(170) Effects of Oral Vitamin D Supplementation in an Experimental Model of Peyronie’s Disease

Introduction While numerous treatments have been proposed for Peyronie’s Disease (PD), the biological mechanisms underlying tunical fibrosis remain only partially understood. Growing evidence points to vitamin D (vitD) as a modulator of inflammatory responses and extracellular matrix remodeling, raising interest in its potential to mitigate fibrotic changes in PD. Objective To evaluate the effects of oral vitD supplementation on collagen deposition and vitD receptors in an experimental model of PD. Methods Thirty-six male Wistar rats were allocated into three groups: control (G1), PD induced and treated with placebo (G2), and PD induced and treated with oral vitamin D (G3). PD was induced by injecting autologous plasma into the tunica albuginea using a previously validated model (Figure 1). VitD was administered orally throughout either 8 or 18 weeks, representing the acute and chronic phases, respectively. Collagen types I and III were quantified using Picrosirius Red staining, and vitD receptor expression was assessed by immunohistochemistry. Results VitD receptors expression did not differ significantly among groups during the acute phase. However, in the chronic phase, both the mean H-score and the percentage of positively stained tissue were significantly higher in Group 2 and 3 compared to Groups 1 (p < 0.05), indicating upregulation of vitD receptor expression in PD experimental model. (Figure 2) In the acute phase, type III collagen levels were similar across groups, with mean ± SD values of 20.90 ± 9.93% in G1, 21.20 ± 12.14% in G2, and 18.59 ± 12.79% in G3(p = 0.54). Likewise, type I collagen also displayed comparable distribution, with 28.44 ± 23.70% in G1, 24.61 ± 14.24% in G2, and 17.56 ± 10.40% in G3 (p = 0.91). These findings indicate that, in the early inflammatory phase, oral vitamin D supplementation does not yet significantly influence collagen deposition, and the extracellular matrix composition remains similar between treated and untreated groups. In the chronic phase, type I collagen demonstrated a progressive reduction from the control group toward the vitamin D–treated group, with mean ± SD values of 38.71 ± 6.35% in G1, 30.20 ± 16.77% in G2, and 26.24 ± 7.96% in G3, though not statistically significant (p = 0.27). Regarding type III collagen, a distinct pattern was observed, with 12.4 ± 8.2% in G1 and markedly higher levels in both PD-induced groups, 30.89 ± 25.74% in G2 and 30.22 ± 13.90% in G3 (p=0.27). In the chronic phase, G2 demonstrated a higher type I/III collagen ratio compared to the vitD–treated group, consistent with a more fibrotic tunical architecture. In contrast, vitD supplementation was associated with a shift toward a lower type I/III ratio, suggesting a less fibrotic and more remodeling-oriented extracellular matrix profile. (Figure 3) Conclusions VitD receptor expression is higher in PD experimental model and vitD supplementation showed a lower type I/III collagen ratio in the tunica albuginea in the chronic phase, indicating possible modulation of extracellular matrix, remodeling and attenuation of fibrotic progression. These findings support a potential antifibrotic and tissue-preserving role for vitD in PD and more studies should be encouraged. Disclosure No