The Effect of High Sugar Intake on the Development of Periradicular                Lesions in Rats with Type 2 Diabetes

Iwama, Atsushi; Nishigaki, Noriyuki; Nakamura, Koki; Imaizumi, Ichiro; Shibata, Naoki; Yamasaki, Masahiro; Nakamura, Hiroshi; Kameyama, Yôichiro; Kapila, Yvonne L.

doi:10.1177/154405910308200416

Cited by 49 publications

(45 citation statements)

References 20 publications

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“…A model of this endodontic infection could be valuable for improving the understanding of disease etiology and progression and effective treatments. There are many reports regarding the induction of periapical lesions and their histological observation in animals including rats (23,24), dogs (25), cats (26), and monkeys (27). Rat models are the most frequently used models for such studies: the morphology of a rat molar is similar to that of a human molar, and the genetic background of these animals is clear, with practically no individual specificity (28).…”

Section: Discussionmentioning

confidence: 99%

Promotion of Endodontic Lesions in Rats by a Novel Extraradicular Biofilm Model Using Obturation Materials

Kuremoto

Noiri

Ishimoto

et al. 2014

Appl Environ Microbiol

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bAlthough extraradicular biofilm formation is related to refractory periapical periodontitis, the mechanism of extraradicular biofilm development, as well as its effect on periapical lesions, is unknown. Therefore, we aimed to develop an in vivo extraradicular biofilm model in rats and to identify and quantify extraradicular biofilm-forming bacteria while investigating the effect of extraradicular biofilms on periapical lesions. Periapical lesions were induced by exposing the pulpal tissue of the mandibular first molars of male Wistar rats to their oral environment. Four weeks later, gutta-percha points were excessively inserted into the mesial root canals of the right first molars (experimental sites) but not the left first molars (control sites). After 6 and 8 weeks of pulp exposure, the presence of extraradicular biofilms was confirmed histomorphologically, and biofilm-forming bacteria were identified by using classical culture methods. The biofilms were observed in the extraradicular area of the experimental sites. Similar species were detected both inside and outside the root canals. The bacterial count, quantified by real-time PCR assays, in the extraradicular area gradually increased in the experimental sites until 20 weeks after pulp exposure. After 8 weeks of pulp exposure, the periapical lesion volume that was measured by micro-computed tomography was significantly larger in the experimental sites than in the control sites (P < 0.05 by Welch's t test). These results suggest that we developed an extraradicular biofilm model in rats and that extraradicular biofilms affect developing periapical lesions. In clinical practice, we encounter patients in whom periapical periodontitis does not heal despite a root canal treatment following general dental procedures. The etiology is considered to be the result of residual bacteria in the lateral branch of the root canal, endodontic reinfection, or both. Recent studies have shown that biofilms that form outside the apical foramen, which are termed "extraradicular biofilm," are also involved in refractory periapical periodontitis (1-4). As the bacteria in biofilms are resistant to the host's immunoreaction and to antibiotics (5), dental biofilm diseases such as caries or periodontitis have been treated by mechanical removal. However, extraradicular biofilm is impossible to remove mechanically with nonsurgical endodontic treatments. As extraradicular biofilms cannot be accessed from the root canal for mechanical removal, the only treatment methods are endodontic surgery and tooth extraction.Current research is focused on developing methods to prevent or control biofilm formation (6, 7). We recently found three analogues of N-acyl homoserine lactone that participate in quorum sensing, a system of bacterial cell-to-cell communication, and inhibit Porphyromonas gingivalis biofilm formation (8). Furthermore, azithromycin, a 15-membered macrolide antibiotic, has an antibiofilm effect on P. gingivalis (9). For clinical applicability, these in vitro effects should be exami...

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Section: Discussionmentioning

confidence: 99%

Promotion of Endodontic Lesions in Rats by a Novel Extraradicular Biofilm Model Using Obturation Materials

Kuremoto

Noiri

Ishimoto

et al. 2014

Appl Environ Microbiol

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“…The susceptibility of leptin deficient (ob/ob) mice to periapical lesion is unknown. GK (Goto-Kakizaki) rats, a model for spontaneous non-insulin-dependent diabetes, fed a regular rodent diet and 30% sucrose solution ad libitum, exhibited significantly enlarged periapical lesions in weeks 2 and 4 post pulp exposure compared to groups of GK rats fed the regular diet and tap water and non-diabetic Wistar rats treated with the same diet regimens (p<0.01 in each observation period) [43]. Streptozotocin-induced diabetic rats, a model for type 1 diabetes, exhibited extended periapical lesions and elevated inflammation vs. control animals in two different studies [44, 45].…”

Section: Periapical Lesion and Type 2 Diabetes Mellitusmentioning

confidence: 99%

Interrelationship Between Periapical Lesion and Systemic Metabolic Disorders

Sasaki¹,

Hirai²,

Martins³

et al. 2016

CPD

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Periapical periodontitis, also known as periapical lesion, is a common dental disease, along with periodontitis (gum disease). Periapical periodontitis is a chronic inflammatory disease, caused by endodontic infection, and its development is regulated by the host immune/inflammatory response. Metabolic disorders, which are largely dependent on life style such as eating habits, have been interpreted as a “metabolically-triggered” low-grade systemic inflammation and may interact with periapical periodontitis by triggering immune modulation. The host immune system is therefore considered the common fundamental mechanism of both disease conditions. An elevated inflammatory state caused by metabolic disorders can impact the clinical outcome of periapical lesions and interfere with wound healing after endodontic treatment. Although additional well-designed clinical studies are needed, periapical lesions appear to affect insulin sensitivity and exacerbate non-alcoholic steatohepatitis. Immune regulatory cytokines produced by various cell types, including immune cells and adipose tissue, play an important role in this interrelationship.

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“…The samples were demineralized with 5% nitric acid (pH 7.4), which was renewed every 2 days. For the histopathologic analysis, the methodology described by Iwama et al (13) was accomplished. Briefly, paraffin blocks containing the mandibles were serially sectioned with average thickness of 6 mm in a mesiodistal plane.…”

Section: Histopathologic Analysismentioning

confidence: 99%

“…Periapical lesion induction was performed as previously described with minor adaptations (13,14). Rats were anesthetized by intraperitoneal injection of a combination of xylazine (10 mg/kg) and ketamine (100 mg/kg).…”

Section: Periapical Lesion Inductionmentioning

confidence: 99%

Effects of the Antioxidant Agent Tempol on Periapical Lesions in Rats with Doxorubicin-induced Cardiomyopathy

Wolle

Zollmann

Etges

et al. 2012

Journal of Endodontics

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The Effect of High Sugar Intake on the Development of Periradicular Lesions in Rats with Type 2 Diabetes

Cited by 49 publications

References 20 publications

Promotion of Endodontic Lesions in Rats by a Novel Extraradicular Biofilm Model Using Obturation Materials

Promotion of Endodontic Lesions in Rats by a Novel Extraradicular Biofilm Model Using Obturation Materials

Interrelationship Between Periapical Lesion and Systemic Metabolic Disorders

Effects of the Antioxidant Agent Tempol on Periapical Lesions in Rats with Doxorubicin-induced Cardiomyopathy

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