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Updated: Jan 29, 2026
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Maternal apical periodontitis is associated with insulin resistance in adult offspring
T V S Tsosura1, F Y Chiba2, M S L C Mattera1
1Department of Basic Sciences, Multicenter Postgraduate Program in Physiological Sciences, SBFis, School of Dentistry, São Paulo State University (UNESP), Araçatuba, Brazil.
Insights
Maternal apical periodontitis (AP) in rats leads to insulin resistance in offspring by affecting insulin signaling and inflammation. Preventing maternal AP is crucial for offspring metabolic health.
Area of Science:
- Endocrinology and Metabolism
- Inflammation Research
- Reproductive Biology
Background:
- Maternal inflammation, such as apical periodontitis (AP), may impact offspring metabolic health.
- Insulin resistance is a growing public health concern with potential developmental origins.
Purpose of the Study:
- To investigate the effects of maternal AP on plasma glucose, insulin, and tumor necrosis factor-alpha (TNF-α) in adult rat offspring.
- To explore how maternal inflammation influences insulin signaling and inflammatory pathways in offspring muscle and adipose tissue.
Main Methods:
- Wistar rats were divided into control, mild (1 AP tooth), and severe (4 AP teeth) maternal AP groups.
- Offspring plasma markers and insulin resistance (HOMA-IR) were measured.
- Western blot analysis assessed insulin signaling (pp185, IRS-1) and inflammation (IKKα/β, JNK) pathways in gastrocnemius muscle (GM) and periepididymal white adipose tissue (pWAT).
Main Results:
- Maternal AP significantly increased offspring plasma insulin and TNF-α levels.
- Insulin resistance and impaired insulin signaling (reduced pp185 phosphorylation) were observed in offspring of mothers with AP.
- Enhanced IKKα/β phosphorylation in GM and pWAT indicated increased inflammation in offspring.
Conclusions:
- Maternal AP is linked to the development of insulin resistance in adult offspring.
- Alterations in insulin signaling and inflammatory pathways mediate the effects of maternal AP on offspring metabolism.
- Preventing maternal AP is vital for ensuring the long-term metabolic health of offspring.
Aim:
To investigate the plasma concentrations of glucose, insulin and tumour necrosis factor-α (TNF-α) of rats with maternal apical periodontitis (AP) and to explore the effect of maternal inflammation on the initial steps of insulin signalling and the inflammatory pathway in the gastrocnemius muscle (GM) and periepididymal white adipose tissue (pWAT) of adult offspring.
Methodology:
Fifteen female Wistar rats were distributed into a control group (CN), a group with 1 tooth with AP (1AP) and a group with 4 teeth with AP (4AP). Thirty days following induction of AP, female rats from all groups were mated with healthy male rats. When male offspring reached 75 days of age, plasma concentrations of glucose, insulin and TNF-α were quantified. Insulin resistance was evaluated by the homoeostasis model assessment of insulin resistance (HOMA-IR) index. Phosphorylation status of pp185 tyrosine, insulin receptor substrate 1 (IRS-1) serine, IκB kinase α/β (IKKα/β) and c-Jun N-terminal kinase (JNK) in the GM and pWAT were measured by Western blot. Analysis of variance was performed, followed by the Tukey's post hoc test. P values <0.05 were considered to be statistically significant.
Results:
Maternal AP promoted insulin resistance, impaired the initial steps of insulin signalling, significantly increased plasma concentrations of insulin (P < 0.001) and TNF-α (P < 0.05), and enhanced IKKα/β phosphorylation in the GM and pWAT (P < 0.05) of adult offspring. However, maternal AP did not affect fasting glycaemia and JNK phosphorylation in the GM and pWAT of adult offspring.
Conclusions:
Maternal AP was associated with insulin resistance in adult offspring through alterations in insulin signalling and inflammation pathways. The study provides information on the impact of maternal AP on the development of metabolic alterations such as insulin resistance in adult offspring and reinforces the importance of preventing maternal AP in order to maintain the general health of offspring.
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