ArticleClinical oral investigations2014
Apoptosis: an underlying factor for accelerated periodontal disease associated with diabetes in rats.
Article in Clinical oral investigations, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed, 12 citations in OpenAlex.
- PINK1 mediated mitophagy attenuates early apoptosis of gingival epithelial cells induced by high glucose.BMC oral health · 2022Article
- Association between metabolic syndrome and periodontitis: The role of lipids, inflammatory cytokines, altered host response, and the microbiome.Periodontology 2000 · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesDiabetes mellitus (DM) is well-established risk factor for periodontal disease. DM can also lead to changes in the number of apoptotic cells in periodontal tissues. The goal of this study was to evaluate apoptosis, depending on DM, in healthy and diseased periodontal soft tissues. MATERIAL AND
methodsA total of 43 adult male Sprague-Dawley rats were used in this study. Experimental periodontitis was created by placing silk ligatures around the cervices of the first mandibular molars. Experimental diabetes was induced by intraperitoneal injection of the diabetogenic agent streptozotocin (STZ). Following the induction of both experimental diseases, the animals were divided into four groups: (1) The healthy group (H) (n = 10); (2) The diabetes group (D) (n = 10); (3) The periodontitis group (P) (n = 11); and (4) The diabetes and periodontitis group (DP) (n = 12). Apoptotic cells were determined by immunohistochemistry, and the frequency of apoptotic cells was evaluated by apoptotic index score.
resultsIt was observed that there was less apoptosis in both the epithelial and gingival connective tissue cells of healthy diabetic tissues than in healthy tissues without diabetes. When periodontal disease existed, apoptosis increased in both the epithelial and gingival connective tissues of diabetic and non-diabetic animals.
conclusionsThere may be differences in the apoptotic mechanisms in the periodontal soft tissues of diabetic and non-diabetic animals. CLINICAL RELEVANCE: Apoptosis may be one of the underlying factors in increased risk for periodontal disease that is associated with diabetes.
Indexed as
Identifiers
What 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.