Abstract
We propose curcumin as a preventive measure to avoid/manage periodontitis (PD), and as a natural immunosuppressant for rheumatoid arthritis (RA). PD, mainly caused by Porphyromonas gingivalis forming biofilm and leading to tooth decay, is a major public health issue and a risk factor for the development of RA in humans. P. gingivalis is able to trigger experimental autoimmune arthritis in animal models and in humans can induce citrullinated peptides, which not only are a source of anti-citrullinated antibodies (ACPAs), but also participate in autoreactive responses and disease development. Curcumin appears to have efficient anti-bacterial activity against P. gingivalis infection and biofilm formation. In addition to antibacterial, anti-oxidant, and anti-inflammatory action, curcumin exerts unique immunosuppressant properties via the inhibition of Th17 pro-inflammatory responses and promotion of regulatory T cells, thus suppressing autoimmunity. We introduce curcumin as a natural product for the management of both PD and RA-related autoreactivity, possibly also as a preventive measure in early RA or individuals at high risk to develop RA.
Highlights
Rheumatoid arthritis (RA) is an autoimmune rheumatic disease characterized by immune-mediated joint inflammation, which leads to joint destruction, loss of joint function, and disability, if left untreated [1,2,3]
The immunopathogenesis of rheumatoid arthritis (RA) has been extensively investigated and it is well established that genetic factors, predominantly HLA-DRB1 shared epitope (HLA-DRB1SE) alleles [5,6], epigenetic, and environmental factors are involved in the development of the disease [1,2,7,8,9,10]
A better understanding of the underlying mechanisms of the disease has led to its therapeutic management with synthetic disease-modifying antirheumatic drugs and novel biological agents that target specific molecules involved in disease pathogenesis, which can prevent joint damage and disease progression, and improve disease prognosis [2,9,11,12,13]
Summary
Rheumatoid arthritis (RA) is an autoimmune rheumatic disease characterized by immune-mediated joint inflammation, which leads to joint destruction, loss of joint function, and disability, if left untreated [1,2,3]. A better understanding of the underlying mechanisms of the disease has led to its therapeutic management with synthetic disease-modifying antirheumatic drugs (sDMARD) and novel biological agents that target specific molecules involved in disease pathogenesis, which can prevent joint damage and disease progression, and improve disease prognosis [2,9,11,12,13] Since these therapies can have potentially toxic side effects, it is very important for practicing physicians to diagnose the disease early and accurately, especially more aggressive forms, in order to select the appropriate treatment [14,15]
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