Osteopenia after gastrectomy, fundectomy or antrectomy:: an experimental study in the rat

Background: Gastrectomy induces osteopenia. In this study, we tested if resection of defined parts of the stomach could reproduce the gastrectomy-evoked osteopenia. Methods: Rats were subjected to gastrectomy (surgical removal of the glandular part of the stomach), fundectomy (extirpation of the acid-producing part, fundus) or antrectomy (extirpation of the gastrin-producing part, antrum). Calvariae, tibiae and femurs were examined at various times after the operations. The calvariae were subjected to transillumination. Calvariae and tibiae were sectioned and analysed by histomorphometry, tibia sections by the aid of a Merz grid and calvaria sections using computer-assisted image analysis. The intact femurs were subjected to computerized microtomography. Results: Gastrectomy (hypogastrinemia) and fundectomy (hypergastrinemia) resulted in osteopenia, while antrectomy (hypogastrinemia) had less effect on bone. Gastrectomy/fundectomy were associated with loss of trabecules in the tibia and with reduced bone volume in both tibia and calvaria. In contrast, there was only little reduction of cortical bone in the femur. Conclusion: Gastrectomy-evoked osteopenia can be reproduced by selective resection of the acid-producing part of the rat stomach (i.e. fundectomy). Antrectomy was less effective. In the long bones, the osteopenia was manifested primarily in trabecular bone and less in cortical bone. The calvaria displayed marked osteopenia. Although the findings indicate that the stomach, notably the acid-producing (oxyntic) mucosa, is important for bone metabolism, the precise mechanisms behind the gastrectomy/fundectomy-evoked osteopenia remain unidentified. Clearly, lack of gastrin is not responsible. The oxyntic mucosa is rich in peptide hormone-producing cells (the so-called ECL cells), with unidentified physiological significance. The ECL cells, which operate under the control of gastrin, have been put forward as a possible source of an osteotropic hormone. (C) 1998 Elsevier Science BN. All rights reserved.