The two immunoinflammatory disorders, rheumatoid arthritis (RA) and Periodontitis (PD) are characterized by synovitis, joint damage, and alveolar bone degradation, are triggered by certain inflammatory mediators and leukocyte invasion, respectively. Rheumatoid arthritis is an infectious disorder which attacks changed self-epitopes and thus affects 1% of the human population, whereas 11% of the worldwide population aged is afflicted by extreme periodontal diseases in which commensal microbes upon the tooth surface is substituted by dysbiosis of the bacterial community that facilitate chronic inflammatory periodontal tissue damage. Periodontitis and RA display similarities in terms of pathogenesis amid variations in aetiology; all diseases entail systemic inflammation fuelled by, degradation of connective tissue, pro-inflammatory cytokines, and bone deterioration. Both the disorders have significant serological, epidemiological, and therapeutic connections and also have some common risk factors like aging and smoking. Laboratory and clinical data supporting this correlation is addressed in this aetiology analysis and the possible pathways involved in connecting both the diseases i.e., periodontitis to RA are described.

The success of implant performance and arthroplasty is based on several factors, including oxidative stress-induced osteolysis. Oxidative stress is a key factor of the inflammatory response. Implant biomaterials can release wear particles which may elicit adverse reactions in patients, such as local inflammatory response leading to tissue damage, which eventually results in loosening of the implant. Wear debris undergo phagocytosis by macrophages, inducing a low-grade chronic inflammation and reactive oxygen species (ROS) production. In addition, ROS can also be directly produced by prosthetic biomaterial oxidation. Overall, ROS amplify the inflammatory response and stimulate both RANKL-induced osteoclastogenesis and osteoblast apoptosis, resulting in bone resorption, leading to periprosthetic osteolysis. Therefore, a growing understanding of the mechanism of oxidative stress-induced periprosthetic osteolysis and anti-oxidant strategies of implant design as well as the addition of anti-oxidant agents will help to improve implants’ performances and therapeutic approaches.