These findings suggest that periopathogens (e.g., P. gingivalis) stimulate the expression of TLR-2 and TLR-4 in the periodontium and activate the mechanisms of local and systemic autoimmunity related to the SLE, which might be, at least partially, associated with the disease in the SLE patients. Here, TLR2 is linked to systemic lupus erythematosus.