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72 m a s s a g e & b o d y wo r k m ay/ j u n e 2 0 2 3 Some people with arthrofibrosis get stuck in this state of active inf lammation, pain, and loss of function, and that is their lifelong experience. But others may move on to the second residual arthrofibrosis stage: inf lammation subsides, scar tissue constricts, and the person is left with persistent stiffness and loss of function. Pain may no longer be a constant problem. However, if this person then pushes the affected joint past a comfortable range of motion and initiates a new inf lammatory process—especially within the first year of recovery when the fibroblasts may still be easy to reactivate—they may reenter that acute stage of pain and scar tissue formation. TREATMENT CONTROVERSIES Because arthrofibrosis is not well understood, we have few strategies to prevent or even lower the risk of its development. Over the past decades, orthopedic surgical and post-surgical protocols have evolved to try to improve long-term outcomes, but we have not seen significant changes in the frequency with which arthrofibrosis develops as a complication. Orthopedists and others may assume that some patients develop arthrofibrosis because they are not compliant with their physical therapy or other postsurgical treatment, but this is probably not the case. Instead, arthrofibrosis is a situation that involves dysregulated inf lammatory and healing responses. The "old school" approach to arthrofibrosis involves aggressive physical therapy, sometimes followed by forceful joint manipulation or manipulation under anesthesia to try to break up internal joint adhesions. Alternatively, surgery to destroy or remove scar tissue may be recommended. In the short term these interventions have been seen to with diabetes are five times more likely to develop frozen shoulder compared to the rest of the population. 4 Most of the literature about arthrofibrosis discusses it in the context of the knee, especially as a surgical complication of ACL repair or total knee replacement. But it has been documented at the elbow, wrist, hip, and ankle. It is often associated with a joint injury or surgery, but it can occur with neurological deficits, and it is an especially common complication of hemophiliac arthropathy: a person with hemophilia may bleed into a joint space, and this is a powerful impetus for the cellular activities that cause arthrofibrosis. Some experts discuss frozen shoulder or adhesive capsulitis as a form of arthrofibrosis. Certainly the cellular processes are the same or similar, but frozen shoulder has some different patterns: it tends to occur in middle- aged women (where arthrofibrosis is more common in younger people); it often has a spontaneous onset (where arthrofibrosis is usually linked to injury or surgery); and while the prognosis for arthrofibrosis is often poor in many cases, most cases of frozen shoulder are expected to have a nearly full recovery, regardless of what kind of intervention is used—at least, that's been the traditional expectation. This belief has recently come under scrutiny, however, and it may be unrealistically optimistic: Many people with frozen shoulder live with long-term pain, stiffness, and loss of range of motion. SIGNS AND SYMPTOMS The symptom patterns we see with arthrofibrosis suggest that this condition appears in two main forms or stages: active and residual. A typical presentation involves a trigger, followed by pain, inf lammation, new scar tissue production, and a decreased range of motion that worsens over a period of time. This active, inf lammatory period may persist for an undetermined amount of time, and it may lead to peripheral and central sensitization: changes in neural processing of nociceptive signals. In fact, this presentation of arthrofibrosis may often be misdiagnosed as complex regional pain syndrome, a pain-processing disorder that usually begins with an injury to an extremity.