Microanatomic studies to define predictive factors for the topography of periarticular erosion formation in inflammatory arthritis

Abstract

Objective. The microanatomic basis for formation of erosions in inflammatory arthritis is incompletely understood but is thought to be related to bare areas and the associated cartilage-synovium junction. The purpose of this study was to test the hypothesis that erosion-prone sites are associated with microdamage in macroscopically normal joints.Methods. Histologic evaluation of erosion-prone sites was performed on 20 collateral ligaments (CLs) from the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints of 5 normal cadavers. In addition, the MCP joints (n ‫؍‬ 17) and PIP joints (n ‫؍‬ 3) of 20 patients with rheumatoid arthritis (RA) were assessed by computed tomography (CT) to ascertain whether the topography of erosion formation in patients with RA corresponded to the cadaveric findings.Results. Absence of a bare area was noted in cadaveric tissue at the periligamentous erosion-prone regions, especially in the distal MCP joints and both distal and proximal PIP joints. Nevertheless, these sites exhibited soft-tissue pathologic features and bony microdamage/cyst formation. Other significant findings included the presence of pannus without inflammatory changes in the regions in which a bare area was absent, and the replacement of bare area regions with fibrovascular synovial tissue in joints without inflammatory changes. The sites of cadaveric tissue microdamage corresponded to CT-determined erosion formation in the MCP and PIP joints of patients with RA, in whom erosions adjacent to the CLs were more common than dorsal or volar erosions.Conclusion. Periarticular erosion formation may not necessarily depend on the presence of a bare area and has a propensity to occur adjacent to ligaments in which bone microdamage is common. These findings suggest that periligamentous locations prone to microdamage may critically influence the topography of erosion formation in inflammatory arthritis.

The Pathogenesis of Rheumatoid Arthritis

“…Thus, "mechanically vulnerable" sites such as the second and third metacarpals are prone to erosive changes. 76 Breach of cortical bone permits synovial access to the bone marrow, which causes inflammation of the bone marrow (osteitis as observed on magnetic resonance imaging), in which T-cell and B-cell aggregates gradually replace marrow fat. 77 It is unclear whether these lesions occur in conjunction with synoviuminduced erosions or whether osteitis necessarily or independently precedes erosion.…”

The role of RANK ligand/osteoprotegerin in rheumatoid arthritis

“…In RA without bone erosions at baseline it has been found that bone erosions preferentially occur at the bone site depraved from periost in the joint, the so-called 'bare area ' [McGonagle et al 2009;Theumann et al 2002]. It is the localization where osteoclasts derived from the synovium can start to attack the nude bone in RA, as osteoclasts can only degrade mineralized tissue and not nonmineralized tissue [Parfitt, 1976].…”

“…Surprisingly, nearly 40% of clinically apparent healthy subjects have small bone erosions when studied with high-resolution quantitative computed tomography (HRqCT) [Stach et al 2010]. Studies of the anatomy of the finger joints has shown that erosions can occur at sites of pressure by ligaments on bone without any sign of RA [McGonagle, 2010;McGonagle et al 2009]. Furthermore, in patients with RA MRI osteitis was more pronounced at sites of pressure, e.g.…”

Structural Basis of Joint Instability as Cause for Chronic Musculoskeletal Pain and Its Successful Treatment with Regenerative Injection Therapy (Prolotherapy)

“…In view of the structural and physiological characteristics of the ligaments and their entheses, an exaggerated response to an insult can occur. This anatomical arrangement may be key to the development of the OA phenotype [67,68]. The imbalance between the breakdown and repair of joint tissues in OA is the result of the activation of joint cells by inflammatory mediators, matrix components and mechanical stress [69].…”