Scoliosis in Chickens: Responsiveness of Severity and Incidence to Dietary Copper

Abstract

The severity and incidence of spinal lesions were manipulated in a line of chickens susceptible to scoliosis by varying their dietary intake of copper. A decrease in expression of the lesion was related to increased intake of copper. The change in expression, however, appeared to be related only indirectly to the defects in collagen cross-linking, maturation, and deposition known to be associated with dietary copper deficiency. Thus, a dietary constituent in the range of normal intakes may act as an environmental factor in the expression of scoliosis.

Common polymorphisms in human lysyl oxidase genes are not associated with the adolescent idiopathic scoliosis phenotype

“…Prior work demonstrated that some mutations in a zebrafish model did not overtly cause the abnormal phenotype, but instead allowed the expression of the phenotype at previously subclinical levels of copper deprivation [14]. Likewise, the incidence and severity of scoliosis in the genetically predisposed chickens were sensitive to dietary copper [15,16]. Measures of copper intake or homeostasis were not available in this population.…”

“…Zebrafish researchers have shown that disrupting lysyl oxidase activity in embryonic fish results in notochord distortion leading to defects of the axial skeleton [14]. Work in a line of chickens susceptible to scoliosis implicated the lysyl oxidases as a causative feature [15,16], but this has not yet been definitively shown. Recent work has investigated the murine lysyl oxidases with bone development [17-19], but a scoliotic phenotype has not been specifically studied in a murine model.…”

Dietary Habits Had No Relationship with Adolescent Idiopathic Scoliosis: Analysis Utilizing Quantitative Data about Dietary Intakes

“…Studies of nutrients affecting spinal development and morphology are scarce, particularly those in humans. There have been a few experimental studies in animals [16,17,18]. Li et al reported that vitamin A deficiency in pregnant rats induced congenital scoliosis in neonates through a defect in retinoic signaling pathway during somitogenesis [16].…”

“…Nutrients for analysis were selected based on the physiology of bone [28] and the results of past studies [13,14,15,16,17,18]. Selected nutrients were protein, calcium, vitamins (D, A, K, B6), and minerals (manganese and copper).…”

“…However, the pathological mechanism between the onset of AIS and calcium/vitamin D intake has not been elucidated. Although other experimental studies in animals suggested that deficiencies of vitamins (e.g., A, B1) and minerals (e.g., copper, manganese) could cause spinal deformity [16,17,18], the effect of these nutrients on AIS has not been investigated.…”