Absence of interleukin 22 affects the oral microbiota and the progression of induced periapical lesions in murine teeth

Oliveira, Katharina Morant Holanda de; Silva, R. A. B. da; Rossi, Andiara De; Fukada, Sandra Yasuyo; Feres, Magda; Filho, Paulo Nelson; Silva, L. A. B. da

doi:10.1111/iej.12274

Cited by 30 publications

(28 citation statements)

References 41 publications

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“…, De Oliveira et al . ). No previous studies have examined the effect of melatonin on the presence and location of bacteria in experimental periapical lesion models.…”

Section: Discussionmentioning

confidence: 97%

Anti‐inflammatory and antiresorptive functions of melatonin on experimentally induced periapical lesions

Sarıtekin¹,

Kaya²,

Aşçı³

et al. 2019

Int Endodontic J

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Aim To investigate the effects of systemically administered melatonin on inflammation and alveolar bone resorption in rats with experimentally induced periapical lesions. Methodology Thirty adult Sprague Dawley rats were divided equally into negative, positive control and melatonin groups. The pulp chambers of their mandibular first molars were exposed to the oral environment to induce experimental periapical lesions in the positive control and melatonin groups. The melatonin group received daily intraperitoneal injections of melatonin at a dose of 10 mg kg−1. After 21 days, the animals were euthanized; the hemi‐mandible parts were prepared for radiological, histopathological, immunohistochemical (IL‐1β, RANK, RANKL, OPG and tartrate‐resistant acid phosphatase (TRAP) and Brown–Brenn (bacteria) evaluations. Data were analysed by Kruskal–Wallis (for non‐parametric data) and one‐way anova tests (for parametric data) (P < 0.05). Results The area of radiographic periapical bone loss was significantly smaller in rats that were given daily intraperitoneal injections of melatonin (P < 0.01). The histopathological scores of the melatonin group were significantly lower than those of positive control group (P < 0.01). Histomorphometrically, the area of periapical bone loss in the melatonin group was significantly smaller than the positive control group (P < 0.01). The expression of IL1‐β, RANK and RANKL was significantly higher in the positive control group, whereas OPG was significantly higher in the melatonin group (P < 0.01). The number of osteoclasts was significantly greater in the positive control group by TRAP staining analyses (P < 0.01). The scores for bacteria localization using Brown–Brenn staining in the melatonin group was significantly lower than that of the positive control group (P < 0.01). Conclusions Melatonin demonstrated antiresorptive effects on bone associated with experimentally induced periapical lesions in rats via its anti‐inflammatory activity. Further studies are necessary to evaluate its possible effects on the healing of periapical lesions.

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“…, De Oliveira et al . ). No previous studies have examined the effect of melatonin on the presence and location of bacteria in experimental periapical lesion models.…”

Section: Discussionmentioning

confidence: 97%

Anti‐inflammatory and antiresorptive functions of melatonin on experimentally induced periapical lesions

Sarıtekin¹,

Kaya²,

Aşçı³

et al. 2019

Int Endodontic J

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“…Apical periodontitis results from polymicrobial infection of the dental pulp and root canal system leading to a progressive destruction of periodontal ligament, cementum, and alveolar bone. The destruction of apical and periapical tissues is mediated by a complex network of cellular and molecular mechanisms, which includes migration of inflammatory cells to the sites of infection and osteoclastogenesis (Wang & Stashenko , Stashenko et al , Nair , De Rossi et al , Fukada et al , da Silva et al , de Oliveira et al , De Rossi et al , Braz‐Silva et al , Jakovljevic et al , Howait et al ). The knowledge of regulatory mechanisms that control the host immune system response to infection is important for a better understanding of the aetiopathogenesis and treatment of immunoinflammatory diseases.…”

Section: Introductionmentioning

confidence: 99%

Effect of intercellular adhesion molecule 1 deficiency on the development of apical periodontitis

Rossi¹,

Lucisano²,

Rossi³

et al. 2019

Int Endodontic J

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Aim To evaluate the specific role of ICAM‐1 in host responses against endodontic infection. Methods Apical periodontitis was experimentally induced in the mandibular first molars of ICAM‐1 knockout and wild‐type (WT) mice by pulp exposure to the oral environment. At 7, 21 and 42 days following pulp infection, the animals were euthanized and the jaws were prepared for analysis under conventional and fluorescence microscopy (histopathologic and morphometric analysis), immunohistochemistry (polymorphonuclear leucocytes), enzyme histochemistry (osteoclasts and cementoclasts) and RT‐PCR (IL‐1 α, TNF‐α, INF‐γ, IL‐10, RANK, RANKL and OPG). A generalized linear model with GLIMMIX procedure with Satterthwaite approximation method of degrees of freedom, Tukey–Kramer, pseudo‐ranking nonparametric, Bonferroni–Holm multiple testing adjustment, analysis of variance (ANOVA) and the Tukey's multiple comparisons tests were used to evaluate the statistical differences between the groups using SAS 9.4 and the GraphPad Prism 5.0 software (α = 0.05). Results Compared to WT mice, ICAM‐1 knockout mice had significantly greater bone resorption (P < 0.05), reduced recruitment of neutrophils to periapical inflammatory tissues (P < 0.05) and an increased number of fibroblasts (P < 0.05) at all experimental periods. The osteoclast number was significantly higher in ICAM‐1 KO than that of WT animals at all times (P < 0.05), while there was no significant difference between the groups regarding cementoclasts. At day 21, the level of IL‐1α, RANK, RANKL and IL‐10 had increased significantly in tissues from ICAM‐1 KO versus WT mice (P < 0.05), while no significant difference was observed in TNF‐α and OPG levels (P > 0.05). Tissue levels of INF‐γ were significantly lower in ICAM‐1 KO than those in WT mice (P < 0.05). Conclusion ICAM‐1 deficiency impaired the host response against endodontic infection, resulting in increased tissue destruction.

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“…Associated inflammation in the gut upregulates epithelial S100A8/A9 [107]. Failure to upregulate S100A8/A9 affects the oral salivary microbiome, changing the course of periapical lesions at the roots of teeth [108]. Whereas “alarmins” act to recruit and activate inflammatory cells, S100A8/A9-dependent intracellular and extracellular AMP activities would appear to protect against and mitigate periodontal infection.…”

Section: Effector Arm Of Innate Intraepithelial Immunitymentioning

confidence: 99%

Autonomous immunity in mucosal epithelial cells: fortifying the barrier against infection

Ross

Herzberg

2016

Microbes and Infection

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Mucosal epithelial cells express an autonomous innate immune response that controls the overgrowth of invaded bacteria, mitigates the harmful effects of the bacteria carried within, and does not rely on other external arms of the immune response. Epithelial cell autonomous innate immunity “respects” the social biology of invading bacteria to achieve symbiosis, and is the primary protective mechanism against pathogens.

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Absence of interleukin 22 affects the oral microbiota and the progression of induced periapical lesions in murine teeth

Cited by 30 publications

References 41 publications

Anti‐inflammatory and antiresorptive functions of melatonin on experimentally induced periapical lesions

Anti‐inflammatory and antiresorptive functions of melatonin on experimentally induced periapical lesions

Effect of intercellular adhesion molecule 1 deficiency on the development of apical periodontitis

Autonomous immunity in mucosal epithelial cells: fortifying the barrier against infection

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