Background
Excessive sugar intake is linked to a potential addiction-like response due to its impact on the brain’s reward system, similar to that seen with drugs such as cocaine. Sugar triggers dopamine release in the brain’s pleasure centers and activates the endogenous opioid system, potentially leading to addictive behaviors such as bingeing, craving and withdrawal. Glucose and fructose are integral to many modern foods, leading to overconsumption and associated health risks like systemic inflammation, gut dysbiosis, and metabolic syndrome. Oral diseases, affecting 3.5 billion people globally, share sugar as a major risk factor. The American Heart Association and World Health Organization recommend limiting sugar intake to reduce these risks. Despite its critical role, the impact of dietary sugars on periodontal inflammation has been underexplored.
Sugar-driven inflammation
Excess dietary sugar contributes to low-grade systemic inflammation, gut barrier dysfunction, and immune dysregulation, all of which are linked to various health conditions, including periodontal inflammation. Fructose consumption, in particular, disrupts tight junction proteins in the intestinal barrier, increasing permeability and allowing bacterial endotoxins to enter the bloodstream. This process, known as endotoxemia, exacerbates systemic inflammation and contributes to the development of NAFLD, which further fuels the inflammatory cycle. NAFLD then perpetuates systemic inflammation, which is linked to diseases such as metabolic syndrome and cardiovascular disease. Sugar-rich diets also directly affect immune function, promoting the production of pro-inflammatory cytokines and oxidative stress, further exacerbating inflammation. This chronic inflammation has a bidirectional relationship with periodontitis.
Studies show that excessive intake of sugar and sugar-sweetened beverages is associated with a higher risk of periodontal disease, particularly in adolescents. High sugar intake is linked to obesity and metabolic syndrome, which are associated with various non-communicable diseases, including type 2 diabetes, cardiovascular disease and cancer. These conditions also have a bidirectional relationship with periodontal inflammation. Moreover, the pro-inflammatory state triggered by NAFLD and obesity exacerbates periodontal inflammation through systemic pathways, including the production of pro-inflammatory cytokines such as TNF-α and IL-6. Future studies using genomic technologies could provide deeper insights into sugar’s impact on gene expression related to inflammation. Nutrigenomics, in particular, may help explore how dietary sugars influence gene expression patterns related to periodontal inflammation and systemic disease progression.
Sugar-induced dysbiosis
The human microbiome, comprising all microbes in the body and their genomic content, plays a vital role in health and disease. Dysbiosis, the disruption of the microbiota’s symbiotic balance, can result from various factors, including diet and lifestyle. The gut microbiota mainly consists of Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria, and Verrucomicrobia. A high-sugar diet is linked to gut dysbiosis, characterized by increased Proteobacteria and Bacteroidetes and decreased Firmicutes and short-chain fatty acid (SCFA) producers, leading to increased intestinal permeability and inflammation. Fructose and sucrose, in particular, have been shown to promote dysbiosis, leading to increased levels of harmful gram-negative bacteria and decreased production of beneficial SCFAs, such as butyrate. This promotes gut barrier dysfunction and systemic inflammation.
Studies in rats and humans show that high fructose and sucrose consumption alters the gut microbiota’s composition, decreases SCFA production, and promotes inflammation and lipid accumulation in the liver. Notably, fructose from whole fruits does not negatively impact gut health. The oral microbiome, containing around 700 bacterial species, is also affected by excessive sugar intake. Short-term sucrose rinses and in vitro studies indicate that high sugar levels can reduce microbial diversity and increase harmful bacteria like Actinomyces and Streptococcus. This dysbiosis in the oral microbiome contributes directly to periodontal inflammation by increasing the abundance of pathogenic species, reducing diversity, and promoting the formation of biofilms that exacerbate gingival inflammation. A systematic review suggests that high sugar consumption significantly contributes to oral dysbiosis, but further research is needed to understand its full microbiological impact.
Clinical relevance
Three factors contribute to periodontal inflammation: dysbiosis of oral biofilms, an unresolved inflammatory response leading to tissue damage and systemic conditions that worsen inflammation. Current strategies for preventing and managing periodontal inflammation mainly focus on controlling biofilms through brushing and professional cleanings. However, a multidimensional approach addressing lifestyle factors is needed. Dietary interventions have shown that a micronutrient-rich, low-sugar diet can significantly reduce gingival inflammation and the presence of pathogens. Probiotic supplementation may be another easy and feasible strategy to buffer inflammtion and resolve pathogenetic mechanisms beneath chronic inflammation and dysbiosis.
Fermented food like yogurt, kefir, kombucha and other less known are naturally rich in lactobacilli (L. casei, L. bulgaricus, L. fermentum, L. plantarum, L. rhamnosus and others), healthy cocci (Streptococcus thermophilus, Str. salivarius, etc.) and bifidobacteria (B. bifidus, B. infantum, B. longum and others). Kefir is also enriched with healthy strains of yeasts as well (Saccharomyces unisporum, Candida kefyri, Kluyveromyces marxianus, K. lactis, etc.) which amplify the diversity of either gut and oral microbiota communities. They represent a most recommended food tipology that should never be missing in our table. Scientific literature now has plenty of proofs linking the diversity and balanced status of microbiota as the primary factor for the human health.
Commercial supplements may represent another possible option for those rejecting dairy and fermented dairy products in their diet. These formulation, often, are integrated with prebiotics i.e. soluble fibers derived from vegetal sources that enhance the vitality of prebiotics and stimulated them to produce cytoprotective and regulatory metabolites. These include the aformentioned SCFAs or short-chain fatty acids (i.e. propionic, butyric, valeric, isovaleric, etc.), along with neurotransmitters like GABA, acetilcholine, serotonin and tyramine. In the gut they exert immunoregulatory activities, while in the liver they control lipid and carbohydrate homeostasis, avoiding thus the onset of insulin-resistance, trygliceride storage (fatty liver) and blood high cholesterol.
Since these conditions represent the spark for the onset of diabetes, cardiovascular diseases, cancers and even autoimmune conditions, it may be concluded that excessive consumption of simple sugars in the daily diet is strongly discouraged. Rather, a varied diet rich in grains (with plenty of fibers) vegetables, fruits, legumes, with dairies, eggs and animal meats as a complement may represent the best way to keep a general good health, starting from the mouth and ending in out guts.
- Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.
Scientific references
Shanmugasundaram S et al. BDJ Open. 2024; 10:78.
He J, Liu Y et al. Clin Oral Investig. 2024; 28(12):675.
Gu M, Ge J et al. BMC Oral Health. 2024; 24(1):1424.
Akbari E et al. Curr Oncol Rep. 2024; 26(11):1388-97.