A Literature Review Submitted to the Council of the College of Dentistry at Hawler Medical University in partial Fulfillment of the Requirement for the B.D.S. degree in Degree
4. Diabetes mellitus
• Type 1 diabetes
– β-cell destruction
• Type 2 diabetes
– insulin resistance
• Gestational diabetes mellitus (GDM)
• Other specific types of diabetes
– Genetic defects in β-cell function, insulin action
– Diseases of the exocrine pancreas
– Drug- or chemical-induced
– Others ..
5. Oral manifestation and complications
of diabetes mellitus
• enlarged gingiva, sessile or pedunculated
gingival polyp, polypoid gingival proliferations,
abscess.
• cheilosis, diminished salivary flow, mucosal
drying, and cracking, burning mouth and
tongue, and with greater predominance of
candida albicans, hemolytic streptococci, and
staphylococci.
6. • increased rate of dental caries
• peripheral diabetic neuropathy may be a risk
factor for severe TMJ dysfunction.
• Geographic and fissured tongue
• lichen planus, recurrent aphthous stomatitis,
and oral fungal infections
7.
8. Mechanisms of interaction between
diabetes and periodontal tissues
• Bacterial pathogens in diabetes mellitus:
Capnocytophaga species , A.
actinomycetumcomitans, C. rectus, C. species,
E. corrodens, F. nucleatum, P. gingivalis, and P.
intermedia.
• glycemic control and alterations in microflora
may increase the susceptibility of diabetics to
periodontal disease.
9. Polymorphonuclear leukocyte function
in diabetes mellitus
• polymorphonuclear leukocyte deficiencies
resulting in impaired chemotaxis, defective
phagocytosis, or impaired adherence .
• Function of polymorphonuclear leukocytes
(PMNs) impaired.
• (GCF) collagenase concentration is higher in
diabetics and it is primarily derived from
PMNs.
• related to poor glycemic control .
10. Monocytes, macrophages and
cytokines in diabetes mellitus
• Higher concentration IL-1β, PGE2, and TNF-α
have been detected in GCF.
• The release of these cytokines in response to
bacterial lipopolysaccharides (LPS) by monocytes
is significantly higher.
• This hyperinflammatory is due to (AGE-RAGE
interaction)
• dysregulation of macrophages cytokine
production, tissue destruction and alveolar bone
loss. alter the function of macrophages and delay
the wound healing
11. Altered collagen metabolism in
diabetes mellitus
• increase collagenasae activity, decreased collagen
synthesis, maturation, and maintenance of collagen.
• In the hyperglycemic state, numerous proteins and matrix
molecules undergo a nonenzymatic glycosylation, resulting
in accumulated advanced glycation end products (AGEs)
• collagen is cross-linked by AGE formation, making it less
soluble and less likely to be normally repaired or replaced
• biologic effect of AGEs is mediated by the receptor for AGEs
(RAGE)
• causing precoagulatory changes, thrombus formation and
thickening of basement membrane of microvasculature
12. Altered wound healing in diabetes
mellitus
• the primary reparative cell in the
periodontium is the fibroblast, which does not
function properly in high-glucose
environments
• The collagen that is produced by these
fibroblasts is susceptible to rapid degradation
by matrix metalloproteinase enzymes
• Gingival microangiopathy, Increased collagen
degradation, and Glycolysation
13. The mechanisms in which periodontal
diseases may affect the diabetic state
• Chronic periodontal diseases have the
potential to exacerbate insulin resistance and
worsen glycemic control
• hyperinflammatory immune cells can
exacerbate the elevated production of
proinflammatory cytokines, this has the
potential to increase insulin resistance and
make it more difficult for the patient to
control diabetes
14. The relationship between diabetes and
periodontitis
• The severity of periodontitis was significantly
higher in diabetic patients compared to non-
diabetic patients
• Poorly controlled diabetics had three fold
increases in risk of having periodontitis compared
to non-diabetics
• this bidirectional relationship between
periodontal disease and diabetes mellitus makes
diabetes a disorder of importance to dentists and
dental hygienists and to patients seen in the
dental office.