Aetiology and Treatment of Arthritis

Describe osteoarthritis and rheumatoid arthritis, and compare their aetiology and treatment.

Rheumatoid arthritis is a chronic, systemic inflammatory disorder. It can affect many tissues and organs but mainly attacks the joints, producing an inflammatory reaction in the lining surfaces that often progresses to destruction of the articular cartilage and ankylosis. Unlike osteoarthritis, which seems to affect both sexes equally (although men at an earlier age), women appear to be more susceptible to RA at a ratio of 3:1.  There also appears to be some geographical bias in occurrence. RA is seen in 0.5 – 1% of the general population, less so in Africa and Asia and is more prevalent in native American tribes (up to 7%). This is possibly due to a higher presence of susceptibility genes HDA DR1 and HDA DR2 in these populations.

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Rheumatoid arthritis can also produce inflammation in the lungs, pericardium, pleura, and sclera, and also nodular lesions, most common in subcutaneous tissue under the skin. One of the key features of the disease is persistent symmetric polyarthritis that affects the hands and feet, although any joint lined by a synovial membrane may be involved. RA tends to exhibit periods of exacerbation (flare) and remission.

Although the cause of rheumatoid arthritis is unknown, autoimmunity is thought to play a pivotal role in its chronicity and progression although an external trigger – e.g. cigarette smoking, infections, trauma, may instigate. A study (Childers, N.F et al,1993) into the role of nightshades (Solanaceae) found a build-up of cholinesterase inhibiting glycoalkaloids and steroids from consumption of the nightshades.

The disease progresses when activated t-cells stimulate b-cells to produce antibodies including RF (against human IgG) and anti-CPP (against cyclic citrullinated peptides) and macrophages to produce pro-inflammatory cytokines. When immune cells no longer see antigens as self-antigens, they get picked up by antigen-presenting cells and carried to the lymph nodes. The antigen-presenting cells then activate CD4 helper cells. T-helper cells stimulate B cells to start proliferating and differentiating into plasma cells to produce specific auto-antibodies against the self-antigens. This results in enzymatic degradation of the collagen and aggrecan resulting in cartilage loss.

Davidson (2018. Pg 1022) outlines a process whereby in normal conditions, chondrocytes are differentiated, but start dividing to produce “nests of metabolically active cells” with simultaneous and accelerated degradation of the cartilage matrix leading to cartilage vulnerable to injury. Fibrillation of the cartilage also occurs, the resultant deep fissures in turn leading to the development of deep clefts, attracting also calcium pyrophosphate and calcium phosphate deposits.

In addition to articular deterioration, systemic involvement may lead to weight loss, low grade fever, and malaise. Additional early onset indications may also include morning joint stiffness lasting more than an hour, swelling on 3 or more joints, an abnormal serum RF, which must be present more than 6 weeks. The severity of RA may fluctuate over time, but chronic RA most commonly results in the progressive development of various degrees of joint destruction, deformity, and a significant decline in functional status. Symptoms include Boutonniere, a deformed position of the fingers or toes, in which the joint nearest the knuckle (the proximal interphalangeal joint) is permanently bent toward the palm whilst the furthest joint (DIP) is bent back away, ulnar deviation of the proximal and metacarpophalangeal joints and ‘Swan neck’ deformity of fingers (hypertension of PIP joints with flexion of DIP joint). Whereas in OA, early signs of disease typically include pain and swelling in the distal and proximal joints.

Although rheumatoid arthritis (RA) can occur at any age, it increases with advancing age. The peak initial onset of RA occurs in individuals aged 40 - 60 years. Due to the higher incidence of this (and other auto-immune conditions) arising in higher levels in women who are post-menopausal, there could be a possible link between lower estrogen levels and the commencement or acceleration of this disease. A 2016 study (Sapir-Koren R et al), found that there was room for more research into this hypothesis.

By comparison, osteoarthritis is a non-inflammatory degenerative joint disease mostly affecting cartilage.  Osteoarthritis (OA) refers to a clinical syndrome of a-symmetrical joint pain accompanied by varying degrees of functional limitation and reduced quality of life. Of the two, osteoarthritis is far more prevalent and risk increases with age, rising especially over age 40 but more often seen in those over 60.

Unlike rheumatoid arthritis, it affects only joint function and does not affect skin tissue, the lungs, the eyes, or the blood vessels. Degeneration of articular cartilage is the key feature of OA. In osteoarthritis, the surface layer of cartilage breaks down and wears away. This allows bones under the cartilage to rub together, causing pain, swelling, and loss of motion of the joint. Over time, the joint may lose its normal shape. Also, small deposits of bone – called osteophytes or bone spurs – may grow on the edges of the joint. Bits of bone or cartilage can break off and float inside the joint space.

Other risk factors include ‘wear and tear’ on the joints via obesity and inactivity, joint injury or long-term overuse of and malformed joints, such as a dysplasia of the hip, playing a role. This is due to non-parallel load distribution across the joint. Davidson (2018) also cites biomechanical factors such as occupation. This is borne out by a study (Kontio T, et.al 2019) suggesting a correlative relationship between heavy manual work and the incidence of OA of the knee.  Interestingly, with obesity, theoretically also cytokines in adipose tissue also play a role. One study (da Silva MR, 2017), found there to be upregulation of neuroimmune markers present in OA with deregulated balance between pro and anti-inflammatory cytokines, but no clear systematic pattern was exhibited amongst participants again necessitating further study.

There appears to be a higher rate of occurrence in people having close relatives with OA, suggesting a level of genetic predisposition.  According to Davidson (2018, pg 1007), “..Genetic factors are recognised as playing a key role in the pathogenesis of OA” and can be caused by gene mutations in the genes responsible for the cartilage matrix.

It has been found that patients with OA are, in part, protected from osteoporosis as bone density increases at the sites distant from the affected joint. Again, this was found to be the case in a study (Shen Y et al, 2013) looking at postmenopausal women with OA. This found supportive evidence that there might be an inverse relationship between OP and OA.

RA sufferers can exhibit a whole range of symptoms from Scleritus scleromalaca to Sjorgens syndrome (dry eyes, mouth), lymphadenopathy, pericarditis, bursitis nodules, tendon sheath swelling, tenosynovitis, amyloidosis, leg ulcers, ankle oedema and many others This would make a diagnosis difficult on symptom presentation alone (due to many of these being present in other autoimmune conditions). Blood tests are used to determine levels of Rheumatoid Factor (RF), a group of proteins created when the body attacks healthy tissue. The difficulty with this is that positive results are also seen in 5% of normal individuals with no presenting symptoms. Tests can also be carried out to see the Erythrocyte Sedimentation Rate (ESR) and levels of C-reactive Protein to determine levels of inflammation present. Anti-CCP is thought to be present in anywhere between 60% and 80% of rheumatoid arthritis patients. Often the anti-CCP antibody will be found in patients’ blood anywhere from 5 to 10 years before they ever exhibit symptoms of rheumatoid arthritis. Diagnosis is complicated by the fact that in some cases, patients can still be diagnosed with rheumatoid arthritis even if they don’t test positive for the various types of antibodies found in rheumatoid arthritis blood tests.

Whilst it is thought that RA tends to exhibit periods of exacerbation (flare) and remission and that OA is persistently degenerative, one study (Prince et al, 2012), found that sustained rheumatoid arthritis remission is uncommon in clinical practice and findings concluded that a minority of patients experience sustained remission.

In the case of OA, diagnosis can be via blood tests for ESR, CRP rates but also a FBC. X-rays may also pick up subchondrial sclerosis, osteophytes, any narrowing of the joint space and the presence of subchondrial cysts.

So, in this way, it seems that the continued progression of the disease in both instances has a similar presentation. Ostensibly once you have it, in the allopathic viewpoint, it’s a case of managing the symptoms as and when they arise.

For OA, this may involve health and behaviour modifications. For example, physical therapy, exercise and weight loss. Drug therapy deployed include paracetamol and NSAIDS, such as ibuprofen and, in advanced cases, steroidal intra-articular injections.

Surgery can also be an option. Arthroscopy is a day surgery, performed via keyhole. It involves cleansing and removing debris from the joint and smoothing out rough or irregular joint surfaces along with the limited removal of inflamed tissues in larger joints. In more severe cases, arthroplasty or total joint replacement is possible.

Orthodox treatment for RA, on the other hand, tends to be more aggressive from the outset. As well as rest and dietary changes, smoking cessation and exercise, pain relief is often given. These include Non-steroidal anti-inflammatories and steroids. Prolonged use of NSAIDS have many side effects ranging from gastrointestinal to visual disturbances, headaches, insomnia, confusion and tinnitus (Hoffman, 2012) and genitourinary issues. DMARDS are used extensively. These can include early use of, Methotrxate. All have side effects ranging from ulcers, alopecia, GI upset, hepatotoxicity to rashes.

Hoffman (2012) cites changes in diet as being useful, underlining one theory that a cause of rheumatism is the accumulation of toxins and waste products in the affected tissue. Chrondroitin sulphate and glucosamine sulphate have also been shown to have a marginal effect in pain and other symptom relief.  A recent study (Honvo, G et al, June , 2019) found pharmaceutical-grade Chondroitin sulfate as effective as celecoxib and superior to placebo in symptomatic knee osteoarthritis.

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