BACKGROUND: The purpose of this study was to examine the biological environment of the esophageal hiatus through analysis of the collagen content within the gastrohepatic ligament (GHL), gastrophrenic ligament (GPL), and phrenoesophageal ligament (PEL) in patients with type I hiatal hernias (HH) and type III paraesophageal hernias (PEH). METHODS: A control group (N=10) and patients with type I HH (N=10) and type III PEH (N=10) were included in the analysis. Specimens of the GHL, PEL, and GPL were collected intraoperatively. Slides stained with sirius red/fast green were created and ten photos at 400xmagnification were taken of each specimen. Axiovision 4.7 (Zeiss) photo analysis software was employed for quantification of collagen I (red) and III (green) by calculating color area (mum2). Statistical significance (p<0.05) was determined using a one-way ANOVA and Fisher's LSD post-test. RESULTS: Cross-polarization microscopy revealed that the collagen I content was similar in the three study groups for the GHL, greater in the type III PEH group and in the control group compared to the type I HH group for the PEL, and greater in the type III PEH group compared to control group for the GPL. Collagen III quantity was greater in the control group than in the type I HH group for each ligament, and greater in the GHL and PEL when compared to the type III PEH group. Type III PEH patients had greater collagen III quantity than did type I HH patients for each ligament. Collagen type I:III ratio of the GHL was greater in both hernia groups compared to the control group. Type III PEH patients contained a higher I:III ratio than both the control and type I HH groups with respect to the PEL. There was no difference in the ratio with evaluation of the GPL for the three groups. CONCLUSION: Evaluation of the esophageal hiatus revealed that patients with PEH have a different biological environment with regard to collagen content compared to control patients. The collagen I:III ratio of the study groups was equal to or greater than the control group. Collagen deficiency in the GE junction supporting ligaments does not appear to be an etiology of PEH formation.
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