Abstract

Structural changes of bone and cartilage are a hallmark of inflammatory joint diseases such as rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS). Despite certain similarities – in particular, inflammation as the driving force for structural changes – the three major inflammatory joint diseases show considerably different pathologies. Whereas RA primarily results in bone and cartilage resorption, PsA combines destructive elements with anabolic bone responses, and AS is the prototype of a hyper-responsive joint disease associated with substantial bone and cartilage apposition. In the present review we summarize the clinical picture and pathophysiologic processes of bone and cartilage damage in RA, PsA, and AS, we describe the key insights obtained from the introduction of TNF blockade, and we discuss the future challenges and frontiers of structural damage in arthritis.

Highlights

  • Structural changes of cartilage and bone resulting from arthritis were recognized in the mid-nineteenth century: witness Baker’s description of bone cysts as a protective mechanism for the joint [1]

  • We summarize the mechanistic concepts of structural damage in these three major joint diseases, we review the achievements of tumor necrosis factor (TNF) blockers – in particular, their contribution to understanding structural damage – and we discuss unanswered questions and future frontiers in the management of bone and cartilage damage in rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS)

  • Since the scoring systems used for the assessment of radiographic damage of PsA are the same as those used for RA, our knowledge about TNF-blocker effects on structural damage are confined to the erosive component of the disease, and it is unclear whether these agents affect enthesiophyte formation

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Summary

Introduction

Structural changes of cartilage and bone resulting from arthritis were recognized in the mid-nineteenth century: witness Baker’s description of bone cysts as a protective mechanism for the joint [1]. Since the scoring systems used for the assessment of radiographic damage of PsA are the same as those used for RA, our knowledge about TNF-blocker effects on structural damage are confined to the erosive component of the disease, and it is unclear whether these agents affect enthesiophyte formation.

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