Hypothesis: Inflammation Infection-bacterial, fungal, viral, protozoal organisms produce toxins or have other chemotactic factors which attract WBC such as neutrophils and macrophages. Chemicals that are produced by infectious organisms or WBC are factors that result in the production of pain, fever, and inflammation. Immune-mediated-The host immune system attacks the cells of the synovium/joint components and damages them. These damaged cells and immune cells release cytokines, interleukins, and other factors. These result in signs of inflammation. Trauma-Trauma damages cartilage or other parts of the joint capsule. These damaged cells release proteins and chemotactic factors/chemicals. These attract WBC to clean up the cellular debris. The WBCs release cytokines that result in further signs of inflammation. Neoplasia-A Neoplasm (a space occupying lesion) causes pressure necrosis of the joint structures. Dying cells release factors that attract WBC resulting in inflammation. Neoplasia is not a very likely cause in this case. Inflammation and Actual Mechanisms Infectious-bacterial products act as chemoattractants. Inflammatory mediators in the plasma in cells are released. These mediators damage the cells of the synovial joint. Bacterial endotoxins cause the release of complements, which cause an aggregation of clotting factors leading to intravascular coagulation. This further leads to prostaglandin formation, which is involved in the production of pain. Infectious causes can include bacteria, viruses, parasites, fungi, rickettsia, mycoplasma, and spirochetes. Immune-mediated-There can be immune-complex deposition in the synovium. In rheumatoid arthritis, there can also be T-Cells, local inflammatory mediators, and cytokines attracted to the joint. Lysosomal enzymes are released in response to the inflammatory response eliciting degradation of the cartilaginous matrix. Deposition of fibrin impairs nutrient metabolite exchange. Mechanical damage adds to the problem. Trauma-A traumatic incident involving crushing or penetration damages the blood vessels and other cells. The damaged cells release factors/chemicals that act as chemoattractants for WBCs. The blood released from the damaged blood vessels also attracts WBCs. Neoplasia-Although this is a very unlikely cause of the symptoms in this case, a space occupying neoplasm of the joint causes pressure necrosis of the joint/joint structures. Dying cells in the joint, release factors that attract WBCs resulting in inflammation. Degenerative Joint Disease-Chondrocytes undergo biochemical and metabolic changes. They release Il-1 and TNF-A which stimulate catabolic metalloproteinases and inhibit collagen and proteoglycan synthesis. Prostaglandins and Il-6 are also produced which lead to matrix degradation and inflammation.