Turkish journal of pharmaceutical sciences · 2020
Investigation of the Peripheral Analgesic Activity of Oxicams and Their Combinations with Caffeine.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Syrova Anna, Lukyanova Larisa, Kozub Svetlana, Zavada Oksana, Levashova Olga, Shaposhnik Viktor
Аннотация
BACKGROUND: Diabetes mellitus (DM) is a common metabolic disorder, and persistent hyperglycemia may impair oral health through various immunological and inflammatory mechanisms, particularly by influencing the onset and healing of apical periodontitis (AP). This systematic review and meta-analysis aimed to evaluate whether poor glycemic control (PGC) is associated with the presence and progression of AP.
MATERIAL AND METHODS: This study was conducted in accordance with the PRISMA 2020 guidelines. A comprehensive search of PubMed, Embase, Google Scholar, and Scopus was performed to identify relevant English-language studies published up to June 2025. Cross-sectional and longitudinal studies examining the association between glycemic control status-defined by glycated hemoglobin (HbA1c) levels-and AP-related outcomes were included. Data were synthesized using RevMan 5.3 software to calculate pooled odds ratios (ORs) and 95% confidence intervals (CIs). Heterogeneity and publication bias were also assessed.
RESULTS: A total of 18 studies comprising approximately 51,070 patients were included. The relationship between PGC and AP was examined across three domains: AP prevalence, the persistence of apical periodontitis in root-filled teeth (AP-RFT), and alterations in local or systemic immune responses. Meta-analysis of AP prevalence (6 studies) revealed that individuals with PGC had a significantly increased risk of developing AP compared to controls (OR=2.38, 95% CI: 1.98-2.86, P<0.00001). Furthermore, meta-analysis of AP-RFT persistence (8 studies) showed that patients with PGC had a significantly higher risk of AP-RFT (OR=2.74, 95% CI: 2.03-3.70, P<0.0001). Several studies also reported elevated levels of inflammatory cytokines and bacterial load in patients with PGC.
DISCUSSION: PGC appears to negatively influence both the development and healing of AP, possibly through immune-inflammatory pathways.
CONCLUSIONS: PGC is closely associated with the occurrence of AP and the failure of periapical healing following endodontic treatment. PGC may aggravate periapical tissue damage and inflammation through proinflammatory immune pathways. Clinicians should consider comprehensive evaluation and individualized management of DM patients during endodontic therapy to improve treatment outcomes and oral health.
MATERIAL AND METHODS: This study was conducted in accordance with the PRISMA 2020 guidelines. A comprehensive search of PubMed, Embase, Google Scholar, and Scopus was performed to identify relevant English-language studies published up to June 2025. Cross-sectional and longitudinal studies examining the association between glycemic control status-defined by glycated hemoglobin (HbA1c) levels-and AP-related outcomes were included. Data were synthesized using RevMan 5.3 software to calculate pooled odds ratios (ORs) and 95% confidence intervals (CIs). Heterogeneity and publication bias were also assessed.
RESULTS: A total of 18 studies comprising approximately 51,070 patients were included. The relationship between PGC and AP was examined across three domains: AP prevalence, the persistence of apical periodontitis in root-filled teeth (AP-RFT), and alterations in local or systemic immune responses. Meta-analysis of AP prevalence (6 studies) revealed that individuals with PGC had a significantly increased risk of developing AP compared to controls (OR=2.38, 95% CI: 1.98-2.86, P<0.00001). Furthermore, meta-analysis of AP-RFT persistence (8 studies) showed that patients with PGC had a significantly higher risk of AP-RFT (OR=2.74, 95% CI: 2.03-3.70, P<0.0001). Several studies also reported elevated levels of inflammatory cytokines and bacterial load in patients with PGC.
DISCUSSION: PGC appears to negatively influence both the development and healing of AP, possibly through immune-inflammatory pathways.
CONCLUSIONS: PGC is closely associated with the occurrence of AP and the failure of periapical healing following endodontic treatment. PGC may aggravate periapical tissue damage and inflammation through proinflammatory immune pathways. Clinicians should consider comprehensive evaluation and individualized management of DM patients during endodontic therapy to improve treatment outcomes and oral health.