Concise reports
Vitamin D receptors in the rheumatoid lesion: expression by
chondrocytes, macrophages, and synoviocytes
University
Department of Medicine, Manchester Royal Infirmary, Oxford Road,
Manchester, M13 9WL
Correspondence to: Dr D E Woolley.
Accepted for publication 15 September 1998
OBJECTIVES
The active
form of vitamin D3, 1
,25 dihydroxyvitamin D3
(1,25D3), through its interaction with vitamin D receptors
(VDR), is reported to effect a variety of anabolic and catabolic
events, especially in bone and cartilage tissues. As cartilage
degradation and tissue remodelling are characteristic features of the
rheumatoid lesion, the distribution and expression of VDR at sites of
cartilage erosion was examined.
METHODSImmunolocalisation
techniques using a rat monoclonal antibody to VDR and an alkaline
phosphatase conjugated avidin/biotin detection system were used to
examine VDR in 18 specimens of cartilage-pannus junction, 10 specimens
of rheumatoid synovium or cartilage tissue, and four primary cultures
of adherent rheumatoid synovial cells (RSC). For comparison, VDR
expression was examined in 10 specimens of normal, healthy age matched
articular cartilage.
RESULTSVDR was
demonstrated in 15 of 18 cartilage-pannus junctions either at the
interface (8 of 18), within the pannus tissue (12 of 18), and by
chondrocytes often close to the erosive lesion (10 of 18). All the
rheumatoid synovial tissue and 5 of 10 cartilage specimens showed cells
with positive staining, but the extent of this was variable. Negligible
VDR staining was observed for normal cartilage. Primary cultures of RSC
also showed variability in both the numbers and proportions of
macrophages or synovial fibroblasts stained for VDR (range 10-50%),
this being more common in cultures with a high proportion of macrophages.
CONCLUSIONSVDR
expression has been demonstrated by most specimens of cartilage-pannus
junction; was associated with various cell types, including
chondrocytes, but not exclusively with CD68+ macrophages.
The focal nature of VDR expression within the rheumatoid lesion
suggests a contributory role for 1,25D3 in the
pathophysiological processes of rheumatoid arthritis.
© 1999 by Annals of the Rheumatic Diseases
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
-
Ranganathan, P.
(2009). Genetics of bone loss in rheumatoid arthritis--role of vitamin D receptor polymorphisms. Rheumatology (Oxford)
48: 342-346
[Abstract] [Full Text] -
Leventis, P., Patel, S.
(2008). Clinical aspects of vitamin D in the management of rheumatoid arthritis. Rheumatology (Oxford)
47: 1617-1621
[Abstract] [Full Text]
- Full Text
- Full Text (PDF)
- Submit a response
- Alert me when this article is cited
- Alert me when eLetters are posted
- Alert me if a correction is posted
- Citation Map
Services
- Email this link to a friend
- Similar articles in this journal
- Similar articles in PubMed
- Add article to my folders
- Download to citation manager
- Request Permissions
Citing Articles
Google Scholar
PubMed
Topic Collections
-
Immunology (including allergy)
-
Connective tissue disease
-
Degenerative joint disease
-
Musculoskeletal syndromes
- Rheumatoid arthritis
Bookmark with
Register for free content
The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.
Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.
