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Mechanism causing post menopausal osteoporosis in RA patients

Mechanism causing post menopausal osteoporosis in RA patients Mechanism causing post menopausal osteoporosis in RA patients
Mechanism causing post menopausal osteoporosis in RA patients Mechanism causing post menopausal osteoporosis in RA patients

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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.

Source:

Bone

Article:

Postmenopausal osteoporosis in rheumatoid arthritis: The estrogen deficiency-immune mechanisms link

Authors:

Chang-Ki Hong et al.

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