Treatment focuses on reducing inflammation, managing symptoms, and preventing joint destruction.
a. Disease-modifying antirheumatic Drugs (DMARDs)
Conventional DMARDs (first-line treatment)
Methotrexate (most commonly used)
Leflunomide
Sulfasalazine
Hydroxychloroquine
Targeted Synthetic DMARDs
Janus kinase (JAK) inhibitors: Tofacitinib, Baricitinib, Upadacitinib
b. Biologic DMARDs (Biologics)
TNF Inhibitors:
Etanercept
Infliximab
Adalimumab
Golimumab
Certolizumab
Non-TNF Biologics:
Abatacept (T-cell inhibitor)
Rituximab (B-cell inhibitor)
Tocilizumab, Sarilumab (IL-6 inhibitors)
c. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Ibuprofen
Naproxen
Celecoxib (COX-2 inhibitor)
d. Corticosteroids
Prednisone (used for flare-ups and short-term symptom control)
2. Lifestyle Modifications
a. Exercise & Physical Therapy
Low-impact activities (e.g., swimming, yoga, cycling)
Strength training to support joint stability
Range-of-motion exercises
b. Diet & Nutrition
Anti-inflammatory diet (Mediterranean diet, omega-3 fatty acids from fish, nuts, and seeds)
Avoid processed foods and excess sugar
c. Weight Management
Reducing excess weight can decrease stress on joints and inflammation.
d. Smoking Cessation
Smoking worsens RA and reduces medication effectiveness.
3. Alternative & Supportive Therapies
Acupuncture
Massage therapy
Heat & cold therapy
Mind-body techniques (meditation, Tai Chi)
Supplements (turmeric, vitamin D, omega-3s)
4. Surgery (For Severe Cases)
Synovectomy (removal of inflamed joint lining)
Joint replacement surgery (hip, knee, or hand joint replacement)
Joint fusion (Arthrodesis)
5. Regular Monitoring & Early Treatment
Early diagnosis and aggressive treatment are essential to prevent irreversible joint damage and maintain function.
Treatments for rheumatoid arthritis include both medication and non-pharmacological measures - the goal being to control joint inflammation and prevent joint damage and disability. Non-pharmacological treatment includes physical therapy, splints and braces, occupational therapy and dietary changes but these do not stop the progression of joint destruction. painkillers and anti-inflammatory drugs, including steroids, suppress symptoms, but do not stop the progression either. Disease-modifying antirheumatic drugs (DMARDs) may slow or halt the progress of the disease. Biological DMARDS like anti-TNF agents are effective but usually avoided in persons with active disease or hypersensitivity to these agent. They have been shown to decrease the number of tender or swollen joints and the pain and disability due to the disease but there is little data about side effects. Alternative medicine is not supported by any evidence.
RA affects between 0.5 and 1% of adults in the developed world with between 5 and 50 per 100,000 people newly developing the condition each year. Onset is most frequent during middle age, but people of any age can be affected. The name is based on the term “rheumatic fever”, an illness which includes joint pain and is derived from the Greek word ῥεύμα-rheuma (nom.), ῥεύματος-rheumatos (gen.) (“flow, current”). The suffix -oid (“resembling”) gives the translation as joint inflammation that resembles rheumatic fever. The first recognized description of RA was made in 1800 by Dr. Augustin Jacob Landré-Beauvais (1772–1840) of Paris.
Anethole, a prominent compound derived from fennel (Foeniculum vulgare), possesses a spectrum of therapeutic properties, including anti-arthritic, anti-inflammatory, antioxidant, and tumor-suppressive effects. However, its specific impact on RA remains underexplored. A study sought to uncover the potential therapeutic value of anethole in treating RA by employing an H2O2 -induced inflammation model with HIG-82 synovial cells. The results demonstrated that exposure to H2O2 induced the inflammation and apoptosis in these cells. Remarkably, anethole treatment effectively countered these inflammatory and apoptotic processes triggered by H2 O2 . Moreover, they identified the aquaporin 1 (AQP1) and protein kinase A (PKA) pathway as critical regulators of inflammation and apoptosis. H2O2 stimulation led to an increase in the AQP1 expression and a decrease in p-PKA-C, contributing to cartilage degradation. Conversely, anethole not only downregulated the AQP1 expression but also activated the PKA pathway, effectively suppressing cell inflammation and apoptosis. Furthermore, anethole also inhibited the enzymes responsible for cartilage degradation. In summary, the findings highlight the potential of anethole as a therapeutic agent for mitigating H2O2 -induced inflammation and apoptosis in synovial cells, offering promising prospects for future Rheumatoid Arthritis Treatments 1).
Findings suggest that patients with rheumatoid arthritis with osteopenia or osteoporosis, particularly those with lower body mass index (BMI), should be screened regularly to determine the status of their cervical spines. 2).