Arthritis is a complaint and a disease afflicting many patients and accounting for >10% of appointments to a generalist practice. Arthritis is multifaceted and can be categorized in several different fashions. For simplicity, this chapter focuses on conditions affecting the anatomic joint composed of cartilage, synovium, and bone. Other discussions would include localized disorders of the periarticular region (eg, tendonitis and bursitis) and systemic disorders that have arthritic manifestations (eg, vasculitides, polymyalgia rheumatica, and fibromyalgia). The chapter discusses three prototypical types of arthritis: osteoarthritis, as an example of a cartilage disorder; gout, as an example of both a crystal-induced arthritis and an acute arthritis; and rheumatoid arthritis, as an example of an immune-mediated, systemic disease and a chronic deforming arthritis.
ESSENTIALS OF DIAGNOSIS
Degenerative changes in the knee, hip, shoulder, spine, or virtually any other joint.
Pain with movement that improves with rest.
Joint deformity and mechanical alteration.
Sclerosis, thickening, spur formation, warmth, and effusion in the joints.
Arthritis is among the oldest identified conditions in humans. Anthropologists examining skeletal remains from antiquity deduce levels of physical activity and work by searching for the presence of the degenerative changes of osteoarthritis (OA). OA is more prevalent among people in occupations characterized by steady, physically demanding activity such as farming, construction, certain sports, and production-line work. Obesity is a significant risk factor for OA, especially of the knee. Heredity and gender play a role in a person’s likelihood of developing OA, regardless of work or recreational activity.
It is increasingly accepted that most OA results, at least in part, from altered mechanics within the joint. Certain metabolic conditions such as hemochromatosis and Gaucher disease involve a genetic defect in collagen/cartilage. Altered mechanics may occur from minor gait abnormalities or major traumas that, over a lifetime, result in repeated stress and damage to cartilage. Repeated trauma may result in microfracture of cartilage, with incomplete healing due to continuation of the altered mechanics. Disruption of the otherwise smooth cartilage surface allows differential pressure on remaining cartilage, as well as stress on the underlying bone. Debris from fractured cartilage acts as a foreign body, causing low-level inflammation within the synovial fluid. Indeed, increasing evidence suggests that inflammation, from damaged cartilage or even as a primary activity, is involved in most OA, and actions taken to reduce inflammation are increasingly used to alter the path to joint damage. These multiple influences combine to alter intrinsic efforts at cartilage repair, leading to progressive cartilage destruction and bony joint change. Current thinking suggests that the process is not immutable, but any intervention would have to be made while the joint is still asymptomatic—an unlikely occurrence.
It is difficult to advise patients on measures to prevent OA. Obese persons should lose weight, ...