Obesity status and change in body mass have been associated with viral infection and distinct gut microbiota signatures in obese and lean patients.74-77 It is currently unclear if the GI bacterial microflora shift precede obesity or are a result of an obesogenic diet. However, in human and animal models, interventions such as roux-en-Y gastric bypass surgery have demonstrated an ability to shift this gut microbiota from one associated with obese to one associated with lean control subjects.78,79 In those animals with newly acquired lean gut microflora, altered overall nutrient acquisition and energy regulation has been seen.79-81 Furthermore, the immediate drop in hyperglycemia in obese subjects who have undergone bariatric surgery, prior to substantial weight loss indicates the surgical procedure itself, and perhaps the alterations in the gut microflora associated with it, have a beneficial effect on comorbid inflammatory conditions separate from those associated with weight loss.79,80,82 Recent studies have also shown increased numbers and proportions of pathogenic periodontal bacteria in obese patients83 and obesity-induced insulin resistence in ginval tissues.84
The primary etiology of periodontal disease is bacterial plaque, in particular virulent bacterial “complexes” and/or “consortia” that are associated with active periodontal disease sites and periodontal disease progression.85-87 In addition, nonsurgical periodontal therapy has been shown to alter the oral microflora significantly.88,89 Due to the direct access of bacteria and bacterial products to the systemic circulation through the ulcerated periodontal pocket epithelium90 as well as the potential mechanism of bacterial-induced signaling and bacterial epitope recognition by epithelial and mucosal immune cells within the alimentary canal,8,91,92 oral bacteria may influence systemic energy metabolism, immune system stimulation, and gut permeability (Figure 5).
Figure 5. Hypotheses for the interaction between oral bacteria and obesity.104
A. Hypothesis 1 - Oral bacteria increase metabolic efficiency.
B. Hypothesis 2 - Oral bacteria increase appetite.
C. Hypothesis 3 - Oral bacteria redirect energy metabolism.