Objectives: Objectives: Systemic sclerosis (SSc) is a chronic connective tissue disease characterized by fibrosis and remodeling of the microvasculature. Increased deposition of collagen and other extracellular matrix components affect not only the skin but the majority of the internal organs including the gastrointestinal (GI) tract. Few reports assessed the morphology of the stomach in SSc. Therefore, we analysed gastroesophageal biopsies obtained during gastroscopical examination from SSc patients to evaluate the expression of markers for fibrosis including a 52-year old female patient, who underwent distal esophageal myotomy and subsequently total gastrectomy.
Methods: Methods: The full-thickness gastric samples were embedded in paraffin. The endoscopic samples were snap frozen in liquid nitrogen and stored at –80°C. In order to investigate tissue fibrosis, the sections were stained by Masson’s thrichrom method and analysed by immunohistochemistry for the expression of connective tissue growth factor (CTGF), collagen type I, and type IV, alpha-smooth muscle actin (alpha-SMA) and endothelin-1 (ET-1). Full-thickness gastric wall biopsies, without inflammatory responses and neoplastic infiltration, from 3 patients which underwent total gastrectomy due to other disease entities, and endoscopic biopsies from 5 controls were also examined.
Results: Results: In SSc gastric wall, Masson’s stain revealed a mild fibrosis in the lamina propria that is more severe in the muscularis mucosae. In the muscle layers, wide areas of focal fibrosis surrounded smooth muscle cells, hereby increasing the intercellular spaces. A marked fibrosis was evident around the vessels. Collagen type I expression mirrored the fibrotic areas revealed by Masson’s stain. Collagen type IV was detectable in the basal lamina around the glands and the vessels in SSc when compared with gastric control samples. In SSc, a strong CTGF expression was evident in the muscularis mucosae, and was focally distributed in the muscle layers when compared with the control. Moreover, the majority of the vessels showed a strong immunopositivity for CTGF in the SSc gastric wall while they were weakly positive in the controls. In SSc the alpha-SMA reactivity was stronger in the lamina propria, muscolaris mucosae, muscle layers and in the vessel walls than in controls, whereas ET-1 positive cells were predominantly located in SSc muscle layers.

Conclusion: Conclusion: Our results show that different markers for fibrosis can be demonstrated in SSc stomach. Moreover, the involvement of gastric wall components in fibrosis most likely is involved in the decreased mobility and atrophy of the stomach in SSc patients.