UCSF

The Western diet, characterized by high consumption of refined, processed grains, has been epidemiologically associated with elevated periodontal disease risk, yet the mechanisms underlying this relationship remain incompletely understood. Grain refinement simultaneously removes dietary fiber and reduces food texture, producing a soft, rapidly fermentable substrate that may promote oral biofilm dysbiosis through two distinct but potentially synergistic pathways: augmented saccharide substrate availability to saccharolytic pioneer species, and loss of the masticatory mechanical challenge that limits biofilm maturation and sustains homeostatic gingival immune signaling. Whether the protective effects of whole grain consumption are attributable to its fiber content, its structural and textural properties, or both has not been experimentally resolved.The present thesis employed a multi-diet murine experimental framework to dissociate the contributions of dietary texture and fiber content to periodontal host-microbe homeostasis. In Chapter 2, Sprague-Dawley rats were fed hard or soft nutritionally matched diets, and dental biofilm abundance was assessed by scanning electron microscopy. In parallel, coarse- and fine-particle wheat digests were used to grow human saliva-derived oral biofilms in vitro, with biofilm architecture characterized by scanning electron microscopy and growth kinetics quantified by 24-hour spectrophotometry. In Chapters 3 and 4, BALB/cByJ mice were assigned to one of five dietary regimens: a Standard Diet (SD), Whole Grain (WG), Processed Grain (PG), Fiber Bar (FB), or Placebo Bar (PB). Within each dietary group, animals were further divided into sham-inoculated and polymicrobial-inoculated subgroups receiving a topical oral lavage of Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum. Gingival inflammatory cytokine profiles (TNF-α, IL-1β, IL-6, IL-23, IL-17A, IL-10) were quantified by multiplex assay, alveolar bone loss was measured by micro-computed tomography, and oral microbial community composition was characterized by 16S rRNA V4 amplicon sequencing with multivariate and differential abundance analyses.Across all experimental chapters, dietary texture emerged as the dominant modifier of periodontal outcomes, with diet consistently explaining more variance than polymicrobial inoculation status. In Chapter 2, hard-diet animals accumulated significantly less dental biofilm than soft-diet counterparts, and fine-particle grain digests supported greater bacterial growth kinetics and larger biofilm surface areas than coarse-particle digests across all digestion intervals. In Chapter 3, WG-fed animals exhibited significantly lower alveolar bone loss and reduced gingival IL-17A levels compared to PG- and FB-fed animals, while no significant differences were observed between FB and PB groups differing only in fiber supplementation. A positive correlation between gingival IL-17A and total alveolar bone loss across all dietary groups implicated IL-17A as a mechanistic intermediate linking dietary texture to periodontal bone outcomes. In Chapter 4, the most statistically robust differences in oral microbial community composition were observed between WG and FB groups, diets differing in fiber form, with WG selectively enriching Lactobacillus and processed grain and fiber bar diets enriching Enterococcus and Staphylococcus. Among inoculated animals, processed grain diet uniquely supported enrichment of Fusobacterium and Prevotella, suggesting that grain refinement creates an ecologically permissive oral environment for periodontal pathogen colonization. Collectively, these findings identify dietary texture—independent of fiber content—as a dominant and mechanistically grounded determinant of periodontal host–microbe homeostasis, with implications for dietary prevention strategies, pediatric oral health policy, and the reduction of the substantial individual and societal costs of periodontal disease and edentulism.