Clinical, radiographic and histologic features suggest that inflammation is central to the pathogenesis of erosive osteoarthritis (OA). Since mediators of inflammation may activate osteoclasts and stimulate release of metalloproteinases in joint cartilage, we hypothesized that patients with erosive OA may have more joint space narrowing and less proliferative bone response (osteophytes, sclerosis) than those with idiopathic nodal OA. Hand radiographs of 33 patients with erosive OA and 33 age and sex matched patients with nodal OA were evaluated for prevalence and severity of joint space narrowing, osteophytes, subchondral sclerosis, subchondral cysts, erosions and subchondral collapse. While the prevalence and severity of OA was greater at each joint in erosive OA than in nodal OA, significant differences (p less than 0.05) were confined largely to the interphalangeal joints. Among patients with erosive OA, radiographic features of OA were more severe in joints with erosive changes than in joints that did not show erosive change (p less than 0.01 in most cases). Notably, when joints with erosive change were excluded, only joint space narrowing was more severe in patients with erosive OA than in the corresponding joints of patients with nodal OA (p less than 0.001). Our analysis did not support the hypothesis that inflammatory mediators modify chondro or osteoneogenesis in erosive OA.