Knowing is not enough; we must apply. Willing is not enough; we must do. —Goethe

Caring optimally for patients with early arthritis is one of the exciting challenges of contemporary rheumatology. Indeed we perceive this to be an urgent societal imperative.

The superb contributions to this timely issue of Rheumatic Disease Clinics frame many of the pertinent issues. These articles inform us and permit us to identify the key questions, and provide an elegant state-of-the-art summary of potential predictors/triggers of inflammatory arthritis, sophisticated imaging (and serologic) methods to establish early/preclinical disease, and principles to guide the therapy for these patients to maximize their opportunity for favorable outcomes.

Several important questions remain unanswered. When does disease begin? This is a critical issue. The autoimmune diathesis that generates disease, when specific enough, is arguably a point of disease onset, and could be more amenable to treatment, even cure, perhaps with different approaches than we use in established disease. Considering that statins are increasingly used in primary and not just secondary prevention of vascular disease, we need not be too timid about considering treatment at this stage.

When should therapeutic intervention occur? What are needed are biomarkers that can guide treatment for both disease subsets and disease severity. In the not too distant future individual genetic profiles, even complete genomic sequences, may contribute not only to risk assessment but also to early diagnosis. It seems likely that our current definitions and subclassifications of rheumatic diseases will change substantially and become more sharply focused with better insight into pathogenesis, and combined use of genetic, epigenetic, immunologic, inflammatory, and tissue-related biomarkers.

In rheumatoid arthritis (RA), have the new disease classification criteria made our task harder because, in an effort to capture patients with earlier RA, a much greater number of patients end up misclassified as RA who actually have a self-limited syndrome?

What are the incremental consequences of delayed therapy, particularly for preclinical illness?

Are there not disease subsets, certainly for RA, which perhaps merit differing approaches?

But most compelling to us is the challenge of assuring that all patients with early arthritis are provided optimal care. Only 41% of RA patients in Canada were started on therapy within 6 months of presumed onset of disease; 78% of the delay was attributable to processes/events occurring before patients saw a rheumatologist. And these data were only for patients who were referred to and seen by rheumatologists. How many never get to rheumatologists or even primary care physicians? While some might view these data as reasonably salutary, we do not; we suspect the experience is worse in the United States and possibly other and underdeveloped countries. For example, at Los Angeles County + University of Southern California medical center there are approximately 1000 patients who will wait around 6 to 12 months for rheumatologic evaluation. We certainly respect the care this (and similar) system(s) will bring to an otherwise underserved, indeed neglected, population. We understand the inherent problems and limitations. But we must not be complacent. We must not settle for less than the best possible care now available.

How, then, will we care for these patients? Someone once suggested that good questions are more important than answers; answers change, good questions do not. However, this query, we believe, demands response. We suggest it will require paradigmatic changes in how health care is provided. Surely there are not enough rheumatologists. Nor is it likely there will be any time soon. Training more is not the solution. In part rheumatologists will have to accept that other health care professionals will need to be a part of any plan to approach this issue; in the past, we have been reluctant to concede that others had the ability or ought to have a prerogative of caring for our patients. But there are probably not enough primary care physicians either, although that may never be known. This means that nonphysicians (nurse practitioners, physician assistants, and/or new, specially trained rheumatology/musculoskeletal disease professionals) will have to assume a prominent role if all patients with early arthritis are to be reached. These caregivers will need to use new approaches, including immediate-access clinics, group visits, algorithms, and communication with patients by telephone and other electronic means, using new applications that are disease-specific and even patient-specific. Supervisory mechanisms will need to be devised, and referrals to rheumatologists will need to be selective.

The Institute of Medicine promulgated goals for health care for this century: care that is safe, timely, patient-centered/personalized, equitable, efficient, and effective (which we would infer includes humanistic and of high quality). The expositions in this issue emphasize the value of prompt, aggressive treatment for early arthritis. It is tempting to reflect on the progress of rheumatology in but a few short years. But we cannot be satisfied until we bring the benefits of our advances to all of our patients. It is our individual and societal responsibility to identify these patients and assure that they have opportunities to receive effective and affordable therapy. Limitations to this are no longer our current art nor our science, but rather our communal resources and will.

Comprehensive medical economic analyses are needed of how to treat RA most effectively and with the least toxicity in the general population. We need to understand the trade-off between the cost and toxicity (and cost of toxicity) of early widespread use of biologics versus the economic benefits of preventing disability. Would it be economically more beneficial to give antimalarials to all patients with a positive anti-CCP antibody rather than very aggressive treatment of clinical RA? Some of these approaches could end up being tested in countries that cannot afford biologics. Do our current clinical measures of disease activity and radiographic anatomy optimally predict disability? Why do we assess structural changes in RA entirely by radiographic measurement of cartilage loss and erosions, some of which are very small, without also considering soft-tissue damage and deformities that are functionally significant? What about the cardiac and pulmonary aspects of rheumatic disease, for which our current so-called disease-modifying antirheumatic drugs, biologic and nonbiologic, may not be working so well?

Even better than remission or cure, of course, would be prevention. At the least we could begin with an organized approach to smoking cessation for individuals who have a family history of RA or who carry the MHC shared epitope.

It should be possible to do much, if not all of this, or certainly do better. We owe it to our patients.