Spinal Deformity in Vitamin D-Deprived Pigs: Why and What Next?: Commentary on an article by Matthew A. Halanski, MD, et al.: "Maternal Diets Deficient in Vitamin D Increase the Risk of Kyphosis in Offspring. A Novel Kyphotic Porcine Model".

Abstract

Commentary In most children, the growing spine has minimal curvature in the coronal plane and sagittal curvatures in the normal range, in apparent defiance of gravity and prevailing muscular forces. Very little is known about how growth is regulated to achieve this, and conversely how growth is poorly regulated in those in whom progressive curvatures develop. In this paper, Halanski and colleagues focus on prenatal and postnatal diet and report a high prevalence of hyperkyphosis in piglets when both sows and the piglets are deprived of vitamin D. However, providing vitamin D in the post-weaning nursery diet was associated with a lower eventual prevalence. The various permutations of maternal vitamin-D and mineral diet during gestation and lactation, together with manipulation of the post-weaning nursery diet, indicate that maternal deprivation of vitamin D during gestation and lactation has a greater effect than the piglet’s post-weaning diet does. Pediatricians and orthopaedic surgeons should take note for 2 reasons identified by Halanski and colleagues: first, these findings may have implications for the health of human children (as both spinal deformity1,2 and maternal vitamin-D deficiency3 are quite common); and second, this paper proposes a novel mammalian model for subsequent use in evaluating procedures for treating spinal deformity. With regard to mechanisms, in these piglets the deformities are apparently idiopathic, in the sense of there being no structural vertebral defect, so this is apparently an abnormal fetal and postnatal development of an essentially normal skeleton. Conversely, infantile spinal deformities in humans are commonly associated with vertebral malformation4, while idiopathic deformities become apparent toward the end of skeletal growth2. Since discs are very narrow in the porcine thoracic spine, it is likely that these deformities result from vertebral rather than discal wedging; they result from altered bone growth. There is a complex interaction between vitamin D and growth hormones systemically5, but the effect on spinal growth here must be more local; apparently, the growth suppression affected only the thoracic vertebrae and only anteriorly. Here, the authors report that the influence of diet on vertebral bone density was subtle (8%) by mineral (ash) content, but not detectable by computed tomography (CT) radiodensity. A companion paper cites other affected traits, including an 11% reduction in body mass growth, a 25% reduction in whole-body bone mineral content, reduced femoral mechanical strength, and abnormalities in the growth plates of femora and vertebrae in piglets; it also gives measurements from maternal serum and milk of vitamin D, parathyroid hormone, and related metabolites6. Overall, the empirical findings provide few clues as to possible underlying mechanisms, so it is unclear how they further our understanding the causes of spinal deformity in humans and its management. Endocrinologists, dieticians, and epidemiologists would probably have to work together to determine whether anything similar is occurring in human populations. Could this model be used to study the treatment of pediatric deformities? Certainly, there is a great need for in vivo platforms for testing treatments. This mammalian model could be quite valuable, as the animals were apparently in good health with considerable spontaneous spinal deformity and substantial residual growth (with growth plates closing between 1 and 4 years of age). However, as a first step, the natural history should be determined more thoroughly. Here, documenting the post-weaning evolution of the kyphosis was hampered by methodological difficulties. Also, the postnatal nutritional regimen was complex (with weaning at 3 to 4 weeks, the nursery diet until 7 weeks, and then the standard diet from 7 to 17 weeks). It will be important to know whether the hyperkyphosis resolves or is retained in untreated animals before treatments can be studied. This is 1 paper in a series reporting on this animal model, but several questions about the relevance to human spinal deformity and its management remain unanswered. However, they are important questions, and pursuing the answers could be productive, valuable steps forward in understanding the clinical problem of the development of spinal deformity.