**Abstract**

The relationship between periodontitis and systemic diseases is an important part of clinical periodontal research, which has been growing steadily. Even though the etiologies of periodontal disease and rheumatoid arthritis (RA) differ, these pathologies have many common features, both being multifactorial diseases characterized by localized chronic inflammatory reactions, which are fuelled by an analogous set of cytokines (among many, the most prominent being Tumour Necrosis Factor (TNF), Interleukin (IL) 6 and 17), leading to high systemic circulating concentrations of inflammatory markers such as C-reactive protein (CRP). It was not until the discovery of peptidylarginine deiminase (PAD) mediated citrullination of proteins by *Porphyromonas gingivalis* that the link between the two diseases was purely speculative. This citrullination initiates a series of events which culminate in the production of anti-citrullinated protein antibodies (ACPA) and, finally, in the clinical manifestation of rheumatoid arthritis. Another common denominator is the bone destruction caused by proinflammatory cytokines secreted by T 17 helper cells (TH17) which is the pathological hallmark of both diseases. Other notable common areas are shared risk factors such as environmental and genetic risk factors. Regarding treatment, neither pathologies have a definitive cure, however, several strategies are employed, some of which are common, such as diet and lifestyle changes, and immunomodulating medication applied locally or systemically.

**Keywords:** periodontal disease, rheumatoid arthritis, cytokines, DMARDS, treatment, microorganisms
