PERIODONTAL DISEASE AMONG COMMUNITY-DWELLING DIABETICS:
EVIDENCE FROM A DIABETES EDUCATION AND PROMOTION EVENT
by
David C. Hay
DMD, Temple University, 2013
Submitted to the Graduate Faculty of
the Multidisciplinary MPH Program
Graduate School of Public Health in partial fulfillment
of the requirements for the degree of
Master of Public Health
University of Pittsburgh
2015
i
UNIVERSITY OF PITTSBURGH
GRADUATE SCHOOL OF PUBLIC HEALTH
This essay is submitted
by
David C. Hay
on
March 31, 2015
and approved by
Essay Advisor:
David Finegold, MD
Professor of Human Genetics
Director Multidisciplinary MPH Program
Graduate School of Public Health
University of Pittsburgh
_______________________________________
Essay Reader:
Pouran Famili, DMD, MDS, MPH, PhD
_______________________________________
Professor, Department of Periodontics and Preventive Dentistry
Professor, Clinical and Translational Science Institute
School of Dental Medicine
University of Pittsburgh
ii
Copyright © by David C. Hay
2015
iii
David Finegold, MD
PERIODONTAL DISEASE AMONG COMMUNITY-DWELLING DIABETICS:
EVIDENCE FROM A DIABETES EDUCATION AND PROMOTION EVENT
David C. Hay, MPH
University of Pittsburgh, 2015
ABSTRACT
Periodontal disease is a chronic inflammatory condition and a major cause of tooth loss. The
public health impact of periodontal disease is great. Nearly half of adults in the United States are
affected by some degree of periodontal disease. The prevalence of periodontal disease increases
with age and is closely related to certain systemic diseases such as diabetes. Diabetes is a chronic
metabolic disease associated with a hyper-inflammatory state. Well-controlled diabetes will help
to improve the periodontal condition, decreasing the public health impact of the disease.
Objective. The objective of this investigation was to study the prevalence of periodontal disease
in a population of community-dwelling adults attending an all-day diabetes awareness and
education event.
Methods. Retrospective study of periodontal disease and its relationship with diabetes. Data
were collected from attendees at the Diabetes Expo in Pittsburgh, Pennsylvania, an event
sponsored by the American Diabetes Association. Informed consent was obtained.
iv
Comprehensive periodontal examinations were performed. Information on age, gender,
education, smoking, diabetes, periodontal disease, and oral health were collected and analyzed.
Results. Participants = 206 individuals; 97 respondents had periodontal disease and 147 did not.
Ninety-three (93) individuals (47.9%) without periodontal disease had diabetes and fifty-four
(54) individuals (36.3%) did not have diabetes; this finding was not significant (p=0.847). Good
oral health was important among the people attending this event. Those with good oral health
had less diabetes compared to people with poor oral health; this finding was statistically
significant (p=0.004).
Conclusion. Retrospective investigation of periodontal disease among community-dwelling
diabetics in this study revealed no significant relationship between diabetes and periodontal
disease (p=0.847), although oral health was an important, significant factor (p=0.004). Further
prospective research with larger sample size is recommended to confirm these findings.
v
TABLE OF CONTENTS
1.0
INTRODUCTION ........................................................................................................ 1
1.1
BACKGROUND ..................................................................................................2
1.1.1
Periodontal disease pathogenesis/Etiology…….……………………………2
1.1.2
Classification of disease………………………………………………………3
1.1.3
Prevalence of disease…………………………………………………………4
1.2
RISK FACTORS………………………………………......................................4
1.2.1
Bacterial plaque and host response………………………………………….4
1.2.2
Smoking ............................................................................................................ 5
1.2.3
Race ............................................................................................................ …...6
1.2.4
Gender .............................................................................................................. 6
1.2.5
Socioeconomic Status ...................................................................................... 7
1.2.6
Age..................................................................................................................... 7
1.2.7
Systemic Disease .............................................................................................. 8
vi
1.3
DIABETES PATHOGENESIS……………………………..............................9
1.3.1
Prevalence....................................................................................................... 11
1.3.2
Risk factors for diabetes................................................................................ 11
1.3.3
Periodontal disease and diabetes .................................................................. 13
2.0
METHODOLOGY..................................................................................................... 16
3.0
RESULTS ................................................................................................................... 17
4.0
DISCUSSION ............................................................................................................. 20
5.0
CONCLUSION........................................................................................................... 22
BIBLIOGRAPHY ....................................................................................................................... 23
vii
LIST OF TABLES
Table 1. Logistical regression test to show the association between individual covariates and the
outcome of interest (Gum Disease)…........................................................................................... 18
Table 2. Multivariate logistical regression…............................................................................... 19
viii
1.0
INTRODUCTION
Periodontitis is a chronic inflammatory disease of the oral cavity, which causes destruction of the
periodontium. The periodontium acts as the support mechanism for the teeth and is made up of
cementum, the periodontal ligament, and alveolar bone. As the periodontium is destroyed, teeth
may become loose and eventually can be lost. The public health impact of periodontal disease is
great. Nearly half of the United States population is affected by some degree of periodontal
disease.1
A major risk factor for periodontal disease is diabetes. Diabetes is a metabolic disease
where those affected either do not produce insulin or are resistant to its action. It is estimated that
27.8% of those with diabetes remain undiagnosed.2 Of those who are aware of their diabetic
status, a large proportion is unable to adequately control their disease. Uncontrolled diabetes can
lead to many systemic complications including damage to microvasculature and compromised
healing. The connection between diabetes and periodontal disease is well documented in the
literature.3-6 The systemic effects of diabetes increase susceptibility to periodontal disease,
making diabetics an at-risk population for periodontitis.
The public health implications of periodontal disease are great. Progressive alveolar bone
loss, if left untreated, will eventually lead to tooth loss and partial or full edentulism. Decreased
masticatory function can have adverse nutritional effects including decreased vegetable intake
1
and high fat, low fiber diets.7 Nutritional tendencies such as these are large factors in the quickly
growing obesity epidemic in the United States.
1.1
BACKGROUND
1.1.1 Periodontal disease and pathogenesis/Etiology
Periodontal disease bears the most significant burden of oral disease. It is one of the world’s
most common dental diseases, highly prevalent worldwide.8,9 The primary etiology of
periodontal disease is bacterial plaque. Historically, any and all plaque biofilm was thought to be
disease causing. However, in 1979, Loesche presented the specific plaque hypothesis, which
states that dental decay and periodontal disease appear to be due to specific bacterial infections
following overgrowth of certain indigenous plaque bacteria.10 If the plaque biofilm is allowed to
form and attach to the tooth surface, an immunological response is mounted by the host to
combat the infection. It is due to this response that periodontal attachment in the form of
cementum, periodontal ligament, and alveolar bone, is destroyed. As destruction of the
periodontium progresses, the epithelial attachment to the tooth migrates down the root, forming a
periodontal pocket. As the depth of the pocket increases, it becomes increasingly difficult, if not
impossible, for the patient to clean. This further promotes biofilm growth and periodontal
destruction. It is only once the biofilm is removed and pockets corrected that the disease process
can be halted.
2
1.1.2 Classification of disease
In its earliest form, periodontal disease manifests as gingivitis. Clinical signs of inflammation are
notable and include edema, redness, and bleeding on probing. Histologically, inflammatory
infiltrates consisting of neutrophils, lymphocytes, and plasma cells are detectable.11 In gingivitis,
the inflammatory process is localized to the gingiva and does not cause destruction of the
periodontium. In some cases the disease remains confined to the gingiva, however, in a
susceptible patient, the lesion will progress and involve the alveolar bone. Once alveolar bone
destruction has occurred, gingivitis has progressed to periodontitis.
As classified by the 1999 International Workshop for a Classification of Periodontal
Disease and Conditions, there are four main forms of periodontitis; chronic periodontitis,
aggressive periodontitis, periodontitis as a manifestation of systemic disease, and necrotizing
periodontal diseases.12 Of these, the most common form is chronic periodontitis.
The degree of periodontal destruction is categorized as mild, moderate or severe. This is
determined based on the amount of clinical attachment loss present throughout the dentition.
Periodontitis is a progressive disease, however, not all individuals progress through the stages at
the same rate. In fact, research clearly demonstrates that some patients do not progress through
the stages at all. In a classic study by Löe et al. on Sri Lankan tea laborers who did not practice
oral hygiene, it was discovered that 8% displayed rapid progression of periodontal disease, 81%
displayed a moderate progression, and approximately 11% displayed no progression at all
beyond gingivitis.13
3
1.1.3 Prevalence of disease
Based on the most recent NHANES study, nearly half of the United States adult population
suffers from some type of periodontal disease1. This corresponds to 64.7 million people with
periodontitis. Moderate periodontitis was most common, with 30% of cases classified. Mild and
severe periodontitis were found to constitute 8.7% and 8.5% of the population, respectively.1
Rates of periodontitis were highest in men, non-Asian Hispanics, smokers, adults with less than a
high school education, and adults below 100% Federal Poverty Levels.1
1.2
RISK FACTORS FOR PERIODONTAL DISEASE
1.2.1 Bacterial Plaque and Host Response
Bacterial plaque is the primary etiology of periodontal disease. While there is a clear, causal
relationship between poor oral hygiene and gingivitis, the relationship of oral hygiene to
periodontitis is less clear.14 Conclusions from numerous studies in populations with poor oral
hygiene reveal that plaque accumulation correlates poorly with severe periodontitis.13, 15, 16 This
has led to the more recent investigation into the critical nature of the host response in the
literature. It has been discovered that bacteria are essential, but insufficient for disease and that
they account for only a small proportion of the variance in susceptibility for disease expression.17
However, hereditary factors can account for roughly 50% of the variance.18 Genetic disorders
4
such as familial cyclic neutropenia, trisomy, and Papillon-Lefevre syndrome are all strongly
associated with an increased susceptibility to periodontal disease due to their effects on
neutrophil number or function.19 More recently, the importance of IL-1 polymorphism has been
investigated. IL-1β, along with TNF-α, INF-γ, and PGE2, is greatly responsible for the
destructive processes affecting the periodontium. These normally protective compounds are
released by macrophages and monocytes when they become activated by lipopolysaccharide
from periodontal pathogenic bacteria. Individuals with a specific IL-1 polymorphism produce
about four times as much IL-1β as those who are genotype negative and are about twenty times
more likely to develop severe adult periodontitis.20
1.2.2 Smoking
Tobacco smoking has also been well documented as an independent risk factor for periodontal
disease, when controlling for other factors such as oral hygiene. Meta-analysis on data
examining the effect of smoking on periodontal attachment loss confirmed smoking as a risk
factor, revealing an odds ratio of 2.8.21 Another review of the literature reveals that smokers are
2.5 to 6 times more likely to develop periodontal disease than non-smokers, and that the number
of cigarettes smoked has a direct correlation with the risk of developing the disease.22 Both
systemic and local effects are known to be detrimental to periodontal health. Clinically, the
gingiva of smokers tends to be more fibrotic and display less bleeding, due to the decrease in
vascularity of the gingiva. Smokers also tend to have larger amounts of plaque, maxillary
anterior palatal attachment loss, and furcation involvement than non-smokers. It has also been
reported that smokers with periodontitis suffer from more severe disease than do similar
periodontitis patients who do not smoke.23
Smoking also renders non-surgical and surgical
5
treatment of periodontal disease less effective.24, 25 In fact, one study reported that approximately
90% of refractory periodontitis cases, periodontitis that does not respond at all to treatment, were
in smokers.26
1.2.3 Race
Based on the most recent NHANES data, periodontal disease is most common among Hispanics
and non-Hispanic blacks with a prevalence of 63.5% and 59.1%, respectively. Non-Hispanic
Asian Americans, with a prevalence of 50.0%, are the next most likely to be affected. The lowest
prevalence reported was 40.8% among non-Hispanic whites1. These results agree with a study by
Albandar et al. which demonstrated that United States subjects of African or Mexican descent
have greater attachment loss than Caucasians.27 However, the true role of race as an independent
risk factor for periodontal disease remains unclear, as the association is significantly reduced
when accounting for other factors such as smoking and socioeconomic status.28 It is quite
possible that the confounding effects of these other variables falsely represent the role of
race/ethnicity in periodontal disease susceptibility.
1.2.4 Gender
A generally consistent finding in all national surveys in the United States since the 1960s1, 29, 30, 31
is that periodontal disease is more prevalent among males than females. Though the true cause of
this trend is unknown, the hypothesis is that males tend to practice less effective oral hygiene,
visit a dentist less regularly, and have more negative attitudes about dental care than women. It is
6
unlikely that a true genetic difference predisposes males to periodontal disease more than
women.
1.2.5 Socioeconomic Status
As is the case with many other diseases, periodontal disease is more common among individuals
of lower socioeconomic status (SES).1,
32
This historically reported relationship is likely
attributable to multiple factors influenced by SES, such as education level and access to regular
dental care. Oral hygiene and attitudes toward oral health are typically higher among the better
educated. Higher SES groups are also more likely to have dental insurance to remove some of
the financial burden of oral care. Furthermore, dentists tend to be more readily available in
geographic locations with a higher SES population. Though the exact relationship is unknown, it
is clear that SES is part of a complex, multifactorial group of variables along with education,
location, and race, which make periodontal disease more prevalent among those of lower SES.
1.2.6 Age
It is clear from multiple cross-sectional surveys1;
33-37
that the prevalence and severity of
periodontal disease increase with age. For example, when examining the 2009-2010 NHANES
data, it showed prevalence rates of clinical attachment loss (CAL) increase with age. In the 30-34
year old age group, prevalence of periodontitis of any severity was 24.4%. Contrast this with the
≥65 year old age group, which displayed a prevalence of 70.1%.33 Of the varying severities of
periodontal disease, moderate periodontitis is the most common, with a prevalence of
approximately 30%. Examining the prevalence of moderate periodontitis amongst different age
7
groups again reveals that older individuals are more likely to exhibit disease. Only 13% of those
aged 30-34 years were found to have moderate periodontitis, whereas 53% of those in the ≥65
year old group were affected.33 Although this data may seem to represent periodontitis as a
disease of aging, this dated theory is no longer accepted.35, 36 The current view recognizes the
greater periodontal destruction observed in the elderly as reflecting lifetime disease accumulation
rather than an age-specific condition.4 It is also notable that the prevalence will likely continue
to rise as the United States population continues to age and, due to advances in oral care, these
elderly persons retain their teeth longer into life.
1.2.7 Systemic Disease
Due to the importance of the host response in the protection from periodontal pathogens, a welldocumented relationship exists between certain systemic diseases and susceptibility to
periodontitis. The most well-defined relationship exists with systemic diseases which negatively
affect neutrophils. The neutrophil is the central element of the host response against invading
periodontal pathogens.38 Innate or acquired defects in number and/or function of neutrophils
reveal the importance of this cell type to the pathogenesis of periodontitis.39 Systemic diseases
affecting the number of neutrophils include agranulocytosis, cyclic neutropenia, familial benign
chronic neutropenia, and systemic lupus erythematosus, among others. Diseases affecting
neutrophil function include leukocyte adhesion deficiency Type I and II, Chédiak-Hagashi
syndrome, Down’s syndrome, and Papillon-Lefèvre syndrome.39 Though many of these diseases
are relatively rare to encounter in clinical practice, they often manifest as severe and rapid
periodontal breakdown. Another well understood relationship exists between periodontitis and
diabetes. This relationship has been well documented in the literature and periodontitis has been
8
labelled as a definitive complication of diabetes.40 Various mechanisms attempting to explain
this relationship have been proposed and will be discussed in detail in a later section. Less clear
relationships have begun to be elucidated more recently with obesity and osteoporosis. Saito et
al.41 was the first to describe a potential relationship with obesity when it was discovered that
patients with body-mass indexes (BMI) ≥30 had a relative risk of 8.6 for periodontitis, compared
to those with BMI ≤20, after adjusting for confounding variables. A plausible mechanism is
found in the discovery that adipose tissue is a complex and metabolically active endocrine organ,
secreting numerous immunomodulatory factors which may affect the periodontium.42 Numerous
other cross sectional studies have investigated this potential relationship with varying results.
Longitudinal studies are needed to further investigate this potential relationship. Osteoporosis
has also been investigated as a possible risk factor for periodontal disease, however mixed results
have been obtained. It has been reported that severe osteoporosis may be associated with less
than favorable attachment level in periodontal disease,43 however a more recent, longitudinal
study by Famili et al. found no such association.44
1.3
DIABETES PATHOGENESIS
Diabetes is a metabolic disease characterized by hyperglycemia deriving from defects of insulin
secretion or insulin action. Uncontrolled diabetes can cause extreme metabolic dysfunction, up to
the failure of multiple human organs, among them the kidneys, eyes, heart, nerve endings and
blood vessels.45 There are two major types of diabetes, accounting for about 99% of cases; Type
I and Type II. More rare forms of the disease, such as gestational diabetes, make up the
remainder of cases.
9
Type I diabetes is characterized by an absolute insulin deficiency due to cellularmediated autoimmune destruction of β-cells in the pancreas.46 There are three known types of
autoantibodies which contribute to β-cell destruction. Islet cell cytoplasmic autoantibodies are
the primary autoantibody type, present in 90% of Type I diabetics. Their presence is highly
predictive of future Type I diabetes.47
Islet cell surface antibodies are also very common in
Type I diabetes cases, present approximately 80% of the time. Some patients with Type II
diabetes have also been found to be Islet cell surface antibody positive.47 Specific antigenic
targets of Islet cells may also be affected, with antibodies against glutamic acid decarboxylase
and insulin being strongly predictive of future Type I diabetes in at risk populations.47 The onset
of Type I diabetes is variable and dependent on the rate of β-cell destruction. The onset of
clinical Type I diabetes marks the completed destruction of the human pancreas’ β-cells.
Type II diabetes is a heterogenous disorder caused by a combination of genetic factors
related to impaired insulin secretion, insulin resistance, and environmental factors such as
obesity, over-eating, lack of exercise, stress and aging.48 It is widely reported as a multifactorial
disease and characterized by the lack of need for insulin to prevent ketoacidosis.47 In contrast to
Type I, it is not considered to be of autoimmune etiology. Normally, plasma glucose
concentrations are maintained within a narrow range through a tightly regulated interaction
between tissue sensitivity to insulin and insulin secretion.49
In Type II diabetic patients this
interaction breaks down, leading to impaired insulin secretion due to a dysfunction of the
pancreatic β-cells and impaired insulin action through insulin resistance.50 The genetic influence
on Type II diabetes is thought to be greater than Type I, however the specific inheritance pattern
and many of the influential genes remain unknown.47
10
1.3.1 Prevalence
In the United States, a total of 29.1 million people or 9.3% of the population have diabetes.2 The
prevalence of diabetes is increasing annually with older individuals, Native Americans,
Hispanics, and non-Hispanic blacks more commonly affected than younger individuals and nonHispanic whites.2 The incidence of diabetes is also increasing, with 1.7 million new cases
reported in 20122 and 1.9 million new cases reported in 201151 compared to 1.3 million cases in
2003 and 800,000 in 1998.52 Of the close to 30 million cases in the United States, approximately
90% are Type II.2 The World Health Organization estimates 177 million Type II diabetics
worldwide and predicts that number doubling by the year 2030,53 with the greatest numbers of
new diabetics likely to occur in developing and emerging societies, due to the global nutrition
crisis rooted dually in hunger and obesity. Most data estimate the prevalence of undiagnosed and
diagnosed Type II diabetes approaches twenty percent.51
1.3.2 Risk factors for Diabetes
The risk factors for Type I diabetes are much less clear than those for Type II. While genetics is
known to play a larger role in Type II, the prevalence of Type I diabetes is increased in those
with a parent or sibling affected by Type I diabetes. According to the American Diabetes
Association,54 the odds of having Type I diabetes if your father has Type I, are 1 in 17. The odds
are less if your mother is affected. If both parents have Type I diabetes, the risk ranges from 1 in
10 to 1 in 4. If either parent suffers from Type II polyglandular autoimmune syndrome, a
relatively common condition among Type I diabetics, the risk for the child is 1 in 2. This
inherited risk alone is not sufficient to cause disease and requires an environmental factor, such
11
as diet or infection.55 Many hypothesized environmental factors, and their relationship to genetic
susceptibility, are still not well understood.
Risk factors for Type II diabetes are better understood and well described in the
literature. Typically grouped into modifiable and non-modifiable, the constellation of risk factors
convey a clear susceptibility to Type II diabetes. Non-modifiable risk factors include age, race,
gender, and family history.56 The risk of developing diabetes increases significantly with age.50
Individuals of African American, Mexican American, and Native American ethnic origin are also
at a higher risk for developing diabetes. The true effect of race is likely confounded by other
factors prevalent among these racial groups including obesity, smoking, and hypertension.57
However, the magnitude of the differences between ethnic groups when exposed to similar
environments implies a significant genetic contribution.56 This genetic contribution is further
reinforced by a higher prevalence of Type II diabetes in those who have a family history of the
disease, though the genes involved in this susceptibility remain unknown.56
The most important modifiable risk factor for Type II diabetes is obesity.56 More than
one-third of American adults and 17% of youth are overweight or obese.58 A longitudinal study
by Chan et al.59 demonstrated obesity to be a powerful predictor of future Type II diabetes. It has
also been demonstrated that interventions aimed at reducing obesity are successful in reducing
the incidence of Type II diabetes.56
While obesity is a problem, data suggest60 that the
distribution of fat may be more important than total fat, with visceral or abdominal fat being the
best indicator for future disease. In close relation to obesity, physical inactivity is also an
important and independent risk factor. Studies have shown61,
62
that for equivalent levels of
obesity, higher levels of physical activity were related with a lower incidence of diabetes. As one
might expect when obesity is a large risk factor, diet seems to have an influence on diabetes
12
susceptibility, though the exact role is difficult to ascertain. It has been reported63 that a high
total calorie and low dietary fiber intake, high glycemic load and a low polyunsaturated to
saturated fat ratio may predispose to Type II diabetes. Lastly, metabolic syndrome has been
shown to increase the risk for both cardiovascular disease and Type II diabetes.64 Metabolic
syndrome is a common presentation in the United States and consists of at least three of the
following clinical findings: abdominal adiposity, low HDL cholesterol, high triglycerides,
hypertension, and impaired fasting glucose. In a prospective cohort study with a large sample
size,64 metabolic syndrome was found to be associated with approximately half of the incident
cases of Type II diabetes over an eight-year period with an age-adjusted relative risk of 6.92
(95% CI 4.47-10.8). While it is clear that many of these risk factors are interdependent, each has
the ability to decrease the incidence of Type II diabetes if targeted in an intervention. These
types of interventions should be the focus of public health and medicine in order to decrease the
prevalence of Type II diabetes.
1.3.3 Periodontal disease and diabetes
The most significant early work establishing relationship between diabetes and periodontal
disease examined the rates of both in a homogenous population of non-insulin dependent
diabetic Native Americans (Pima Indians)65,66,67 with Löe (1993)68 definitively labelling
periodontal disease as the sixth complication of diabetes. Grossi and Genco established in the
mid-1990s69, 70 that treatment of periodontal disease would have a beneficial effect on the Type II
diabetes condition, reducing glycated hemoglobin; longitudinal research71 around the same time
showed that poor control of Type II diabetes had a positive association on the severity and extent
of periodontal disease. This was further supported by Kaur5 which demonstrated that patients
13
with poorly controlled diabetes are at a greater risk for the development of periodontal diseases,
as well as a more severe disease course than non-diabetics. The bidirectional nature of the
relationship between the two diseases suggested by Löe was then subsequently confirmed by
Taylor in 2001.4 By 2005, Genco and Grossi laid groundwork toward defining an inflammatory
model linking cytokine production in periodontal disease with the metabolic dysfunction created
by obesity in diabetes.72
This model was expanded upon and, more recently, three major mechanisms explaining
the link were presented.3 First, diabetic patients display impaired neutrophil activity consisting
of a reduced chemotactic response and decreased phagocytic activity.73,74 The importance of
neutrophil function for periodontal health has been well documented and is evidenced by the
severe periodontal destruction seen in those suffering from genetic conditions negatively
affecting neutrophil number or function. The diabetic hyper-inflammatory state is being
increasingly demonstrated in the literature. While normally pro-inflammatory cytokines, such as
interleukin-1β, play a protective role, over-expression can lead to extensive tissue destruction.3
One study compared the gingival levels of IL-1β in well controlled and poorly controlled Type II
diabetics; revealing significantly higher IL-1β levels in the poorly controlled group.75
Furthermore, TNF-α has been shown to be increased in obese women.76 demonstrating the ability
of adipose tissue in Type II diabetics to produce another pro-inflammatory cytokine, possibly
contributing to periodontal destruction. The last proposed mechanism centers on the role of
advanced glycation end-products (AGE). These end products are used as an indicator of diabetic
control over the long-term, but also have been shown to lead to a hyper-inflammatory state with
increased secretion of IL-1, IL-6, and TNF- α.77 It has also been suggested78 that AGE correlates
with an increased level of destructive reactive oxygen species in the gingiva. AGE not only
14
enhances the inflammatory response, but may also reduce bone formation, interfering with
remodeling and healing once periodontal treatment is completed.3 While research continues to
unveil the details of the connection between diabetes and periodontal disease, these proposed
mechanisms provide a valid framework for the interaction and underscore the importance of
neutrophil function, pro-inflammatory cytokines and bone metabolism.
15
2.0
METHODOLOGY
This was a retrospective study analyzing periodontal exam data and diabetic health surveys
collected as part of the American Diabetes Association Diabetes Expo in Pittsburgh,
Pennsylvania, an annual diabetes health education and promotion event. This study was
approved by the Institutional Review Board (IRB) of the University of Pittsburgh (IRB#:
PRO15010133). Attendees to the Expo were given the opportunity to have a free complete
periodontal examination as one of the various health screenings available and educational
pamphlets about the relationship between periodontal disease and diabetes were provided to
participants. Information on age, gender, education, smoking, diabetes, periodontal disease and
oral health were collected and analyzed.
16
3.0
RESULTS
Data were collected on 206 people; 47 respondents had periodontal disease and 147 did not have
periodontal disease, periodontal disease being defined as probing depth 4mm or more. Ninetythree (93) individuals [47.9 percent] without periodontal disease had diabetes and fifty-four (54)
individuals [36.3 percent] did not have diabetes [p=0.847 and not significant]. Eighty-six (86)
individuals [44.3 percent] with diabetes and without periodontal disease reported good oral
health, versus only fifteen (15) individuals with diabetes and periodontal disease who reported
good oral health, a difference p=0.004, which was significant. Education was not significant,
p=0.182. Bleeding upon probing among both diabetics and non-diabetics with periodontal
disease was significant, p=0.003 (Table 1).
17
Table 1.
Logistical regression test to show the association between individual covariates and the outcome of interest
(GumDisease).
*GumTreatment, OralHealth, and GumBleeding are statistically important for predicting the outcome variable.
18
Table 2.
Multivariate logistical regression.
GumDisease
Odds Ratio
Std. Err.
z
P>|z|
anticenter
2.32
1.41
1.38
0.167
[0.704, 7.61]
gumtcenter
22.0
12.1
5.62
0.000
[7.49, 64.6]
Gender
1.02
0.454
0.04
0.969
[0.425, 2.44]
Education
0.710
0.134
-1.81
0.071
[0.490, 1.03]
Diabetes
1.38
0.616
0.72
0.471
[0.575, 3.31]
gumbcenter
1.77
0.770
1.31
0.190
[0.754, 4.15]
MouthRinses
1.30
0.255
1.34
0.180
[0.886, 1.91]
OralHealth
0.512
0.151
-2.26
0.024
[0.294, 0.918]
1.03
1.17
0.03
0.977
[0.111, 9.58]
_cons
[95% Conf. Interval]
*Controlling for GumTreatment, Antibiotic, Gender, Education, Gumbleeding, MouthRinses, and OralHealth, the odds of
having GumDisease vs. not having GumDisease in patients with diabetes is 1.38.
19
4.0
DISCUSSION
Various studies have shown the effect of diabetes on periodontal disease, and vice versa. One
large study by periodontists and endocrinologists combined found that periodontal disease may
contribute to the increased mortality rates among diabetics,79 while others80 have rationalized
that advanced periodontitis is associated with higher HbA1C in both diabetic and non-diabetic
individuals, with the effect being greater in patients with progressive periodontitis. Minimal
evidence supports any association between periodontal disease and diabetes complications. No
studies have considered the level of periodontal disease associated with a likelihood of diabetes
complications.
Periodontal disease can cause problems for patients with diabetes, in whom the diabetes
can be more severe and progress more rapidly than in diabetics who do not have periodontal
disease. Control and prevention of periodontal disease may be more important in patients with
diabetes. Uncontrolled periodontal disease may affect control of diabetes, and the opposite could
be true. It is established that this effect can be modified by good oral hygiene and control of any
existing periodontal disease.81, 82
Results from this research show that not all individuals with diabetes have periodontal
disease. In our sample of 206 individuals on whom we performed complete periodontal
examinations, 29 had both periodontal disease and diabetes, while 93 individuals with diabetes
did not have periodontal disease, a difference that was not statistically significant (p=0.847).
20
Table 1 shows the importance of oral health, specifically that individuals with good oral health
have less chance of having diabetes. Periodontal treatment was shown to be a significant factor
on the effect of diabetes (p=0.001). Multivariate logistical regression analysis (Table 2) was
shown, controlling for periodontal treatment, gender, education, bleeding upon probing and oral
health. The odds of having periodontal disease versus not having periodontal disease among
patients with diabetes in our sample was 1.38, a difference that was not statistically significant
(p=0.847).
Results from our research show that in individuals with diabetes who are aware of their
illness and make attempts to control their glycemic condition, the prevalence of periodontal
disease was low. These results, however, reflect only cross-sectional analysis with a convenience
sample and the finding requires prospective study with larger sample sizes to confirm.
21
5.0
CONCLUSION
Retrospective study of periodontal disease among community-dwelling diabetics in this research
revealed no significant relationship between diabetes and periodontal disease (p=0.847), though
oral health was an important, significant factor (p=0.004). While the public health implications
of periodontal disease are vast, it appears that quality glycemic control in the diabetic population
can help to alleviate the burden. Further prospective research with a larger sample size is
necessary to confirm this finding.
22
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