ArticleOdontology2026
Diabetes mellitus influences Toll-like receptors 2 and 4 in experimental apical periodontitis of Wistar rats.
Article in Odontology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
The aim of this study was to investigate the inflammatory profile and immunostaining expression of Toll-like receptors 2 and 4 (TLR2 and TLR4) in periapical tissues of control and diabetic rats (DM) with induced apical periodontitis (AP), correlating these findings with the progression of root canal contamination. Forty male Wistar rats were divided into four groups: Group C-control rats, Group AP-rats with AP, Group DM-rats with diabetes, and Group DM + AP-rats with DM and AP. DM was induced using streptozotocin, and AP was induced by dental pulp exposure of the first mandibular molar to the oral environment. After 30 days, the jaws were removed and processed for histologic and bacterial analysis, as well as immunochemical assays for TLR2 and TLR4. Two-way analysis of variance was used (P < 0.05). Inflammatory infiltrate was moderate in the AP group and severe in the DM + AP group (P < 0.05). There was a greater presence of bacteria disseminated in the apical region in the DM + AP group when compared with the AP group (P < 0.05). TLR2 and TLR4 levels were significantly higher in the DM + AP group when compared to the AP group (P < 0.05). Diabetes increases the inflammatory infiltrate in AP, causing significant overexpression of TLR2 and TLR4 in the periapical inflammatory tissues of diabetic rats. By activating TLRs, diabetes exacerbates the immune response in AP, increasing inflammation and influencing the progression of bacterial contamination.
Indexed as
Identifiers
40632348What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.