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Histomorphometric assessment of bone biopsies from foals fed diets high in phosphorus and digestible energy
Author(s) -
Savage C. J.,
McCarthy R. N.,
Jeffcott L. B.
Publication year - 1993
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.1111/j.2042-3306.1993.tb04861.x
Subject(s) - osteoid , cancellous bone , bone remodeling , bone resorption , cortical bone , medicine , resorption , phosphorus , endocrinology , chemistry , zoology , anatomy , biology , organic chemistry
Summary Bone turnover was estimated from biopsy cores from the wing of ilium in 24 mixed‐bred foals, aged 4.5–6.5 months and divided into 4 groups. A control group was fed according to NRC recommendations for foals growing at 0.65 kg/day, experimental groups diet for 16–18 weeks with additions of phosphorus (P, 388% of control level), digestible energy (DE, 129% of control level) or crude protein (CP, 126% of control level). Bone biopsies were taken in Week 7/8 and again at the end of the trial. In the first biopsy no significant differences between dietary groups were found. Cortical bone porosity increased over time (P = 0.001) in foals fed High P (17.09 ± 2.25% vs 22.41 ± 2.62%). At the end of the study cortical bone porosity was greater (P = 0.02) in foals fed excess P than in other groups. In High P fed foals the extent of osteoid covered surfaces of cancellous bone decreased over time (P = 0.03), and there was a trend towards increased resorption surfaces in the cancellous bone with a subsequent slight decrease in cancellous bone volume. Cortical bone porosity tended to increase in foals fed High DE (P = 0.07) yet no significant alteration was seen in cancellous bone volume. Joint lesions of dyschondroplasia (DCP) were found at post mortem in foals fed High DE and High P. However, only minor changes in the measurements of bone remodelling were found by histomorphometric analysis. Changes in foals fed High P were consistent with a mild form of nutritional secondary hyperparathyroidism, although no clinical signs were noted.