Diet-induced Generalized Periodontitis in Lewis Rats

Author:

Messer Jonathan G1,La Stephanie2,Kipp Deborah E2,Castillo Evelyn J1,Yarrow Joshua F3,Jorgensen Marda4,Wnek Russell D3,Kimmel Donald B1,Aguirre José Ignacio5

Affiliation:

1. Department of Physiological Sciences, University of Florida, Gainesville, Florida

2. Department of Nutrition, University of North Carolina–Greensboro, Greensboro, North Carolina

3. Department of Research Service, Veterans Affairs Medical Center, North Florida–South Georgia Veteran Health System, Gainesville, Florida

4. Department of Pediatrics, Division of Endocrinology, Diabetes, and Metabolism, College of Medicine, University of Florida, Gainesville, Florida

5. Department of Physiological Sciences, University of Florida, Gainesville, Florida;, Email: aguirrej@ufl.edu

Abstract

Periodontitis is an important public health concern worldwide. Because rodents from the genus Rattus are resistant to spontaneous periodontitis, experimental periodontitis must be initiated by mechanical procedures and interventions. Due to their exacerbated Th1 response and imbalanced Th17 regulatory T-cell responses, Lewis rats are highly susceptible to inducible inflammatory and autoimmune diseases. We hypothesized that feeding Lewis rats a diet high in sucrose and casein (HSC) would alter the oral microenvironment and induce inflammation and the development of periodontitis lesions without mechanical intervention. A baseline group (BSL, n = 8) was euthanized at age 6 wk. Beginning at 6 wk of age, 2 groups of Lewis rats were fed standard (STD, n = 12) or HSC (n = 20) chow and euthanized at 29 wk of age. We evaluated the degree of periodontitis through histology and μCT of maxillae and mandibles. The HSC-induced inflammatory response of periodontal tissues was assessed by using immunohistochemistry. Gene expression analysis of inflammatory cytokines associated with Th1 and Th17 responses, innate immunity cytokines, and tissue damage in response to bacteria were assessed also. The potential systemic effects of HSC diet were evaluated by assessing body composition and bone densitometry endpoints; serum leptin and insulin concentrations; and gene expression of inflammatory cytokines in the liver. Placing Lewis rats on HSC diet for 24 wk induced a host Th1-immune response in periodontal tissues and mild to moderate, generalized periodontitis characterized by inflammatory cell infiltration (predominantly T cells and macrophages), osteoclast resorption of alveolar bone, and hyperplasia and migration of the gingival epithelium. HSC-fed Lewis rats developed periodontitis without mechanical intervention in the oral cavity and in the absence of any noteworthy metabolic abnormalities. Consequently, the rat model we described here may be a promising approach for modeling mild to moderate periodontitis that is similar in presentation to the human disease.

Publisher

American Association for Laboratory Animal Science

Subject

General Veterinary,General Biochemistry, Genetics and Molecular Biology

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