We aim to define the role of systemic, low grade, chronic inflammation in the development of sarcopenia and therefore study patients with rheumatoid arthritis and patients with osteoarthritis as controls, on cellular and functional level. Until now…
ID
Source
Brief title
Condition
- Immune disorders NEC
- Musculoskeletal and connective tissue disorders NEC
Synonym
Research involving
Sponsors and support
Intervention
Outcome measures
Primary outcome
1. On a cellular level: differences in satellite cell number, proliferative
potential of myoblasts, differential capacity of myoblasts, cellular capacity
to react to the exposure to oxidative stress, presence of muscle atrophy.
2. On a systemic level: differences in the systemic inflammatory status, number
of lymphocyte subsets.
3. On a functional level: differences in handgrip strength, leg press strength,
isometric knee extensor strength.
4. On an imaging level: differences in muscle architecture.
Secondary outcome
No secondary outcome.
Background summary
Sarcopenia is a universal, age-related loss of muscle mass associated with a
loss of strength and function resulting in muscle weakness. It often leads to
progressive disability and loss of independence. The development of sarcopenia
has also been associated with increased mortality. Despite its clinical
importance, the pathophysiology leading to sarcopenia is not well understood.
Environmental factors, such as a sedentary life style and malnutrition
contribute to sarcopenia; other possible causes of sarcopenia include systemic
changes such as a decreased growth hormone production and increased
inflammatory cytokine secretion.
One of the hallmarks of rheumatoid arthritis (RA) is chronic inflammation,
which leads to the destruction of the cartilage, bone and ligaments causing
deformity of the joints. Cytokines, such as TNF-α, IL-1β and IL-6, play a key
role in driving synovial cell activation leading to joint destruction. Synovium
and synovial fluid contain more cytokine activity compared to control patients
with osteoarthritis (OA), whereas, on systemic level, a reduced release of
INF-γ during whole blood stimulation tests is seen in RA patients versus
controls. In RA patients with minimally involved knee involvement, weakness of
the quadriceps is significantly present, which could underline a possible role
of systemic inflammation in the onset and progression of sarcopenia in RA
patients.
Study objective
We aim to define the role of systemic, low grade, chronic inflammation in the
development of sarcopenia and therefore study patients with rheumatoid
arthritis and patients with osteoarthritis as controls, on cellular and
functional level. Until now, there has not been a detailed investigation of the
physiological, cellular and molecular consequences of RA on sarcopenia in a
clinically well defined population.
Study design
Case (rheumatoid arthritis patients) - control (osteoarthritis patients) study.
Study burden and risks
No potential risks are expected. While the patients participating in this study
may not directly derive any immediate benefits, the results of the study should
improve the understanding of the pathogenesis of sarcopenia.
Albinusdreef 2
2333 ZA Leiden
Nederland
Albinusdreef 2
2333 ZA Leiden
Nederland
Listed location countries
Age
Inclusion criteria
rheumatoid arthritis
osteoarthritis
age 45-70 years
Exclusion criteria
no
Design
Recruitment
Followed up by the following (possibly more current) registration
No registrations found.
Other (possibly less up-to-date) registrations in this register
No registrations found.
In other registers
| Register | ID |
|---|---|
| CCMO | NL20629.058.07 |