Download 2. Oral Complications in Diabetes

Contents
1 Diabetes, Clinical Dentistry and Changing Paradigms
Battling and Insidious Foe
A Challenge for Dentists
A Biology of Complexity
How Diabetes Occurs
IDDM
NIDDM
Promoting Health, Preventing The Disease
Conclusion
For Additional Information
2 Oral Complications in Diabetes
Summary
Caries (Tooth Decay)
Periodontal Disease
Saliva
Other Pathological Features of the Oral Cavity
References
3 Oral Opportunistic Infections: Links to Systemic Diseases
Diabetes Mellitus
Preterm Low Birth Weight Babies
Diseases Associated With Diabetes
4 Detection and Prevention of Periodontal Disease in Diabetes
Overview
Gingivitis
Thrush
Pathophysiology
Progress of Periodontal Disease
Diabetic Control
Oral Factors
Natural Dentition
Oral Hygiene
Acute Infections
Oral Surgery
Diabetes Control
Risk of Infection
References
5 Oral Complications of Diabetes: A Guide for Dental Hygienists
Oral Complications
Dental Management
Diabetic Emergencies
The Role of Diet
Planning Dental Treatment
Dental Tips for Patients With Diabetes
6 Oral Complications of Diabetes: A Guide for Patients
What is the relationship between poor oral health and diabetes?
What is the link between diabetes and periodontal disease?
Controlled Diabetics Have New Reason to Smile
How does periodontal disease develop?
How is periodontal disease treated?
Since I have diabetes, do I need to do anything to prepare for oral surgery?
Are other oral problems linked to diabetes?
Keep your teeth
How can you protect your teeth and gums?
Things to keep in mind
1. Diabetes, Clinical Dentistry and Changing
Paradigms
The infectious diseases that took the young lives of our ancestors in the early part of the 20th
century have been replaced at the end of the century with chronic and degenerative diseases.
This has awakened a new respect for and interest in cancer, heart disease, dementia, dwarfism,
periodontal diseases, chronic pain, osteoporosis, arthritis and rheumatism—all known since
time immemorial but, until recently, only as a faint background to the acute tragedies of assorted
fevers and plagues.
Our changing demographics indicate that nearly 20 percent of all Americans will be 65 years of
age or older by the year 2010. We are beginning to appreciate the changing patterns of disease—
disease that is chronic, that affects older people, that debilitates but does not necessarily kill.
These patterns are reflected in the goal of the health professions. Our challenge now is not to
extend life, but to improve the quality of the human condition throughout the lengthened
lifespan—a changing paradigm.
Battling an Insidious Foe
Slowly evolving and symptomless, chronic noninfectious diseases are mysterious and
frightening. Because it is hard to imagine being sick when you feel fine, by the time signs and
symptoms do appear, it usually means that the disease has progressed to a serious stage.
For many people, diabetes is just such a disease. Diabetes is a disease of metabolism, an
alteration of what Claude Bernard, a 19th-century French physiologist, called the "milieu
interieur," a malfunction of the mechanisms that regulate sugar utilization which results in
hyperglycemia. Between 13 and 15 million Americans are believed to have the disease, and
about half are unaware of their condition.
Early detection is important because diabetes can lead to life-threatening complications_heart
disease, blindness, neuropathies (including chronic facial and oral pain), periodontal diseases,
tooth loss, stroke, kidney failure and even gangrene. In 1993, about 400,000 deaths resulting
from any cause are estimated to have occurred in people with diabetes. 1 Only heart disease and
cancer kill more Americans than diabetes and its complications.
A Challenge for Dentists
Diabetes poses a significant public health challenge for the United States. Some 800,000 new
cases are diagnosed each year, or 2,200 per day. The changing demographic patterns in the
Unites States are expected to increase the number of people who are at risk for diabetes and
who eventually develop the disease. Diabetes is a chronic disease that usually manifests itself
as one of two major types: Type 1, mainly occurring in children and adolescents 18 years and
younger, in which the body does not produce insulin and thus insulin administration is required
to sustain life; or Type 2 occurring usually in adults over 30 years of age in which the body's
tissues become unable to use its own limited amount of insulin effectively. While all persons
with diabetes require self-management training, treatment for Type 2 diabetes usually consists
of a combination of physical activity, proper nutrition, oral tablets and insulin. Type 1 diabetes
has been sometimes referred to as juvenile or insulin-dependent diabetes; and Type 2 diabetes
has been referred to as adult-onset or noninsulin dependent diabetes.
Controlling the blood glucose level is the most important step for the diabetic to prevent tooth
and gum problems. However, maintenance of good oral hygiene cannot be overemphasized. The
diabetic patient who is well managed medically and whose glucose levels are controlled can
receive any indicated dental treatment. Because infection aggravates diabetes our ultimate goal
should be to stress early care to help prevent complications of gum and periodontal disease.
Important management for effective oral hygiene include antibiotics, calculus and plaque
removal.
A number of major complications of diabetes present major challenges to oral health
professionals: acidosis, hypoglycemic coma and hypoglycemia, neuropathy, kidney diseases,
peripheral vascular diseases, heart disease, stroke, digestive diseases and opportunistic
microbial infections such as those of the mouth associated with gingivitis, periodontal disease
and candidiasis. Therefore, oral health professionals have major opportunities for health
promotion, disease prevention, diagnosis and therapy related to diabetes.
Some studies have shown a possible improvement in diabetic control (as measured by glucose
levels) after treatment for periodontal disease. A reduction in inflammation associated with oral
infection is believed to reduce harmful effects that lead to poor metabolic control. The
management of diabetic patients presents another critical reason for dentists to obtain
comprehensive dental and medical information before initiating diagnostic and treatment
procedures.
In addition, people with all types of diabetes who use tobacco products face a significant risk of
severe periodontal disease. In one study, 30 percent of patients aged 19 years and older who
had insulin-dependent diabetes mellitus, or IDDM, also had periodontal disease. In Pima Indians
with non-insulin-dependent diabetes mellitus, or NIDDM, tooth loss is 15 percent higher than that
among those without diabetes, and the incidence of periodontal disease is 2.6 percent higher.
Prevalence of gingivitis, periodontal attachment loss, bone loss and tooth loss are
characteristics of patients with IDDM.
A Biology of Complexity
Diabetes is an excellent example of a biology of complexity, which reminds us that health is
really a profound and intricate balance of the components of the human body throughout life.
Reduced blood circulation to the legs leading to sores and ulcers; kidney failure; and
neurological, circulatory, reproductive and ocular problems are frequent and confounding
complications in patients with diabetes that reflect the biological complexity associated with
chronic and degenerative diseases.
Six hormones are important in regulating fuel metabolism in humans. In general terms, insulin is
the primary anabolic hormone (linked with synthesis and storage of body fuels), while the other
five hormones subserve catabolic functions (that is, breakdown and oxidation of stored fuels for
the provision of energy in the absence of food intake). The primary hormones involved in
diabetes are insulin and glucagon. The biological regulation that maintains a balance between
anabolic and catabolic functions is at the heart of diabetes.
Types of diabetes.
Of the estimated 13 to 15 million people in the United States who have diabetes, between 90 and
95 percent have NIDDM, also called Type II diabetes. The second form of diabetes is IDDM, also
called Type I. IDDM affects an estimated 800,000 people. The cost to the U.S. economy of both
types is about $92 billion per year, with $45 billion in direct medical costs and $47 billion in
indirect costs (such as disability, work loss and premature mortality). 1
A third type of diabetes—gestational diabetes—has been found to develop in some pregnant
women. The condition appears to be transient in that it disappears when the pregnancy is over,
but women who have it appear to have an increased susceptibility to developing NIDDM in later
years.
Identifying those at risk.
Diagnostically, people at high risk of developing diabetes can be identified through analysis of
accumulated glucose in blood and saliva. Hyperglycemia can be associated with unusual
changes in the microbial ecology of the oral cavity, resulting in gingivitis, periodontal disease
and oral candidiasis. Studies in clinic, community and hospital populations indicate that people
with diabetes have a higher risk of developing bacterial and yeast infections, including
asymptomatic bacteriuria, infections in surgical wounds and group B streptococcal infections.
How Diabetes Occurs
Diabetes is a disorder of metabolism, which is the way the body uses digested food for growth
and energy. Most digested food is broken down by digestive enzymes into glucose, which
circulates in the blood stream and is taken up by the cells for growth and energy. For the
glucose to get into the cells, the hormone insulin must be present.
Insulin reacts with the insulin receptor at the cell membrane, allowing glucose to enter the cell.
Insulin is synthesized in the pancreas, a gland 5 to 6 inches in length tucked behind the
stomach. The pancreas is a compound organ containing several types of cells that function
independently. It is mainly composed of acinar cells, which synthesize and secrete various
digestive enzymes through the pancreatic duct into the duodenum. The pancreas also contains
quite different cells in areas called the islets of Langerhans. The islets produce internal
secretions, including the hormone insulin in the beta cells, the hormone glucagon in the alpha
cells and somatostatin in the delta cells, which may regulate the synthesis of both insulin and
glucagon.
Insulin functions to reduce the concentration of glucose in the blood in at least four processes:




to stimulate (probably by altering membrane permeability) the muscles to remove more
glucose from the blood;
to stimulate both the muscles and the liver to convert more glucose into glycogen for
storage;
to inhibit the liver from producing glucose from glycogen or other stored materials;
to stimulate the muscles and liver to oxidize carbohydrates at a more accelerated rate.
Scientists did not begin to understand the causes of diabetes until the latter part of the 19th
century. By 1889, two German physicians, Johann von Mering and Oskar Minkowski, observed
that removal of the pancreas resulted in the excretion of sugar into the urine and the
development of several symptoms associated with diabetes—excessive thirst, frequent
urination, glucose in blood and urine, coma, visual disorders involving retinopathy, neuropathy
and kidney disease.
IDDM
The precise cause of diabetes is not known. Scientists assume that IDDM may be more than one
disease and may have a number of different causes. For example, a number of scientific groups
have provided evidence that IDDM is influenced by multiple genes that confer susceptibility—
genes that are prevalent as risk factors in some families but not in other families. IDDM usually
occurs in children and adults younger than 30 years of age and thus is known as juvenile
diabetes. IDDM occurs equally among males and females, is more common among whites and is
very rare in most Asian-, African- and Native American populations. Some Northern European
countries, including Finland and Sweden, have high rates of IDDM.
IDDM exhibits 30 to 50 percent concordance in identical or monozygotic twins, suggesting that
the disorder depends on environmental factors as well as genes. Additional evidence suggests
that IDDM susceptibility genes are not linked to, but interact with, the human leukocyte antigen
system.
Type I diabetes mellitus, or IDDM, is thought to result from the destruction of pancreatic beta
cells. Genetic susceptibility to IDDM is encoded by several genes near the insulin gene on
chromosome 11. Presumably, IDDM is primarily an autoimmune disease associated with a loss
of tolerance for several pancreatic islet cell protein molecules, including insulin; glutamic acid
decarboxylase, or GAD; and tyrosine kinase, or IA-2, proteins. When these molecules in the beta
cells are exposed to the immune system as foreign (by becoming altered in some manner), they
are no longer given tolerance or protection from immunological attack. The immune system
produces antibodies against these normal cell components (autoantibodies), attacks these
molecules and in the process destroys the beta cell.
With reduced or eliminated beta cells, the pancreas produces little or no insulin. The body is
then unable to use glucose for energy and glucose accumulates in the blood, giving rise to the
abnormally high glucose levels that are the hallmark of hyperglycemia and diabetes. The kidneys
overwork to filter the excess glucose into the urine, and the body becomes dehydrated as a
result. The body breaks down its stores of fat and protein to provide more glucose to the cells
"starving in the midst of plenty." If the breakdown of fat continues unchecked, acidic by
products called ketones accumulate. These ketones, combined with dehydration, induce coma
and eventually death. However, subclinical abnormal processes precede the apparent rapid
onset of IDDM.
A number of research laboratories, including some supported by the NIDR, have identified
antibodies to autoantigens associated with the pancreatic beta cells before there is any apparent
diabetes. It is hoped that early detection of this autoimmune attack on the beta cells could allow
for a counterattack to halt the antibody production and prevent the disease.
Another very recent discovery has been that IDDM shows familial patterns, suggesting an
inherited disease process. Scientific investigations have discovered that selective mouse and
human characteristics are produced by imprinting—that is, a developmental, often tissuespecific, form of gene regulation by which only one of the two parental alleles or genes is
expressed, while the other imprinted allele is repressed. Imprinting has been found for a number
of genes that are physically located in the chromosome 11p15 region (for example, insulinlike
growth factor, insulin like growth factor receptor, insulin). Imprinting may explain the observed
parental effects on IDDM-associated susceptibility.
Treating IDDM.
Treatment of diabetes requires therapeutic insulin coupled with a dietary plan, a daily exercise
program and tests for blood glucose levels taken several times a day.
Once trigger autoantigens for IDDM have been identified and their structure determined, it
should be feasible, with existing technology, to design and fabricate highly specific, sensitive
and clinically effective therapeutics. These therapeutics could be designed to remove the small
group of circulating T lymphocytes that are involved in the initiation of the autoimmune disease.
The rest of the T cells required by the body for immune protection would be left intact. In other
preliminary studies of newly diagnosed patients with IDDM, surviving beta cells have been
protected by agents such as cyclosporine, steroids and azathioprine, all of which reduce the
overall population of T cells or inhibit their activation.
NIDDM
The most common form of diabetes is NIDDM, or adult-onset Type II diabetes. About 90 to 95
percent of all people with diabetes have NIDDM. This type usually develops in adults older than
40 years of age and is most common in adults older than age 55 years. About 80 percent of
people with NIDDM are overweight.
In NIDDM, the pancreas usually produces insulin, but the body is not able to use it effectively.
Resistance is linked to high blood pressure, high levels of fat in the blood and aging. The result
of this chronic and degenerative disease is the same as that of IDDM—an abnormal
accumulation of glucose in the blood (hyperglycemia), coupled with an inability to use the
available glucose as metabolic fuel.
In asymptomatic people, the diagnosis of diabetes is usually made by measuring glucose
tolerance. The criteria for a diagnosis of impaired glucose tolerance is shown in the box
("Criteria for Impaired Glucose Tolerance").
Criteria for Impaired Glucose Tolerance
Fasting Glucose Concentration




Venous plasma < 140 milligrams/deciliter
(7.8 millimolars)
Venous whole blood < 120 mg/dL (6.7 mmol/L)
Capillary whole blood < 120 mg/dL (6.7 mmol/L)
Glucose Concentration at Two Hours After Ingesting 75 Grams Oral Glucose
 Venous plasma 140 and < 200 mg/dL (7.8 and 11.1 mmol/L)
 Venous whole blood 120 and < 180 mg/dL (6.7 and 10.0 mmol/L)
 Capillary whole blood 140 and < 200 mg/dL (7.8 and 11.1 mmol/L)
Glucose Concentration at Midtest (1/2 Hour, 12 Hour or 11/2 Hours) After Ingestion 75 G Oral
Glucose
 Venous plasma 200 mg/dL (11.1 mmol/L)
 Venous whole blood 180 mg/dL (10.0 mmol/L)
 Capillary whole blood 200 mg/dL (11.1 mmol/L)
In contrast to IDDM, NIDDM is more common in older people, especially older women who are
overweight. The prevalence is higher among African-Americans, Hispanics and Native
Americans. Compared with the prevalence in non-Hispanic whites, diabetes prevalence is 60
percent higher in African-Americans and 110 to 120 percent higher in Mexican-Americans and
Puerto Ricans. Native Americans have the highest prevalence of diabetes in the world. Among
American Pima Indian adults, essentially 50 percent of the population has NIDDM.
The changing demographics of the United States suggest that the prevalence of diabetes will
increase profoundly by 2010, when 20 percent of our nation will be composed of people 65 years
of age and older. Also contributing to this probable increase is the fact that Hispanics and other
at-risk minority groups make up the fastest-growing segments of the U.S. population.
There is strong genetic linkage evidence of NIDDM genes on chromosome 12. What is emerging
is that "risk factors" for NIDDM include genetically determined susceptibility genes as well as
environmental and behavioral issues such as exercise, weight, diet and a family history of
diabetes.
Treating NIDDM.
People with NIDDM often can control their condition by losing excessive weight through diet and
exercise. Approximately 40 percent of people with Type II diabetes use insulin, and of this group,
49 percent use orally administered medications. Ten percent use a combination of insulin and
oral medications.
Before the discovery of insulin in 1921 and its clinical use, the only specific therapy for diabetic
patients was to reduce carbohydrate intake to an absolute minimum—near starvation levels. But
insulin—however momentous its discovery—is not a cure for diabetes. When a person is
hyperglycemic, the injection of insulin will relieve the symptoms. (When a diabetic patient is
hypoglycemic, the symptoms can be relieved with sugar.) However, the intricate balance
between insulin, blood sugar and intermediary metabolism is very complex. The levels can vary
with stress, exercise, illness and even the time of day.
Glucose levels in the blood are monitored as often as necessary but usually several times a day.
Monitoring can be easily done by placing a drop of blood on a strip of treated paper that gives a
color indication of the glucose level or that is analyzed to produce a numeric readout of the
blood-glucose concentration.
Several studies have found that with frequent monitoring of glucose levels and intensive insulin
therapy and monitoring, many of diabetes' serious clinical complications can be reduced or at
least delayed. With this goal in sight, there has been increased research focusing on health
promotion, early diagnosis, improved therapy through enhanced insulin delivery and monitoring
systems, biomimetic approaches to design and fabricate functional beta-cell replacements, and
improved drugs, which can address a number of the problems associated with the etiology and
pathogenesis of diabetes.
Insulin is usually administered to a person with diabetes by intramuscular injection.
The amount of insulin needed is determined individually, taking into consideration height,
weight and physical activity. Insulin can be injected with an insulin pen. Some people use an
insulin pump, a device that delivers a continuous supply of insulin through a needle inserted
into the body. Insulin is delivered at two rates: a low, steady rate (basal rate) for daylong
coverage, and extra boosts (bolus doses) to cover meals or when needed. The device is batteryoperated and can be clipped to a belt. Pumping devices inserted under the skin are also being
developed.
Other methods of delivering insulin to a person with diabetes are still in the research stages of
development_for example, methods of pancreatic transplantation and transplantation of the
islets of Langerhans. Studies are also being conducted in which functional donor beta cells are
protected by a surrounding, synthetic, limiting membrane when inserted into the recipient. This
membrane inhibits production of antibodies against the transplanted "foreign" cells, yet the beta
cells remain viable and can still secrete insulin by diffusion of essential nutrients from the
vasculature.
Other treatments for NIDDM.
Besides insulin, three classes of drugs have been sold for treatment of NIDDM. A fourth class
was approved for sale by the Food and Drug Administration at the end of January. The first class
of medications is the sulfonylurea group, which functions primarily to stimulate insulin
production in the pancreas. There are several of these drugs on the market.
The second class of medications is the biguanide group, which functions by decreasing the
amount of sugar secreted by the liver and improves insulin sensitivity. Only one drug in this
group, metformin, has been approved.
The third class of medications is the alpha glucosidase inhibitor group. The FDA-approved drug
in this class, acarbose, was developed to inhibit the digestive process and thereby prevent the
breakdown of starchy food in the small intestines. This strategy is effective in inhibiting or
delaying the absorption of sugar into the blood and prevents sudden surges of glucose that
occur after food ingestion.
Troglitazone (Rezulin) is the fourth class of drug, which recently was approved by the FDA. It
consists of a thiazolidinedione molecule and an insulin-resistance inhibitor. Troglitazone can
reduce or eliminate the need for additional insulin. Studies are in progress to determine if
troglitazone is effective in treating IDDM and to determine the effects of combining it with the
other classes of drugs.
Promoting Health, Preventing The Disease
In light of the biological complexity associated with diabetes as a chronic and degenerative
disease, the most significant course of action is health promotion and disease prevention. One
of the factors increasingly shown to be important in health promotion and disease prevention is
diet.
In February 1997, as part of a 20-year-old Nurses Health Study project, a study described 65,173
women 40 to 65 years of age who were followed up for 6 years to determine the prevalence of
diabetes; 915 developed the disease. The study found that those who ate a low-fiber starchy diet
and drank numerous soft drinks had 2.5 times the prevalence of diabetes as women who ate less
of these starchy foods and soft drinks and more fiber or roughage, specifically more fiber from
whole-grain cereals. The evidence suggests that people with diets high in sugar and low in fiber
were likely to develop a chronic and elevated demand for insulin. If the pancreas cannot respond
to that need and insulin resistance exacerbates the effect, diabetes will likely be the result.
Disease prevention requires health care professionals to be able to identify the at-risk
population. In September 1996, a group from the Whitehead Institute for Biomedical Research in
Cambridge, Mass., identified a chromosomal area that appears to harbor a diabetes-related gene.
This is the second such region involving NIDDM found in 1996. Pinpointing the actual gene(s)
could lead to a diagnostic test that identifies people at risk and eventually leads to cost-effective
prevention and treatment strategies.
In response to the growing emphasis on prevention of diabetes, the Centers for Disease Control
and Prevention and the National Institutes of Health announced late last year a national diabetes
prevention study. Researchers will recruit 4,000 people in 25 academic health science centers
who have higher-than-normal blood sugar levels but do not as yet have diabetes. Thirty-five to
40 percent of the participants would be expected to develop diabetes. The participants will be
divided into four groups. The first group will make lifestyle changes such as improved diet and
increased exercise. The other three groups will be given standard advice on exercise and diet
along with metformin or the newly approved drug troglitazone, or a placebo. The groups will be
followed up for 5 years.
Conclusion
Before diabetes can be optimally managed and eventually prevented, there is much more to be
learned and to be understood about human behavior, environmental risk factors and their
interactions within the biology of a developing human being. Without scientific and
technological progress and significantly improved public health and education efforts, diabetes
will increase in prevalence and continue to have a tremendous impact on the aging population
and the American economy. The changing paradigm for the next century asks each of us to
consider how we can improve the quality of life for all Americans throughout their lifespan.
For Additional Information
American
Associations
of
444
N.
Michigan
Chicago,
Ill.
1-312-644-2233
or
Diabetes
Educator
1-800-TEAMUP4
or
Offers diabetes treatment and education programs
Diabetes
Ave.,
Suite
Access
Educators
1240
60611
1-800-338-3633
Line:
1-800-832-6874
American
Diabetes
1660
Duke
Alexandria,
Va.
1-703-549-1500
or
Funds research and educational activities
Association
St.
22314
1-800-232-3472
Juvenile
Diabetes
Foundation
(JDF)
432
Park
Ave.
New
York,
N.Y.
1-212-889-7575
or
Offers research, training, support groups and family activities
International
South
10016-8013
1-800-533-2873
National
Institute
of
Diabetes
and
Digestive
and
Kidney
Diseases
National
Diabetes
Clearinghouse
1
Information
Way
Bethesda,
Md.
20892-3560
1-301-654-3327
Offers information, education and referral service; publications; newsletter
National
Information
Building
31
Bethesda,
1-301-496-4261
Institute
of
31,
Center
Dental
Room
Drive
Md.
MSC
Research
Office
2C35
2290
20892-2290
National
Oral
Health
Information
Clearinghouse
1-301-402-7364
Offers pamphlets: "Detection and Prevention of Periodontal Disease in Diabetes", "Dental Tips
for Diabetics"
2. Oral Complications in Diabetes
by Harald Loe, DDS, and Robert J. Genco, DDS, PhD
Summary
Data regarding oral complications in diabetes prior to the insulin era are scarce, possibly due to
the limited scope of oral health care of that time and the short life span of the insulin-requiring
diabetic patient. During the past 40 years, much data have been generated emphasizing the
frequent occurrence of oral afflictions in patients with insulin-dependent diabetes mellitus
(IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). Perhaps the most important
finding is that periodontal disease is more severe and occurs with higher frequency in diabetic
patients (both NIDDM and IDDM), especially if the diabetes is not well controlled and there are
other complications, such as retinopathy. The reason for the greater occurrence of periodontal
destruction in diabetes is not clear. However, studies of the periodontal flora find similar
microorganisms in diabetic and nondiabetic individuals, suggesting that alteration in host
responses to periodontal pathogens account for these differences in periodontal destruction.
For example, increased susceptibility to infection by periodontal bacteria associated with altered
phagocyte functions and reduced healing capacity associated with altered collagen metabolism
may explain, in part, the increased levels of periodontal disease in diabetes.
Caries in the crowns of teeth appear to be greater in adults with poor control of IDDM. However,
the prevalence of root caries requires further studies. Oral infections aside from dental caries
and periodontal disease are often more severe. Life- threatening deep neck infections and
palatal ulcers exemplify the severity of these conditions. Mucosal abnormalities and oral
bacterial and fungal infections may reflect undiagnosed diabetes or identify poorly controlled
diabetes. Successful management of oral infections, including periodontal diseases, seems to
depend on establishing metabolic control in diabetic patients. Knowledge of oral co-morbidity
among people with diabetes is generally poor and suggests the need for appropriate health
education and health promotion to improve the oral health of diabetic patients.
Caries (Tooth Decay)
Children with IDDM have been reported to have caries incidence that is higher, lower 2-4, or
similar to that of nondiabetic children. This contradiction may possibly be explained by cohort
characteristics, degree of diabetes control, and degree of adherence to dietary prescriptions.
Adult patients with poor control of their IDDM seem to have more coronal caries 5-7. In the
general population, the frequency of root caries increases with age and is three times more
prevalent in those age >= 65 years compared with young adults 8. However, very few studies have
reported on the incidence of root-surface caries as a significant problem in older patients with
IDDM or NIDDM9.
Periodontal Disease
Periodontal disease is the most prevalent oral complication in IDDM and NIDDM patients and has
been labeled the "sixth complication of diabetes mellitus." 10. Numerous studies have shown
both increased prevalence and severity of periodontal disease in patients with IDDM. Diabetic
children and adults with less than optimal metabolic control show a tendency towards higher
gingivitis scores 11-17. Early case reports suggested that diabetic adolescents and teenagers may
suffer from periodontitis. In a more recent study, the prevalence of periodontal disease was 9.8%
in 263 patients with IDDM, compared with 1.7% in people without diabetes 19. Most of the
periodontal disease was found in those age 11-18 years (Figure 1).
However, earlier rapid periodontal destruction was not found in adolescent patients with IDDM in
Finlandl5. This difference may be related to different levels of metabolic control in participants of
the two studies. For example, case reports suggest a strong relationship between rapid
periodontal breakdown and elevated blood glucose levels20.
Patients with IDDM of > 10 years duration had greater loss of periodontal attachment compared
with those of <10 years duration. 2l. This was found to be particularly true for patients age >=35
years (Figure 2). More recently, it was reported that IDDM patients age 40-50 years with long
IDDM duration had significantly more sites with advanced periodontal destruction and alveolar
bone loss than people without diabetesl7. It has also been demonstrated2l and confirmedl6 that in
IDDM patients with retinal changes the loss of periodontal attachment is significantly larger than
in IDDM patients without retinal changes (Figure 3).
Several studies have clearly demonstrated that IDDM patients with poor long-term control of
diabetes have increased extent and severity of periodontal disease, whereas those who maintain
good metabolic control have minimal periodontal problems. Patients with IDDM of long duration
who have retinopathy tend to exhibit more loss of periodontal attachment as they reach age 4050 years. Good oral home care and frequent professional checkups and care are important for
these patients22.
Few studies have dealt with NIDDM subjects. In a study of Pima Indians, 40% of whom have
NIDDM, diabetic patients age <40 years had increased attachment loss, and alveolar bone loss
was associated with increased glucose intolerance 23. Periodontal tissue loss increased with age
and was higher in people with diabetes compared with people without diabetes in all age groups
(Figure 4). Alveolar bone loss also increased with age and was substantially more frequent in
patients with NIDDM compared with nondiabetic people age 5-44 years (Figure 5) .
Toothlessness was 15 times higher in the diabetic than in the nondiabetic group. Indeed, 30% of
these young adults with NIDDM had no teeth. The odds ratio for subjects with NIDDM for
increased risk of periodontal destruction was 3.43 (95% confidence interval (CI) 2.28-5.16) 24. In
this population, the age and sex adjusted incidence of periodontal disease in subjects with
NIDDM was 75 cases per 1,000 person-years, which was substantially higher than the rate of 29
cases per 1,000 person-years in subjects without diabetes25 (Table 1).
Early studies of the pathogenesis of periodontal disease in diabetic patients centered on the
general feature of "basement membrane thickening" 26 and possible changes in the
vasculature27-29. More recent studies have focused on the role of the periodontal infection 15, the
microflora of dental plaque 30, collagen metabolism31,32, leukocyte function 33, and other aspects
of the host response 34-35. All of these factors may individually or synergistically contribute to
periodontal disease.
The reason for the greater occurrence of periodontal destruction in diabetics is not clear.
However, studies of the periodontal flora find similar microorganisms in diabetic and
nondiabetic people 30,36, suggesting that alteration in host responses to periodontal pathogens
account for these differences in periodontal destruction. For example, increased susceptibility to
infection by periodontal bacteria associated with altered phagocyte functions and reduced
healing capacity associated with altered collagen metabolism may explain, in part, the increased
levels of periodontal disease in diabetic patients.
Table 1: Incidence of Periodontal Disease in Pima Indians by Diabetes Status
Age- and sex adjusted incidence
Diabetes Status
(new cases/1,000 person-years)
Nondiabetic
28.9
NIDDM
75.5
Relative risk
2.6
The response to treatment suggests that the periodontal lesions are eminently treatable 37,38and
that eradication of the infection and the inflammatory foci may reduce insulin requirements 39.
The knowledge among people with diabetes of oral co-morbidity is generally poor 40 and
suggests the need for appropriate health education and health promotion to improve the oral
health of diabetic patients.
Saliva
Reduced salivary secretion has been a frequent finding in experimental diabetes in animals 41 as
well as in IDDM patients. A non-inflammatory non-neoplastic enlargement of the parotid gland is
believed to occur in 25% of patients with moderate to severe diabetes and especially in IDDM
patients with poor metabolic control42. The etiology of this condition is unknown, but it is
speculated that the enlargement occurs in response to decreased insulin production or that the
Sjogren's syndrome may underlie this symptom43. Also, the possibility that in some cases these
enlargements may be due to a low degree of mumps infection has been mentioned 44. Increased
concentration of Ca++ in both parotid and submandibular saliva of IDDM subjects 45 might
explain the frequently reported increase in calculus formation in such patients. However, in wellcontrolled individuals with altered glucose metabolism, salivary gland function does not seem to
be significantly impaired 46.
Other Pathological Features of the Oral Cavity
Other pathology associated with diabetes includes oral infections other than those responsible
for dental caries and periodontal destruction. Case reports on life-threatening deep neck
infection from a periodontal abscess 47 and fatal palatal ulcers 48 exemplify the severity of these
conditions. To what extent such incidents are part of the broader issue of increased occurrence
of infection in people with diabetes, or may have strictly a local etiology, is open to question. In
addition to these infections, other localized or regional infections such as mucormycosis,
"malignant otitis media", necrotizing cellulitis, urinary tract infections, skin infections, and
pneumonia have also been found more often in poorly controlled diabetic patients than in
others.
There are also indications that patients with elevated salivary glucose levels carry candida
intraorally more often than those with lower glucose levels 49. Moreover, a study of 40 patients
with lichen planus found that 11 patients (28%) had overt or latent diabetes, compared with none
of the control groups50, the implication being that diabetes may be related to the pathogenesis of
lichen planus. The evidence for an immunological defects 51 and deficient leukocyte functions
superimposed on the metabolic abnormality of diabetes seems increasingly convincing.
Finally, it should be mentioned that diabetes may initially manifest with oral symptoms other
than thirst52. Mucosal abnormalities, such as erosive lichen planus, burning tongue, and gingival
bleeding, as well as sialorrhoea and sialosis, have been found in undiagnosed NIDDM, most of
which resolved on treatment directed at improving glycemic control 52.
Dr. Harald Loe is Former Director, National Institute of Dental Research, National Institutes of
Health, Bethesda, MD and University Professor, Department of Periodontology, University of
Connecticut Dental School, Farmington, CT; Dr. Robert J. Genco, is Distinguished Professor and
Chair, Department of Oral Biology, School of Dentistry, State University of New York, Buffalo,
NY.
Source:
National
1
Bethesda, MD 20892-3560
Diabetes
Information
Information
Clearinghouse
(NDIC)
Way
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3. Oral Opportunistic Infections:
Links to Systemic Diseases
Diabetes Mellitus
The destructive inflammatory processes that define periodontal disease are closely intertwined
with diabetes. Persons with noninsulin-dependent diabetes mellitus (NIDDM) are three times
more likely to develop periodontal disease than nondiabetic individuals. Add smoking to the mix,
and the chances of developing periodontitis with loss of tooth-supporting bone are 20 times
higher. An increased risk for destructive periodontal disease also holds for persons with insulindependent diabetes mellitus (IDDM).
Much of what is known about the periodontal complications of diabetes has been learned from
the Pima Indians of Arizona, who have the highest reported rates of NIDDM in the world. NIDCRsupported research in the Pima community has shown that periodontal infection is more
prevalent, more severe, and develops at an earlier age in this population than in nondiabetic
persons. As diabetes increases in severity, the rate at which vital tooth-anchoring bone is lost
accelerates. Pima Indians with NIDDM are 15 times more likely to be edentulous than those
without diabetes. Now there is evidence that a history of chronic periodontal disease can disrupt
diabetic control, suggesting that periodontal infections may have systemic repercussions. The
exact nature of this complex relationship is not clear. It is likely, however, that increased genetic
susceptibility to infection, impaired host response, and the excessive production of collagenase
found in periodontal disease may all play important roles in NIDDM. Similarities in the etiology of
periodontal and other complications of diabetes have also emerged.
Studies have shown, for example, that hyperglycemia is the common basis for diabetic
complications in the eyes, kidneys and nerves. Glucose in high concentrations attaches to other
molecules, stimulating chemical reactions that produce advanced glycosylation end products.
These large molecules accumulate in tissues, causing damage and disrupting normal function.
Scientists suspect that these cellular reactions figure as well in the tissue destruction seen in
periodontal disease.
Investigators are also examining the interplay between periodontal infection and metabolic
control. Acute viral and bacterial infections are known to induce insulin resistance, which
disrupts blood glucose control. Factors including stress, fever, catabolism, and elevated levels
of hormones antagonistic to insulin such as growth hormone, cortisol, and glucagon likely play
a role in the development of insulin resistance during infection.
It is possible, then, that chronic gram-negative infections with persistent production of bacterial
toxins, like periodontal disease, could have the same deleterious effect. If so, would elimination
or control of periodontal infection improve metabolic control of diabetes?
To explore this hypothesis, researchers designed a treatment protocol specifically to manage
diabetes-associated periodontitis in a group of Pima Indians with poorly controlled NIDDM. They
found that debridement (deep cleaning to remove hardened plaque below the surface of the
gingiva), combined with an antimicrobial solution and a 2-week regimen of the antibiotic
doxycycline — chosen for its anticollagenase activity — resulted in significant short-term
improvement in the concentration of hemoglobin A1c, a measure of average blood glucose
levels over 3 months. A control group receiving only debridement did not share the gains in
periodontal health, improved hemoglobin A1c levels, and reduced hyperglycemia that the
treatment group experienced.
These findings offer evidence that chronic infections such as periodontal disease worsen
glycemic control and that eliminating these infections could enhance metabolic control in
persons with diabetes. Additional large-scale studies are needed to further evaluate the effects
of treating periodontitis on blood glucose levels. Future research should also examine, in other
populations, the relationship between severe periodontal disease and poor glycemic control that
has been evidenced in the Pima Indian community.
While work proceeds on the oral complications of diabetes, other studies are exploring the
molecular pathogenesis of the disease. NIDCR researchers have identified an important marker
protein, IA-2ß, for insulin-dependent diabetes mellitus, an autoimmune disorder which affects
close to one million people in the United States alone. Destructive autoantibodies, which attack
the body’s own insulin-producing beta cells, are the basis of the existing, labor intensive
diagnostic test for IDDM. However, the recent identification of target proteins in the pancreas,
such as IA-2ß, that react with these autoantibodies makes it possible to develop a rapid and
effective test to screen large populations for IDDM.
IA2ß, when used in combination with two other known marker proteins, IA-2 and GAD65,
recognized autoantibodies in 90 percent of persons with IDDM. The presence of autoantibodies
to the marker proteins in otherwise normal individuals was also highly predictive in identifying
those at risk of developing the disease. In addition, these proteins are candidates for immune
tolerance studies, which attempt to prevent the development of destructive autoantibodies and
subsequent IDDM.
The investigators are hopeful that their demonstration of the proteins as major targets of the
autoimmune attack will aid in uncovering the actual cause of the disease process.
Preterm Low Birth Weight Babies
Emerging evidence may link severe periodontal disease in pregnant women to a sevenfold
increase in the risk of delivering preterm low birth weight babies. NIDCR-supported researchers
estimate that as many as 18 percent of the 250,000 premature low-weight infants born in the
United States each year may be attributed to infectious oral disease.
The emotional, social, and economic costs associated with these small babies are staggering.
Hospital costs alone surpass $5 billion annually. When costs to society in terms of suffering and
managing long-term disabilities often associated with prematurity are considered, this figure
escalates dramatically.
In a recent study, mothers of preterm low-weight newborns were found to have significantly
more severe periodontal disease than did mothers of full-term, normal weight babies.
Investigators believe that the molecular pathogenesis may be similar to that characterized for
other maternal, bacterial, opportunistic infections, such as genitourinary infections, that are
associated with low-weight preterm births.
Scientists theorize that oral pathogens release toxins that reach the human placenta via the
mother’s blood circulation and interfere with fetal growth and development, which has been
shown to occur in animal studies. The oral infection also prompts accelerated production of
inflammatory mediators PGE2 and TNF that normally build to a threshold level throughout
pregnancy, then cue the onset of labor. Instead, the elevated levels of these inflammatory
mediators trigger premature delivery.
Taking into account all the known risk factors for premature birth, the researchers could identify
no other reason for the relationship they had found between severe periodontal disease and
preterm low-weight births. Additional research is needed to confirm this intriguing finding and to
determine if treating and preventing periodontal disease would reduce the incidence of these
high risk births.
Table 1: Oral Manifestations of Common Secondary Causes of Diabetes
Cause
Manisfestations
Glucagonoma
Glossitis, angular stomatitis
Pheochromocytoma
Neurofibromas of lips or cheeks (in von ecklinghausen’s
mocytoma disease), neuromas of mucosal surfaces (in multiple
endocrine neoplasia type 2B), capillary or cavernous
hemangiomas (in Sturge-Weber syndrome)
Cushing’s syndrome
Round face with “chubby cheeks,” acne, hirsutism, thinning, of
skin on cheeks, oral candidiasis, periodontal disease, impaired
healing after dental procedures
Acromegaly
Macrognathia with tooth splaying, prognathism, macroglossia
Alcoholism
Bilateral generalized
enlargement
salivary
gland
(especially
parotid)
Table 2: Oral Manifestations of Other Autoimmune Diseases That May Coexist With Type 1
Diabetes
Cause
Manisfestations
Hypopituitarism
Delayed eruption of primary and secondary dentition, retarded
growth with tooth crowding, malocclusion
Hypothyroidism
Dysgeusia, macroglossia secondary to edema, abnormal tooth
development (short roots, hypo-plastic enamel and dentin),
underdevelopment of jaw with maxillary overbite, periodontal
disease
Table 2: Oral Manifestations of Other Autoimmune Diseases That May Coexist With Type 1
Diabetes
Hyperthyroidism
disease)
(Graves’ Periodontal disease
Addison’s disease
Lowered threshold for the sensation of saltiness,
hyperpigmentation of the gums and mucous membranes
Vitiligo
Hypopigmentation of the skin around the mouth
Pernicious anemia
Glossodynia, metallic taste, “raw beef” tongue
Diseases Associated With Diabetes
Diabetes mellitus is associated with many diseases that have oral manifestations. An astute
clinician must always consider the secondary causes of diabetes in a patient with
hyperglycemia. Table 1 outlines the oral manifestations of some of these causes. In addition, the
diagnosis of Type 1 diabetes, or autoimmune destruction of the pancreatic cells, should prompt
the physician to consider the possibility of other autoimmune diseases. Table 2 outlines the oral
manifestations of autoimmune diseases that may coexist with Type 1 diabetes.
4. Detection and Prevention of Periodontal
Disease in Diabetes
Periodontal problems can complicate the management of diabetes, and poorly controlled
diabetes may aggravate periodontal diseases. About 85% of the U.S. population probably has
some degree of periodontal disease, including the most common form, chronic adult
periodontitis1.
Because the prevalence of both chronic periodontitis and diabetes increases with age,
establishing a relationship between them in the older age groups is extremely difficult. Recent
studies in which the age relationship of periodontal disease is accounted for show that in Type 2
diabetics, periodontal disease is more severe and more prevalent than in nondiabetics. These
studies further show that adult diabetes patients have greater tooth loss from periodontal
disease than nondiabetics of comparable age. However, it is generally accepted that adults
whose diabetes is well-controlled do not have more gingivitis or destructive periodontitis than
nondiabetics2, 3.
Although definitive proof of a cause-effect relationship between glycemic control and
periodontal disease is not available, an increased susceptibility to acute lateral periodontal
abscesses has been reported in uncontrolled diabetes mellitus. A study of patients with
longstanding diabetes, accompanied by retinal changes, showed an increased severity of
periodontal diseases4.
Severity of Periodontal Disease Among Diabetic and Non-Diabetic Pima Indians
Periodontal tissue loss, measured in millimeters along the tooth root, is a key indicator of
periodontal disease severity. For the Pima Indians of Arizona, a population with the highest rate
of diabetes in the world, periodontal infection and tooth loss are significant complications of the
diabetic condition.
Diabetes and periodontal disease do seem to be related in children and adolescents. The
frequency and severity of gingivitis increase in prepubertal diabetic children5, especially in
those with poor metabolic control6. In the l2- to l8-year-old age group in the United States, the
prevalence of periodontitis in all forms is about 3%7. However, the prevalence appears to be far
higher, ranging from 11 to 16%, among those in the same group with insulin-dependent diabetes
mellitus (IDDM)2, 5.
In uncontrolled IDDM in both juveniles and adults, most observers agree that it is not unusual to
find acute fulminating periodontitis, characterized by rapidly progressive pocket formation and
bone loss, and frequently complicated by acute abscesses 5.
Gingivitis
Gingivitis, characterized by inflamed and bleeding gums, is a precursor to chronic periodontitis,
although not all gingivitis progresses to periodontitis. Gingivitis results from bacterial
colonization at the gum margin and in the sulcus between the margin and the tooth. These
bacteria and their products have direct inflammatory effects and also evoke an immunological
response. Although these responses are mainly protective, they also cause progressive
destruction of the connective tissue fibers, resorption of alveolar bone around the tooth, and
deepening of the gingival sulcus or pocket8. The resulting condition is called periodontitis,
formerly known as pyorrhea.
Thrush
Diabetics have elevated glucose levels in oral fluids when blood glucose is high, and these
glucose elevations can influence the microbial flora, the composition of bacterial plaque, and the
mixture of organisms at the bottoms of the periodontal pockets. Elevated glucose levels may in
particular encourage the growth of Candida albicans, the causative agent in thrush, and oral C.
albicans counts have been reported to be higher in diabetics than nondiabetics.
Normal,
Gingiva
Periodontitis
Healthy Gingivitis
Advanced
Periodontitis
Pathophysiology
In addition to elevated glucose levels, other pathophysiological changes in diabetics may
predispose the diabetic to periodontal disease. These changes include decreases in leukocyte
chemotaxis, phagocytosis, and bactericidal activity, as well as decreased cellular immunity9.
Impaired neutrophil function may reduce resistance to periodontal infection during periods of
poor diabetic control and local relative insulin insufficiency10.
Other factors contributing to periodontal disease in diabetics may be vascular changes,
including statis in the microcirculation, and altered collagen metabolism.
Dental infections themselves may worsen the diabetic state. As in other infections, dental
infections result in hyperglycemia, mobilization of fatty acids, and acidosis. Exacerbation of
dental infection may undermine good control that has been achieved in diabetes, and initial
control may be difficult or impossible in a newly diagnosed diabetic with active dental infection.
Dental disease, especially severe periodontal disease, may also hamper systemic management
by making chewing painful or difficult, leading the diabetic to select foods that are easier to
chew but that may be dietetically inappropriate.
Diabetic Control
Dental infection in diabetes may rapidly cause a series of adverse metabolic consequences,
including coma. Rapidly progressive periodontitis in adults, unlike the chronic form, is less
responsive to conventional treatment such as subgingival scaling, debridement, and plaque
control; and with continuing bone loss around the teeth, exacerbations may occur. Therefore,
preventing infection through local measures and reducing susceptibility to infection by
maintaining good control of diabetes are primary steps in the prevention of periodontal
complications.
Oral Factors
Local factors, such as smoking and wearing dentures, particularly when dentures are worn
continuously, may promote candidal colonization in the mouth. Attention to these predisposing
factors could reduce the incidence of thrush in diabetes.
Natural Dentition
Because of the importance of diet in diabetes, diabetic patients need to
be aware of the desirability of maintaining their own teeth. Most diabetic
patients who lose their teeth become edentulous because of periodontal
disease. Dentures may not be completely satisfactory replacements
because the size and form of the remaining alveolar ridge for proper fit
may be diminished. In addition, diabetic individuals may not tolerate full
dentures well, especially when diabetes is poorly controlled, because of
mucosal soreness and the need for frequent relining of the dentures.
Every effort should therefore be made to preserve a healthy, functional,
natural dentition so that diabetics may chew proper foods efficiently and
comfortably.
As noted above, teenage diabetics may be at increased risk for periodontal infections and need
to be especially counseled about preventive measures. Diabetes in the mother may have an
influence on tooth development in the offspring, resulting in disturbances of mineralization of
the primary dentition (hypoplasia of the enamel). There may also be a correlation between
congenital dental defects and degree of diabetic control during pregnancy.
Oral Hygiene
Periodontitis can be arrested by local treatment aimed at plaque and calculus removal and
improved oral hygiene, all of which are directed toward eradicating pathogenic bacteria that
cause periodontal disease. Periodontitis is a bacterial infection strongly correlated with poor
oral hygiene, and proper care of the mouth, teeth, and gums is especially important for diabetic
patients.
Diabetic patients should have a dental examination every 6 months and should be sure to tell
their dentists that they are diabetic.
Acute Infections
When a patient with diabetes is found to have advanced periodontal disease, most dental
treatment should be deferred until the diabetes is reasonably controlled. Acute infections,
however, require immediate attention, including draining acute abscesses and administering
broad-spectrum antibiotics. Complete metabolic control of diabetes may not be possible while
dental infection is still present. However, if blood glucose can be reduced, the acute periodontal
condition may subsequently improve.
Oral Surgery
Once infection has subsided, any necessary tooth extractions can be performed. When diabetes
is under good control, oral surgery can be carried out as in a nondiabetic.
Dental appointments should be scheduled in the morning, generally about an hour and a half
after breakfast and the morning insulin.
Diabetes Control
Patients should be informed that periodontal infection may make it more difficult to control
diabetes and conversely, poor diabetic control may increase susceptibility to periodontal
infection.
Risk of Infection
Patients should know that diabetics may be more likely to get gum infections than nondiabetics,
and the infections may take longer to heal. Long standing infection may lead to loss of teeth.
Oral examination by the physician should be an integral part of regular diabetes checkups.
Newly diagnosed diabetics should be referred to a dentist for a thorough oral evaluation.
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Mashimo, P.A., Yamamoto, Y., Slots, J., Park, B.H., and Genco, R.J.: The Periodontal
Microflora of Juvenile Diabetics. J. Periodontol. 54:420, 1983.
Schneir, M.L., Ramamurthy, N.S., and Golub, L.M.: Extensive Degradation of Recently
Synthe sized Collagen in Gingiva of Normal and Streptozotocin-Induced Diabetic Rats.
J. Dent. Res. 63:23, 1984.
Johnson, J.E., III: Infection and Diabetes. Diabetes Mellitus: Theory and Practice. Edited
by M. Ellenberg and H. Rifkin. New York: McCraw-Hill, 1970, pp. 734-745.
Grahnen, H. and Edlund, K.: Maternal Diabetes and Changes in the Hard Tissue of
Primary Teeth. I. A Clinical Study. Odontol. Rev. 18:1957, 1967.
5. Oral Complications of Diabetes
A Guide for Dental Hygienists
Dental hygienists should be aware of certain symptoms that may indicate undetected diabetes in
a patient. Oral symptoms such as xerostomia, an increase in tooth decay, candidiasis, and
periodontal disease may signal that the patient is diabetic.
Oral Complications
Xerostomia is a decrease in the flow of saliva resulting in dry mouth. More than just an
uncomfortable feeling, it can cause soreness, ulcers, infection and tooth decay. Saliva helps
control the growth of germs that cause tooth decay and oral infections. If the glucose levels in
the diabetic are not well controlled, they are at more risk for gum infection. Once an infection
begins in a diabetic it takes longer to heal, which means that the infection lasts longer and the
patient is at more risk for periodontal disease. A severe infection can also make it difficult for the
patient to control the blood glucose level.
Saliva plays an important role in washing the sticky foods away that help form plaque and also
helps to strengthen the teeth with minerals. Plaque is the major bad guy of gum disease for any
healthy person, but for the diabetic individual the mouth�s germ-fighting powers are weaker and
the patient has a higher risk for gum disease. The high blood glucose level accentuates the
response to plaque. Glucose concentrations allow the growth and colonization of the bacteria
that give rise to gum disease.
Chronic inflammation of the gums can result in loss of attachment to the teeth, formation of
pockets, and as these pockets become deeper there is more area for bacteria to grow giving rise
to infections. Bone surrounding the teeth can be damaged which eventually can lead to loss of
teeth. Bleeding gums and inflammation are two most visible signs of periodontal disease.
Dry mouth can cause oral tissues to dehydrate increasing the risk of candidiasis. This fungus
thrives on high glucose levels leaving diabetics more prone to fungal infections. If they are
taking antibiotics, smoking, or wearing dentures, the risk of candidiasis increases even more.
Dental Management
To reduce the risk of candidiasis, if the patient smokes recommend that the patient quit. Let him
or her know that you can offer some smoking cessation programs that can help the patient quit
smoking. If the patient wears dentures, advise the patient that wearing the dentures during the
day and taking them out at bedtime will help reduce the risk of fungal infections. Educate the
patient on the importance of cleaning the dentures and the mouth before bedtime.
Urge the patient to brush and floss teeth several times a day. Mouthwashes with antimicrobial
agents can benefit in certain situations. Recommend a soft toothbrush and a fluoride toothpaste.
After each brushing the patient should rinse the brush thoroughly to help reduce bacteria from
growing on the brush, and to change the brush every 3 months.
Ask your patients if they have problems with infections or glucose control. Schedule them for
morning appointments after they have had their breakfast. Regular meal schedules are an
important factor in managing the disease. Make sure that they have taken their normal
medications before their appointment and encourage dental checkups every six months. If
periodontal surgery is required, a consultation with their physician is needed to inquire if an
antibiotic would be needed to help prevent infection. If use of a local anesthetic is indicated, use
a vasoconstrictor drug and avoid giving excessive epinephrine to prevent elevating blood
glucose.
Diabetic Emergencies
While treating a diabetic patient, the hygienist must be able to recognize and manage any
complications or emergencies that might possibly occur with the dental visit. Two complications
would be hyperglycemia and hypoglycemia. These could be evident in an undiagnosed diabetic
or a known diabetic. Hypoglycemia is more life-threatening. The insulin-dependent diabetic is
likely to encounter these complications. The type of diabetes would be indicated with a review of
the medical history before treating the patient.
Hyperglycemia is a high blood glucose level and can manifest in several different ways
depending on the severity of the diabetes. Clinical sign of hyperglycemia would be bright red
color appearance of the face. The skin would be hot and dry which would indicate dehydration.
The heart rate is rapid and the blood pressure may be lower than normal which would also
indicate dehydration. A fruity-sweet odor of acetone may also be observed. If these signs should
occur, because hypoglycemia is more life threatening, the condition should be treated as if it
were hypoglycemia until it is proven otherwise, and oral glucose should be administered.
Hypoglycemia is low blood glucose level and occurs most commonly with diabetes. The patient
usually appears pale, the skin is cold and wet, and the patient may have an intoxicated
appearance. The patient may have shallow breathing and the level of consciousness is altered.
Oral carbohydrates should be administered. It is recommended that if the patient is known to
have had these episodes, candy or just plain sugar should be set out nearby. Sometimes the
patient is able to let you know it is coming on and will tell you that he or she needs some form of
sugar.
The Role of Diet
Fermentable carbohydrates (six-carbon sugars) provide substrate for cariogenic bacteria,
especially Streptococcus mutans, and can promote tooth decay. Food form determines
cariogenic potential. Sticky, long-lasting carbohydrates (such as sugar- containing hard candies,
chewing gums, breath mints, and cough drops) have the greatest decay-producing potential.
Next in line for cariogenicity are solid, sticky foods, such as cakes, cookies, raisins, bananas,
dried fruits, chewy candies, and jams. Cereals, crackers, and pretzels are also in this category,
even though not considered sticky sweet, since they take longer to leave the mouth and
surrounding tissues. The least cariogenic carbohydrates are those in a liquid form, such as soft
drinks, juices, frozen desserts, gelatin, and puddings, since they are rapidly cleared by the
mouth and generally do not adhere to teeth.
The frequency of meals also contributes to periodontal disease risks. Each meal or snack
containing fermentable carbohydrate produces a 20- to 30-minute exposure to bacterial acid.
Prolonged exposure to these acids should be avoided whenever possible.
Nutrient composition of various foods also plays an important role in oral health. Nuts and
peanut butter are cariostatic (inhibiting tooth decay) and provide a protective coating to tooth
enamel. Cheese, which is also cariostatic, promotes alkaline-rich saliva that reduces plaqueforming bacteria.
Planning Dental Treatment
When patients with diabetes are scheduled for oral surgery or extensive dental work, the
diabetes team needs to be consulted about possible changes in insulin or oral hypoglycemic
drug dosages. If the patient is not in good metabolic control and time permits, every effort
should be made to improve blood glucose control.
Patients need to be aware of how long a dental procedure will last. If dental work is scheduled
when insulin might be peaking, consider rescheduling the procedure. In most cases, patients
should eat their usual meal, and the dental team should confirm that the patient has eaten before
the procedure has begun. If sedation or extensive surgery is needed, fasting may be indicated.
The diabetes team needs to be consulted in these cases, and medications may need to be
changed.
Dentists who treat patients with diabetes on a regular basis often have blood glucose testing
equipment, glucose tablets, and glucagon available in their offices. Although hypoglycemia
usually is avoidable with proper precautions, patients may wish to talk with their dentist about
possible hypoglycemia and steps to be taken by the dental team.
Dentists sometimes are the first to spot hyperglycemia. Important clues are dry mucous
membranes and acetone breath. The diagnosis can be confirmed by blood glucose testing.
Patients with acetone breath and those progressing to severe hypotension and loss of
consciousness need to be sent to a medical facility immediately.
Restorative dental work (dentures, bridgework, and tooth fillings) often requires a soft diet that
minimizes biting or chewing of foods. If raw fruits and vegetables are normally part of a specific
patient�s meal plan, suggest cooked or canned choices until soreness and swelling are gone.
Patients with dentures initially need to avoid nuts and seeds that could become wedged under
the prostheses. Sick-day management guidelines that incorporate carbohydrate replacement
should be given to patients who feel too ill to consume even a soft diet after a dental procedure.
There is no substitute for careful examination, meticulous education, and active treatment. As a
hygienist, it is important to be able to recognize signs and symptoms of this disease and aid the
patient to minimize additional complications to the already complicated disease.
Dental Tips For Patients With Diabetes
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Be careful with between-meal snacks. When you just want a snack, plain popcorn or
vegetables are good low-calorie choices that do not promote tooth decay. When a more
substantial snack, such as crackers or cereal, is part of your meal plan, pair those foods
with a liquid (milk or juice) or with cheese, which slows bacterial growth.
Avoid frequent use of glucose tablets, sugared or chewy candies, or driped fruits, fruit
roll-ups, or raisins for treating hypoglycemia. If you have, or are afraid you might have,
frequent bouts of low blood glucose, ask your diabetes educators about adjusting your
meals or insulin to keep blood glucoses where they should be.
Pay attention to your mouth. Always let your physician or dentist know if something
changes or does not seem right.
See your dentist at least every 6 months.
Remove plaque after meals and snacks. Brushing is preferable, but if that is not
possible, rinsing with water or chewing sugarless gum is acceptable.
Brush your teeth properly with a soft-bristled toothbrush.
Floss between teeth at least once a day.
Use other cleaning aids recommended by your dentist.
Do not smoke or chew tobacco.
6. Oral Complications of Diabetes
A Guide for Patients
If you have diabetes, you know the disease can harm your eyes, nerves, kidneys, heart and other
important systems in the body. Did you know it can also cause problems in your mouth? People
with diabetes have a higher than normal risk of periodontal diseases.
What is the relationship between poor oral health and diabetes?
It is well known that people who have diabetes have a higher than normal risk of periodontal
(gum) disease. Other oral complications of diabetes can include infections, poor healing, and
fungal infections.
What is the link between diabetes and periodontal disease?
Periodontal diseases are infections of the gum and bone that hold the teeth in place. In
advanced stages, they lead to painful chewing problems and even tooth loss. Like any infection,
gum disease can make it hard to keep your blood sugar under control.
Periodontal diseases are infections of the gum and bone that hold the teeth in place. In
advanced stages, they lead to painful chewing problems and even tooth loss. Like any infection,
gum disease can make it hard to keep your blood sugar under control.
Diabetic Control.Like other complications of diabetes, gum disease is linked to diabetic control.
People with poor blood sugar control get gum disease more often and more severely, and they
lose more teeth than do persons with good control. In fact, people whose diabetes is well
controlled have no more periodontal disease than persons without diabetes. Children with IDDM
(insulin-dependent diabetes mellitus) are also at risk for gum problems. Good diabetic control is
the best protection against periodontal disease.
Studies show that controlling blood sugar levels lowers the risk of some complications of
diabetes, such as eye and heart disease and nerve damage. Scientists believe many
complications, including gum disease, can be prevented with good diabetic control.
Blood Vessel Changes.Thickening of blood vessels is a complication of diabetes that may
increase risk for gum disease. Blood vessels deliver oxygen and nourishment to body tissues,
including the mouth, and carry away the tissues� waste products. Diabetes causes blood
vessels to thicken, which slows the flow of nutrients and the removal of harmful wastes. This
can weaken the resistance of gum and bone tissue to infection.
Bacteria.Many kinds of bacteria (germs) thrive on sugars, including glucose - the sugar linked to
diabetes. When diabetes is poorly controlled, high glucose levels in mouth fluids may help
germs grow and set the stage for gum disease.
Smoking.The harmful effects of smoking, particularly heart disease and cancer, are well known.
Studies show that smoking also increases the chances of developing gum disease. In fact,
smokers are five times more likely than nonsmokers to have gum disease. For smokers with
diabetes, the risk is even greater. If you are a smoker with diabetes, age 45 or older, you are 20
times more likely than a person without these risk factors to get severe gum disease.
Controlled Diabetics Have New Reason to Smile
CHICAGO - November 22, 1999 - Diabetes has long been known to increase the risk of severe
periodontal disease. A study released today in the November issue of the Journal of
Periodontology found that poorly controlled Type 2 diabetic patients are more likely to develop
periodontal disease than well-controlled diabetics are. In addition, the study further explains why
diabetics are more susceptible to severe periodontal disease.
The study concluded that poorly controlled diabetics respond differently to bacterial plaque at
the gum line than well-controlled diabetics and non-diabetics, possibly due to elevated serum
triglycerides. Poorly controlled diabetics have more harmful proteins (cytokines) in their gingival
tissue, causing destructive inflammation of the gums. In turn, beneficial proteins (growth
factors) are reduced, interfering with the healing response to infection.
"Increased serum triglyceride levels in uncontrolled diabetics seem to be related to greater
attachment loss and probing depths, which are measures of periodontal disease," said
Christopher Cutler, D.D.S., Ph.D., the study�s lead researcher. "Diabetic patients should
certainly be aware of their blood sugar levels, but it�s also important they have their serum
triglycerides and cholesterol levels checked by their physician on a regular basis. Reducing
cholesterol and serum triglyceride levels, preferably through diet and exercise, may be the most
important changes that diabetics can make to improve their quality of life, as well as their oral
health."
The American Academy of Periodontology is encouraging diabetics to get a periodontal
evaluation during National Diabetes Month in November, as recent research also has found that
having periodontal disease makes diabetes more difficult to control. "We have a classic vicious
cycle going on," said Cutler.
"Controlling your periodontal disease may help you control your diabetes," added Jack Caton,
D.D.S., M.S., President of the American Academy of Periodontology (AAP). "Therefore, diabetic
patients should be sure both their medical and dental care provider are aware of their medical
history and periodontal status."
How does periodontal disease develop?
Gingivitis. Poor brushing and flossing habits allow dental plaque - a sticky film of germs - to
build up on teeth. Some of these germs cause gum disease. The gums can become red and
swollen and may bleed during toothbrushing or flossing. This is called gingivitis, the first stage
of periodontal disease.
Gingivitis can usually be reversed with daily brushing and flossing and regular cleanings by the
dentist. If it is not stopped, gingivitis could lead to a more serious type of gum disease called
periodontitis.
Periodontitis. Periodontitis is an infection of the tissues that hold the teeth in place. In
periodontitis, plaque builds and hardens under the gums. The gums pull away from the teeth,
forming "pockets" of infection. The infection leads to loss of the bone that holds the tooth in its
socket and might lead to tooth loss.
As plaque builds up, the gums become inflamed and, in time, affected teeth may loosen and
could be lost.
There are often no warning signs of early periodontitis. Pain, abscess, and loosening of the teeth
do not occur until the disease is advanced. Since periodontitis affects more than just the gums,
it cannot be controlled with regular brushing and flossing. Periodontitis should be treated by a
periodontist (a gum disease specialist) or by a general dentist who has special training in
treating gum diseases.
How is periodontal disease treated?
Plaque Removal. Treatment of periodontitis depends on how much damage the disease has
caused. In the early stages, the dentist or periodontist will use deep cleaning to remove
hardened plaque and infected tissue under the gum and smooth the damaged root surfaces of
teeth. This allows the gum to re-attach to the teeth. A special mouthrinse or an antibiotic might
also be prescribed to help control the infection.
Deep cleaning is successful only if the patient regularly brushes and flosses to keep the plaque
from building up again.
Periodontal Surgery. Gum surgery is needed when periodontitis is very advanced and tissues
that hold a tooth in place are destroyed. The dentist or periodontist will clean out the infected
area under the gum, then reshape or replace the damaged tooth-supporting tissues. These
treatments increase the chances of saving the tooth.
If you have diabetes...
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It's important for you to know how well your diabetes is controlled and to tell your
dentist this information at each visit.
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See your doctor before scheduling treatment for periodontal disease. Ask your doctor to
talk to the dentist or periodontist about your overall medical condition before treatment
begins.
You may need to change your meal schedule and the timing and dosage of your insulin
if oral surgery is planned.
Postpone non-emergency dental procedures if your blood sugar is not in good control.
However, acute infections, such as abscesses, should be treated right away.
For the person with controlled diabetes, periodontal or oral surgery can usually be done in the
dentist�s office. Because of diabetes, healing may take more time. But with good medical and
dental care, problems after surgery are no more likely than for someone without diabetes.
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Once the periodontal infection is successfully treated, it is often easier to control blood
sugar levels.
Since I have diabetes, do I need to do anything to prepare for oral
surgery?
Yes, prior to any treatment, it is important that your physician and periodontist talk to each other
to discuss your overall medical condition. You should have morning appointments after you
have eaten and taken your insulin. If your diabetes is poorly controlled, it will be difficult to
provide treatment and may require you to be admitted to the hospital. Healing after oral surgery
may take longer because of diabetes, but with good medical and dental care there should be no
more problems than for an individual without diabetes.
Are other oral problems linked to diabetes?
Dental Cavities. Young people with IDDM have no more tooth decay than do nondiabetic
children. In fact, youngsters with IDDM who are careful about their diet and take good care of
their teeth often have fewer cavities than other children because they don�t eat many foods that
contain sugar.
Thrush. Thrush is an infection caused by a fungus that grows in the mouth. People with diabetes
are at risk for thrush because the fungus thrives on high glucose levels in saliva. Smoking and
wearing dentures (especially when they are worn constantly) can also lead to fungal infection.
Medication is available to treat this infection. Good diabetic control, no smoking, and removing
and cleaning dentures daily can help prevent thrush.
Dry Mouth. Dry mouth is often a symptom of undetected diabetes and can cause more than just
an uncomfortable feeling in your mouth. Dry mouth can cause soreness, ulcers, infections, and
tooth decay.
The dryness means that you don�t have enough saliva, the mouth�s natural protective fluid.
Saliva helps control the growth of germs that cause tooth decay and other oral infections. Saliva
washes away sticky foods that help form plaque and strengthens teeth with minerals.
One of the major causes of dry mouth is medication. More than 400 over-the-counter and
prescription drugs, including medicines for colds, high blood pressure or depression, can cause
dry mouth. If you are taking medications, tell your doctor or dentist if your mouth feels dry. You
may be able to try a different drug or use an "artificial saliva" to keep your mouth moist.
Good blood glucose control can help prevent or relieve dry mouth caused by diabetes.
Keep your teeth
Serious periodontal disease not only can cause tooth loss, but can also cause changes in the
shape of bone and gum tissue. The gum becomes uneven, and dentures may not fit well. People
with diabetes often have sore gums from dentures.
If chewing with dentures is painful, you might choose foods that are easier to chew but not right
for your diet. Eating the wrong foods can upset blood sugar control. The best way to avoid these
problems is to keep your natural teeth and gums healthy.
How can you protect your teeth and gums?
Harmful germs attack the teeth and gums when plaque builds up. You can stop plaque build-up
and prevent gum disease by brushing and flossing carefully every day.
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Use a piece of dental floss about 18 inches long.
Using a sawing motion, gently bring the floss through the tight spaces between the
teeth.
Do not snap the floss against the gums.
Curve the floss around each tooth and gently scrape from below the gum to the top of
the tooth several times.
 Rinse your mouth after flossing.
 Gently brush teeth twice a day with a soft nylon brush with
rounded ends on the bristles.
 Avoid hard back-and-forth scrubbing.
 Use small circle motions and short back-and-forth motions.
 Gently brush your tongue, which can trap germs.
 Use a fluoride toothpaste to protect teeth from decay.
Check Your Work. Dental plaque is hard to see unless it is stained. Plaque can be stained by
chewing red "disclosing tablets" sold at grocery stores and drug stores or by using a cotton
swab to smear green food coloring on the teeth. The color left on the teeth shows where there is
still plaque. Extra flossing and brushing will remove this plaque.
Dental Check-ups. People with diabetes should have dental check-ups at least every 6 months,
or more often if recommended by their dentist. Be sure to tell your dentist you have diabetes.
Frequent dental check-ups are needed to find problems early when treatment is most effective.
See your dentist as soon as possible if you have any problem with your teeth or mouth.
Preventing or controlling gum disease depends on teamwork. The best defense against this
complication of diabetes is good blood sugar control, combined with daily brushing and flossing
and regular dental check-ups.
Things to keep in mind
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Protect your teeth and gums by brushing and flossing daily.
See you dentist at least every 6 months and as soon as possible if you have a problem
with your teeth and gums.
Make sure you tell your dentist that you have diabetes.
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Controlling your diabetes will make it easier to control your oral health and controlling
your oral health will make it easier to control your diabetes.
Source:
Periodontal
Disease
&
Diabetes:
National
Institute
of
Dental
and
National
Institutes
31
Center
Drive
Bethesda, MD 20892-2290
A
Guide
for
Craniofacial
of
MSC
Patients
Research
Health
2290