2016
DOI: 10.1016/j.lfs.2016.04.033
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Delayed healing of oral mucosa in a diabetic rat model: Implication of TNF-α, IL-1β and FGF-2

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Cited by 52 publications
(58 citation statements)
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References 43 publications
(54 reference statements)
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“…31 The topical application of liquid smoke is capable of reducing the production of TNF-α. 15 The mechanism by which it does so is the inhibiting of reactive oxygen species (ROS), and signaling NFқB for the production of TNF-α.…”
Section: Discussionmentioning
confidence: 99%
“…31 The topical application of liquid smoke is capable of reducing the production of TNF-α. 15 The mechanism by which it does so is the inhibiting of reactive oxygen species (ROS), and signaling NFқB for the production of TNF-α.…”
Section: Discussionmentioning
confidence: 99%
“…Similar results have been reported for wounds in the skin and mucosa of diabetic animals. Brizeno et al also demonstrated that the diabetes increased vascular permeability in the cheek mucosa of the ulcerated rats. This change appeared to be related to the diabetic state and not to the ulceration because a similar level was observed in the mucosa of the normoglycemic ulcerated animals and the non‐ulcerated control animals on the 5th day after trauma, which was not observed in the diabetic animals.…”
Section: Discussionmentioning
confidence: 93%
“…This is relatively consistent with other similar studies. Brizeno et al investigated the differences in the healing of ulcerated oral mucosal lesions in diabetic rats compared with those of normal rats. Their results revealed that healing was delayed in cheek mucosal lesions in the diabetic animals.…”
Section: Discussionmentioning
confidence: 99%
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“…Fibroblast growth factor 2 is normally expressed in the basal and parabasal layers of the oral mucosa epithelium, while FGFR‐1 is expressed in the upper layers (Figure ). Brizeno et al studied the effects that diabetes has in the oral mucosa healing process, demonstrating that diabetic rats expressed less FGF‐2 than normoglycemic controls and therefore had a significant delay in the angiogenesis and neocollagenesis processes, impairing the wound repair mechanism. Fujisawa et al applied FGF‐2 to treat impaired oral ulcers by different factors in rabbits, and it was able to promote wound healing of the mucosal lesions, by promoting the proliferation of fibroblasts and keratinocytes.…”
Section: Fgf‐2/fgfr‐1 Expression In Normal Oral Mucosa and During Oramentioning
confidence: 99%