A Review of the Relationship between Obesity and Periodontal Diseases Volume 1 - Issue 3
Jiabao Sun BA, Kristin Williams and Leena Palomo*
Department of Periodontology, School of Dental Medicine, Case Western Reserve University, USA
Received: July 29, 2017; Published: August 10, 2017
Corresponding author: Leena Palomo, Department of Periodontology, School of Dental Medicine, Case Western Reserve University, 2124 Cornell Road,Cleveland, Ohio 44106, USA
Aim: To explore the influence of obesity/overweight on development and treatment outcome of periodontal diseases (PD), and to explore
possible mechanisms of interaction between obesity and PD.
Methods:A literature search was conducted using the PubMed and Go Pubmed databases.
Conclusion: Obesity and PD can exert similar pathogenic effects via common pathways, and can influence each other bidirectionally.
Elucidating the relationship between obesity and PD allows for the development of care guidelines and recommendations for clinicians and
the public.
Obesity and periodontal diseases (PD) are very prevalent
among U.S. adults during recent years [1-4]. Since both can lead to
severe chronic health conditions and impair people’s life quality
by exerting similar influences [5-10], a clear understanding of the
association between obesity and periodontal diseases is warranted
to reduce health and medical costs in the U.S. [5] The objective of
this review is to explore the influence of obesity/overweight on
development and treatment outcome of PD, and to explore possible
mechanisms of interaction between obesity and PD.
PubMed and Go Pubmed were used to search for related
preclinical, observational, clinical studies and meta-analyses
that investigated the relationship between obesity and PD. They
were reviewed to determine the association and to summarize
mechanisms of interaction between the conditions. Combinations
of “obesity” or”overweight” or “fat-induced obesity” or “weight
changes” AND“gingivitis” or “periodontitis” or “periodontal diseases”
were used as key terms. Studies conducted in the past six years
PD and obesity can cause and/or facilitate the development
and progression of similar systemic diseases and conditions,
which include metabolic syndrome [9-16], type 2 diabetes mellitus (T2DM) [17,18], cardiovascular diseases (CVD) [19-21], alveolar
bone loss [22-24], rheumatic diseases[17,25-34], and a series
of cancers [32-38]. Because of the pro-inflammatory cytokines
and adipokines released by adipocytes [9-16], obesity has been
consistently shown to be significantly associated with increased
risk and worsened prognosis of metabolic syndrome, T2DM, CVD,
breast cancer and pancreatic cancer. Meanwhile, PD has been
found to have similar relationship with these diseases because
of the pro-inflammatory effects caused by virulent factors and
antigens of periodontal pathogens such as Fusobacterium species,
T. denticolaand P.gingivalis [37-41]. Fusobacterium species have
even been detected in pancreatic tissues of patients suffering from
pancreatic ductal adenocarcinoma [38]. At the same time, although
alveolar bone loss is the hallmark of PD [22], it has been found
that each unit increase in BMI is associated with a 5% increase in
the risk of alveolar bone loss, and that every 1% increase in waist
circumference to height ratio is associated with 3% increase in risk
of progression of alveolar bone loss [23,24].
PD and obesity are very likely to interact through their
shared inflammatory pathways to influence diseases mentioned
above [42]. Although they initiate inflammation via different
mechanisms [39,40,43-45], their similar effects on the same
set of biomarkers involved in pathogenesis indicate that lots of
common inflammatory pathways are involved in subsequent steps
[14,40,42]. Among these biomarkers, resistin, TNF-alpha, and IL-6 are commonly tested for [46,47]. PD elevates levels of these
biomarkers mainly through bacterial invasion [39,41,46,48,49].
For instance, lipo polysaccharide of P. gingivalisis able to induce the
secretion of resistin from neutrophils [46]. Karilysin, a proteolytic
enzyme of T. forsythia, can induce the release of active TNF-alpha
[39,50]. Moreover, PD increases serum IL-6 by lowering the
methylation level of IL-6 DNA promotor in patients’ gingival tissue
and peripheral tissue [48,49]. Increased levels of these biomarkers
in obese individuals are mainly due to the excessive amount of
adipose tissues [31,51,52].
It is noteworthy that resistin [46,51,53-58], TNF-alpha [50,59-
61], and IL-6 [62-69] can participate in many pathogenic pathways.
For example, adipose tissue-released TNF-alpha can activate the
NF-κB pathway, causing reduced adipocyte insulin sensitivity and
increased expression of endothelial cell adhesion proteins, ICAM-
1 and VCAM-1, which will lead to endothelial proliferation and
increase the risk of atherosclerosis [59,60]. IL-6 can also participate
in the NF-κB pathway to promote the transition of human vascular
interstitial cells toward an osteoblastic phenotype, inducing aortic
valve mineralization and vascular inflammation [66]. Furthermore,
IL-6 has been found to participate in mechanisms impairing
glycemic control [67-69].
Besides exerting similar pathogenic mechanisms on a set of
conditions, PD and obesity can influence each other directly as well
[70,71]. Studies have consistently demonstrated that obesity and its
various endpoints are positively associated with increased risk and
severity, and worse treatment outcome of PD [72-80]. Since visceral
adipose tissue releases more pro-inflammatory cytokines than
subcutaneous fat, central adiposity tends to induce more severe oral
connective tissue breakdown and inflammation in periodontium
[75-77]. Moreover, obesity can alter the expression of essential
microRNAs of gingival tissues to facilitate PD progression [80].
On the other hand, since PD has been observed to elevate serum
level of leptin [81-85], PD may inhibit the progression of obesity
[86,87]. Non-surgical treatments of PD can also significantly reduce
the serum level of inflammatory biomarkers, and even improve the
glycemic control in patients with metabolic syndrome [79,87].
In conclusion, PD and obesity can collectively influence the
risk of many chronic systemic diseases, as well as several types
of cancers, due to their shared signaling pathways, including
adipokine-related pathways and leptin. Furthermore, because
of the bidirectional relationship between obesity and PD, wellmanaged
periodontal status is likely to prevent progression of
many obesity-induced diseases. Weight loss may also improve
the health of periodontium. Last but not the least, elucidating the
relationship between obesity and PD allows for the development of
care guidelines and recommendations for clinicians and the public.
ISSN: 2574 -1241
