Psoriatic cutaneous inflammation promotes human monocyte differentiation into active osteoclasts, facilitating bone damage.
Annunziata RaimondoSerena LemboRoberta Di CaprioGiovanna DonnarummaGiuseppe MonfrecolaNicola BalatoFabio AyalaAnna BalatoPublished in: European journal of immunology (2017)
Psoriatic arthritis (PsA) is a chronic inflammatory arthropathy that can be associated with focal bone erosions. Psoriasis usually precedes the psoriatic arthritis onset by an average of 10 years, but this relation is not yet fully elucidated. Pro-inflammatory cytokines, such as IL-33, OPN, IL-17, and TNF-α are involved in both psoriasis and PsA pathogenesis as well as in bone homeostasis. In this study, we have demonstrated that IL-33, OPN, IL-17, and TNF-α induced the release of a wide range of pro-osteoclastogenic factors from the skin, such as RANKL, that promote monocyte differentiation in osteoclasts. The addition of osteoprotegerin, a RANKL inhibitor, to monocyte cultures treated with supernatant from stimulated skin did not completely deplete osteoclast formation, suggesting that skin produced several additional pro-osteoclastogenic mediators, which could act in a RANKL-independent manner. Moreover, we have found that RANKL serum levels as well as osteoclast number and activity in psoriatic patients with and without arthritis, was influenced by severity of cutaneous disease. Our data demonstrate that psoriatic cutaneous inflammation contributes to bone damage.
Keyphrases
- bone loss
- rheumatoid arthritis
- oxidative stress
- endothelial cells
- soft tissue
- prostate cancer
- disease activity
- dendritic cells
- ankylosing spondylitis
- high glucose
- anti inflammatory
- diabetic rats
- peripheral blood
- bone mineral density
- wound healing
- nuclear factor
- drug induced
- electronic health record
- atopic dermatitis
- body composition
- radical prostatectomy
- systemic lupus erythematosus
- machine learning
- data analysis
- deep learning