A Prospective Study on Inflammatory Cytokines and Bone Metabolism Mediators in Patients Affected by Rheumatoid and Psoriatic Arthritis treated with Adalimumab
Abstract:Rheumatoid (RA) and Psoriatic arthritis (PsA) are characterized by extensive synovitis resulting in bone destruction in both diseases and new bone formation in PsA.
“…Furthermore, treatment with anti-TNFα in PsA has demonstrated inhibition of radiographic progression and this seems to correlate to a reduction in circulating osteoclast precursors, indicating an osteoclast directed effect of TNFα [ 167 ]. Although most studies have found that the levels of TNFα and related cytokines are somewhat lower in PsA than those in RA, the role of TNFα in inflammation and joint destruction does not seem particularly different [ 168 , 169 ].…”
Osteoarthritis, rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis, all have one clear common denominator; an altered turnover of bone. However, this may be more complex than a simple change in bone matrix and mineral turnover. While these diseases share a common tissue axis, their manifestations in the area of pathology are highly diverse, ranging from sclerosis to erosion of bone in different regions. The management of these diseases will benefit from a deeper understanding of the local versus systemic effects, the relation to the equilibrium of the bone balance (i.e., bone formation versus bone resorption), and the physiological and pathophysiological phenotypes of the cells involved (e.g., osteoblasts, osteoclasts, osteocytes and chondrocytes). For example, the process of endochondral bone formation in chondrocytes occurs exists during skeletal development and healthy conditions, but also in pathological conditions. This review focuses on the complex molecular and cellular taxonomy of bone in the context of rheumatological diseases that alter bone matrix composition and maintenance, giving rise to different bone turnover phenotypes, and how biomarkers (biochemical markers) can be applied to potentially describe specific bone phenotypic tissue profiles.
“…Furthermore, treatment with anti-TNFα in PsA has demonstrated inhibition of radiographic progression and this seems to correlate to a reduction in circulating osteoclast precursors, indicating an osteoclast directed effect of TNFα [ 167 ]. Although most studies have found that the levels of TNFα and related cytokines are somewhat lower in PsA than those in RA, the role of TNFα in inflammation and joint destruction does not seem particularly different [ 168 , 169 ].…”
Osteoarthritis, rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis, all have one clear common denominator; an altered turnover of bone. However, this may be more complex than a simple change in bone matrix and mineral turnover. While these diseases share a common tissue axis, their manifestations in the area of pathology are highly diverse, ranging from sclerosis to erosion of bone in different regions. The management of these diseases will benefit from a deeper understanding of the local versus systemic effects, the relation to the equilibrium of the bone balance (i.e., bone formation versus bone resorption), and the physiological and pathophysiological phenotypes of the cells involved (e.g., osteoblasts, osteoclasts, osteocytes and chondrocytes). For example, the process of endochondral bone formation in chondrocytes occurs exists during skeletal development and healthy conditions, but also in pathological conditions. This review focuses on the complex molecular and cellular taxonomy of bone in the context of rheumatological diseases that alter bone matrix composition and maintenance, giving rise to different bone turnover phenotypes, and how biomarkers (biochemical markers) can be applied to potentially describe specific bone phenotypic tissue profiles.
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