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In postmenopausal
RA-OP patients, the extent of RANKL production, contributing to more
significant net bone loss was found to be higher than in non-RA postmenopausal
OP patients.
Rheumatoid arthritis (RA) is characterized, by systemic bone loss, reaching ~50% prevalence of osteoporosis in postmenopausal women. This prevalence is found roughly double when compared with age-matched non-RA women. Postmenopausal RA women are more suitable to sero-positive for the anti-citrullinated peptide antibody (ACPA). The extensive review of recent scientific literature leads to propose several mechanisms as responsible for the accelerated bone loss in ACPA (+) RA postmenopausal women.
Estrogen deficiency associated with menopause is believed to play a significant role in the pathophysiology of osteoporosis. Withdrawal of Estrogen leads to immune dysregulation manifested in a skewed distribution of T-helper cell subsets, and enhanced reactivity of T-helper-17 (Th17) cells. It results in a shift toward elevated levels of inflammatory cytokines, especially TNFα, IL-17, and RANKL, as well as accelerated net bone loss.
The proposed interaction between estrogen deficiency and RA-genetic risk alleles promotes enhanced Th17-cell autoreactivity, manifested by ACPA (+) RA. Such interactions exacerbate the inflammatory conditions and cause massive bone destruction.
TNFα and IL-17 play a dual role in RA
because they excite bone resorption and inhibit bone formation.
The RA-unique factor, the pathogenic
appearance of ACPA, promotes an inflammation independent-mechanism, resulting
in direct osteoclast genesis and bone resorption.
Bone
Postmenopausal osteoporosis in rheumatoid arthritis: The estrogen deficiency-immune mechanisms link
Chang-Ki Hong et al.
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