in the pathogenesis of
obesity.2 Obesity is either an independent
factor or aggravating factor for a variety
of non-communicable diseases, including
cardiovascular diseases, osteoarthritis, type2
diabetes and cancer.2,16
Worldwide, obesity has nearly tripled since
1975, contrary to other major global risks such
as tobacco use and childhood malnutrition,
which are declining.12,15 Increase in prevalence
occurs in developed and developing countries,
and will continue to grow in the future.17 In
2016, 1.9 billion adults aged 18years and older
were overweight. Out of these, over 650 million
adults were obese. Approximately 13% of the
world’s adult population (11% of men and 15%
of women) were obese.12 ese trends project
65 million additional obese adults in the United
States and 11 million additional obese adults
in the United Kingdom by 2030.17 e large
increments in obesity over the past years have
focused on a number of potential contributors,
including increases in caloric intake, declining
levels of physical activity, changes in the
composition of diet, and changes in the gut
microbiome.15
Periodontitis
Periodontitis is a chronic inammatory disease
of bacterial origin that aects the supporting
and surrounding structures of the teeth.18
Historically, all individuals were considered
equally susceptible to develop periodontitis.
Poor oral hygiene, biolm accumulation and
possibly occlusal trauma were sucient to
initiate disease.19
Predisposition to periodontal disease is
highly variable and depends on the host’s
response to periodontal pathogens.20 The
current aetiological concept implies a bacterial
infection as the primary cause. Porphyromona
gingivalis, Prevotella intermedia, Tannerella
forsythia, Campylobacter rectus, Eubacterium
nodatum, Treponema denticola, Fusobacterium
nucleatum, and Eikenella corrodens have been
closely associated to periodontitis.21
Aer the publication of several studies by Van
Dyke, Oenbacher and Heaton, the existence of
certain risk factors (genetic and acquired) that
can modulate the susceptibility or resistance of
the host to periodontitis, is accepted. Hence,
this disease has a multifactorial aetiology.19,22,23
ere is great interest in developing indicators
that allow for identification of susceptible
individuals and to identify modiable risk
factors that can prevent or alter the course
of periodontitis.19 With the recent discovery
of possible associations between periodontal
disease and systemic health, the research on
susceptibility to periodontitis has taken a
broader and more signicant meaning.19
e prevalence of periodontitis varies in
different regions of the world, according
to the case denition used and the studied
population.20 In the United States, the National
Health and Nutrition Examination Survey
(NHANES 2009–2014), reported in a sample of
10,683 participants aged 30years or older that
42.2% of adults presented periodontitis with
a distribution of 7.8% for severe periodontitis
and 34.4% for non-severe periodontitis (mild
or moderate).24 e mean age of the population
examined was 50.8 years. Periodontitis
was greatest among men (50.2%), Mexican
Americans (59.7%), adults below 100% of
the federal poverty levels (60.4%), current
smokers (62.4%), and those who self-reported
diabetes (59.9%).24 In general, the occurrence
of periodontitis decreases with improved
quality of life. It tends to be more common
in economically disadvantaged populations.25
Individuals from Yemen, Israel, North of
Africa, South Asia and the Mediterranean
present a greater prevalence of periodontitis
compared to Europeans.25
Biological plausibility
e underlying biological mechanisms of the
association between obesity and periodontitis
involve adipose tissue-derived cytokines
and hormones (also known as adipokines).26
Obesity is associated with a chronic low-grade
inammatory state due to increased expression
of pro-inflammatory adipokines and
diminished expression of anti-inammatory
adipokines.27 Pro-inammatory adipokines
includeTNF-α, IL-6, leptin, resistin, among
others. In addition to the numerous adipokines
with pro-inammatory eect, adipose tissue
secretes a smaller number of anti-inammatory
factors including adiponectin.27
Many researchers agree that the most
important mediators related to obesity and
periodontitis are TNF-α, IL-6, which are
involved in the pathophysiology of both
diseases.8 It appears that pro-inammatory
biomarkers show a pleiotropic effect and
can target specific cells by controlling
activation of cells, cell proliferation and
function in the periodontium. As a result,
raised pro-inammatory biomarkers levels
such as TNF-α and IL-6 cause periodontal
tissue destruction.26 Leptin is a pleiotropic
cytokine secreted by adipocytes, linked
Classification BMI
Disease risk
(relative to normal weight and waist circumference)
Men<102cm
Women<88cm
Men≥102cm
Women≥88cm
Underweight <18.5 – –
Normal range 18.5–24.9 – –
Overweight 25 –29.9 Increased High
Obesity: ≥30 – –
Obesity class I 30–34.9 High Ver y high
Obesity class II 35–39.9 Very high Very high
Obesity class III ≥40 Extremely high Extremely high
Table1 The international classification of adult underweight, overweight and obesity,
according to BMI and risk of comorbidities. Adapted from Obesity: preventing and
managing the global epidemic. World Health Organization, Defining the problem, p. 9,
Copyright (2000)
236 BRITISH DENTAL JOURNAL | VOLUME 227 NO. 3 | AUGUST 9 2019
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© The Author(s), under exclusive licence to British Dental Association 2019
to several systemic diseases. Besides the
control of appetite, leptin stimulates energy
expenditure and modulates lipid and bone
metabolism, haematopoiesis, coagulation, the
function of pancreatic beta cells, and insulin
sensitivity.14,28 Furthermore, leptin regulates
the immune system and inflammatory
response, with mainly pro-inflammatory
behaviours.14 An experimental study
demonstrated that leptin negatively interferes
with the regenerative capacity of periodontal
ligament cells, suggesting that leptin may be
one of many pathologic links between obesity
and compromised periodontal healing.28
Adiponectin is a circulating hormone that is
involved in glucose and lipids metabolism;
its levels are lower in subjects with obesity,
insulin resistance, or type2 diabetes. is
substance improves insulin sensitivity
and may have anti-atherogenic and anti-
inflammatory properties.27 In contrast,
resistin exhibits a potent pro-inammatory
eect and is involved in several inammatory
diseases.29 In humans, this cytokine forms part
of inammatory processes.27 Zimmermann
etal.30 measured serum and gingival
crevicular uid levels of adipokines in obese
and normal-weight subjects, with and without
chronic periodontitis. They found that in
serum, resistin levels were higher whereas
adiponectin levels were lower in groups
with periodontitis.30 e role of resistin in
inflammatory periodontal disease has yet
to be claried. Further research will shed
light into the precise biological mechanism
responsible for the association between these
two diseases.
Studies
e initial report of this association in humans
was established in 1998 by Saito etal.5 who
studied 241 Japanese subjects aged 20 to
59. Periodontal status was measured by the
community periodontal index of treatment
needs (CPITN). Aer adjusting for confounding
variables such as age, sex, oral hygiene status and
smoking history, the estimated odds ratio (OR)
for periodontitis was 3.4 (95% CI, 1.2–9.6) in
overweight and 8.6 (95% CI, 1.4–51.4) in obese
subjects. Further studies from Japan,31,32,33 the
United States8,34 and South Korea35 also found
that obesity was associated with an increased
risk of periodontitis.
Al-Zahrani etal., in a sample size of 13,655
participants from the NHANES III, reported
a signicant association between overall and
abdominal obesity, with the prevalence of
periodontitis in young participants (ages
18–34) with an adjusted OR of 2.27 (95%
CI, 1.4–3.4).7 In Brazil, Dalla Vecchia etal.36
evaluated the relationship between overweight,
obesity and periodontitis. Overweight and
obesity were assessed by BMI using the
WHO criteria and periodontitis was dened
as ≥30% of teeth with clinical attachment
loss≥5 mm. e authors found that obesity
was only associated with periodontitis in non-
smoker women (OR 3.4, 95% CI, 1.4–8.2). e
association between periodontitis and obesity,
but not overweight, is conrmed by Khader
etal.6 who, in a sample of 340 Jordanian adult
subjects, reported that the association was
not dierent between normal and overweight
participants. Obese subjects had three times
the probability of having periodontitis
compared to subjects with normal weight (OR
2.9, 95% CI, 1.3–6.1). A more recent study by
Eke etal.24 analysed 10,683 participants aged
30years or older from the NHANES 2009–
2014. ey found that periodontitis was more
prevalent among people with co-occurring
chronic conditions. Periodontitis signicantly
co-occurred with diabetes and increasing
number of missing teeth but not with obesity.24
Although most evidence has come from
cross-sectional studies, stronger evidence has
come from longitudinal studies. Linden etal.37
evaluated the association between obesity
and periodontitis in a group of 60–70-year-
old Western European men. ey assessed
the periodontitis at two levels, as suggested
by Tonetti and Claey.38 Obesity increased
prevalence of periodontitis (OR 1.77, 95%
CI, 1.2–2.6) when they used a low-threshold
denition (at least two teeth with≥6mm loss
of attachment and at least one site with a pocket
of≥5 mm). However, with a high-threshold
definition (≥15% of sites with attachment
loss≥6 mm and at least one site with pocket
of ≥6 mm) obesity was not significantly
associated with periodontitis.37 A prospective
study in Finland by Saxlin etal.,39 of 214 non-
diabetic subjects who had never smoked,
concluded that body weight was weakly but
not statistically signicantly associated with
the development of periodontal infection (RR
1.3, 95% CI, 0.7–2.1). However, the authors
stated that the results of their study should
be interpreted cautiously due to its small
size.39 Gorman etal.40 in a longitudinal study
with criteria for periodontitis which met the
Reference (authors, year) Age range
(years)
Studies
included
OR or RR
95% (IC) Main results
Chaffee and Weston, 2010.3
Systematic review and meta-analysis >18 28 OR 1.35
(1.23 –1.47)
Positive association between obesity and periodontitis. Inability to distinguish the
temporal ordering of events
Suvan etal., 2 011.4
Systematic review and meta-analysis >18 19 OR 1.81
(1.42–2.30)
Association between BMI overweight and obesity and periodontitis. The magnitude
is unclear. Insufficient evidence to provide guidelines to clinicians on the clinical
management of periodontitis in overweight and obese subjec ts
Moura-Grec etal., 2014 .54
Systematic review and meta-analysis >15 31 OR 1.30
(1.25 –1.35)
Obesity was associated with periodontitis. The risk factors that aggravate these
diseases should be better clarified to elucidate the direction of this association
Nascimento etal., 2015.55
Systematic review and meta-analysis >18 5RR 1.33
(1.21–1.47)
Positive association between weight gain and new cases of periodontitis; due that
only prospective longitudinal studies were included. Results are originated from
limited evidence and its results should be interpreted with precaution
Martinez-Herrera etal., 2 017.56
Systematic review >18 28 –
Nineteen observational studies and nine clinical trials. Obesity was associated with
periodontitis in 17 observational studies. Insulin resistance could be implicated in
the association between both diseases
Khan etal., 2018 .57
Systematic review
13–17 to
18–34 25 –Of 25 studies included, 17 showed an association between obesity and
periodontitis in adolescents and young adults (OR ranged from 1.1–4.5)
Table2 Systematic reviews and meta-analysis that have evaluated the association between obesity and periodontitis
BRITISH DENTAL JOURNAL | VOLUME 227 NO. 3 | AUGUST 9 2019 237
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© The Author(s), under exclusive licence to British Dental Association 2019
threshold (two or more teeth with alveolar
bone loss≥40%, probing pocket depth≥5mm,
or clinical attachment loss≥5 mm) found
that overall obesity and central adiposity
are associated with an increased hazard of
periodontal disease progression events in men
(41–72% higher).40
Signicant variability exists in the denitions
used to identify periodontitis, with few studies
that meet stringent criteria for periodontitis.
For example, one study utilised loss of clinical
attachment as the only diagnostic criterion
for periodontitis,36 which is inappropriate
because this disease cannot be reected by
measurements of a single variable.41 Loss of
clinical attachment is considered a physiological
condition that takes place during the ageing
process. Even though it is one of the clinical
signs of periodontitis, it may occur in the
absence of this disease.42 In other studies, the
criterion used to dene periodontitis included
shallow pockets and was>3.5mm,5,31 which
could be considered low-level periodontal
damage. e use of low thresholds results in a
higher number of subjects with periodontitis.
The lack of consensus across accepted case
denitions for periodontitis also complicates
the comparison of prevalence estimates across
surveys.43 The strength of the association
between obesity and periodontitis may be
overestimated due to the denitions used in the
evaluated studies. Currently, it is recommended
to use the case denitions originally developed
by the Centre for Disease Control, and the
American Academy of Periodontology (CDC/
AAP) to provide standardised clinical case
definitions for population-based studies
of periodontitis.41,44 The case definition for
periodontitis requires ≥two interproximal
sites with attachment loss≥3mm, and≥two
interproximal sites with probing depth≥4mm
not on same tooth, or one site with probing
depth≥5 mm).41 Use of these standards could
facilitate comparison of periodontal prevalence
estimates worldwide.43
Most of the studies that showed a positive
association between obesity and periodontitis
are cross-sectional,5,6,7,31,32,36 in which the
prevalence of periodontitis and obesity were
ascertained at a single point in time and
therefore a temporal sequence or cause and
eect cannot be determined.45 Cross-sectional
studies describe the frequency and distribution
of events of health and disease. Although they
are also used to explore and generate research
hypotheses, they only provide information
from one observation performed at a single
point in time. erefore, to reach a causal
relationship, it is necessary to develop studies
specically designed for this purpose.45
Furthermore, the risk factors that
aggravate these conditions must be
clarified to determine the direction of the
association. An example is diabetes mellitus
is a metabolic disorder characterised by the
presence of hyperglycaemia due to defective
insulin secretion, defective insulin action
or both.46 It is well established that obesity
is an independent risk factor for type 2
diabetes.47,48 Recent studies have identified
links between obesity and diabetes involving
pro-inammatory cytokines, deranged fatty
acid metabolism, insulin resistance, and
cellular processes such as mitochondrial
dysfunction and endoplasmic reticulum
stress.48,49,50 Numerous epidemiological studies
also document the association between type2
diabetes and periodontitis.51,52 In fact, Löe
described periodontal disease as the sixth
complication of diabetes.53 This statement
implies that diabetes can be a confounding
variable of the association between obesity and
periodontitis, and thus should be controlled
when performing cross-sectional studies.
Several systematic reviews and meta-
analysis evaluated the relationship between
obesity and periodontitis in the last decade
(Tabl e 2).3,4,54,56,57 Chaee and Weston3 found
a positive association between these two
diseases in 41 of the 70 studies included in their
review. A meta-analysis of 28 studies reported
an OR of 1.35 (95% CI, 1.23–1.47) for the
association between obesity and periodontitis.
Suvan etal.4 reported a stronger association
between both conditions with an OR of 1.81
(95% CI, 1.42–2.30) from a meta-analysis
of 19 studies. Nascimento etal.,55 in a meta-
analysis from prospective longitudinal studies,
concluded that subjects who became obese
had an increased relative risk of 1.33 (95%
CI, 1.21–1.47) of developing periodontitis
compared with counterparts who stayed
within normal weight. e results do provide a
clear positive association between weight gain
and new cases of periodontitis. However, the
authors stated that this conclusion should be
interpreted carefully due to limited evidence. A
more recent meta-analysis included 25 studies
from 12 countries, from which 17 showed an
association between obesity and periodontitis
(OR ranged from 1.1–4.5).57 ese systematic
reviews concluded that it is possible to nd
a high prevalence of periodontitis in obese
subjects.
The influence of obesity on
periodontal treatment
The relationship between body weight and
periodontitis appears clearer when the inuence
of obesity in periodontal disease treatment is
studied. Interventional studies provide the
strongest evidence of a causal relationship and
can provide further evidence for the benet
of eliminating the risk factor.19 Lakkis etal.58
evaluated whether weight loss by bariatric
surgery in initially obese subjects can improve
the response to non-surgical periodontal
therapy. ey found a statistically signicant
improvement in the response of these subjects
to periodontal treatment compared to obese
subjects (the control group). Probing depth
had a mean reduction of 0.45mm vs 0.28mm,
the reduction in clinical attachment loss was
0.44 mm vs 0.3 mm, the percentage of sites
with bleeding on probing 16% vs 15% and
the gingival index was 1.03 vs 0.52 in the
bariatric surgery group vs the control group,
respectively. Although these measurements
have a statistically signicant impact (p<0.05),
the clinical relevance may be debatable.
ese results contrast with those reported by
Zuza etal.59 who showed that non-surgical
periodontal treatment allows the reduction of
all clinical parameters of inammation in obese
and normal-weight subjects, supporting that
obesity does not negatively aect the success
of periodontal therapy. Altay etal.60 reported
similar ndings.
Gerber etal.,9 in a systematic review, reported
that obesity has a clear negative eect on the
outcome of non-surgical periodontal therapy in
ve of eight studies. e remaining three studies
did not report treatment dierences between
obese and normal-weight participants. However,
the authors stated that the included studies did
not correspond to the highest level of quality.
Nascimento etal.61 and Papageorgiou etal.62
found no dierences in clinical periodontal
parameters between obese and non-obese
subjects in the included studies in their meta-
analysis. In summary, obesity does not appear
to play a negative role in the treatment outcome
of non-surgical periodontal therapy. However,
the available evidence is variable.
Conclusion and future perspective
The present review suggests a positive
association between these two conditions with
a general direction that could be from obesity
to periodontitis. e relationship between these
238 BRITISH DENTAL JOURNAL | VOLUME 227 NO. 3 | AUGUST 9 2019
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© The Author(s), under exclusive licence to British Dental Association 2019
two disorders could travel through multiple
pathways. However, these results should be
interpreted cautiously due to the heterogeneity
of criteria to assess periodontitis and the paucity
of longitudinal studies, which hamper our
ability to determine the relative contribution
of periodontitis to obesity. Further research
should take into consideration an adequate
denition of cases of periodontitis based on
the criteria previously established by the CDC/
AAP. Presently, there is limited evidence to
recommend changes in treatment planning.
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BRITISH DENTAL JOURNAL | VOLUME 227 NO. 3 | AUGUST 9 2019 239
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