Although the exact process is unknown, there are a few hypotheses for the generation of<unk> s. It has been observed that<unk> s frequently form over extensor sites and areas vulnerable to trauma. The trauma causes inflammatory particles to build up and leads to a secondary inflammatory response which ultimately causes fibrin release and necrosis. Another hypothesis suggests that the inflammation of blood vessels activates complement components, which leads to the deposit of<unk>  factors and fibrin. The<unk>  is the most common cutaneous manifestation of<unk>  arthritis (RA).<unk>  arthritis involves chronic inflammation of synovial membranes, which leads to degradation of articular cartilage and the juxta-articular bone. Inflammation is caused by T cells, B cells and monocytes when endothelial cells are activated. Neovascularization, or the growth of new blood vessels, serves as an additional marker for<unk>  arthritis. A hyperplastic synovial lining layer can be caused by the expansion of synovial fibroblast and macrophage cells. This expansion of the synovial membrane, sometimes referred to as "pannus," can lead to bony erosions and cartilage degradation at the site of the cartilage-bone junction in the periarticular bone. It is important to note that the cause of<unk>  arthritis is unknown. It is speculated that genetic and environmental factors can both contribute to the development of<unk>  arthritis. Gene loci and antigens, such as HLA class II antigens, have been seen as closely associated with<unk>  arthritis. Environmental risk factors include smoking, periodontitis, viral infections and gut, mouth and lung microbiomes. Researchers have noted that Prevotella species, which are expanded in the gastrointestinal tract in early RA, and Porphyromonas gingivalis, which is associated with periodontitis, may have a role in pathogenesis.
Rheumatoid nodule
Villonodular synovitis
Plasma cell granuloma
Eosinophilic granuloma
Fibrin ring granuloma
Palindromic rheumatism
Colloid nodule
Cold nodule