Osteoarthritis: Can We Do Better?

Abstract

Osteoarthritis (OA) is the most common form of arthritis, affecting approximately 32.5 million adults in the United States. OA is characterized as a degenerative joint disease or "wear and tear" arthritis. Symptoms experienced by patients include, but are not limited to, swelling, stiffness, pain or aching, and decreased range of motion. The majority of individuals impacted by OA are over the age of 65. OA has long been thought of as an inevitable part of aging. Patients are typically diagnosed after the onset of symptoms once irreversible damage has occurred, such as the breakdown of bone and cartilage. Along with clinical presentations, medical professionals often relied on radiographic images to confirm the diagnosis of OA. Limited research has looked into how to catch OA early and stage patients in a pre-OA state, possibly preventing irreparable damage that is observable radiographically. This article presents the history, diagnosis, and classes of OA. In addition, we present multiple diagnostic tools currently used and others under investigation, including OA-specific biomarkers and electroarthrography (EAG). These tools show promise as aids in early OA diagnosis and intervention, ultimately slowing down or altogether stopping the progression of OA. In conjunction or individually, these techniques, if further developed, stand out as promising mechanisms that may decrease the current OA burden on the healthcare system.

Systemic inflammatory biomarkers are novel predictors of all-cause and cardiovascular mortality in individuals with osteoarthritis: a prospective cohort study using data from the NHANES

“…Although OA has traditionally been considered a noninflammatory form of arthritis, extensive evidence now demonstrates that chronic low-grade inflammation plays an integral role in OA onset and progression [ 26 , 27 ]. Local inflammation within joint tissues promotes cartilage destruction and synovitis through effects on cartilage-degrading enzymes, apoptosis, and matrix proteins [ 28 , 29 ]. Systematically, higher circulating levels of inflammatory mediators may accelerate OA severity through mechanisms including increased bone resorption and impaired muscle function [ 30 , 31 ].…”