Dickkopf-1 (Dkk-1) serum levels in systemic sclerosis and rheumatoid arthritis patients: correlation with the Trabecular Bone Score (TBS).

Abstract:

:The aim of this research was to determine any correlations between Dickkopf-1 serum levels (Dkk-1, a natural inhibitor of the Wnt signaling pathway promoting osteoclastogenesis) and the Trabecular Bone Score (TBS), in systemic sclerosis (SSc) and rheumatoid arthritis (RA) patients. It also aimed at determining any difference in Dkk-1 serum levels between SSc and RA patients and a control group (CNT) of healthy subjects. A prospective study was carried out in 60 SSc and 60 RA patients and 60 CNT. Dkk-1 serum levels were evaluated by the ELISA method (Quantikine Human Dkk-1 Immunoassay, R&D System, Minneapolis, USA). The severity of microvascular damage was evaluated by nailfold videocapillaroscopy (NVC patterns: "Early," "Active," "Late"), in the SSc patients. TBS analysis and bone mineral density (BMD, g/cm2) were measured in all patients/subjects. The SSc patients showed higher Dkk-1 serum levels than RA (p < 0.004) and CNT (p < 0.0001) patients. SSc patients, showing the "Late" NVC pattern had statistically higher Dkk-1 serum levels than patients with either the "Active" or "Early" (p < 0.004) patterns. Only in the "Late" NVC pattern group of SSc patients was there a significant negative correlation between Dkk-1 and TBS values (p < 0.0001). The increased Dkk-1 serum levels and decreased TBS values observed suggest a diffuse bone damage in SSc patients with advanced disease, as demonstrated by the concomitant presence of the "Late" NVC pattern. Moreover, the bone remodeling in SSc seems even higher than that in RA patients.

journal_name

Clin Rheumatol

journal_title

Clinical rheumatology

authors

Ruaro B,Casabella A,Paolino S,Pizzorni C,Ghio M,Seriolo C,Molfetta L,Odetti P,Smith V,Cutolo M

doi

10.1007/s10067-018-4322-9

subject

Has Abstract

pub_date

2018-11-01 00:00:00

pages

3057-3062

issue

11

eissn

0770-3198

issn

1434-9949

pii

10.1007/s10067-018-4322-9

journal_volume

37

pub_type

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