Reviewing inflammatory markers in joint pain and arthropathies

In this video, from our Inflammatory Marker Essentials course, we'll review inflammatory markers in joint pain and inflammatory arthropathies, including connective tissue disorders, RA, seronegative arthropathies, gout / pseudogout, and septic arthritis.

Pete Yunyongying, MD FACP
Pete Yunyongying, MD FACP
9th Nov 2021 • 3m read

In this video, from our Inflammatory Marker Essentials course, we'll review inflammatory markers in joint pain and inflammatory arthropathies, including connective tissue disorders, RA, seronegative arthropathies, gout / pseudogout, and septic arthritis.

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Clinicians encounter inflammation daily and there are lots of inflammatory markers to consider. Which should you order for your patient? Here, you’ll learn the strengths and limitations of each marker, when they’re useful, and when they’re not. We’ll look at laboratory markers of inflammation as well as radiologic and clinical signs so you can take your diagnostic skills to the next level.

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Video transcript

Joint pain is one of the most common presenting symptoms in all clinical settings, from the general practice office, to the emergency department and inpatient or ICU setting. First, let's review basic anatomy of a joint using the knee as an archetype. The joint itself is composed of two or more bones coming together. The joint surface itself is rarely bone on bone, but lined with cartilage. The joint space is lubricated with synovial fluid, all of which is encased in a joint capsule of soft tissue.

Tendons and ligaments add structural stability to the joint and insert onto bone in areas called the endthesis. Bursa serves as pulleys and add shock absorption to the mechanical stresses and lie between these structures. When considering patients presenting with joint pains, consider two categories of diseases. First is inflammatory arthritis and the other is non inflammatory arthralgias. In inflammatory arthritis, we have out of control inflammation that leads to destruction of the bone.

Traditional examples of this include rheumatoid arthritis, and lupus, other common considerations are psoriatic arthritis, associated inflammatory bowel diseases and post infectious arthritis. Non inflammatory arthritis has been traditionally described as wear and tear or mechanical damage to a joint. The prototypical example of this is osteoarthritis. The main distinction between the two diagnostic categories has been whether there are inflammatory markers suggesting systemic inflammation.

The presumption has been that without markers of systemic inflammation, we have non inflammatory arthralgias. That distinction is used to determine the management of the two syndromes, one with systemic anti- inflammatories and the other with correction of the biomechanical issues leading to disease. With new research however, we are finding that this distinction is an oversimplification of pathophysiology. It appears that osteoarthritis is the final common pathway for biomechanical damage to a joint. This may be due to accumulation of physical trauma to an otherwise normal joint, or biomechanical malalignment of the joint leading to chronic micro trauma.

The damage however, is likely due not just to mechanical stress, but mediated by localized inflammation. Some would say it's just semantics, that it really doesn't matter if non inflammatory arthritis is mediated by some inflammation and there is some truth here. The two categories still have great clinical value. Inflammatory arthropathies tend to have much more profound systemic inflammation, whereas non inflammatory arthropathies tend to have much more localized inflammation. But the two categories do have overlap, with some arguing that the two categories are probably best thought of as extremes of a spectrum rather than two distinct categories.

This is highlighted most notably by ankylosing spondylitis, and valeted spondyloarthropathy. These these are immune mediated systemic disorders that lead to enthesitis or inflammation of the soft tissue that connects ligaments and tendons to bone. Clinically, they have fewer signs of systemic inflammation like in rheumatoid arthritis. However, unlike osteoarthritis, the inflammation does not appear to be incited by mechanical trauma, but by an autoimmune process. In brief, inflammation related to joint pain is a rapidly evolving field of research, with many questions still left to be answered.

One thing is becoming clear though, the natural history and development of inflammatory arthropathies show there is a progression from controlled inflammation to out of control inflammation, rather than a simple on off switch. Clinically, this means that joint pain that presents with few markers of systemic inflammation resembling non inflammatory arthritides may evolve into a condition that more closely resembles inflammatory arthritides, like rheumatoid arthritis many years later. More research is needed to better understand whether one category truly progresses to the other category, but that is beyond the scope of this discussion. The use of inflammatory markers to follow progression or success of treatment is also a major management strategy. With the revelation that inflammation is what drives the biomechanical damage of non inflammatory arthropathy, it remains to be seen if there are specific inflammatory markers that are useful in managing osteoarthritis and its related disorders.