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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.
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 aecting 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
eects 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
inammatory 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 dierent 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 dened as abnormal or excessive fat
accumulation that may impair health.10 e
World Health Organisation (WHO) denes
overweight as a BMI≥25kg/m2 and obesity as
a BMI≥30 kg/m2 (Ta b l e 1).10 BMI is dened
as the weight in kilograms divided by the
square of the height in meters (kg/m2).10 is
traditional BMI classication underestimates
risk in Asian and South Asian people.11 A
separate guideline for this population classies
overweight as a BMI between 23 and 24.9kg/
m2 and obesity as a BMI≥25kg/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 inuence the
relationship between BMI and body fat.13
Alternative measures that reect 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
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© 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≥102cm (40 inches) in
men and ≥88cm (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 proles.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, type2
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 18years 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 inammatory disease
of bacterial origin that aects the supporting
and surrounding structures of the teeth.18
Historically, all individuals were considered
equally susceptible to develop periodontitis.
Poor oral hygiene, biolm accumulation and
possibly occlusal trauma were sucient 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
Aer the publication of several studies by Van
Dyke, Oenbacher 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 modiable 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 signicant meaning.19
e prevalence of periodontitis varies in
different regions of the world, according
to the case denition 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 30years 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
inammatory state due to increased expression
of pro-inflammatory adipokines and
diminished expression of anti-inammatory
adipokines.27 Pro-inammatory adipokines
includeTNF-α, IL-6, leptin, resistin, among
others. In addition to the numerous adipokines
with pro-inammatory eect, adipose tissue
secretes a smaller number of anti-inammatory
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-inammatory
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-inammatory 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<102cm
Women<88cm
Men≥102cm
Women≥88cm
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
Table1 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
GENERAL
© 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 type2 diabetes. is
substance improves insulin sensitivity
and may have anti-atherogenic and anti-
inflammatory properties.27 In contrast,
resistin exhibits a potent pro-inammatory
eect and is involved in several inammatory
diseases.29 In humans, this cytokine forms part
of inammatory 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 claried. 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). Aer 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 signicant 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 dened
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 conrmed by Khader
etal.6 who, in a sample of 340 Jordanian adult
subjects, reported that the association was
not dierent 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
30years or older from the NHANES 2009–
2014. ey found that periodontitis was more
prevalent among people with co-occurring
chronic conditions. Periodontitis signicantly
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 Claey.38 Obesity increased
prevalence of periodontitis (OR 1.77, 95%
CI, 1.2–2.6) when they used a low-threshold
denition (at least two teeth with≥6mm 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 signicantly 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 etal., 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 etal., 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 etal., 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 etal., 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 etal., 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)
Table2 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≥5mm,
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
Signicant variability exists in the denitions
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 reected 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 dene periodontitis included
shallow pockets and was>3.5mm,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
denitions 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 denitions used in the
evaluated studies. Currently, it is recommended
to use the case denitions 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≥3mm, and≥two
interproximal sites with probing depth≥4mm
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
eect 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
specically 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-inammatory 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 type2
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 Chaee 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 inuence
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 benet
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 signicant
improvement in the response of these subjects
to periodontal treatment compared to obese
subjects (the control group). Probing depth
had a mean reduction of 0.45mm vs 0.28mm,
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 signicant 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 inammation in obese
and normal-weight subjects, supporting that
obesity does not negatively aect 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 eect on the
outcome of non-surgical periodontal therapy in
ve of eight studies. e remaining three studies
did not report treatment dierences 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 dierences 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
denition 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
GENERAL
© The Author(s), under exclusive licence to British Dental Association 2019
... Obezite ve periodontitis prevelansı ile ilişkili sistematik derlemelerde, çalışma verileri obez hastaların normal vücut ağırlığına sahip bireylere göre periodontal hastalığın herhangi bir formunun daha sıklıkla görüldüğünü göstermiştir, buna ek olarak obez hastalarda vücut ağırlığının artması ile periodontitis şiddetinin arttığı bulgulanmıştır. 86,87 Aşırı kilolu/obez vakalarda periodontal hastalık insidansı ve progresyonuna dair çocuklar ve yetişkinlerde yapılan iki uzun dönem klinik çalışmanın özeti ise obezitenin periodontal hastalıkların başlangıcı ve/veya ilerlemesini artırdığı yönündedir. 88 Obezitenin periodontal tedaviyi takiben iyileşme üzerine etkisine dair, sistematik derlemelerde kesin ifadeler henüz yoktur, buna etken ise yapılan çalışmalarda örneklem sayısının az olması ve yüksek düzeyde heterojenliğe sahip sınırlı sayıda çalışma olmasıdır. ...
... 91 Son yıllarda yapılan çalışmaların sonuçları da ,obez bireylerin geleneksel risk faktörlerinden (yaş, cinsiyet, ve sigara kullanımı gibi) bağımsız olarak periodontitise yakalanma olasılığının daha fazla olduğunu göstermektedir. [86][87][88] Aşırı kilolu ve obez bireylerde oral/periodontal mikrobiyom kompozisyonuna dair raporlar henüz az sayıdadır. Gözlemsel bir çalışma sonuçlarına göre, obezitenin özellikle obez ve kronik periodontitisli hastalarda ve aynı zamanda periodontitisi olmayan obez bireylerde de periodontal patojenlerin artan oranlarıyla ilişkili olduğu bildirilmiştir. ...
... 94 Pratisyen hekimlere, obez hastalarında olası artmış periodontitis riskinin ve bunun obezite ilişkili kardiyovasküler risk artışına katkıda bulunma potansiyelinin farkında olmaları önerilmektedir. 73,85,86 Obezite yönetiminin bunu azalttığı henüz kanıtlanmamış olsa da, periodontal tedavi kesinlikle kanıtlanmıştır ve bu nedenle kapsamlı tedavinin zorunlu bir parçası olmalı, hatta diyabetli hastaları tedavi eden profesyoneller tarafından hastalar periodontal değerlendirmelere yönlendirilmelidir. Periodontal tedaviye yanıtı iyileştirmek, inflamasyonu azaltmaya katkı için diş hekimleri aşırı kilolu/obez hastalara yaşam şeklinde değişikliklere yönelik tavsiyeler, diyet tedavisi, davranışsal tedavi, ilaç tedavileri ve cerrahi prosedürler hakkında bilgi vermelidir. ...
... These two diseases are frequently associated with inflammatory responses [13,14], insulin resistance [15,16], and metabolic syndrome [17,18] and have been postulated to interact with each other through these pathways. Chronic periodontitis (CP) has also been linked to various systemic conditions, including cardiovascular disease [19], diabetes [20], obesity [21], and dyslipidemia [22]. In particular, interest in the interaction between these two conditions has increased as a result of studies demonstrating that chronic periodontitis can exacerbate NAFLD progression by increasing the level of systemic inflammation [23,24]. ...
... Obesity is a well-established risk factor for chronic periodontitis, primarily mediated through systemic inflammation. Elevated BMI, waist circumference, and body fat are strongly associated with increased risks of periodontitis, with inflammatory mediators such as TNF-α and IL-6 playing critical roles [21]. It provides strong epidemiological evidence linking severe periodontitis to an increased risk of atherosclerotic CVD, with possible mechanisms involving systemic inflammation and the presence of periodontal pathogens in atherothrombotic tissues [40]. ...
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Background: Chronic periodontitis (CP) and metabolic dysfunction-associated steatotic liver disease (MASLD) have emerged as interconnected conditions with shared mechanisms, such as systemic inflammation and metabolic dysregulation. However, the risk of CP in the newly classified subgroups of steatotic liver disease (SLD), including MASLD and metabolic alcohol-associated liver disease (MetALD), has not been extensively studied. This study investigated the association between SLD subtypes and the incidence of CP in a nationwide cohort. Methods: This retrospective cohort study used data from the Korean National Health Insurance Service database. The study included 115,619 participants aged 40 and older who underwent health screenings between 2009 and 2010. The participants were classified into four groups: normal without risk factors, normal with risk factors, MASLD, and MetALD. The primary outcome was the incidence of CP as defined by ICD-10 codes and dental treatment records. Hazard ratios (HRs) were calculated using the Cox proportional hazards model and adjusted for demographic, clinical, and lifestyle factors. Results: Over a mean follow-up of 7.4 years, individuals with MASLD and MetALD had significantly higher risks of developing CP compared with the normal group without risk factors (MASLD: adjusted HR 1.14, 95% confidence interval (CI): 1.11–1.17; MetALD: adjusted HR 1.21, 95% CI: 1.15–1.27). The risk was more pronounced for severe CP, particularly for those with MetALD (adjusted HR 1.29, 95% CI: 1.22–1.36). Subgroup and sensitivity analyses confirmed these findings across the various definitions of hepatic steatosis and metabolic risk factors. Conclusions: This study reveals that individuals with MASLD and MetALD are at an elevated risk of developing CP, highlighting the need for integrated care strategies that address both periodontal health and metabolic liver conditions. These findings underscore the importance of periodontal health management in reducing the risk of CP among SLD populations.
... With the continuous advancement of oral implant technology, clinical research confirms the feasibility of immediate implants for periodontitis patients. Periodontitis is a prevalent periodontal disease seen in clinical practice (Arboleda et al., 2019). As the name suggests, it is a chronic inflammation of the tissue surrounding the tooth, which leads to the gradual loss of attachment. ...
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Background With the advancement of oral implant technology, immediate implant placement is believed to be feasible for periodontitis patients. However, there is a lack of high-quality clinical studies regarding this approach. This study aimed to observe the short-term implant survival rate and conditions of peri-implant tissues in periodontitis patients who received immediate implants without systematic periodontal treatment. Methods This retrospective study included 95 patients and 234 implants treated at the Stomatological Hospital of Jinan University from June 2017 to December 2022. Patients were classified according to the 2018 AAP/EFP periodontal classification system, with Stage determined by CBCT-assessed marginal bone loss (MBL) and Grade estimated based on annual bone loss rate, smoking status, and diabetes history. Immediate implant placement was performed following atraumatic tooth extraction, with bone defects augmented using Bio-Oss bone graft and covered with Bio-Gide collagen membrane as needed. Patients were followed up for 12 months, during which implant survival, modified sulcus bleeding index (mSBI), modified plaque index (mPLI), marginal bone loss (MBL), and peri-implant probing depth (PPD) were assessed. Results A total of 95 patients (234 implants) were included, with a mean age of 58.59 years. The distribution of Stage II-IV and Grade A-C periodontitis was recorded. Preoperative assessments showed a significant increase in P-PDD, CAL, and MBL with greater disease severity (p < 0.001). One-year follow-up data indicated an implant survival rate of 97.86%, with Kaplan-Meier survival analysis revealing significantly lower survival rates in Stage IV and Grade C patients (p < 0.05). Postoperative soft tissue health assessment showed significant differences in mSBI and mPLI between stages (p = 0.002, p = 0.007) but not grades (p > 0.05). PPD did not differ significantly among groups (p > 0.05), whereas MBL was significantly higher in Stage IV than in Stage II and III (p < 0.001), though no significant differences were observed across grades (p > 0.05). Clinical and radiographic evaluations demonstrated favorable implant outcomes, with most patients reporting high satisfaction. These findings reinforce the viability of immediate implant placement in periodontitis patients, demonstrating high short-term success rates across different disease severities. While disease severity and progression rate may influence clinical outcomes, appropriate case selection, meticulous surgical techniques, and comprehensive postoperative care can lead to predictable and favorable implant success, even in patients with periodontitis.
... A previous epidemiological study assessed the effect of obesity on the onset and progression of periodontitis. Results showed that elevated body mass index, WC, percentage of subcutaneous fat, and blood lipid levels are associated with an increased risk of developing periodontitis [1]. In terms of the underlying biological mechanism for this association, adipose tissue-derived cytokines, such as tumor necrosis factor-alpha and interleukin-6, can affect systemic metabolism and contribute to the development of low-grade systemic inflammation [24]. ...
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Background The rising obesity rates are accompanied by an increasing prevalence of insulin resistance (IR) associated with obesity. To ascertain the best index for replacing IR, this study aimed to investigate the possible association between IR, which was assessed using the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), and the triglyceride–glucose (TyG) index and its derived indexes and periodontitis. Methods The association between the indicators of IR and periodontitis was assessed via multivariate-adjusted logistic regression analyses using data from the National Health and Nutrition Examination Survey (NHANES) 2009–2014. In addition, subgroup analyses and receiver operating characteristic curve analyses were conducted to explore possible influencing factors. Results Our study encompassed 1,588 participants, and 41.0% were diagnosed with periodontitis. Based on the multivariate logistic regression analysis, a higher TyG-waist-to-height ratio (WHtR) (odds ratio [OR] = 1.14, 95% confidence interval [CI]: 1.02–1.27, P = 0.0244) and HOMA-IR score (OR = 1.00, 95% CI: 1.00–1.00, P = 0.0028) were associated with an increased risk of periodontitis. Conversely, the TyG index, TyG-adjusted for body mass index, and TyG-adjusted for waist circumference (WC) were not associated with periodontitis. According to further subgroup analyses and interaction result analyses, sex affected the association between the TyG index, TyG-WC, and TyG-WHtR and periodontitis (P < 0.05 for interaction). Moreover, the influence of age regulated the association between periodontitis and both TyG and HOMA-IR score. In terms of diagnostic accuracy, the area under the receiver operating characteristic curve analysis revealed that HOMA-IR score and TyG-WHtR slightly outperformed the TyG index, TyG-body mass index, and TyG-WC. Thus, they can be robust markers for assessing IR-related periodontitis risk. Conclusion A consistent and positive association was found between HOMA-IR score and TyG-WHtR and the odds of periodontitis prevalence. Hence, HOMA-IR score and TyG-WHtR were significantly associated with periodontitis in this cross-sectional study. However, prospective studies are needed to determine whether higher TyG-waist-to-height ratio and HOMA-IR score can predict the occurrence of periodontitis.
... A literature search reveals that the prevalence of periodontitis was high in obese patients and there exists a positive association between obesity and periodontitis (Kongstad et al. 2009;Arboleda et al. 2019;Saito et al. 2001). However, to date, only one study has assessed the relationship between body mass index and the severity of periodontitis (Çetin et al. 2022). ...
Article
Full-text available
Objectives This study aimed to assess the relationship between body mass index (BMI) classification and the severity of periodontitis, recognizing that both obesity and periodontitis involve chronic inflammatory processes, which may exacerbate one another. Materials and Methods A cross‐sectional study was conducted on a convenience sample of 162 consecutive outpatients who reported to the Department of Periodontics, Saveetha Dental College and Hospitals in Chennai from March 2023 to September 2023. Age, gender, Russell's periodontal index, and BMI were recorded. The association between age, gender, BMI, and severity of periodontitis was analyzed using linear‐by‐linear χ² association. Ordinal logistic regression analysis was employed to assess the odds ratio (OR) of age, gender, and BMI with the severity of periodontitis. Results A statistically significant association was observed between age, gender, BMI, and the severity of periodontitis (p < 0.05). Participants aged 35‐60 years had an OR of 1.305 for severe periodontitis (95% CI: 0.754–1.561). Males exhibited a higher risk of severe periodontitis (OR: 1.171; 95% CI: 0.894–2.485). Obese participants showed an OR of 1.417 for severe periodontitis compared to overweight participants (OR: 0.683; 95% CI: 0.817–1.629). Conclusions Severe periodontitis was more prevalent among obese individuals, followed by overweight individuals. Obesity may be considered a potential risk indicator for the development and progression of periodontitis.
... Metabolic syndrome is characterized by a combination of metabolic disorders that become evident when an individual exhibits three or more interconnected risk factors, including abdominal obesity, arterial hypertension, dyslipidemia and hyperglycemia (Alberti et al., 2009;Lamster & Pagan, 2017). It is believed that the heightened release of cytokines originating from adipose tissue promotes low-grade systemic inflammation, which is eventually associated with inflammatory diseases, such as chronic oral inflammation (Arboleda et al., 2019). ...
Article
Aim This study aimed to explore the possible bidirectional interrelations between fructose‐induced metabolic syndrome (MS) and apical periodontitis (AP). Methodology Twenty‐eight male Wistar rats were distributed into four groups ( n = 7, per group): Control (C), AP, Fructose Consumption (FRUT) and Fructose Consumption and AP (FRUT+AP). The rats in groups C and AP received filtered water, while those in groups FRUT and FRUT+AP received a 20% fructose solution mixed with water to induce MS. The groups AP and FRUT+AP had the pulp of their right mandibular first molar exposed to induce AP. Food consumption, murinometric measurements, blood glucose levels and glucose tolerance were monitored. Fifty‐six days after the start of the experiment, the animals were euthanized, and serum samples were collected for metabolomic analysis. Mandibles, livers and right kidneys were also collected. The area and volume of the periapical lesions were calculated using micro‐computed tomography. Histopathological evaluation was performed. Kruskal–Wallis followed by the Student–Newman–Keuls or Mann–Whitney tests and one‐way anova followed by Tukey's or Independent t ‐test were used for non‐parametric and parametric data, respectively ( p < .05). Multivariate analysis and variable importance in projection score were applied to assess metabolite profile differences among groups ( p < .05). Results FRUT and FRUT+AP groups showed significantly increased fluid intake, body mass, abdominal circumference, blood glucose levels, liver weight and visceral fat weight ( p < .05), indicating the development of MS. The analyses of the metabolite profile suggest increasing glucose, histidine, lactate, fatty acid and phenylalanine in the FRUT+AP group. There were no significant differences in volume and area of periapical lesions in micro‐CT analyses ( p = .1048 and p = .7494, respectively). Histopathological analysis of the hemimandibles demonstrated areas of inflammatory response, necrosis and microabscess in the periapical region. Hepatic histopathological observations indicated notable differences in cell appearance, with the FRUT and FRUT+AP groups showing signs of microsteatosis. Kidney analysis revealed Bowman's space dilation in the FRUT and AP groups, while the FRUT+AP group exhibited retracted Bowman's space, suggesting a possible alteration in renal filtration capacity. Conclusions MS had no impact on the progression of AP in rats. However, AP exacerbated the systemic state affected by MS, with changes in liver and kidney tissues and metabolite levels.
... These proteins are bioactive molecules with hormonal properties and a structure similar to cytokines produced by the adipose tissue [22] the greater the amount of adipose tissue, the higher the levels of leptin, interleukin IL-1 and IL-6, and tumor necrosis factor (TNF)-α. Increasing inflammatory cytokine levels in the gingival crevicular fluid hasten the progression of periodontal disease [23,24]. Hence, there is positive scientific evidence of the link between periodontal disease and overweight/obesity [23]. ...
Article
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Background: The pediatric population is one of the social groups most affected by oral pathology, and overweight and/or obesity is increasingly frequently observed. This work presents a study of the prevalence of oral disease in the school population in Mallorca and its relationship with overweight/obesity. Methods: A cross-sectional study was carried out with a sample of 718 students aged 5–6 (n = 255), 12 (n = 230) and 15 years (n = 233). The WHO criteria for diagnosing and coding examined teeth and overweight/obesity prevalence values. To explore the differences in data, the mean was analyzed using the Student’s t-test or a one-way analysis of variance followed by the Bonferroni post hoc analysis. Results: Results found that students aged 15 years have a caries prevalence rate of 45.49%, higher than those aged 12 (27.39%). The presence of dental calculus in 15-year-old students is 52.8%, even higher than in 12-year-olds (30%). Students aged 6 and 12 with lower weight percentiles have fewer healthy teeth than those with higher percentiles. Conclusions: The schoolchildren have experienced a decrease in caries and an increase in periodontitis, with weight percentile potentially influencing the number of healthy teeth.
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Objective: To investigate the relationship between body mass index and periodontal diseases by conducting a comprehensive survey to assess daily eating habits and self-care of oral hygiene. Material and Methods: We recruited 357 patients from the outpatient clinic of the Periodontology Department at Baskent University Hospital. All the patients completed a comprehensive survey after their periodontological examination. The questionnaire asked about their daily eating habits and oral hygiene self-care during the last six months. Results: Patients with periodontitis had higher body-mass-index (BMI) than those with gingivitis (26.9 ± 4.3 kg/m² vs 24.7 ± 3.8 kg/m², respectively, p=0.000). The periodontitis group had higher tea consumers than those with gingivitis (46,7% vs. 30,3%, respectively, p=0.001). The group with gingivitis had higher coffee consumers than those with periodontitis (17.7% vs 3.8 %, respectively, p=0.000). There were more diabetic patients in the periodontitis group (10.9% vs. 2.9%, respectively, p=0.003). The percentage of cases with periodontitis was 71.4% in obese patients. The frequency of periodontitis was significantly correlated with the BMI (Pearson correlation 0.2229, p=0.000). Conclusion: Individuals with a higher BMI were more likely to have periodontitis, consume more tea, and have diabetes.
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Background Periodontal disease (PD) is a prevalent, preventable and treatable oral infection associated with substantial morbidity globally. There is little information from population‐representative cohort studies about the sociodemographic, educational and other early life factors that stratify PD risk. Methods We used data from the U.S. ‘High School and Beyond’ (HS&B:80) study, which has followed a nationally representative sample of 26,820 people from high school in 1980 through midlife in 2021. Data from the 1980s include information about education, early life circumstances, spatial location and demographic attributes. Data from 13,080 sample members who responded in 2021 include indicators of self‐reported PD diagnosis. Results People with higher degrees and course grades have a lower risk of midlife PD. Rural adolescents and those who attended private schools are also at lower risk. We find little evidence of heterogeneity in correlates of midlife PD by gender or race/ethnicity. Conclusions The quantity and characteristics of people's schooling and their location of residence are associated with midlife PD.
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Background: Studies have identified a possible link between obesity, overweight, and gingival inflammation. The objective of this study was to investigate whether overweight and obesity are associated with a higher prevalence of gingival bleeding among university students. Methods: Data were collected from 2089 students in 2016 through a self-administered questionnaire. Gingival inflammation was assessed with the question, “Does your gum bleed when you brush your teeth?” Responses were classified as “yes” or “no”. Body mass index (BMI) was assessed based on self-reported weight and height, following WHO standards: Normal (<25), Overweight (25–30), and Obesity (>30). A Poisson regression model was applied to analyze the association between BMI categories and gingival bleeding prevalence. Results: The prevalence of gingival inflammation was 50.8% and the prevalence of obesity and overweight was 8% and 23%, respectively. Obese individuals demonstrated a 32% higher prevalence of gingival bleeding compared to those with a normal BMI (PR=1.32, 95%CI [1.17–1.49]). Overweight students showed no significant association with gingival bleeding (PR=1.01, 95%CI [0.91–1.13]). Conclusion: Obesity was associated with a higher prevalence of gingival bleeding, while overweight status showed no significant association. These results suggest that obesity, rather than overweight, is associated with increased gingival inflammation.
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Background: This report presents weighted average estimates of the prevalence of periodontitis in the adult US population during the 6 years 2009-2014 and highlights key findings of a national periodontitis surveillance project. Methods: Estimates were derived for dentate adults 30 years or older from the civilian noninstitutionalized population whose periodontitis status was assessed by means of a full-mouth periodontal examination at 6 sites per tooth on all non-third molar teeth. Results are reported according to a standard format by applying the Centers for Disease Control and Prevention/American Academy of Periodontology periodontitis case definitions for surveillance, as well as various thresholds of clinical attachment loss and periodontal probing depth. Results: An estimated 42% of dentate US adults 30 years or older had periodontitis, with 7.8% having severe periodontitis. Overall, 3.3% of all periodontally probed sites (9.1% of all teeth) had periodontal probing depth of 4 millimeters or greater, and 19.0% of sites (37.1% of teeth) had clinical attachment loss of 3 mm or greater. Severe periodontitis was most prevalent among adults 65 years or older, Mexican Americans, non-Hispanic blacks, and smokers. Conclusions: This nationally representative study shows that periodontitis is a highly prevalent oral disease among US adults. Practical implications: Dental practitioners should be aware of the high prevalence of periodontitis in US adults and may provide preventive care and counselling for periodontitis. General dentists who encounter patients with periodontitis may refer these patients to see a periodontist for specialty care.
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Background: Obesity is a very prevalent chronic disease worldwide and has been suggested to increase susceptibility of periodontitis. The aim of this paper was to provide a systematic review of the association between obesity and periodontal disease, and to determine the possible mechanisms underlying in this relationship. Material and methods: A literature search was carried out in the databases PubMed-Medline and Embase. Controlled clinical trials and observational studies identifying periodontal and body composition parameters were selected. Each article was subjected to data extraction and quality assessment. Results: A total of 284 articles were identified, of which 64 were preselected and 28 were finally included in the review. All the studies described an association between obesity and periodontal disease, except two articles that reported no such association. Obesity is characterized by a chronic subclinical inflammation that could exacerbate other chronic inflammatory disorders like as periodontitis. Conclusions: The association between obesity and periodontitis was consistent with a compelling pattern of increased risk of periodontitis in overweight or obese individuals. Although the underlying pathophysiological mechanism remains unclear, it has been pointed out that the development of insulin resistance as a consequence of a chronic inflammatory state and oxidative stress could be implicated in the association between obesity and periodontitis. Further prospective longitudinal studies are needed to define the magnitude of this association and to elucidate the causal biological mechanisms.
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Background: Obesity and periodontitis are important chronic health problems. Obesity is associated with an increased prevalence of periodontitis. Whether obesity also affects the outcome of non-surgical periodontal therapy is to date still unclear. Methods: A systematic review of studies referenced in SCOPUS, MEDLINE, PubMed, Cochrane, CINAHL, Biosis and Web of Science was performed. Titles, abstracts and finally full texts were scrutinized for possible inclusion by two independent investigators. Quality and heterogeneity of the studies were assessed and the study designs were examined. Probing pocket depth reduction was analyzed as primary surrogate parameter for therapeutic success after non-surgical periodontal therapy. Results: One-hundred-and-fifty-nine potentially qualifying studies were screened. Eight studies fulfilled the inclusion criteria and were analyzed. Three of eight studies failed to show an influence of obesity on pocket depth reduction after non-surgical therapy. The remaining five studies documented a clear negative effect on the outcome of non-surgical periodontal therapy. The finally included studies did not correspond to the highest level of quality (RCTs). Due to the heterogeneity of the data a meta-analysis was not possible. Conclusion: The literature on the effect of obesity on the treatment outcome of non-surgical periodontal therapy remains controversial. The data, however, support that obesity is not only a factor associated with poorer periodontal health but might also result in inferior response to non-surgical treatment of periodontitis.
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To investigate the cytokine profile as biomarkers in the gingival crevicular fluid (GCF) of chronic periodontitis (CP) patients with and without obesity. MEDLINE/PubMed, EMBASE, Science direct, and SCOPUS databases were combined with hand searching of articles published from 1977 up to and including May 2016 using relevant MeSH terms. Meta-analyses were conducted separately for each of the cytokines; resistin, adiponectin, TNF-α, leptin, IL-6, IL-8, and IL-1β. Forest plots were produced reporting standardized mean difference of outcomes and 95% confidence intervals. Eleven studies were included. Three studies showed comparable levels of leptin among obese and non-obese patients with CP. Four studies reported comparable levels of interleukin (IL)-6 and resistin whereas five studies reported comparable levels of adiponectin. Two studies reported similar levels of CRP in patients with periodontitis with and without obesity. One study showed higher levels of tumor necrosis factor-alpha in obese patients with CP. One study showed higher levels of IL-1β and IL-8 in obese patients with CP. The level of localized periodontal inflammation may have a greater influence on the GCF proinflammatory biomarker levels as compared to systemic obesity. Whether patients having chronic periodontitis with obesity have elevated proinflammatory GCF biomarkers levels than non-obese individuals remains debatable.
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Objective: To determine population-average risk profiles for severe and non-severe periodontitis in US adults (30 years and older) using optimal surveillance measures and standard case definitions. Methods: We used data from the 2009-2012 National Health and Nutrition Examination Survey (NHANES), which for the first time used the "gold standard" full-mouth periodontitis surveillance protocol to classify severity of periodontitis following the suggested CDC/AAP case definitions. The probabilities of periodontitis by socio-demographics, behavioral factors, and co-morbid conditions, were assessed using prevalence ratios (PR) estimated by the predicted marginal probability from multivariable generalized logistic regression models. The analyses were further stratified by gender for each classification of periodontitis. Results: The likelihood of periodontitis increased with age for overall and non-severe relative to non-periodontitis. Compared to non-Hispanic whites, periodontitis was more likely among Hispanics (aPR=1.38; 1.26-1.52) and non-Hispanic blacks (aPR=1.35; 1.22-1.50), whereas severe periodontitis was most likely among non-Hispanic blacks (aPR=1.82; 1.44-2.31). There was at least a 50% greater likelihood of periodontitis among current smokers compared to non-smokers. Among males, the likelihood of periodontitis among adults 65 years and older was greater (aPR=2.07; 1.76 - 2.43) than adults 30-44 years old. This probability was even greater among women (aPR=3.15; 95% CI 2.63 - 3.77). The likelihood of periodontitis was higher among current smokers relative to non-smokers regardless of gender and periodontitis classification. Periodontitis was more likely among men with un-controlled diabetes compared to persons with no diabetes only. Conclusions: An assessment of risk profiles for periodontitis in US adults based on gold standard periodontal measures show important differences by severity of disease and gender. Cigarette smoking, specifically among current smokers remains an important modifiable risk for all levels of periodontitis severity. The higher likelihood of periodontitis in older adults and in males with uncontrolled diabetes is noteworthy. These findings could improve the identification of target populations for effective public health interventions to improve periodontal health of US adults.
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Aim The aim of this study was to systematically review the literature to answer the questions: (i) “Is periodontal treatment effective to improve clinical and immunological conditions in obese subjects?”; (ii) “Do obese subjects present different clinical and immunological response after periodontal therapy when compared to non-obese subjects?” Methods Searches were performed in six databases up to August 2014. Interventional studies were included if the following data were described: (1) Obesity/overweight assessment; (2) definition of periodontal disease; (3) periodontal therapy; (4) inflammatory marker in serum/plasma, and/or clinical parameters of periodontal disease. Assessment of quality was performed with the Downs and Black scale. Meta-analyses were conducted with the available data. Results Of 489 articles, 5 were included, and only 3 proceeded to meta-analysis of clinical outcomes. Included studies presented fair methodological quality. Statistical analysis demonstrated that periodontal therapy in obese subjects was effective to improve clinical outcomes. No clinical differences between post-therapy results of obese and non-obese were observed. Effects of periodontal therapy on inflammatory markers remain unclear. Conclusions Periodontal treatment seems to be effective to improve healing in obese individuals. No differences on periodontal healing between obese and non-obese subjects were observed; however, only limited and fragile base of evidence was available for analysis. Clinical relevance Periodontal treatment is effective to improve clinical and immunological periodontal parameters in adults. Also, obesity seems to not modify the periodontal healing after treatment.
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Obesity is a chronic disease that is strongly associated with an increase in mortality and morbidity including certain types of cancer, cardiovascular disease, disability, diabetes mellitus, hypertension, osteoarthritis, and stroke. In adults, overweight is defined as a body mass index (BMI) of 25 kg/m(2) to 29 kg/m(2) and obesity as a BMI of greater than 30 kg/m(2). If current trends continue, it is estimated that, by the year 2030, 38% of the world's adult population will be overweight and another 20% obese. Significant global health strategies must reduce the morbidity and mortality associated with the obesity epidemic.
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In recent years, it has become apparent that the pathogenesis of periodontal diseases is more complex than the presence of virulent microorganisms. In fact, it is now widely accepted that susceptibility to periodontitis varies greatly between individuals who harbor the same pathogenic microflora. To date, the bulk of evidence points to the host response to bacterial challenge as a major determinant of susceptibility. In this review, we will assess the data implicating various inherited and acquired risk factors for susceptibility to periodontal diseases.