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A syndrome of acute onset of inflammation over interphalangeal joints heralding deforming osteoarthritis may be intermediate between degenerative and rheumatoid joint diseases. The syndrome appears predominantly in women of menopausal age and is remarkably symmetrical. In a prospective study of 170 propositi, later changes more characteristic of rheumatoid arthritis than of generalized or erosive osteoarthritis developed in 15.3%.

Osteoarthritis was seen as a stepchild of rheumatology until very recently. Veterinarians took an interest in it because they had racehorses and racing greyhounds to take care of, whose economic value to their owners made it worthwhile. But medicine had little to offer, especially as osteoarthritis was thought to be part of ageing, like the greying of hair, and few distinctions were made in the clinical presentations. The terminology of degenerative or wear-and-tear arthritis reflected this view. It held little interest for most clinicians. The name, osteoarthritis, implicitly acknowledges that inflammation plays a part in the presentation, and the nodal deformities of interphalangeal joints have aroused some curiosity since the early 18th century; but little else has been done to distinguish osteoarthritis from other forms of arthritis. For therapy, there were thermal spas for those who could afford to go to them, and surgeons performed osteotomies on the lower extremities of some crippled by hip and knee arthritis. What has changed to attract clinicians, biologists, geneticists, pathologists and orthopaedists now? For one thing, there is the recognition that osteoarthritis represents a final common pathway for all insults to the joints (1). Also, we now know that osteoarthritis does not arise de novo but has antecedents that may be remote in time or, because of their severity (as in athletic injuries), more recent. That characterizes osteoarthritis as a dynamic process worthy of study, and has led to therapeutic advances that may not yet be able to halt the progression but can afford relief from pain and disability. To that end, scales and tests permit clinical assessment of severity, and molecular biology offers explanations of pathogenesis. The clinical definitions that emphasize changes made visible by X-ray--such as joint (space) narrowing owing to cartilage loss and osteophytes (or spurs, which are reparative processes that increase the articular surface), buttressing, increased density of juxta-articular bone, and eburnation--cannot distinguish between symptomatic and relatively asymptomatic osteoarrhritis. The majority of people have relatively mild symptoms, if any at all, with perhaps some sensitivity to weather changes, occasional limitations of motion, and mild-to-moderate pain. As they do not seek medical consultation, a vast industry caters for them, with, for example, herbals, omega fatty acids from fish oils, simple analgesics for self-medication, and topical products such as capsaicin. Imports from Asia include the Ayurvedic pharmacopaeia (mostly herb-derived), yoga, and acupuncture. For the majority, moral support and time spent--more difficult to provide in today's hectic medical environment--bear fruit. For an appreciable minority, however, osteoarthritis behaves as a true disease. Fraying and fibrillation of cartilage result from the elaboration of proteolytic and cullagenolytic enzymes by the chondrocytes that initially attack the matrix within which they are embedded (2). Synovitis develops, with elaboration of cytokines that further attack the cartilage. Oedema and increased vascularity develop in response. …