Endocrine disorder and
hormonal changes on
periodontium
contents




Diabetes mellitus
Female sex hormones
Corticosteroid hormone
Hyperparathyroidism

DIABETES MELLITUS

is a medical disorder characterized by varying or
persistent hyperglycemia with disturbance of
carbohydrate fat and protein metabolism.
Physiologic role of insulin
foods
broken down into glucose
the circulatory system
Most cells require the presence of
insulin to allow glucose entry
excluding those in the brain and
central nervous system
used by tissue cells for energy and growth.
glucose
concentrations
resulting in its utilization
by the cells and thus
decreased
blood glucose
concentrations
insulin secretion
occurs
glucose is able to exit
the
bloodstream
and enter the tissues
AMERICAN DIABETES ASSOCIATION: Modified
Type 1 DIABETES
 Immune mediated
 Non immune mediated\ idiopathic
Type 2 Diabetes
 Predominantly insulin resistant
 Predominantly secretory defect
OTHER SPECIFIC TYPES:
 Genetic defects in beta cell function
 Genetic defects in insulin action
 Disease of the exocrine pancreas
 Endocrinopathies
 Drug\Chemical induced
 Infections
 Other genetic problems
CLASSIC COMPLICATIONS OF DIABETES
 In addition to dysregulation in carbohydrate, lipid and protein
metabolism, type 1 and type 2 diabetes are associated with a classic
group of microvascular and macrovascular complications
1.RETINOPATHY
2.NEPHROPATHY
3.NEUROPATHY
4.MACROVASCULAR DISEASE (accelerated
atherosclerosis)
5.ALTERED WOUND HEALING
DIAGNOSIS OF DIABETES
 The diagnosis of diabetes through
 Signs and symptoms and
 By laboratory evaluation.
Laboratory evaluation.
 Urine analysis
 Blood glucose levels
In 1997, the American Diabetes Association provided the
most current laboratory diagnostic parameters for diabetes
Laboratory Methods*
 Symptoms of diabetes plus casual (nonfasting) plasma
glucose >200 mg/dL.
 Casual glucose may be drawn at any time of day without
regard to time since the last meal.
 Fasting plasma glucose > 126 mg/dL. Fasting is defined as
no caloric intake for at least 8 hours.
 Two-hour postprandial glucose > 200 mg/dL during an oral
glucose tolerance test. The test should be performed using a
glucose load containing the equivalent of 75 g of anhydrous
glucose dissolved in water.

Categories of fasting plasma glucose (FPG)
 1. FPG <110 mg/dL = normal fasting glucose
 2. FPG > 110 mg/dL and <126 mg/dL = Impaired
fasting glucose (IFG)
 3. FPG > 126 mg/dL = provisional diagnosis of
diabetes (must be confirmed on subsequent day)
Glycohemoglobin test /Glycosylated hemoglobin assay.
 This test measures the amount of glucose bound to the
hemoglobin molecule on red blood cells.
 Glucose binds irreversibly to hemoglobin to form
glycosylated hemoglobin and will remain bound for the
lifespan of the red blood cell, ranging from about 30 to 90
days.
 This process is an example of AGE formation. The higher
the blood glucose levels over time, the greater is the
percentage of glycosylated hemoglobin.
 The glycosylated hemoglobin value is proportional to the
blood glucose levels; thus, this test gives a measure of the
blood glucose status over the preceding 30 to 90 days.






Two different glycosylated hemoglobin tests are
available: the hemoglobin A1 (HbA1) test and. the
hemoglobin A1c (HbA1c) test.
HbA1c is commonly used
4% to 6% normal
< 7% Good diabetes control
7% to 8% moderate diabetes control
>8% action suggested to improve glycemic control


ORAL DISEASES AND DIABETES
Oral complications of diabetes may include






alterations in salivary flow and constituents
increased incidence of infection
burning mouth
altered wound healing and
increased prevalence and severity of periodontal disease.
Dry mucosal surfaces are easily irritated and often
provide a favorable substrate for the growth of
fungal organisms
Increased incidences of
candidiasis
Alterations in salivary flow
Dental caries
rates
 Increase levels of glucose
concentrations in saliva and GCF
Xerostomia may result from the
 diabetic condition
 other drugs for treatment of related complications or
unrelated disorders.
 Diabetic neuropathy may disturb sympathetic and
parasympathetic pathways which control salivary
flow

Mechanisms of Diabetic Influence on Periodontium
 A number of possible mechanisms have been
proposed by which diabetes may affect the
periodontium. These are primarily related to
 changes in the subgingival microbiota,
 GCF glucose levels
 periodontal vasculature
 host response, and
 collagen metabolism.
Periodontal wound healing- Increased blood glucose
levels in diabetes are reflected in increased levels of
GCF glucose.
 In vitro studies show decreased chemotaxis of
periodontal ligament fibroblasts to PDGF when
placed in a hyperglycemic environment compared
with normoglycemic conditions.
 Thus adversely affect events and the local host
response to microbial challenge.

Changes affecting vasculature
There is increase in thickness of gingival capillary
endothelial cell basement membranes and the walls
of small blood vessels

Increased thickness of small vessel walls results in
narrowing of the lumen,

impair oxygen diffusion and nutrient provision
across basement membranes.

altering normal periodontal tissue homeostasis.
HOST DEFENSE
Defects in polymorphonuclear leukocyte (PMN)
 adherence,
 chemotaxis, and
 phagocytosis have been observed in some
individuals with diabetes.
 Many of these PMN abnormalities can be corrected
with improved glycemic control.
 Defects affecting this first line of defense against
subgingival microbial agents may result in
significantly increased tissue destruction.

Collagen metabolism- Collagen is the primary
constituent of gingiva connective tissue and the
organic matrix of alveolar bone.

Changes in collagen metabolism contribute to
alterations in wound healing and to periodontal
disease initiation and progression.
.




Increased collagen breakdown through stimulation
of collagenase activity has been observed in the
periodontium of diabetic patients.
Sustained hyperglycemia results in AGE
modification of existing collagen, with increased
cross-linking.
The net effect of these alterations in collagen
metabolism is a rapid degradation of recently
synthesized collagen by host collagenase and a
predominance of older, highly cross-linked AGE
modified collagen.

Since collagen production and degradation
exist as a highly balanced homeostatic
mechanism, changes in collagen metabolism
result in altered wound healing in response to
physical or microbial wounding of the
periodontium.

Impaired wound healing is a well-recognized
complication of diabetes and may affect any
tissue site, including the periodontium.
PROPOSED MODEL FOR
TWO-WAY RELATIONSHIP
BETWEEN PERIODONTAL
DISEASE AND DIABETES
MELLITUS
The classic complications of diabetes may be closely
associated with periodontal disease in these
individuals, lending further credence to the concept
that periodontal disease may be the “sixth
complication of diabetes.” (Loe H 1993)


Since periodontal infection adversely affect
glycemic control in diabetes, elimination of
pathogenic organisms should have a positive impact
on glycemic control proving the two way
relationship
In case studies of patients with poorly controlled
diabetes and periodontitis, improvement in
metabolic control has been noted coincident with
improvement in periodontal health following
treatment.
Response to Periodontal therapy in diabetic patient
Patients with poorly controlled diabetes often have a
less favorable response to treatment than those with
well-controlled diabetes.
Gram-negative
Periodontal infections
Periodontal Treatment
Increased
Insulin resistance
Improved
Insulin sensitivity
Worsened
Glycemic control.
Improved
Glycemic control.



Thus, metabolic control of diabetes may be an
important variable in the onset and progression of
periodontal disease.
Patients with well-controlled diabetes may be
similar to nondiabetic individuals.
In addition, other factors such as smoking or poor
plaque control may adversely affect the response to
periodontal therapy in diabetic individuals, just as
they may in a nondiabetic person.
Female sex hormones
puberty

Puberty occurs between age of 11-14 in most
women. Production of sex hormone increases
and then remains relatively constant during the
remainder of the reproductive phase

Puberty is often accompanied with an
exaggerated response of the gingiva to plaque
Gingival finding in puberty




Pronounced inflammation
Bluish red discoloration
Edema
Gingival enlargement
Gingival changes associated with
menstrual cycle





Gingival changes associated during menstrual
cycle are attributed to hormonal imbalance
Increases prevalence of gingivitis
Bleeding gums
Incresed gingival exudate
Bloated or tense feeling in the gums
Gingival disease in pregnancy
Oral contraceptives
Hormonal contraceptives aggrevate the gingival response to
local factors in a similar manner to that seen in pregnancy. It is
mainly seen in women taking oc pills for more than 1 ½ years
Menopausal gingivostomatitis




The gingiva and oral mucosa are
dry,shiny,pale to red color, bleeds easily
Fissuring occurs in mucobuccal fold
Atrophy of epithelium, areas of ulceration,
burning sensations in oral cavity are common
symptoms
Extreme sensitivity to thermal changes
Hyperparathyroidism








Radiographically
Alveolar osteoporosis
Widening of periodontal ligament space
Loss of lamina dura
Brown cysts
Oral changes
1. ,malocclusion
2. tooth mobility
THANK YOU