Introduction: Carpal tunnel syndrome (CTS) is the most common type of compressive neuropathy in the human body, manifesting itself through dysfunction in the innervation area of the median nerve. Dupuytren's disease (DD) is a condition characterized by chronic progressive fibrosis of the palmar fascia that leads to flexion deformities of the fingers. The precise molecular mechanism of fibrosis in CTS and DD is unclear, and only certain profibrotic factors have been investigated so far. The aim of this dissertation is to examine the expression of molecules related to the fibroblast growth factor receptor (FGFR) signaling pathway in the palmar tissues of patients with CTS and DD. Materials and methods: In this cross-sectional study tissue samples of the palmar fascia and flexor retinaculum of 15 patients with CTS and macroscopically affected and unaffected palmar fascia of 15 patients with DD were used. The samples were stained with hematoxylin and eosin and Mallory trichrome staining for the purpose of morphological analysis, and immunofluorescence staining for the proliferation marker Ki-67, FGFR1, FGFR2, connective tissue growth factor (CTGF), transforming growth factor β (TGF-β) and syndecan-1. The expression of the mentioned factors was quantified by counting positive cells in the blood vessels, connective tissue and sweat glands of the tested samples. Quantitative polymerase chain reaction analysis was also performed to determine the expression of FGFR1 and FGFR2 genes on the same tissues. Results: Changes in the density of collagen fibers are present in the macroscopically unaffected palmar fascia of patients with DD. Cell proliferation of blood vessels and surrounding connective tissue was increased in palmar fascia samples from subjects with DD compared to healthy palmar fascia. Significant differences in the expression of FGFR1, FGFR2 and CTGF were observed in blood vessel walls and surrounding connective tissue cells in the analyzed groups, with altered expression even in macroscopically unaffected tissues of patients with DD. In the eccrine sweat glands of patients with DD, we found altered expression of FGFR1, FGFR2, CTGF, TGF-β and syndecan-1. The expression of the investigated factors is generally higher in samples of macroscopically unaffected palmar fascia compared to the affected fascia of patients with DD. No significant differences were found in the expression of messenger ribonucleic acid for FGFR1 and FGFR2 genes among the sample groups analyzed. Conclusions: Increased expression of profibrotic factors in the macroscopically unaffected palmar fascia of patients with DD dictates the need for more extensive excision during surgical treatment and the investigated factors can serve as potential targets for the development of pharmacological therapeutic strategies aimed at fibrosis associated with CTS and DD. Eccrine sweat glands have a potential role in the pathophysiology of DD.