A team of researchers from Brazil and Israel review in a recent paper the evidences linking systemic lupus erythematosus and periodontal disease. The study entitled “Possible evidence of systemic lupus erythematosus and periodontal disease association mediated by Toll-Like Receptors-2 and 4 (TLR2, TLR4)” was published in the Clinical & Experimental Immunology journal.
Systemic Lupus Erythematosus (SLE) is a chronic systemic autoimmune disease characterized by the misguided attack of body tissues by the immune system. SLE onset and development are associated with genetic predisposition and environmental factors such as exposure to sun light. Periodontal disease is a chronic inflammatory infectious disease, triggered by microbes that colonize the tissues that surround and support the teeth, i.e. periodontal tissues. The inflammatory process that characterizes this disease results in periodontal tissue destruction and might lead to teeth loss.
In this paper, researchers present evidences that the biological mechanisms leading to SLE and periodontal disease have similarities. The team focused in a special type of proteins present in the membranes of immune cells called Toll-like receptors, which modulate immune responses against foreign pathogens. These proteins are found in higher amounts in the immune cells of patients with SLE and periodontal disease, suggesting that both diseases share analogous immune response pathways.
Toll-like receptors are crucial in periodontal disease development, and are responsible for recognizing the bacteria that infect the periodontal tissues and for initiating the strong inflammatory processes that characterize this condition. In SLE, Toll-like receptors activity is dysregulated, leading to an increase in antibody production and disease progression. Researchers believe that periodontal disease might accelerate SLE by maintaining a high expression of Toll-like receptors in immune cells. Toll-like receptors overexpression results in an excessive activation of immune responses, promoting the onset and progression of autoimmune reactions typical in SLE. These concepts are supported by the fact that periodontal treatment reduces Toll-like receptor numbers and therefore SLE symptoms.
It thus seems that Toll-like receptors play an important role in development of both diseases. Nonetheless, the underlying mechanisms leading and connecting both SLE and periodontal disease are still elusive. Authors finish their review suggesting the implementation of studies to further investigate the relationship between the two diseases and search for novel ways to minimize the effects of periodontal disease in SLE patients.
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