There are a range of rheumatoid inflammations of the joints. Key provocations to focus on in relieving these are infections, diet and especially gut wall and microbiome health.
Autoimmunity and the joints
Among the several different forms of joint inflammation or arthritis, two common forms are osteoarthritis (linked to ‘wear and tear- though with some immunological components) and gout (caused by the deposition of uric acid crystals). There are three forms classically identified as of autoimmune origin: rheumatoid arthritis, ankylosing spondylitis and psoriatic arthritis. In each of the three the joints (as well as other connective tissues) are targeted by the body’s immune defences. Thus they share common features and with other autoimmune diseases so do read the first article in this series to understand the core principles.
Rheumatoid arthritis (RA) was first formally described in 1800, though this picked up on an older concept of ‘rheumatism’, from the ancient Greek-derived word rheum, which was seen as the abnormal flow of toxic ‘humours’ or body fluids. Still recognised as a discharge from the eyes, rheum was earlier seen to move to, and inflame, muscles and joints.
RA itself has widely been thought of as absent in Europe in earlier times, found only after the colonisation of the Americas (where most archaelogical evidence of deformities has been found). A modern assessment is that it probably was always present globally but its incidence increased only with longer life spans, perhaps with the importation of tobacco – and smoking – from the Americas, and with pollution in the Industrial Revolution (smoke and pollution are known precipitating factors in susceptible individuals). It is also likely that there are infective factors that may have become more prominent in the last two centuries. In relation to the schema outlined in the first article of this autoimmune series, RA has shown increasingly strong links to infections (and see below).
In another interesting insight, the ancient link between the airways, where ‘rheum’ comes from, and the joints shows that connections between this condition and at least some infections were well established. New scan technologies now demonstrate that autoimmune-related injuries in the small airways can anticipate RA by years. These can result in the accumulation of cell debris and progressive fibrosis. Prractitioner have long known to check out lung health in treating RA.
Epstein Barr virus (EBV) has long been suspected in the pathogenesis of RA and other implicated viruses include specific parvoviruses and retroviruses. The list of associated bacterial infections include Prevotella copri (normally a prominent member of the healthy gut and mouth microbiomes) and Porphyromonas gingivalis associated with gum problems.
In RA patients the prevalence of periodontal disease is significantly higher than expected, and increases with age and disease duration. In a controlled clinical trial of patients with RA and periodontitis, non-surgical periodontal treatment was effective on improving the gum symptoms, improving the RA symptoms and reducing the presence of pathogens, especially Porphyromonas gingivalis. It may be that this organism converts mouth proteins into those that stimulate T and B cells to recognize the same antigens in joints: a form of molecular mimicry.
So another thesis is that its appearance in Europe after Ameerican colonisation is that also coincided with the sugar trade – and the rise of gum disease!
A quick conclusion: brush your teeth – very well – and especially after eating sugar!
A growing body of evidence supports an even more radical hypothesis than mimicry: RA may be a form of reactive arthritis induced by translocation of microbes directly to joints. Traces of Prevotella copri have indeed been found in the joints of RA sufferers – and not those with osteoarthritis.
Once again the focus shifts to the gut and the integrity of the gut wall. There is evidence that antibodies produced on the gut surface (IgAs) to engage with threatening antigens out in the gut, unusually move through into the deeper tissues in RA sufferers.
RA patients also show significant differences in the composition of gut microbiome. Some of the relevant organisms are able to affect gut wall integrity and are implicated in raising inflammation as a result. It is even likely that the relief afforded by standard anti-rheumatic drugs like methotrxate and hydrocloroquine may in part be linked by their beneficial effects on the gut microbiome. There are encouraging prospects that dietary changes might reduce the development of RA. Probiotics and increased plant foods have been shown to reduce RA factors and by contrast the increasing levels of RA in the population have been well tied to the ‘westernisation’ (ie high fats sugars and processed foods) of the popular diet. For a comprehensive review of these prospects the paper below is worth reading.
There was also a traditional link between SpAs and dysentery. People with AS have been shown to more likely have bacterial infection of the lower small intestinal wall, damaged intestinal gut wall integrity and mucosal barrier.
People with SpAs have shown increased levels of Ruminococcus gnavus in their gut microbiome, consistent with the known proinflammatory role of this bacteria and its association with inflammatory bowel disease. In AS sufferers there is a high prevalence of inflammatory bowel disease with subclinical previous gut infections. There is also a reduction in levels of bacteria (like Firmicutes) that produce metabolites (SCFAs) protecting the gut wall.
For a much deeper dive into factors that influence rheumatoid conditions you could try the following review papers
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