MODUL

Group H
Background:
A 55-year-old female patient visit Unairs Faculty of Dentistrys dental
clinic with symptoms such as dry mouth, burning sensation, and
difficulty in swallowing since 1 month ago. Maxillary and mandibulary
teeth are rocking and lower front teeth dislodged without any retraction
/ trauma. Patients have never seen a doctor or a dentist. In family
history it is mentioned that his father suffered from diabetes mellitus.
Main Issue
What is the diagnosis for the patient on the case above?

Purposes of Writing
This paper aims to explain the diagnosis for the patient on the case above and
understand how to manage it based on clinical case priorities for dental care.

Benefits of Writing
The benefit is to learn how to make a proper diagnosis for patients based on their
medical background and clinical symptoms and how to manage it based on
clinical case priorities for dental care.
 ORAL MANIFESTATION OF DM
High glucose concentrations in the It has been suggested that the
blood correlate with the high salivary sensation of burning mouth in
glucose concentration and crevicular diabetics occurs via stimulation of
fluid
the capsaicin receptor by Candida
Elevated salivary glucose metabolites, since capsaicin
concentrations reduced salivary flow receptors are responsible for the
rates and low salivary pH salivary flow
detection of pain-producing
rates and salivary glucose levels are
chemical and thermal stimuli
inversely correlated
 Periodontitis
an inflammatory disease of the supporting tissues of the
teeth caused by specific microorganisms or groups of
specific microorganisms, resulting in progressive
destruction of the periodontal ligament and alveolar bone
with increased probing depth formation, recession, or
both.
 Clinical signs
Loss of attachment
Periodontal pocket
Changes in density and height of subjacent alveolar bone
Recession of the marginal gingiva
Continous BOP on sequential visits sign of inflammation and potential
of subsequent attachment lost
 Classification
Chronic Periodontitis
Aggressive Periodontitis
Periodontitis as a manifestation of systemic disease
 Periodontitis as a manifestation of systemic disease
Periodontitis as a manifestation of Chronic periodontitis modified by the
systemic disease systemic condition

Systemic condition is the major Periodontal destruction Is clearly the

predisposing factor & local factors result of local factors but has been
are not clearly evident exacerbated by such conditions as
DM or HIV infection

 SUPPORTING EXAMINATION
DIABETES PERIODONTITIS
A1c test or plasma glucose tests Radiography
Fuzziness & disruption of lamina dura crestal
cortication continuity
HbA1c >6.5%
Continued periodontal bone loss & widening of
the periodontal space
Random plasma glucose >200 mg/dl
Destructive process extends across the
Fasting plasma glucose >126 mg/dl alveolar crest

The height of the interdental septum is

2-h postload glucose >200 mg/dl progressively reduced
 Associations between
diabetes and periodontitis
 DIABETES PERIODONTITIS
Periodontitis and diabetes are common, complex, chronic diseases with an
established bidirectional relationship.

Diabetes (particularly if glycaemic control is poor) is associated with an

increased prevalence and severity of periodontitis; severe periodontitis is
associated with compromised glycaemic control.
 DIABETES PERIODONTITIS
The mechanisms that underpin the links between these two conditions are
not completely understood, but involve aspects of immune functioning,
neutrophil activity, and cytokine biology.

There is emerging evidence to support the existence of a two-way

relationship between diabetes and periodontitis, with diabetes increasing
the risk for periodontitis, and periodontal inflammation negatively
affecting glycaemic control.
 PATHOGENESIS OF PERIODONTITIS WITH DIABETES
There is an alterations that the host immune inflammatory response may have a
major influence on the increased prevalence and severity of periodontal
destruction seen in diabetes.

The function of immune cells, including neutrophils, monocytes, and

macrophages, is altered in diabetes. Neutrophil adherence, chemotaxis, and
phagocytosis are often impaired, which may inhibit bacterial killing in the
periodontal pocket and significantly increase periodontal destruction.
 PATHOGENESIS OF PERIODONTITIS WITH DIABETES
The immune system may not function properly in people with diabetes, thereby
increasing the risk of periodontal disease.

There is a damage to capillaries (the small delicate blood vessels) in the gums
may reduce the blood supply to the gums, thereby limiting the actions of
defense cells.

And wound healing is impaired in diabetes, and therefore, healing in the gums
is also reduced.
Conceptual Mapping
 DISCUSSION
information gained by asking specific questions, either of
ANAMNE the patient or of other people who know the person and
can give suitable information.
SIS
Intraoral
Examinatio performed by the dentist to determine existing conditions
n
Extraoral
Examinatio an extra-oral examination of the head and neck should

n be performed by the dentist

 DISCUSSION
DISCUSSION

Additional Diagnostic
Test

Periodontiti
Diabetes Xerostomia
s
- Fasting Plasma - Radiography - Measure the
Grucose test (FPG) saliva flow
- Random Plasma
Glucose test (RPG)
- HbA1c
 DISCUSSION
HYPOTHESIS Periodontitis Modified by Systemic
Disease

Systemic factors modify all forms periodontitis principally through their

effects on the normal immune and inflammatory defenses. Diabetes (IDDM
and NIDDM) is associated with an increased risk of periodontitis. The level of
diabetic control is an important factor in this relationship.
Bibliography
Casanova L, Hughes FJ, and Preshaw PM. 2014. Diabetes and periodontal disease: a two way
relationship. Br Dent J; 217(8): 433-7.
Preshaw PM, Alba AL, Herrera D, Jepsen S, Konstantinidis A, Makrilakis K, and Taylor R. 2012.
Peridontitis and diabetes: a two-way relationship. Diabetologia; 55(1): 21-31.
Naguib G, Al-Mashat H, Desta T, Graves D. 2014. Diabetes prolongs the inflammatory response to a
bacterial stimulus through cytokine dysregulation. J Invest Dermatol;123:87-92.