Effects of dietary phosphorus and calcium on induction of dyschondroplasia in foals

Abstract

SummaryThirty mixed‐bred foals aged 2.5–6.5 months (mean age 4.4 ± 1.0 months,) with no clinical or radiographic lesions indicating dyschondroplasia (DCP) were each fed 1 of 4 diets for 16–18 weeks. Twelve foals were fed a Control diet according to NRC recommendations. Six foals were fed a diet ˜388% NRC recommended level for P; another 6 foals were fed a diet with ˜342% NRC level for Ca and the remaining 6 foals were fed a diet which contained both ˜342% NRC level for Ca and ˜129% NRC level for digestible energy (DE). Diets were formulated using different rice‐based pellets and oaten chaff, with added maize oil for the High DE diet, and additions of limestone (CaCO3) for the High Ca and sodium monophosphate (5.5% of the pellet) for the High P.Foals fed excess DE (High Ca/DE group) had slightly greater average daily gains, humeral lengths and wither heights, but these were not significantly different from foals fed the Control diet. Clinical and radiographic signs of DCP were seen in 7 foals; 4 foals fed High P and 3 foals fed High Ca/DE. Suspicious joint lesions of DCP were identified at post mortem in 13 foals (1 Control, 5 High P, 2 High Ca, 5 High Ca/DE). Histologically confirmed lesions of DCP were found in multiple joints and growth plates in 15 foals (2 Control, 5 High P, 2 High Ca, 6 High Ca/DE). The lesions were more numerous and severe in the foals fed High P and High Ca/DE than in the foals fed the Control and High Ca diets. High levels of dietary Ca did not appear to induce lesions of DCP in foals fed ˜100% NRC recommendation for dietary DE, or reduce the incidence in foals concurrently fed high dietary DE. High levels of P intake resulted in the formation of lesions in foals fed the basal level of DE (˜100% NRC DE), although the mechanism by which this occurred has not been elucidated.