| dc.description | In adult salmon of the sea centres in southern Chile, a jaw deformation (JD) has been identified. It affects the dental and hyomandibular bones, which bend ventrally up to 90° of their normal position. The deformation affects also the dental articular bone. This pathology is related to weight loss and increased mortality of the salmons. It was empirically postulated that a probable cause for this anomaly was food from vegetal origin in the diet of the fishes (which are carnivores) Therefore, the present work aims at comparing the biostructure of jaw bone of salmons fed either with vegetal (soja and gluten) formulation or animal formulation, mostly fish powder. Fifty specimens were analyzed from Puerto Montt, 35 having JD and 15 normal control. Samples were obtained in June, July and September 1999. (group 1) and March, Sept and October, 2000 (group 2). Group 1 was fed mostly with vegetal flour and group 2 with fish flour. Each group was subdivided in two subgroups, one of healthy animals and the other of fishes with JD. Jaw and articular bones were fixed in 10% formaldehyde and 1% glutaraldehyde and processed for histology (hematoxylin.eosin, Alcian blue, Masson trichrome) histochemistry (Syrius red and von Kossa) and scanning electron microscopy (SEM). The mandibular bone of group 1 with JD presented large amounts of osteoid tissue compared with its control. Collagen I disminishes and its architecture and composition changes, collagen III increases. No significant difference was found in calcium content between normal and JD fishes. SEM shows that the dental bone close to the joint in the fishes with JD displayed a disorganized structure and no trabecular formation, compared to controls, In group 2, these pathological findings were less evident, both macro- and microscopically. Results suggest that JD is of multifactorial origin; the primary cause can be a genetic or congenital alteration of the Jaw cartilage. There should be susceptibility for presentation of the defect in this group of fishes, but its expression is triggered by deficit of phosphorous of animal origin in food, so that this pathology is not seen in fishes with adequate nutrition. | |
