Aveneu Park, Starling, Australia

most 0.3- 0.7%. (Carmona et al., 2002

most important
cause of inability and disability if not properly treated.

 

 

Epidemiology

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RA influences
roughly 1% of the population around the world. In the most recent years, a few
epidemiological investigations of RA have been distributed, indicating
varieties in the frequency and pervasiveness of RA crosswise over populations.
The majority of the investigations have been created in nations from the North
Europe and North America, evaluating prevalences of 0.5– 1.1%. (Tobón et al., 2010). Another investigation
made for the most part in nations from South Europe revealed bring down
pervasiveness around 0.3- 0.7%. (Carmona et
al., 2002 and Guillemin et al.,
2005). The most reduced pervasiveness information have been accounted for in
zones from Africa and Asia, and the most noteworthy in Native American
populaces. Truth be told, the pervasiveness of RA is 10 times higher among
Canadian or Native Americans than Europeans (3% and 0.3%, separately).
(Molokhia and McKeigue 2000) (El-Gabalawy et
al., 2011)

 

Pathogenesis

Although the exact cause for the development of rheumatoid arthritis is
unknown but a number of medical studies and reports have suggested a number of
factors . These factors not only
involve the genetic but also  environmental factors are considered contributory to
the progression of this disease. While etiology of rheumatoid arthritis is
unknown, medical evidences suggest that RA develops more often in individuals
with inherited genetic and individual risk factors or exposed to environmental
trigger (Krzysztof et al., 2015).
Rheumatoid arthritis involves a complex interplay among genotype, environmental
triggers, and chance.( Iain et al.,
2011)

 

Genetic
Factors

Genome-wide
association studies have identified greater than 100 percent  genetic susceptibility loci associated with
RA, many of which are commonly present in the general population (Okada et al., 2014). The long-established
association with the human leukocyte antigen (HLA)–DRB1 locus has been
confirmed in patients who are positive for rheumatoid factor or ACPA; alleles
that contain a common amino acid motif (QKRAA) in the HLA DRB1 region, termed
the shared epitope, confer particular susceptibility. (Gregersen et al., 1987). Candidate gene
approaches, genome-wide

 

 

association
studies (GWAS), and trans-ethnic GWAS meta-analyses have identi ed a number of
RA risk genes, such as HLA-DRB1, PTPN22, STAT4, CCR6, TNFAIP3, PADI4, CD40, and
FCRL3, many of which are involved in the functions of immune cells, including T
cells, B cells, and macrophages (Okada et
al., 2014 and Yamamoto et al., 2015).

 

Environmental
Factors

Environmental
factors, such as stress, smoking, excessive coffee drinking and the make-up of
the microbial population in the bowel, have all been implicated in higher
susceptibility to RA. (Rod Hughes 2016). Of the several environmental factors
that have been investigated in relation to RA, the evidence implicating
cigarette smoking as a risk factor remains by far the most robust. (Kulveer and
Paul .2016). A greater intake of vitamin D reduced the incidence of RA in older
woman (Merlino et al., 2004).
Exposure to silica through the respiratory tract increased the risk of
developing RA (Stolt et al., 2005) Other environmental factors, including high
birth weight, obesity, and lower socioeconomic status, have also been found to
be associated with a higher risk of RA. Similarly, environmental exposures,
such as ultraviolet light and silica dust, have also been linked with increased
RA risk. In contrast, lifestyle factors, such as longer duration of
breastfeeding and moderate alcohol intake, may be protective (Karlson and Deane
2012;  Lahiri et al., 2012).

Infectious
agents (e.g., Epstein–Barr virus, cytomegalovirus, proteus species, and
Escherichia coli) and their products (e.g., heat-shock proteins) have long been
linked with rheumatoid arthritis, and although unifying mechanisms remain
elusive, some form of molecular mimicry is postulated. ( Kamphuis et al.,2005)

 

Epigenetic
Factors

Several
epigenetic mechanisms, including posttranslational histone modi cations, DNA
methylation, and microRNAs (miRNAs), determine the species chromatin structure,
consequently in sequencing gene transcription without altering the DNA sequence
itself (Basset et al., 2009).
Rheumatoid arthritis serves an example of a chronic inflammatory disorder in
which miRNAs modulate the inflammatory process in the joints, with the
potential to serve as biomarkers for both the inflammatory process and the
potential for therapeutic response. (Victoria et al., 2012).

 

Clinical
Manifestations

Several
general symptoms can represent a major problem during the course of RA, many of
them also being present before its diagnosis. Weight loss, fever, prolonged
early morning stiffness, fatigue, generalised muscle weakness, low mood, and
depression are often responsible for a significant loss in the quality of life
of patients. Fatigue is reported in 40 80% of RA patients as their most
disabling symptom (Balsamo S et al.,2014).
Gradual onset polyarthralgia with symmetrical, intermittent and migratory joint
involvement, especially in the hands and feet are most typical clinical
presentations of RA.

 

Diagnosis

The diagnosis
is based primarily on the clinical history and physical examination with
support from selected laboratory tests. RA is diagnosed through its distinctive
effects on the joints and in skin, and the diagnosis is reinforced by the
presence in serum of the rheumatoid factor (RF), although its presence is not
mandatory for diagnosis of RA. (Treatment of rheumatoid arthritis and other
inflammatory disorders: Sample chapter from Biological Therapeutics) Elevated
inflammatory markers, such as CRP and ESR, are usually found in association
with RA, but may be normal in some people, especially early in the disease.
When a patient presents with early arthritis (EA), a quick and de?nite
diagnosis is needed to initiate early treatment. Antinuclear antibodies (ANA)
and anti-double-stranded (anti-ds) DNA antibodies may be present in patient
with RA (Yukawa et al., 2011).
Oxidized, nitrated and glycated amino acids combined with hydroxyproline and
anti-CCP antibody status provided a plasma-based biochemical test of relatively
high sensitivity and specificity for early-stage diagnosis and typing of
arthritic disease (Usman Ahmed 2016). The early start of disease-modifying
antirheumatic drugs (DMARDs) may improve clinical and radiographic outcomes.
1–5 A diagnosis of EA may involve several steps, from the detection and
con?rmation of arthritis to the ?nal diagnosis by a rheumatologist (Charlotte et al., 2017)

 

 RA are often characterized by the presence of
autoantibodies. Rheumatoid factor is not specific for RA and may be present in
patients with other diseases, such as hepatitis C, and in healthy older
persons. Anti-citrullinated protein antibody is more specific for RA and may
play a role in disease pathogenesis(Balsa et
al., 2010). Approximately 50 to 80 percent of persons with RA have
rheumatoid factor, anti-citrullinated protein antibody, or both. (Scott et al., 2010). Patients with RA may have
a positive antinuclear antibody test result, and the test is of prognostic
importance in juvenile forms of this disease. 19 C-reactive protein levels and
erythrocyte sedimentation rate are often increased with active RA, and these
acute phase reactants are part of the new RA classification criteria (Aletaha et al., 2010).

 

Treatment

Rheumatoid
arthritis (RA) is a progressive chronic disease whose treatment is still often
symptomatically driven, mainly as a result of incomplete characterization of
the underlying disease process. Currently, there is no preventive treatment or
cure for RA. However, exciting advances in the understanding of rheumatoid
arthritis (RA)  and its pathogenesis are
providing new hope for those suffering from this debilitating disease The
primary treatment is usually disease-modifying anti-rheumatic drugs (DMARDs),
which reduce synovitis and systemic inflammation. Presently, treatment options
for RA include glucocorticoids (systemic or intraarticular), conventional
synthetic disease Modifying anti-rheumatic drugs (csDMARDS) and biologics
(bDMARDs). Methotrexate (MTX), sulfasalazine (SSZ), hydroxychloroquine (HCQ)
and leflunomide (LEF) are considered csDMARDS. Biologics include tumor necrosis
factor inhibitors like infliximab, adalimumab, etanercept, certolizumab, and
golimumab. New biologics include abatacept, rituximab and tocilizumab
(BerkantAvci et al., 2015). Many of
the past and current therapies offer little more than symptomatic relief. Even
the so-called disease modifying antirheumatic drugs (DMARDs) do not halt the
progression of this disease, but rather decrease the onset of disability by 30%
(Ann Pittier 2000).

 

Treatment
Alternatives

As the side
effects of synthetic drugs are common and usually unavoidable, new experiments
search for naturally derived therapeutic medications such as bovine
lactoferrin, which has anti-inflammatory properties (Smolen et al., 2014). Diverse strategies to
develop novel treatments for rheumatoid arthritis which specifically target
those patients who do not respond to available medications, including
biologics, are currently being explored. New potential therapeutic approaches
which may become available as part of standard therapeutic regimens include the
propagation of regulatory T cells and—in the future—of regulatory B cells. New
biologic disease-modifying antirheumatic drugs (b-DMARDs) against
interleukin-17 and -6, granulocyte-macrophage colony-stimulating factor, and
complement component 5 are now standard components of clinical treatment
programs. In addition, recent data indicate that bispecific monoclonal antibody
therapies may be more effective than monoclonal antibody monotherapies. It is
also becoming apparent that the use of more toxic b-DMARDs against B cells, a
therapeutic strategy already being applied in the treatment of haematological
diseases, may also be efficacious for treating B cell-mediated autoimmune
diseases. Undoubtedly, more small molecules will be developed in the future,
and combination therapies with, for example, kinase inhibitors and b-DMARDs,
will most likely be tested. Finally, immunoproteasome inhibitors will become
available for patients with B cell-mediated autoimmunities, which are
refractory to currently available treatment options. The new and exciting
extension of current treatment options for rheumatoid arthritis, biosimilars,
will not be discussed in this review as details on these agents are available
in recently published reports( Joachim. 2016).

 

Use of herbal
medicine is becoming more popular due to their negligible toxic effects and
rare side effects. Studies by Ankit Anwar et
al., 2017 have identified many natural plant products with significant
therapeutic potential against RA. These plant products might be responsible for
alleviating the inflammation and reducing the symptoms of the disease.

 

The employment of stem cells to treat rheumatoid
arthritis, a debilitating and even life-threatening condition, has the
potential to drastically improve the quality of life of sufferers by a factor
which cannot be provided by current therapies or medicines, and even provide a
route to a lifelong cure, for which there is 

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