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L i s te n to T h e A B M P Po d c a s t a t a b m p.co m /p o d c a s t s o r w h e reve r yo u a cce s s yo u r favo r i te p o d c a s t s 71 intervention; other resources include people with joint restrictions, but who don't necessarily pursue surgery, as persons with arthrofibrosis. For this reason, estimates of how common it is range from accounting for 0.2 percent of post-surgical knee problems to 73 percent of post-ankle-fracture problems. PATHOPHYSIOLOGY To talk about the processes involved in arthrofibrosis, we need to look at what might be the body's most interesting cell, the myofibroblast. If you went to massage school in my era (the early '80s), you might have learned that connective tissue is composed mainly of protein fibers suspended within a f luid or solid medium. Those fibers (varieties of collagen, elastin, and others) can be organized or disorganized, and they can be dense or loosely arranged. These variables give connective tissues their properties of strength, stretchiness, resistance, and different levels of stiffness and hardness. And embedded within this extracellular matrix we find the fibroblasts: literally, "fiber builders," cells whose job is to produce new protein fibers and maintain the health of the connective tissue structure. Since that time, our understanding of the construction, maintenance, and repair processes of connective tissue has evolved. Now we know that under certain circumstances (namely, mechanical distortion and/or exposure to pro- inf lammatory chemicals), fibroblasts become more complex. Fibroblasts migrate to areas of injury, and they may change. From being smooth and spindle-shaped, they become broad and f lat, and they develop numerous outreaching branches. Perhaps most importantly, they develop internal actin fibers that make them behave like smooth muscle cells: myofibroblasts are contractile. They play a vital role in wound healing, as they pull on damaged structures and produce ECM to help "glue" and pull injured surfaces together. In short, they make scar tissue (Image 1). Under normal conditions, fibroblasts migrate to an injured area, transform into myofibroblasts, proliferate as needed, and help knit the damaged tissue. Then their work is done, and they die. But in arthrofibrosis, they don't; they just keep churning out ECM. Healthy myofibroblastic activity is important, but it can become pathologic when those cells don't know when to stop and joint function is diminished instead of restored: "On a cellular level arthrofibrosis is characterized by upregulated myofibroblast proliferation with reduced apoptosis, adhesions, aggressive synthesis of ECM that can fill and contract joint pouches and tissues and often also heterotrophic ossification. Although ECM is necessary for healing and wound repair, dysregulation of production and degradation leads to pathologic fibrosis." 3 1 Normally, myofibroblasts disappear after they have done their work of making scar tissue and healing the wound. However, if there is an ongoing inflammatory stimulus then myofibroblasts can create a feedback effect and keep themselves activated. They can then become immortal, much like cancer cells do, and continue to create scar tissue, TGF-ß, and inflammatory cytokines. Courtesy of International Arthrofibrosis Association. Fibroblasts TGF-ß and inflammatory cytokines from insult + Scar tissue (collagen) Contraction, adhesions Myofibroblasts Arthrofibrosis can damage internal joint structures, but external structures like bursae or fat pads may also become infiltrated with myofibroblasts and scar tissue. These may be continually irritated with movement, leading to more inf lammation, and more ECM. In addition, excessive ECM may interfere with local blood f low, leading to hypoxia, which triggers the secretion of inf lammatory cytokines. Ironically, that is the factor that keeps those myofibroblasts busy, and so a vicious circle is born: more ECM, less blood f low, more inf lammation, and more ECM, ad infinitum. It appears that some people have a genetic predisposition for this dysfunctional overactivity of myofibroblasts and scar tissue formation. Some studies have begun to find connections and overlap in people who have frozen shoulder, Dupuytren's contracture, idiopathic pulmonary fibrosis, and other fibrotic problems. It may be that this population is also prone to developing this common complication of joint injuries or surgeries. In addition, research points to connections between inf lammation-based diseases like osteoarthritis, type 2 diabetes, and others to a risk for fibrotic conditions. We see this in the finding that people