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A comparative quantitative morphometric study of cell apoptosis in synovial membranes in psoriatic, reactive and
A Ceponis1, J Hietanen, M Tamulaitiene
1Department of Anatomy, Institute of Biomedicine, University of Helsinki, Helsinki University Central Hospital, Invalid Foundation, Finland.
Objectives:
Inflammatory arthritides/synovitides such as psoriatic (PsA), reactive (ReA) and rheumatoid (RA) arthritis share numerous immunopathological features, but develop different patterns of joint involvement. To investigate whether distinctive cell apoptosis may play a role in this context, we have assessed synovial cell apoptosis in situ in PsA and ReA, and compared it with RA and 'non-inflammatory' controls.
Methods:
TdT-mediated dUTP nick end-labelling (TUNEL) of DNA breaks complemented immunoperoxidase staining for CD68 or LCA as the specific cell markers.
Results:
The proportion of apoptotic synovial lining cells was high in PsA, ReA and RA compared to values in controls (P < 0.05). No differences existed between these inflammatory arthritides in numbers or type of apoptotic lining cells. In RA, however, in contrast to PsA and ReA, apoptotic lining cells were clustered or, in a small subset of samples, were very low in number. Prominent apoptosis of inflammatory cells in the sublining in ReA has accounted for higher overall apoptotic cell numbers in synovial stroma (sublining + perivascular inflammatory cell infiltrates) in this condition than in RA or PsA (P < 0.05).
Conclusions:
No disease-specific pattern in the phenotype of apoptotic synovial lining cells could be suggested in any of the inflammatory arthritides studied. However, topological differences in the lining and quantitative differences in the inflammatory cell apoptosis in synovial stroma may in part explain the occurrence of the prominent synovial lining cell hyperplasia distinguishing RA from ReA and PsA. On the other hand, relatively frequent inflammatory cell apoptosis may contribute both to the downregulation of synovial inflammation and to the control of synovial lining hyperplasia in ReA.