Rheumatoid Arthritis
Rheumatoid Arthritis is defined a chronic disorder as a result of
inflammation, affecting mostly the flexible (synovial) joints and
tissues and organs in the body. The disease affects more women than in
men and generally occurs after the ages of 40 and diminishes the quality
of life of many elders.
B.1. Causes
The probable causes of Rheumatoid Arthritis may include the following
1. Abnormal autoimmune response
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized
by chronic synovitis that progresses to destruction of cartilage and
bone. Scientists in the study of Abnormal networks of immune
response-related molecules in bone marrow cells from patients with
rheumatoid arthritis as revealed by DNA microarray analysis, indicated
that abnormal regulatory networks in the immune response and cell cycle
categories were identified in BM mononuclear cells from RA patients,
indicating that the BM is pathologically involved in RA(10).
2. Abnormal lipid profile
In the study to observe the association between inflammation
status/autoimmune antibodies and plasma lipid in patients with
rheumatoid arthritis (RA), found that (1) There were 12.9%, 10.2% and
14.2% patients with elevated TC, LDL-C and TC respectively, patients
with reduced HDL-C accounted for 43.6%. (2) C(3) was higher in elevated
TC group than normal TC group (P < 0.05). ESR and CRP were
significantly higher in decreased HDL-C group than in normal HDL-C group
(P < 0.05). CRP, C(3) and C(4) were significantly higher in elevated
LDL-C group than in normal LDL-C group (P < 0.05). (3) Multiple
stepwise regression analysis showed that C(3) was positively correlated
with TC (R(2) = 0.067, P < 0.05). Both ESR and CRP were negative
correlated with HDL-C (R(2) = 0.202, P < 0.05). CRP and anti-CCP were
positively correlated with LDL-C (R(2) = 0.129, P < 0.05). ESR and
C(4) were positively correlated with AIP (R(2) = 0.046, P <
0.05)(11).
3. Genetic susceptibility
In exploring the overlap between T1D, CeD and RA, there is strong
evidence that variation within the TAGAP gene is associated with all
three autoimmune diseases. Interestingly a number of loci appear to be
specific to one of the three diseases currently studied suggesting that
they may play a role in determining the particular autoimmune phenotype
at presentation(12). Others suggest that this CCR5 promoter polymorphism
seems to play an important role in determining different clinical
courses in both forms of rheumatoid arthritis(13).
4. Inflammatory and infectious connections
Chronic inflammation of the joint can result of thickens the synovium,
of that affect the cartilage and bone within the joint.Some researchers
suggested that rheumatoid arthritis (RA) is a associated with the T
helper 17 cells (Th17) as major effector cells in several chronic
inflammatory states(14). Others indicated that Periodontal infection (P.
gingivalis) carries a unique risk for development of autoimmune
antibodies associated with RA. Patients with RA have either lost many
teeth or usually have severe periodontitis. Additional research, both in
regards to basic mechanisms as well as clinical studies, are necessary
before it can be said that there are causative links between RA and
periodontitis(15).
5. Etc.
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Sources
(10) http://www.ncbi.nlm.nih.gov/pubmed/21679443
(11) http://www.ncbi.nlm.nih.gov/pubmed/22321280
(12) http://www.ncbi.nlm.nih.gov/pubmed/20854658
(13) http://www.ncbi.nlm.nih.gov/pubmed/22665517
(14) http://www.ncbi.nlm.nih.gov/pubmed/21616040
(15) http://www.ncbi.nlm.nih.gov/pubmed/22347541
Health Researcher and Article Writer. Expert in Health Benefits of Foods, Herbs, and Phytochemicals. Master in Mathematics & Nutrition and BA in World Literature and Literary criticism. All articles written by Kyle J. Norton are for information & education only.
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