The first thing to say about arthrofibrosis is that everybody with it is different, and if you have rheumatoid arthritis (RA) (or other chronic inflammatory condition) your RA will have a powerful influence on your situation. Therefore, you can't be treated the same as other people with arthrofibrosis.
I will explain, but it's complicated. Arthrofibrosis is a dysregulated (disordered) healing response, which kicks in after surgery or injury. In a healthy situation the healing response stops once healing is complete, but in fibrosis the cells that make the scar tissue and inflammation (called myofibroblasts) don't die as they would normally do. These myofibroblasts are activated by a signalling molecule that the body makes, called TGF-β, and there is a positive feedback effect, because myofibroblasts themselves also make TGF-β, so these two factors "feed" each other.
In fact, TGF-β is well known to be the "bogey man" of fibrosis, wherever fibrosis occurs in the body (fibrosis can affect any soft tissue)1. And TGF-β is also known to be an important player in RA2 so it is not unexpected for arthrofibrosis to develop after surgery if you have RA. RA is a known risk factor for arthrofibrosis3. Unfortunately, because it is so important to normal functioning, it is not easy to safely reduce the amount of TGF-β.
The outcome of all this is that, in my opinion, it is unwise for a person who has rheumatoid arthritis with post-surgery arthrofibrosis to have further surgery or manipulation under anaesthesia (MUA), because it will drive an even stronger healing response that could make the situation even worse. It is even a gamble for otherwise healthy people with arthrofibrosis to have more injurious procedures4.
Pharmaceutical preparations called TNF-α antibodies are well-known treatments for RA, and the science suggests that such treatment should also benefit arthrofibrosis, since TNF-α and TGF-β also have positive feedback loops and reducing TNF-α will reduce TGF-β. The downsides of TNF-α antibodies are an increased risk of infection, and a small increased risk of cancer, plus patients need to have blood tests every 6 months or so to check everything out.
There aren't usually any other side-effects, since it is not a drug in the usual sense. There are a number of varieties of TNF-α antibodies, including Humira and Simponi. Simponi is only injected once a month, Humira is injected once a fortnight - they are only skin injections and patients do it themselves at home with an auto-pen.
Another medication that may help recovery is Metformin. This is a very safe medication whose mechanism of action is not properly understood. It reduces the risk of cardiovascular events and reduces TGF-β. In contrast, long-term (more than a week) use of non-steroidal anti-inflammatories (NSAIDS) is not recommended because they can prevent the resolution of inflammation4.
Otherwise, the advice is familiar, "keep icing and elevating as much as possible if the knee is feeling hot". Also, it is really important that patients avoid pushing through the pain during exercise. Pushing through the pain will increase any inflammation, including the levels of TGF-β, and this is very unwise especially in the early phase of arthrofibrosis. A stationary bike is often helpful on the "no resistance" setting, but again, if it makes the knee more painful, cut back or stop. One needs to re-calibrate what is possible. Swimming can also help but one needs to keep the legs straight when kicking. Hiring a Continuous Passive Motion machine (CPM) with a computer controller should increase ROM, but patients will need to use it a lot in the early phase, at least once a day, perhaps even twice. Be careful not to damage the knee by pushing the bending or straightening too hard, you don’t want to tear anything. The important thing is to reduce inflammation as much as possible. If medications and the medical situation allow it, a patient can take low dose aspirin (80 to 100 mg/day) plus high dose omega 3 fatty acids (fish oil). These will help the body to produce resolvins, the molecules that are the “stop signal” for inflammation.
1 Vallee, A. & Lecarpentier, Y. TGF-beta in fibrosis by acting as a conductor for contractile properties of myofibroblasts. Cell Biosci 9, 98, doi:10.1186/s13578-019-0362-3 (2019).
2 Pohlers, D. et al. TGF-beta and fibrosis in different organs - molecular pathway imprints. Biochim Biophys Acta 1792, 746-756, doi:10.1016/j.bbadis.2009.06.004 (2009).
4 Usher, K. M. et al. Pathological mechanisms and therapeutic outlooks for arthrofibrosis. Bone Research 7, doi:10.1038/s41413-019-0047-x (2019). (FULL ARTICLE)