Osteoarthritis Phenotyping Makes Progress, but Will Targeted Treatments Follow?

Clinical medicine ― and rheumatology in particular ― is frequently about pattern recognition. As we age in our profession and as our patient panels grow, we develop a gestalt, so that the most seasoned of us can recognize polymyalgia rheumatica, rheumatoid arthritis, psoriatic arthritis, or gout within a few minutes of meeting a patient.

Dr Karmela Chan

But osteoarthritis (OA) confounds us. Why do some people have more pain than others? Is knee OA biologically the same as spine degenerative disc disease? How is it that some folks have horribly misshapen hands but feel no pain at all? And speaking of hands, what is erosive osteoarthritis even?

OA has become a leading contributor to years lived with disability, as tracked by the Global Burden of Disease Collaborative Network. Yet our treatment options are embarrassingly limited.

To improve outcomes in OA, we need to do a better job of defining it and understanding mechanisms behind it. Though we do not typically think of "phenotypes" when we think of OA, we also instinctively know that the "wear-and-tear" conception of OA is not the whole picture either, as illustrated by those pesky Heberden nodes.

Historically, many attempts have been made to phenotype OA based on a variety of dimensions, such as joint involvement, pain, psychological profiles (eg, depression, coping ability, catastrophizing behavior), comorbidities (metabolic syndrome), imaging features, or disease trajectory.