Periodontitis and Rheumatoid Arthritis: The Same Inflammatory Mediators?

Abstract

The strict link between periodontitis (PD) and rheumatoid arthritis (RA) has been widely demonstrated by several studies. PD is significantly more frequent in RA patients in comparison with healthy subjects: this prevalence is higher in individuals at the earliest stages of disease and in seropositive patients. This is probably related to the role of P. gingivalis in inducing citrullination and leading to the development of the new antigens. Despite the many studies conducted on this topic, there is very little data available concerning the possibility to use the same biomarkers to evaluate both RA and PD patients. The aim of the review is to summarize this issue. Starting from genetic factors, data from literature demonstrated the association between HLA-DRB1 alleles and PD susceptibility, similar to RA patients; moreover, SE-positive patients showed simultaneously structural damage to the wrist and periodontal sites. Contrasting results are available concerning other genetic polymorphisms. Moreover, the possible role of proinflammatory cytokines, such as TNF and IL6 and autoantibodies, specifically anticyclic citrullinated peptide antibodies, has been examined, suggesting the need to perform further studies to better define this issue.

The Role of NF-κB in Physiological Bone Development and Inflammatory Bone Diseases: Is NF-κB Inhibition “Killing Two Birds with One Stone”?

“…Rheumatoid arthritis (RA) is a chronic inflammatory disease with progressive joint destruction over time [6][7][8]. Biologics such as anti-TNF-α antibodies have been shown to be effective in cases where existing drugs have not been effective [47].…”

“…Biologics such as anti-TNF-α antibodies have been shown to be effective in cases where existing drugs have not been effective [47]. The characteristic feature of RA is the proliferation and infiltration of synovial cells and angiogenesis of the joint area [6][7][8]. In the joint area, the overproduction of inflammatory cytokines such as IL-1, TNF-α, IL-6, and IL-17, adhesion molecules, and MMPs and the induction of osteoclasts are involved in bone and cartilage destruction in RA [6][7][8].…”

“…The characteristic feature of RA is the proliferation and infiltration of synovial cells and angiogenesis of the joint area [6][7][8]. In the joint area, the overproduction of inflammatory cytokines such as IL-1, TNF-α, IL-6, and IL-17, adhesion molecules, and MMPs and the induction of osteoclasts are involved in bone and cartilage destruction in RA [6][7][8]. Recently, biological products, such as anti-TNF-α neutralized antibody (etanercept, infliximab, and adalimumab, etc.,) and anti-IL-6 neutralized antibody (tocilizumab), which are drugs created by biotechnology, have been used for rheumatoid arthritis.…”

Use of TNF Inhibitors in Rheumatoid Arthritis and Implications for the Periodontal Status: For the Benefit of Both?

“…Both diseases show similarities in the prevailing cytokines within the tissues. Overexpression of TNF is at stake in both diseases and causes an imbalance in cytokine levels and therefore damage of soft tissues, progressing to bone, where osteoclasts are further activated by TNF-a (2)(3)(4). Furthermore RA patients are prone to develop periodontitis, possibly due to an increase of circulating TNF levels and/or deteriorated motor skills needed for oral hygiene maintenance as a result of damage in the joints.…”

Salivary and serum cathelicidin LL‐37 levels in subjects with rheumatoid arthritis and chronic periodontitis

“…This is due to observed shared risk factors, immuno-genetics and tissue destruction pathways in both diseases. 9,10 Cathelicidin antimicrobial peptide LL-37 has been suggested as a possible mechanistic link for CP and RA besides its role as a very potent human antimicrobial peptide. 11 It is expressed by epithelial cells (skin, ocular, airways, oral, intestine), macrophages, natural killer cells and neutrophils.…”