Developments concerning amyloidosis associated with rheumatic diseases or often causing musculoskeletal symptoms are reviewed. The pathogenesis, clinical manifestations, diagnosis, and therapy of amyloid A, amyloid light-chain, and amyloid beta 2-microglobulin amyloidosis are discussed from the standpoint of a clinical rheumatologist. The biology of the precursor protein serum amyloid A (SAA) has been extensively studied, and a new assay for SAA has been developed. In amyloid beta 2-microglobulin amyloidosis, modified beta 2-microglobulin may function as a pathogenic factor that initiates an inflammatory reaction in which macrophages produce cytokines that induce osteoclastogenesis and bone resorption. Further experience with serum amyloid P component scintigraphy in the diagnosis and monitoring of amyloidosis has accumulated. Guidelines for the dosage of colchicine in the treatment of amyloidosis associated with familial Mediterranean fever have been published. In amyloid light-chain amyloidosis, intensive chemotherapy in combination with bone marrow transplantation or autologous stem-cell infusion has potential therapeutic significance.