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Review
. 2007:43:233-44.
doi: 10.1111/j.1600-0757.2006.00168.x.

Diabetic periodontitis: a model for activated innate immunity and impaired resolution of inflammation

Hamdy Nassar  1 , Alpdogan Kantarci, Thomas E van Dyke
Affiliations
Review

Diabetic periodontitis: a model for activated innate immunity and impaired resolution of inflammation

Hamdy Nassar et al. Periodontol 2000. 2007.
No abstract available

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Figures

Fig. 1
Fig. 1
Pathways of pathogenesis in diabetic periodontitis. Diabetes initiates a series of innate immune responses through production of advanced glycated end-products (AGEs) as a result of hyperglycemia. Innate immune responses via neutrophils and monocytes lead to proinflammatory cytokine production and will generate oxidative stress through the activities of protein kinase C beta (PKC-β) and PKC-α, respectively. These mediators of host response, in turn, result in inflammatory processes, which would further complicate the glycemic control through insulin resistance. Periodontal disease has a direct effect on the deterioration of diabetic state through the chronic inflammatory changes. All these processes could be potentially blocked through the use of anti-inflammatory mediators. AGE, advanced glycated end-products; PKC, protein kinase C; IL-1β, interleukin-1β; TNF-α, tumor necrosis factor-α; MMPs, matrix metalloproteinases; PGE2, prostaglandin E2; LTB4, leukotriene B4; LXA4, lipoxin A4; ATL-α, aspirin-triggered lipoxin-α.
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