Abstract
Tissue turnover, especially in the skin, is altered in systemic sclerosis (SSc), leading to tissue accumulation. The objective was to examine type III, IV, and VI collagens turnovers in SSc and investigate longitudinal alterations in relation to modified Rodnan Skin Score (mRSS). We included patients fulfilling the 2013 ACR/EULAR criteria for SSc (limited cutaneous [lcSSc, n = 20], diffuse cutaneous SSc [dcSSc, n = 23]) and healthy controls (HC, n = 10). Biomarkers of type III, IV, and VI collagens formation (PRO-C3, PRO-C4, PRO-C6) and degradation (C3M, C4M, C6M) were measured in serum. The fibrotic index of the individual collagens (FICol) were calculated. The fibrotic index of type III and VI collagens (FICol3 and FICol6) were increased in dcSSc compared to lcSSc (FICol3: 1.4 vs. 0.8, P = 0.0001; FICol6: 1.2 vs. 0.9, P = 0.03). The fibrotic index of type IV collagen (FICol4) was not different between the groups but was 1.5 times higher than HC (HC: 6.9, lcSSc 10.4, dcSSc: 10.5). Both FICol3 and FICol6 correlated with mRSS with rho’s of 0.59 (P < 0.0001) and 0.35 (P = 0.04). Furthermore, FICol3 steadily decrease over the disease course. Examining collagen turnover and specific collagens could be beneficial in following patients’ skin fibrosis and possibly identifying progressors.
Highlights
Systemic sclerosis (SSc) is a dynamic disease in which the literature suggests that microvascular damage leads to damage to endothelial cells resulting in fibrosis by activation of fibroblasts[1,2]
The turnover of type III (FICol3) and VI (FICol6) collagens were increased in diffuse cutaneous SSc (dcSSc) compared to limited cutaneous SSc (lcSSc) (FICol[3]; lcSSc: 0.8, dcSSc: 1.4, P = 0.0001, fibrotic index of the individual collagens (FICol)[6]; lcSSc: 0.9, dcSSc: 1.2, P = 0.03; Fig. 1)
Type III and VI collagens formation were significantly higher in dcSSc compared to lcSSc (PRO-C3; lcSSc: 31.4 ng/ml, dcSSc: 51.2 ng/ml, P = 0.01, PRO-C6; lcSSc: 4.7 ng/ml, dcSSc: 8.2 ng/ml, P = 0.1)
Summary
Systemic sclerosis (SSc) is a dynamic disease in which the literature suggests that microvascular damage leads to damage to endothelial cells resulting in fibrosis by activation of fibroblasts[1,2]. Fibrosis is both seen around the blood vessels and in the deeper interstitial matrix of the affected tissues. The synthesis of collagen is known to be upregulated in SSc, and the focus of the literature has primarily been on the two main collagens found in skin; type I and III collagens These are usually found in the interstitial matrix, where they act as the “skeleton” of tissue as the skin. We studied the change in collagen turnover over time and in relation to the modified Rodnan Skin Score (mRSS)
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