Is It Possible to Defeat Arthritis?



What is Arthritis?
Arthritis manifests through the structural damage of the joints under the impact of their chronic inflammation (Senthelal, Li, Goyal, Bansal, & Thomas, 2020). Pain is the predominant symptom of arthritis. Arthritis is not synonymous with arthralgia in scenarios where pain does not necessarily originate under the impact of joint(s) inflammation. The articular pathology predominantly leads to the development of arthritic pain in the affected patients. The pain patterns potentially deteriorate the health-related quality of life of arthritic patients.             
What is the Mechanism of Arthritic Pain Development? 
Arthritis-related pain develops through the induction of the following mechanisms (Kidd, Langford, & Wodehouse, 2007). 
1.     The articular pain receptor sensitization occurs under the influence of mediators belonging to tissues, bone, and synovium. 
2.     The pain receptor stimulation occurs abruptly under the impact of mechanical stimuli, including standing and walking activities that eventually lead to the localization of arthritic pain. 
3.     The topical and systemic therapies attempt to control the production of inflammatory mediators in arthritis patients. 
4.     The pain patterns of the arthritis patients emanate under the impact of non-noxious stimuli and environmental (toxic) factors that potentially interact with the genes of the arthritis patients, thereby leading to the development of peripheral and central sensitizations. 
5.     The limited threshold of the peripheral sensitizations triggers localized pain and tenderness in arthritis patients. 
6.     The central sensitizations induce diffusely modified pain perceptions while triggering tenderness and regional or referred pain. 
7.     The patients affected with rheumatoid arthritis and osteoarthritis experience neural sensitizations that potentially trigger their localized pain patterns. 
8.     Rheumatoid arthritis triggers spinal neurons following topical capsaicin application that expands the anatomical regions of punctate hyperalgesia. 
9.     The spinal neuronal excitations in rheumatoid arthritis patients elevate the level of their joint tenderness and pain perceptions. 
10.  The somatic structures along with their inputs and descending inhibitory controls trigger the spinal nociceptive processing in the arthritis patients. 
11.  The genetic attributes and pain episodes of the arthritis patients deteriorate their daily activities as well as health-related quality of life. 
12.  The arthritis patients encounter the impact of numerous inflammatory and pain mediators that warrant the administration of multiple therapeutic interventions. 
13.  The therapies including NSAIDs (non-steroidal anti-inflammatory drugs), TENS (transcutaneous electrical nerve stimulation), and acupuncture interventions assist in mitigating the inflammatory/pain mediators in the arthritis patients. 
14.  The arthritis patients’ social and psychological factors play a pivotal role while exaggerating or reducing the intensity and/or severity of their pain patterns. 
15.  The environmental factors impact cortical or supraspinal levels in a manner to alter nociceptive processing in arthritis patients that eventually disrupts their behavior and pain perceptions to many folds.      
16.  The arthritis patients affected with central sensitization rarely acquire relief from the administration of spinally/peripherally active therapies. 
17.  The arthritis patients’ cortical tissues and their opioid/prostanoid receptors prove to be the therapeutic targets for their pain management. 
18.  The non-pharmacological interventions including cognitive behavior therapy and education assist the arthritis patients to increase their overall pain perception control levels. 
What Causes Arthritis?
Arthritis and its types develop under the influence of the following factors (IQWiG, 2020) (Poudel & Lappin, 2020) (Akhondi & Gupta, 2020). 
1.     Autoimmune diseases potentially elevate the risk of arthritis. 
2.     The disruption of healthy cells by the body’s defense mechanism due to autoimmune complications triggers inflammatory responses that lead to the development of arthritis and its clinical complications. 
3.     Genetic predisposition also determines the risk of arthritis complications. 
4.     Bacterial and viral infections elevate the predisposition of individuals towards arthritis.  
5.     Smoking for extended-term triggers the onset of rheumatoid arthritis in high-risk people. 
6.     The most commonly impacted joints in rheumatoid arthritis include toe joints, ankle joints, knee joints, hip joints, finger joints, wrist joints, elbow joints, and shoulder joints. 
7.     Metabolic complications, including hypercalcemia, pseudogout, serum uric acid elevation, and gout increase the risk of arthritis. 
8.     Traumatic conditions or injuries increase the risk of osteoarthritis, particularly among elderly people.  
9.     Inflammatory arthritis progresses through the development of reactive arthritis, immune-related arthritis, crystal-induced arthritis, and infectious arthritis. 
10.  Some of the arthritis causing pathogens include Rubella, Enterovirus, Parvovirus, Coccidiomycosis, Sporotrichosis, Borrelia burgdorferi, Brucellosis, Mycobacterial species, Anaerobic bacteria, Neisseria gonorrheae, Streptococcal pneumoniae, and Staphylococcus aureus. These organisms variably impact populations based on their geographic locations and age patterns. 
11.  Monomicrobial infection leads to the development of septic arthritis. 
12.  The joint space (penetrating) trauma increases the risk of polymicrobial infections and associated arthritis. 
13.  Intravenous drug abuse and/or traumatic conditions lead to the development of gram-negative bacterial infections and septic arthritis. 
14.  Pseudogout and gout due to monosodium urate crystals’ deposition trigger the development of crystal-induced arthritis. 
15.  Gout develops under the impact of hyperuricemia. 
16.  Overconsumption of protein-rich food items, uric acid elevation, and renal uric acid secretion increases the risk of arthritis and its comorbidities. 
17.  Gout also develops under the impact of chronic kidney disease, loop diuretics/thiazide administration, alcoholism, obesity, and the male gender. 
18.  The inflammatory response due to calcium pyrophosphate crystal accumulation increases the risk of pseudo-gout. 
19.  The accumulation of calcium pyrophosphate crystals occurs due to several conditions including hemochromatosis, familial chondrocalcinosis, and joint trauma. 
20.  The conditions including systemic sclerosis, Sjogren syndrome, polymyositis, dermatomyositis, SLE (systemic lupus erythematosus), and rheumatoid arthritis increase the risk of immune-related arthritis. 
21.  The joint infections that cause reactive arthritis assimilate inside the body in a manner that makes the recovery of respective pathogens almost impossible from the affected joints. 
22.  Some of the urogenital and gastrointestinal pathogens causing arthritis include Campylobacter, Shigella, Salmonella, Yersinia, and Chlamydia trachomatis.  
23.  Familial Mediterranean fever increases the risk of infective arthritis. 
24.  The non-articular causative factors of arthritis include somatoform pain disorder, depression, and hypothyroidism. 
What are the Various Types of Arthritis and their Risk Factors? 
Evidence-based clinical literature reveals almost 100 types of arthritic conditions that impacted the health and wellness of more than ninety-one million individuals in 2015 (Akhondi & Gupta, 2020). Some of the arthritic conditions along with their predisposing attributes or risk factors are documented below (Medical News Today, 2020). 
1.     Arthritis emanating from psoriasis and/or colitis
2.     Ankylosing arthritis 
3.     Reactive arthritis 
4.     Rheumatoid arthritis 
5.     Mechanical/degenerative arthritis 
6.     Infectious arthritis 
7.     Osteoarthritis 
8.     Metabolic arthritis 
9.     Septic arthritis 
10.  Childhood or juvenile idiopathic arthritis 
11.  Fibromyalgia 
12.  Psoriatic arthritis 
13.  Gout 
14.  Sjogren’s Syndrome 
15.  Scleroderma 
16.  Systemic Lupus Erythematosus 
What is the Pathophysiology of Arthritis? 
Arthritis and its types develop under the impact of the following pathological processes (Poudel & Lappin, 2020). 
1.     Inflammatory arthritis develops following the accumulation of inflammatory cells across the synovial membrane. 
2.     The synovial accumulation of granulocytes, lymphocytes, and macrophages worsens the arthritis symptoms.  
3.     The synovial fibroblast hyperplasia elevates the level of joint/cartilage deterioration in arthritis patients. 
4.     Synovial infection is a predominant finding in inflammatory arthritis. 
5.     The immune complexes of the viruses like enteroviruses, Parvoviruses, and Rubella infect skin and joints, thereby leading to the development of skin rash, arthralgia, and arthritis. 
6.     The interaction of environmental and genetic factors leads to the development of rheumatoid arthritis. 
7.     MHC (major histocompatibility complex) genes and HLA (human leukocyte antigen) predominantly enhance the risk of rheumatoid arthritis.   
8.     Smoking increases the expression of peptide arginine deiminase inside alveolar macrophages that supports the formation of citrulline from arginine. 
9.     The interaction of the adaptive immune system with neoantigens triggers the inflammatory processes of rheumatoid arthritis. 
10.  The increased activity of anti-citrullinated protein antibodies and protein citrullination elevates the immune reactivity pattern in rheumatoid arthritis patients. 
11.  The inflammatory mechanisms in gout reciprocate with the joint-related accumulation of monosodium crystals. 
12.  The inflammatory cascade in gout is triggered after neutrophil activation that induces the release of lysosomal enzymes and superoxide in the joints of the affected patients. These processes begin under the impact of MSU crystal-immunoglobulin binding.       
How Could You Diagnose Arthritis? 
The assessment of the following conditions is paramount to the clinical diagnosis of arthritis (Poudel & Lappin, 2020). 
1.     Inflammatory arthritis progresses with anemia of chronic disease, thrombocytosis, and CRP/ESR elevation. The assessment of these clinical parameters is, therefore, highly necessary for the assessment of inflammatory arthritis. 
2.     Joint stiffness is another significant finding that substantiates arthritis development. However, the activity-induced reduction in joint stiffness is a predominant finding of inflammatory arthritis. 
3.     Osteoarthritis manifests with the development of stiffness that lasts for less than sixty minutes and gains intensity after physical activity. 
4.     The joint pain assessment should be accompanied by the affirmation of non-articular or articular symptoms. 
5.     Acute arthritis based on pseudo-gout, gout, or infection is accompanied by the pain of fewer than 42 days/six-weeks duration. The extension of symptom duration beyond 6-weeks tenure supports the clinical finding of chronic arthritis. 
6.     The arthritis condition that impacts fewer than 3 joints is classified as oligo-arthritis. 
7.     The arthritis condition that impacts more the 2 joints is categorized as polyarthritis. 
8.     Arthrocentesis is the preferred diagnostic approach to rule out crystal-induced or infectious arthritis. 
9.     Rheumatoid arthritis is associated with erosions that require radiological examination. 
10.  Some of the significant lab investigations for arthritis include crystal search, culture, gram stain, differential count, and hemogram. 
11.  The clinically significant septic arthritis associates with a single swollen painful joint and fever. Therefore, the assessment of body temperature and joints is highly needed to rule out septic arthritis. 
12.  The synovial fluid aspiration for joint infection assessment should precede the administration of antibiotics. 
13.  The synovial fluid requires laboratory assessment based on crystal evaluation, differential leucocytes count assessment, culture, and gram staining. 
14.  An increase in polymorphonuclear lymphocytes above 20,000 mm-cube reveals the development of septic arthritis. 
15.  The elevation of polymorphonuclear lymphocytes above 2000-20,000 mm-cube indicates crystal deposition and autoimmune process activation under the impact of inflammatory arthritis. 
16.  Pseudo-gout is marked by the deposition of rhomboid-shaped crystals.  
17.  Gouty arthritis progresses with the deposition of needle-shaped yellow crystals.
18.  Rheumatoid arthritis affirmation is based on clinical assessments including CRP/ESR elevation, anti-citrullinated protein antibody, and rheumatoid factor elevation. 
19.  Spondyloarthropathy is revealed by one or more of the several complications including inflammatory eye disease, inflammatory bowel disease history, and inflammatory back manifestations. 
20.  The differential diagnoses include psoriatic arthritis, Lyme arthritis, juvenile idiopathic arthritis, osteoarthritis, and ankylosing spondylitis. 
How Could You Treat Arthritis?
EULAR (European League Against Rheumatism) has recommended the following treatment algorithm for rheumatoid arthritis management (Kohler, Gunther, Kaudewitz, & Lorenz, 2019) (Wilsdon & Hill, 2017). 
1.     The treatment phase-I is based on the administration of conventional synthetic DMARDs (Disease-Modifying Anti-Rheumatic Drugs) with methotrexate followed by short-term administration of glucocorticoids (in reduced dosage). 
2.     The patients with methotrexate contraindications should receive sulfasalazine/leflunomide combination. 
3.     6-months of consistent phase-I treatment focuses on improving the RA (rheumatoid arthritis) symptomatology. 
4.     The failure of phase-I therapy necessitates the administration of phase-II intervention. 
5.     The phase-II therapy begins with the administration of Il-6 inhibitor, or abatacept/TNF inhibitor or a combination of sulfasalazine, leflunomide, and methotrexate. 
6.     The phase-II intervention should acquire its therapeutic goals within a tenure of 6-months. 
7.     The phase-III treatment follows the failure of the phase-II intervention. 
8.     The phase-III treatment warrants the administration of biologic DMARD including rituximab, or Il-6 inhibitor, or abatacept, or TNF inhibitor. 
9.     The phase-III therapy also requires a duration of 6-months for achieving the therapeutic targets.
10.  The targeted arthritis management therapy requires the administration of tofacitinib and/or Janus Kinase Inhibitors. 
Osteoarthritis management reciprocates with the following conservative measures (Sen & Hurley, 2020) (Wu, Goh, Wang, & Ma, 2018). 
1.     Physical therapy 
2.     Analgesia 
3.     Arthroplasty 
4.     Reduction of joint overloading/physical activities for pain management 
5.     Exercise to enhance endurance 
6.     Weight loss
7.     Joint unloading through crutch, cane, splint, and brace
8.     Administration of oral/topical NSAIDs and acetaminophen 
9.     Glucocorticoid/intra-articular injections for pain management 
10.  Duloxetine therapy
Is There a Way to Prevent Arthritis?
The reduction in modifiable risk factors is the only viable strategy to reduce the risk of osteoarthritis. Some of these approaches are mentioned below (Deane, 2013). 
1.     Antimicrobial therapy to reduce the risk of autoimmunity development after contracting an infectious disease 
2.     Smoking cessation 
3.     Immunomodulatory therapy   
4.     Enhancement of socioeconomic status 
5.     Protection from occupational dust 
6.     Nutritional/dietary management 
7.     Reduction in alcoholism 
8.     Statin therapy 
9.     Stress management 
10.  Regular exercise 
Is There Any Herbal Remedy for Treating Arthritis?
The below-mentioned polyherbal formulations claim to treat arthritis and its signs/symptoms (Choudhary et al. 2015). 
1.     Majoon Suranjan 
2.     Sudard 
3.     Tongbiling (TBL-II)
4.     Rumalya Forte Tablet 
5.     Rumalya Liniment 
6.     Artha Cure Oil 
7.     Artha Cure Capsule 
8.     Rheumarthro Gold Capsule 
9.     Ortho Joint Oil 
10.  Rheuma Off Gold 
11.  HLXL (Huo Luo Xiao Ling Dan)
12.  GHJTY (Ganghwaljetongyeum) 
The researchers also claim the therapeutic advantages of the following plant species in arthritis management(Choudhary et al. 2015).
1.     Xanthium strumarium Linn. (XS)(Family-Compositae)
2.     Vitex negundo Linn. (VN)(Family-Verbenaceae)
3.     Trigonella foenum-graecum Linn. (TF)(Family-Papilionaceae)
4.     Terminalia chebula Retz. (TC)(Family-Combretaceae)
5.     Sida rhombifolia Linn. (SR)(Family-Malvaceae)
6.     Saussurea lappa Clarke. (SL)(Family-Compositae)
7.     Ruta graveolens Linn. (RG)(Family-Rutaceae)
8.     Punica granatum Linn. (PG)(Family-Lythraceae)
9.     Piper longum Linn. (PL)(Family-Piperaceae)
10.  Phyllanthus amarus Schum and Thomm. (PA)(Family-Euphorbiaceae)
11.  Lantana camara Linn. (LC)(Family-Verbenaceae)
12.  GY (Family-Fabaceae)
13.  Curcuma longa Linn. (CL)(Family-Scitaminaceae)
14.  Coriander sativum Linn. (CS)(Family-Umbelliferae)
15.  Cinnammomum zeylicanium Blume. (CZ)(Family-Lauraceae)
16.  Cannabis sativum Linn. (CT)(Family-Urticaceae)
17.  Caesalpinia sappan Linn. (CP)(Family-Leguminosae)
18.  Boswellia serrate Roxb. (BS)(Family-Burseraceae)
19.  Boerhaavia diffusa Linn. (BD)(Family-Nyctagineae)
20.  Aristolochia bracteolate Lam. (AB)(Family-Aristolochiaceae)
21.  Alstonia scholaris Linn. (AS)(Family-Apocynaceae)

References

Akhondi, H., & Gupta, N. (2020). Polyarticular Arthritis. In StatPearls. Treasure Island (Flordia): StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK537170/
Choudhary, M., Kumar, V., Malhotra , H., & Singh , S. (2015). Medicinal plants with potential anti-arthritic activity. Journal of Intercultural Ethnopharmacology, 4(2), 147-179. doi:10.5455/jice.20150313021918
Deane , K. (2013). Can Rheumatoid Arthritis Be Prevented? Best Practice & Research Clinical Rheumatology, 27(4), 467-485. doi:10.1016/j.berh.2013.09.002
IQWiG. (2020). Rheumatoid arthritis: Overview. In InformedHealth.org. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK384455/
Kidd, B. L., Langford , R. M., & Wodehouse, T. (2007). Arthritis and pain. Current approaches in the treatment of arthritic pain. Arthritis Research and Therapy, 9(3). doi:10.1186/ar2147
Kohler, B. M., Gunther, J., Kaudewitz, D., & Lorenz, H. M. (2019). Current Therapeutic Options in the Treatment of Rheumatoid Arthritis. Journal of Clinical Medicine, 8(7). doi:10.3390/jcm8070938
Medical_News_Today. (2020). What are the causes and types of arthritis? Retrieved from https://www.medicalnewstoday.com/articles/7621
Poudel, P., & Lappin, S. L. (2020). Inflammatory Arthritis. In StatPearls. Treasure Island (Florida): StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK507704/#_article-23507_s2_
Sen, R., & Hurley , J. A. (2020). Osteoarthritis. In StatPearls. Treasure Island (Florida): StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK482326/
Senthelal, S., Li, J., Goyal, A., Bansal , P., & Thomas , M. A. (2020). StatPearls. In Arthritis. Treasure Island (Florida): StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK518992/
Wilsdon, T. D., & Hill, C. L. (2017). Managing the drug treatment of rheumatoid arthritis. Australian Prescriber, 40(2), 51-58. doi:10.18773/austprescr.2017.012
Wu, Y., Goh, E. L., Wang, D., & Ma, S. (2018). Novel treatments for osteoarthritis: An update. Open Access Rheumatology, 10, 135-140. doi:10.2147/OARRR.S176666







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