Anyhow, in order to research in this aspect of RA, perhaps the following recent full text review article could help you check the various factors implicated in the disease pathogenesis. You may then consider researching on a point of interest or easy to study one:
One year in review 2018: pathogenesis of rheumatoid arthritis. Calabresi E, Petrelli F, Bonifacio AF, Puxeddu I, Alunno A. Clin Exp Rheumatol. 2018 Mar-Apr;36(2):175-184
Im not sure what you mean by referring to RA as Amavata! In Ayurvedic Medicine, Amavata is a disease in which vitiation of Vata Dosha and accumulation of Ama take place in joints (similar to rheumatoid arthritis in modern practice). Good Luck
The etiology of Rheumatoid Arthritis is multifactorial, wide-ranging and not fully or definitely characterised, like most autoimmune diseases. However several contributory factors have been elucidated, and these include genetics, hormones and infection.
Genetics
- HLA DRB1
- STAT4
- TRAF1
- C5
- PTPN22
- familial clustering occurs
The endocrine component
- deficiency of dehydro-epi-androsterone
- deficiency of cortisol
- female sex hormones (70% of patients are women)
- Nulliparity
- Lack of Breastfeeding
Infection
- usually low virulence organisms, which are difficult to culture and capable of causing destruction of periarticular tissue
- May be due to molecular mimicry, bystander effect or adjuvant priming effect
First, I agree with prior answers. Second, consider that there is probably not a single cause for initiation, development, and progression of rheumatoid arthritis in all patients; instead there may be multiple triggers and one or more may be the initiating factor in a given patient. There are also predisposing factors which can increase the chances that a specific person, when faced with a potential RA trigger, does not resolve the incident and instead develops RA symptoms. Some predisposing factors include various genetic variants (eg. the HLA DRB1 shared epitope), skewing towards female dominant hormonal balance, inflammatory milieu, and relatively recent emotional trauma that causes stress.
A 2012 Medical Hypothesis article (1) cited many articles describing different types of potential causes for rheumatoid arthritis, including different infections, joint trauma, sensitivities to foods, and environmental factors (including smoking). One common theme in many of these studies was the short lag time (3 to 6 months) between the potential precipitating event, onset of symptoms, and RA diagnosis. Another theme suggested that different subpopulations of RA patients may have distinct or overlapping precipitating events. Subsequently, several articles have brought up the possibility that lung abnormalities may precede the development of RA in some patients (2,3).
Anecdotally, several colleagues with recent diagnosis of RF seronegative but ACPA+ RA have mentioned extensive ongoing dental problems for 1 to 2 years. It may be useful to consider that long-term dental and gum infections may trigger anti- ACPA antibodies at least in some patients. Early RA patients have a higher rate of periodontal disease (4), and it may be worthwhile to consider peridontal disease as a potential trigger in some patients (5) and not just a consequence of the disease.
As part of your efforts to identify etiologic factors, you may want to consider asking patients about events prior to the onset of symptoms, especially within 3 months or 6 months of the onset of RA symptoms and subsequent diagnosis.
Good luck!
Kathy
Selected references
1. Molnar-Kimber KL, Kimber CT. Each type of cause that initiates rheumatoid arthritis or RA flares differentially affects the response to therapy. Med Hypotheses. 2012;78(1):123-129.
2. Chatzidionisyou A, Catrina AI. The lung in rheumatoid arthritis, cause or consequence? Curr Opin Rheumatol. 2016;28(1):76-82.
3. Demoruelle MK, Solomon JJ, Fischer A, Deane KD. The lung may play a role in the pathogenesis of rheumatoid arthritis. Int J Clin Rheumtol. 2014;9(3):295-309.
4. Wolff B, Berger T, Frese C, et al. Oral status in patients with early rheumatoid arthritis: a prospective, case-control study. Rheumatology (Oxford). 2014;53(3):526-531.
5. Totaro M, Cattani P, Ria F, et al. Porphyromonas gingivalis and the pathogenesis of rheumatoid arthritis: analysis of various compartments including the synovial tissue. Arthrit Res Ther. 2013;15(3):R66.