Potential Role of Free Fatty Acids in the Pathogenesis of Periodontitis and Primary Sjögren's Syndrome

Abstract

Clinical studies have shown that metabolic disorders such as type 2 diabetes and dyslipidemia are associated with increased risk of oral-related diseases, such as periodontitis and Sjögren's syndrome. Although changes in the immune system are critical in both of these metabolic disorders and oral-related diseases, the mechanism underlying the interaction between these diseases remains largely unknown. Obesity and type 2 diabetes are known to be associated with higher concentrations of free fatty acids in blood. Among free fatty acids, saturated fatty acids such as palmitic acid have been demonstrated to induce inflammatory responses mainly via the innate immune systems, and to be involved in the pathogenesis of type 2 diabetes in tissues such as adipose tissue, liver, pancreas, and skeletal muscle. Here, we highlight recent advances in evidence for the potential involvement of palmitic acid in the pathogenesis of periodontitis and Sjögren's syndrome, and discuss the possibility that improvement of the lipid profile could be a new strategy for the treatment of these diseases.

Keywords: Sjögren’s syndrome; free fatty acid; metabolic disorder; periodontitis; type 2 diabetes.

Figure 1

Proposed model of influence of Pal on pathogenesis of periodontitis. AB: alveolar bone, C: cementum, CV: capillary vessel, E: enamel, GE: gingival epithelium, GF: gingival fibroblast, Mo: monocyte, Mφ: macrophage, Ne: neutrophil, OC: osteoclast.

Figure 2

Potential mechanism of involvement of Pal in the pathogenesis of SS. APC: antigen presenting cell, CV: capillary vessel, SGEC: salivary gland epithelial cell.