Inducing Apical Periodontitis in Mice

Goldman, Elisheva; Reich, Eli; Abramovitz, Itzhak; Klutstein, Michael

doi:10.3791/59521

Cited by 10 publications

(10 citation statements)

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“…Samples were placed in a cylindrical sample holder and about 300 microtomographic slices were acquired, covering the entire crown volume of each hemi-jaw. Sample scans were aligned as described by Goldman et al [ 40 ]. Briefly, 3 points of alignment in the first molar were chosen: the mesial apical constriction, the coronal part of the mesial canal, and the distal apical constriction.…”

Section: Methodsmentioning

confidence: 99%

Phage Targeting Streptococcus mutans In Vitro and In Vivo as a Caries-Preventive Modality

et al. 2021

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Dental caries is a common infectious disease worldwide. Current conventional therapies lack specific antimicrobial effects against Streptococcus mutans, a key bacterium that induces caries. A promising alternative approach is bacteriophage (phage) therapy. Recently, SMHBZ8 phage targeting S. mutans was isolated and characterized. The aim of this study was to evaluate the caries-prevention efficacy of SMHBZ8 using in vitro and in vivo caries models. Hemi-mandibles dissected from euthanized healthy mice were subjected to caries-promoting conditions in vitro. Jaws treated with phage therapy in suspension and in formulation with a sustained-release delivery system showed no carious lesions, similar to control and chlorhexidine-treated jaws. Subsequently, SMHBZ8 phage suspension also prevented carious lesion development in a murine caries model in vivo. In both models, caries lesions were analyzed clinically and radiographically by µCT scans. This study shows how SMHBZ8 phage therapy targeting S. mutans can serve as an efficient caries-prevention modality, in suspension or with a sustained-release delivery system, by in vitro and in vivo mouse models.

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Section: Methodsmentioning

confidence: 99%

Phage Targeting Streptococcus mutans In Vitro and In Vivo as a Caries-Preventive Modality

et al. 2021

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“…The aim of this study was to investigate the effect of age on the development of AP. We chose an established mouse model for induced AP [ 6 , 7 , 8 ]. In our experiments we compared two age groups of mice: young mice (6–8 weeks), and mid-age mice (termed adults: 8–10 months) as a model for the difference in development of AP in adolescence and adult age.…”

Section: Resultsmentioning

confidence: 99%

“…The young group were mice aged 6–8 weeks, and the adult group were aged 8–10 months on the first day of the experiment. Apical periodontitis was induced as previously described [ 6 ]. Briefly, mice were anesthetized with ketamine–medetomidime (concentration of 70 mg/kg ketamine hydrochloride (Vetoquinol, CAS 1867-669) and 0.9 mg/kg medetomidine hydrochloride ((Cepetor, CP-pharma GmbH, CAS 86347-15-1) diluted in PBS), and the pulp of the first mandibular molar (M1) on the right side was exposed in the mesial and distal pulp horns.…”

Section: Methodsmentioning

confidence: 99%

“…During the course of the experiment the animals’ weight was monitored and the animals received soft food daily in order to reduce pain during chewing and to encourage biofilm formation. The teeth were left to become contaminated by the oral flora for 42 days as previously described [ 6 , 9 ]. After this time period, the animals were anesthetized with ketamine (162.5 mg/kg)-xylazine (75 mg/kg, Eurovent Animal Health, CAS 7361-61-7) and euthanized by cervical dislocation.…”

Section: Methodsmentioning

confidence: 99%

“…The aim of the current study was to investigate how age affects the progression of AP in a mouse model. For this purpose, we chose to use a mouse model of induced apical periodontitis for our investigation [ 6 , 7 , 8 ] and compared different age groups with the same genetic and environmental conditions.…”

Section: Introductionmentioning

confidence: 99%

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A Mouse Model for Studying the Development of Apical Periodontitis with Age

Goldman

Reich

Roshihotzki

et al. 2021

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Older age is associated with reduced immune function. Our aim was to study how age affects the development of apical periodontitis (AP). AP was induced in two age groups of mice (young vs. adult). Histological samples were stained by Hematoxylin Eosin, Brown and Brenn, and Tartrate-Resistant Acid Phosphatase. In addition, the samples were scanned by Micro-Computerized-Tomography (micro-CT) to evaluate apical constriction and periapical lesion size. Cell density in the periapical region was computationally assessed. Moreover, lesion immune cell populations were characterized by flow cytometry and immunofluorescence. The young group presented more canals with necrotic radicular pulp compared to the adults. There was no difference in bacteria location in the canals between the groups. Apical constriction size was larger in the young mice compared to the adults. The periapical cell density was higher in the young group, while the dominant immune cells in the lesions were neutrophils, which also exhibited the highest young/adult ratio. Immunofluorescence demonstrated neutrophils in the lesion. More osteoclasts were present in the lesions of the young mice, in correlation to the higher volume of bone resorption in this group. Overall, we conclude that the immune reaction to AP stimuli was attenuated in the adult mice compared to the young.

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