title: Periapical lesion progression with controlled microbial inoculation in a type I diabetic mouse model.
abstract: Uncontrolled or poorly controlled diabetes mellitus may be a risk factor for the development of large and/or debilitating periapical infections. The objectives of this investigation were to: (i) determine the effect of diabetes mellitus on the pathogenesis of periapical lesions with or without specific bacterial inoculations at the exposure sites, and (ii) test the sensitivities of two microbiological techniques in detecting the persistence of the bacterial inoculum in exposed pulps of nonobese diabetic (NOD) mice. Periapical lesions were induced in first molars of 29 female NOD mice and 31 BALB/c controls. Acute (1-2 wk) or chronic (5 wk) exposures were either inoculated with a mixture of facultative and anaerobic bacteria or exposed to oral flora without inoculations. After death the teeth in the chronic groups were analyzed for the presence of the inoculated bacteria by culturing and by polymerase chain reaction amplification of 16S rDNA. Periapical lesion size was measured histomorphometrically and the interleukin-6 content was measured immunohistochemically. The mortality among NOD mice with inoculated and sealed exposures was 83%, compared with 29% for BALB/c mice. In the inoculated and uninoculated chronic NOD mice groups, 38% of the animals versus none of the BALB/c mice died. The chronic uninoculated NOD mice lost significantly more weight at the time of death than controls. Polymerase chain reaction was more sensitive than culturing in detecting the inoculated anaerobic bacteria. In the animals that survived to the predetermined time periods, lesion size and interleukin-6 content in NOD and BALB/c mice were not statistically different.
authors.affiliation: Department of Endodontology, School of Dental Medicine, University of Connecticut Health Center, Farmington 06030-1715, USA.
authors.forename: Ashraf
authors.initials: A
authors.lastname: Fouad
authors.forename: Jody
authors.initials: J
authors.lastname: Barry
authors.forename: Jessica
authors.initials: J
authors.lastname: Russo
authors.forename: Justin
authors.initials: J
authors.lastname: Radolf
authors.forename: Qiang
authors.initials: Q
authors.lastname: Zhu
mesh_terms: D000208:Acute Disease; D000704:Analysis of Variance; D000818:Animals; D001431:Bacteriological Techniques; D001862:Bone Resorption / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology; D002423:Cause of Death; D002908:Chronic Disease; D003782:Dental Pulp / Q000382:microbiology; D003789:Dental Pulp Exposure / Q000382:microbiology; D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000382:microbiology; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D016967:Fusobacterium nucleatum / Q000235:genetics / Q000502:physiology; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000032:analysis; D051379:Mice; D008807:Mice, Inbred BALB C; D016688:Mice, Inbred NOD; D010462:Peptostreptococcus / Q000235:genetics / Q000502:physiology; D010483:Periapical Diseases / Q000382:microbiology* / Q000473:pathology / Q000503:physiopathology; D016133:Polymerase Chain Reaction; D018713:Prevotella intermedia / Q000235:genetics / Q000502:physiology; D012336:RNA, Ribosomal, 16S / Q000032:analysis; D013223:Statistics as Topic; D013291:Streptococcus / Q000235:genetics / Q000502:physiology; D015431:Weight Loss
chemical_list: D015850:Interleukin-6; D012336:RNA, Ribosomal, 16S