SYNOVIAL LINING, ENDOTHELIAL AND INFLAMMATORY MONONUCLEAR CELL-PROLIFERATION IS SYNOVIAL MEMBRANES IN PSORIATIC AND REACTIVE ARTHRITIS - A COMPARATIVE QUANTITATIVE MORPHOMETRIC STUDY
A. Ceponis et al., SYNOVIAL LINING, ENDOTHELIAL AND INFLAMMATORY MONONUCLEAR CELL-PROLIFERATION IS SYNOVIAL MEMBRANES IN PSORIATIC AND REACTIVE ARTHRITIS - A COMPARATIVE QUANTITATIVE MORPHOMETRIC STUDY, British journal of rheumatology, 37(2), 1998, pp. 170-178
The extent of synovial cell proliferation in situ and its relationship
to the destructive potential of rheumatoid arthritis (RA) is a matter
of continuing debate, Notably, the situation has not been elucidated
in other inflammatory arthritides [i.e. reactive (ReA) and psoriatic (
PsA)], which, although they share some histopathological similarities
with RA, develop different patterns of joint involvement, In order to
estimate the proliferation of synovial cells in situ in PsA and ReA, a
nd to compare this with RA and with 'non-inflammatory' joint lesions,
we have utilized immunostaining of the Ki-67 antigen complemented with
Ki-67/CD68 or Ki-67/leucocyte common antigen (LCA, clones 2B11 and PD
7/26) double stainings to assess the extent of mononuclear inflammator
y cell proliferation. Synovial samples analysed were from 33 patients:
RA (n = 8), PsA (n = 13)? ReA (n = 6) and six 'non-inflammatory contr
ols' (degenerative or traumatic joint lesions). Thickening of the syno
vial lining (in particular in RA) and perivascular accumulations of mo
nonuclear inflammatory cells, predominantly lymphocytes, were characte
ristic features in all synovitides. In contrast to the thickened avasc
ular synovial lining in RA, in 5/13 cases with PsA, blood vessels were
observed in the lining. The percentage of lining cells expressing Ki-
67 antigen was higher in RA (median = 4.7, interquartile range [Q3-Q1]
= 3.9, mean [95%, CI] = 3.5 [1.7-5.2], P = 0.0063), PsA (median = 1.2
, [Q3-Q1] = 1.9, mean [95% CI] = 1.6 [0.7-2.5], P = 0.007) and ReA (me
dian = 1.4, [Q3-Q1] = 2.3, mean [95% CI] = 1.6 [0.1-3.1], P = 0.0235)
than in controls (median = 0.1, [Q3-Q1] = 0.45, mean [95% CI] = 0.2 [0
.07-0.5]). In this respect, the differences between different forms of
the inflammatory arthritides were not statistically significant (P >
0.05). In RA, PsA and ReA, the percentage of labelled cells in the inf
lammatory mononuclear cell-rich areas was higher than in controls. The
percentage of proliferating endothelial cells was also significantly
higher in RA, PsA and: ReA than in controls. However, in RA, endotheli
al expression of Ki-67 antigen was often seen in small blood vessels,
whereas in PsA, Ki-67 antigen was preferably expressed in the medium t
o large blood vessels. Synovial lining cells of the monocyte/macrophag
e lineage (type A synoviocytes), but not stromal monocytes, demonstrat
ed modest proliferation in situ. These results indicate that although
proliferation of synovial lining fibroblasts is a prominent feature in
RA, the extents to which this, or in situ proliferation of lymphocyte
s, contribute to the histopathology of PsA, ReA and RA are comparable.
Vascular involvement is suggested by the proliferation of endothelial
cells in RA, PsA and ReA in an overlapping manner, but, based on topo
logical differences, such a response may represent diverse pathologica
l features, such as angiogenesis, vascular enlargement and reparative
responses to injury.