Resumen

CASTANEDA, S; GARCES-PUENTES, MV  y  BERNAD PINEDA, M. Pathophysiology of osteoporosis in chronic inflammatory joint diseases. Rev Osteoporos Metab Miner [online]. 2021, vol.13, n.1, pp.32-38.  Epub 17-Mayo-2021. ISSN 2173-2345.  https://dx.doi.org/10.4321/s1889-836x2021000100006.

The immune system and the bone often share the same anatomical niches and spaces, as there is a close functional relationship between both of them. As a consequence, there is a constant interaction between them and a bidirectional flow of information between the immune cells and those of the bone tissue (osteoclasts, osteoblasts and osteocytes) often unknown, in which multiple inflammatory mediators and various growth and cell differentiation factors are involved. This leads to a very close interaction between inflammation and bone loss. In fact, osteoporosis (OP) is one of the most frequent systemic complications in chronic inflammatory diseases (CIDs). The prevalence of OP in CIDs depends on each pathological scenario. Rheumatoid arthritis (RA) is a paradigmatic disease which causes chronic inflammation, where the presence of OP is frequent and shows even prior to the appearance of the first symptoms of the RA. The pathogenesis of RA-associated OP is complex and includes the cooperation of multiple pro-inflammatory cytokines that promote osteoclastogenesis and inhibit bone formation. Tumor necrosis factor alpha (TNF-α) and different interleukins (IL), such as IL-1, IL-6 and IL-17, stand out among all, IL-6 having a relevant hierarchical role. In this study, we review the role of pro-inflammatory cytokines in bone and joint destruction in different CIDs, giving special emphasis to RA, as we set out the bases of possible pathways that open new therapeutic horizons in the their framework.

Palabras clave : osteoporosis; rheumatoid arthritis; psoriatic arthritis; ankylosing spondylitis; pathophysiology; interleukins; IL-6; treatment.

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