Diabetes mellitus (DM) and periodontitis are both chronic
inflammatory diseases, which contribute significantly to morbidity and are a
major health care burden. The interrelationship between DM and periodontitis
has been studied for many years. It has been accepted that the supposed interrelationship
between DM and periodontitis is a two-way relationship. In this sense, the
presence of one condition tends to increases the risk and severity of the
other, and vice versa. However, the mechanisms for this two-way relationship
still remain unknown.
DM is a chronic metabolic disorder, involving impaired
glucose homeostasis. DM poorly controlled is characterized by high blood
glucose levels that result in an increased formation of protein glycosylation
leading to amplified formation of so-called advanced glycation end products.
AGEs are glucose products that have the ability to attract and stimulate
inflammatory cells to produce inflammatory cytokines such as tumor necrosis
factor alpha (TNF-α), Prostaglandin E2 (PGE2), and interleukin-1β (IL-1β) and
matrix metalloproteinases (MMPs) that together with increased generation of
reactive oxygen species may raise the
risk of periodontal attachment and/or alveolar bone loss and contribute to
diabetic complications.
AGEs combined with pro-inflammatory cytokines can motivate
fibroblast apoptosis and impair periodontal wound healing. It is known that,
the expression of these pro-inflammatory mediators is regulated by the T helper
cells. In addition, the polymorphonuclear neutrophils are important in the
first line of defense
in periodontal disease process, as periodontitis. However, exacerbate
response may transpose this protective action of polymorphonuclear neutrophils
into destroyers. Thus, the host immune-inflammatory responses would be
protective or destructive.
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