Diabetes Mellitus:

1) Influence of diabetes on periodontium:

1.1 Oral Manifestations:

Cheilosis, mucosal drying and cracking, burning mouth and tongue, diminished salivary flow,
and an increased rate of dental caries.
These changes are less likely to be observed in patients with well-controlled diabetes.
Individuals with controlled diabetes have a normal tissue response, a normally developed
dentition, a normal defense against infections, and no increase in the incidence of caries.
Effect on periodontium: A tendency toward an enlarged gingiva, sessile or pedunculated
gingival polyps, polypoid gingival proliferations, abscess formation, periodontitis, and loosened
teeth. Severe gingival inflammation, deep periodontal pockets, rapid bone loss, and frequent
periodontal abscesses often occur in patients with poorly controlled diabetes and poor oral
hygiene.
Adults who are 45 years of age or older with poorly controlled diabetes were 2.9 times more
likely to have severe periodontitis than those without diabetes. The likelihood was even greater
(4.6 times) among smokers with poorly controlled diabetes.
As with other systemic conditions associated with periodontitis, diabetes mellitus does not
cause gingivitis or periodontitis, but evidence indicates that it alters the response of the
periodontal tissues to local factors, thereby hastening bone loss and delaying postsurgical
healing. Frequent periodontal abscesses appear to be an important feature of periodontal
disease in patients with diabetes.

1.2 Bacterial Pathogens:

The glucose content of gingival fluid and blood is higher in individuals with diabetes than in
those without diabetes with similar plaque and gingival index scores. The increased glucose in
the gingival fluid and blood of patients with diabetes could change the environment of the
microflora, thereby inducing qualitative changes in bacteria that may contribute to the severity
of periodontal disease observed in those with poorly controlled diabetes.
Patients with type 1 diabetes mellitus and periodontitis have been reported to have a
subgingival flora that is composed mainly of Capnocytophaga, anaerobic vibrios, and
Actinomyces species. Porphyromonas gingivalis, Prevotella intermedia, and Aggregatibacter
actinomycetemcomitans, which are common in periodontal lesions of individuals without
diabetes, are present in low numbers in those with the disease. However, other studies have
found scarce Capnocytophaga and abundant A. actinomycetemcomitans and black-pigmented
Bacteroides as well as P. intermedia, Prevotella melaninogenica, and Campylobacter rectus.
Black-pigmented species—especially P. gingivalis, P. intermedia, and C. rectus—are prominent
in severe periodontal lesions of Pima Indians with type 2 diabetes.
1.3 Polymorphonuclear Leukocyte Function
The increased susceptibility of patients with diabetes to infection has been hypothesized as
being caused by polymorphonuclear leukocyte (PMN) deficiencies that result in impaired
chemotaxis, defective phagocytosis, or impaired adherence. In patients with poorly controlled
diabetes, the functions of PMNs, monocytes, and macrophages are impaired. As a result, the
primary defense mounted by PMNs against periodontal pathogens is diminished, and bacterial
proliferation is more likely.

1.4 Altered Collagen Metabolism:

Chronic hyperglycemia adversely affects the synthesis, maturation, and maintenance of
collagen and extracellular matrix. In the hyperglycemic state, numerous proteins and matrix
molecules undergo a nonenzymatic glycosylation, thereby resulting in accumulated glycation
end-products (AGEs). The formation of AGEs occurs at normal glucose levels as well; however,
in hyperglycemic environments, AGE formation is excessive.
Collagen is cross-linked by AGE formation, which makes the collagen less soluble and less likely
to be normally repaired or replaced. Cellular migration through cross-linked collagen is
impeded, and, perhaps more importantly, tissue integrity is impaired as a result of damaged
collagen that remains in the tissues for longer periods (i.e., collagen is not renewed at a normal
rate). As a result, collagen in the tissues of patients with poorly controlled diabetes is older and
more susceptible to pathogenic breakdown (i.e., less resistant to destruction by periodontal
infections.

2) Effect of periodontal infection on glycemic control:

In a longitudinal study of patients with type 2 diabetes, severe periodontitis was associated
with the significant worsening of glycemic control over time. Individuals with severe
periodontitis at the baseline examination had a greater incidence of worsening glycemic control
over a 2- to 4-year period as compared with those without periodontitis at baseline.
Among diabetic patients with periodontitis, periodontal therapy may have beneficial effects on
glycemic control. This may be especially true for patients with relatively poor glycemic control
and more advanced periodontal destruction before treatment. Numerous systematic reviews
and meta-analyses have consistently shown that periodontal therapy is associated with a
statistically significant and clinically relevant improvement in glycemic control in patients with
diabetes and periodontitis.
in a study of subjects with type 1 and type 2 diabetes with periodontitis, periodontal therapy
was associated with a significant improvement in glycemic control overall in those with type 2
diabetes but not in those with type 1 disease, despite improvement in the periodontal
condition of both groups.

2.1 Periodontal Infection Associated With Glycemic Control in Diabetes

It is well known that systemic inflammation plays a major role in insulin sensitivity and glucose
dynamics. As discussed previously, periodontal diseases can induce or perpetuate an elevated
systemic chronic inflammatory state, which is reflected in increased serum CRP, IL-6, and
fibrinogen levels seen in many people with periodontitis. Inflammation induces insulin
resistance, and such resistance often accompanies systemic infections. Increased serum levels
of several cytokines, including TNF-α and IL-6, are associated with increased insulin resistance.
This mechanism would explain the worsening of glycemic control associated with severe
periodontitis.
Periodontal treatment designed to decrease the bacterial insult and reduce inflammation may
result in decreased systemic inflammation, restoring insulin sensitivity over time and thereby
resulting in improved metabolic control. This mechanism may also explain differences in the
glycemic response to periodontal therapy between individuals with type 1 and type 2 diabetes.
Because type 2 diabetes is strongly associated with insulin resistance, periodontal therapy that
reduces systemic inflammation may improve insulin sensitivity and result in improved glycemic
control. Conversely, type 1 diabetes is not strongly associated with insulin resistance, so
reduced inflammation after periodontal therapy may not have a major effect on insulin
sensitivity in patients with type 1 disease, which would minimize the impact of periodontal
treatment in these patients.

3) Managment of Diabetic Patient in a dental Clinic:

3.1 Undiagnosed Diabetic patient

If the patient has any of these signs or symptoms (Polyphagia, Polydipsia, polyuria, unexplained
weight loss) or the clinician suspects diabetes, the following procedures should be performed:
 Consult the patient’s physician.
 Analyze laboratory tests, including fasting blood glucose and casual glucose test results.
 Rule out acute orofacial infection or severe dental infection; if present, provide
emergency care immediately.
 Establish the best possible oral health through nonsurgical debridement of plaque and
 calculus. Institute oral hygiene instruction.
 Limit more advanced care until the diagnosis has been established and good glycemic
control obtained.

3.2 Already diagnosed patient

If a patient is known to have diabetes, it is critical that the level of glycemic control be
established before initiating periodontal treatment. The fasting glucose and casual glucose tests
provide snapshots of the blood glucose concentration at the time the blood was drawn; these
tests reveal nothing about long-term glycemic control. The primary test used to assess glycemic
control in a known diabetic individual is the glycated hemoglobin (HbA1c).
The therapeutic goal for many patients is to achieve and maintain an HbA1c below 8%. Patients
with relatively well-controlled diabetes (HbA1c <8%) usually respond to therapy in a manner
similar to nondiabetic individuals. Poorly controlled patients (HbA1c >10%) often have a poor
response to treatment, with more postoperative complications and less favorable long-term
results. When possible, an HbA1c of less than 10% should be established before surgical
treatment is performed.
Systemic antibiotics are not needed routinely, although evidence indicates that tetracycline
antibiotics in combination with scaling and root planing may positively influence glycemic
control. If the patient has poor glycemic control and surgery is absolutely needed, prophylactic
antibiotics can be given; penicillin are most often used for this purpose.

The following guidelines should be observed before treating patient in dental

office:
 Patients should be asked to bring their glucometer to the dental office at each
appointment.
 As a general guideline, well-controlled diabetic patients having routine periodontal
treatment may take their normal insulin doses as long as they also eat their normal
meal. If the patient is restricted from eating before treatment (e.g., for conscious
sedation), normal insulin doses need to be reduced. If the procedure is going to be
particularly long, the insulin dose before treatment may need to be reduced. Likewise, if
the patient will have dietary restrictions after treatment, insulin or sulfonylurea dosages
may need to be reduced.
 Patients should check their blood glucose before any long procedure to obtain a
baseline level. Patients with a blood glucose level at or below the lower end of normal
before the procedure may become hypoglycemic intraoperatively. It is advisable to have
the patient consume some carbohydrate before starting treatment. For example, if a 2-
hour procedure is planned and the pretreatment glucose level is 70 mg/dL (i.e., lower
end of normal range), providing 4 ounces of juice preoperatively may help prevent
hypoglycemia during treatment. If the pretreatment glucose level is excessively high,
the clinician should determine whether the patient’s glycemic control has been poor
recently. This can be done with thorough patient questioning and by determining the
most recent HbA1c values. If glycemic control has been poor over the preceding few
months, the procedure may need to be postponed until better glycemic control is
 established. If glycemic control has been good and the current high glucometer reading
is a fairly isolated event, the surgical procedure may proceed.
 If the procedure lasts several hours, it is often beneficial to check the glucose level
during the procedure to ensure that the patient does not become hypoglycemic.
 After the procedure, the blood glucose can be checked again to assess fluctuations over
time.
 Any time the patient feels the symptoms of hypoglycemia, the blood glucose level
should be checked immediately. This may prevent the onset of severe hypoglycemia, a
medical emergency.

3.3) Management of Hypoglycemia:

Checking the pretreatment glucose with the patient’s glucometer, checking again during a long
procedure, and checking again at the end of the procedure provides a better understanding of
the patient’s insulin pharmacodynamics and can help prevent hypoglycemia.
If hypoglycemia occurs during dental treatment, therapy should be immediately terminated.
If a glucometer is available, the blood glucose level should be checked.

Treatment guidelines include the following:

Provide approximately 15 g of oral carbohydrate to the patient
 4 to 6 ounces of juice
 3 or 4 teaspoons of table sugar
 Hard candy with 15 g of sugar
If the patient is unable to take food or drink by mouth or if the patient is sedated
 Give 25 to 30 mL of 50% dextrose intravenously
 Give 1 mg of glucagon intravenously (i.e., glucagon results in rapid release of stored
glucose from the liver), or
 Give 1 mg of glucagon intramuscularly or subcutaneously (if no intravenous access).