Effect of bone and analytical method on assessment of bone mineralization in response to dietary phosphorus, phytase, and vitamin D in finishing pigs.

A total of 882 pigs [PIC TR4 × (Fast LW × PIC L02); initially 33.2 ± 0.31 kg] were used in a 112-d study to evaluate the effects of different bones and analytical methods on the assessment of bone mineralization response to changes in dietary P, phytase, and vitamin D in growing pigs. Pens of pigs (20 pigs per pen) were randomized to 1 of 5 dietary treatments with 9 pens per treatment. Dietary treatments were designed to create differences in bone mineralization and included: 1) P at 80% of NRC (2012) standardized total tract digestible (STTD) P requirement, 2) NRC STTD P with no phytase, 3) NRC STTD P with phytase providing an assumed release of 0.14 % STTD P from 2,000 FYT/kg, 4) high STTD P (128% of the NRC P) using monocalcium phosphate and phytase, 5) diet 4 with additional vitamin D3 from 25(OH)D3. On d 112, one pig per pen was euthanized for bone, blood, and urine analysis. Additionally, 11 pigs identified as having poor body condition which indicated a history of low feed intake (unhealthy) were sampled. There were no differences between treatments for final body weight, average daily gain, average daily feed intake, gain to feed, or bone ash measurements (treatment × bone interaction) regardless of bone ash method. The response to treatment for bone density and bone mineral content was dependent upon bone sampled (density interaction, P = 0.053; mineral interaction, P = 0.078). For 10th rib bone density, pigs fed high levels of P had increased (P < 0.05) bone density compared with pigs fed NRC levels with phytase, with pigs fed deficient P, NRC levels of P with no phytase, and high STTD P with extra 25(OH)D3 intermediate, with no differences for metacarpals, fibulas, or 2nd ribs. Pigs fed extra vitamin D from 25(OH)D3 had increased (P < 0.05) 10th rib bone mineral content compared with pigs fed deficient P and NRC levels of P with phytase, with pigs fed industry P and vitamin D, and NRC P with monocalcium intermediate. Healthy pigs had greater (P < 0.05) serum Ca, P, vitamin D concentrations, and defatted bone ash than those unhealthy, with no difference between the two health statuses for non-defatted bone ash. In summary, differences between bone ash procedures was more apparent than differences between diets. Differences in bone density and mineral content in response to dietary P and vitamin D were most apparent with 10th ribs.

The effect of bone and analytical methods on the assessment of bone mineralization response to dietary phosphorus, phytase, and vitamin D in nursery pigs.

A total of 360 pigs (DNA 600 × 241, DNA; initially 11.9 ±â€…0.56 kg) were used in a 28-d trial to evaluate the effects of different bones and analytical methods on the assessment of bone mineralization response to dietary P, vitamin D, and phytase in nursery pigs. Pens of pigs (six pigs per pen) were randomized to six dietary treatments in a randomized complete block design with 10 pens per treatment. Dietary treatments were designed to create differences in bone mineralization and included: (1) 0.19% standardized total tract digestibility (STTD) P (deficient), (2) 0.33% STTD P (NRC [2012] requirement) using monocalcium phosphate, (3) 0.33% STTD P including 0.14% release from phytase (Ronozyme HiPhos 2700, DSM Nutritional Products, Parsippany, NJ), (4) 0.44% STTD P using monocalcium phosphate, phytase, and no vitamin D, (5) diet 4 with vitamin D (1,653 IU/kg), and (6) diet 5 with an additional 50 µg/kg of 25(OH)D3 (HyD, DSM Nutritional Products, Parsippany, NJ) estimated to provide an additional 2,000 IU/kg of vitamin D3. After 28 d on feed, eight pigs per treatment were euthanized for bone (metacarpal, 2nd rib, 10th rib, and fibula), blood, and urine analysis. The response to treatment for bone density and ash was dependent upon the bone analyzed (treatment × bone interaction for bone density, P = 0.044; non-defatted bone ash, P = 0.060; defatted bone ash, P = 0.068). Thus, the response related to dietary treatment differed depending on which bone (metacarpal, fibula, 2nd rib, or 10th rib) was measured. Pigs fed 0.19% STTD P had decreased (P < 0.05) bone density and ash (non-defatted and defatted) for all bones compared to 0.44% STTD P, with 0.33% STTD P generally intermediate or similar to 0.44% STTD P. Pigs fed 0.44% STTD P with no vitamin D had greater (P < 0.05) non-defatted fibula ash compared to all treatments other than 0.44% STTD P with added 25(OH)D3. Pigs fed diets with 0.44% STTD P had greater (P < 0.05) defatted second rib ash compared to pigs fed 0.19% STTD P or 0.33% STTD P with no phytase. In summary, bone density and ash responses varied depending on bone analyzed. Differences in bone density and ash in response to P and vitamin D were most apparent with fibulas and second ribs. There were apparent differences in the bone ash percentage between defatted and non-defatted bone. However, differences between the treatments remain consistent regardless of the analytic procedure. For histopathology, 10th ribs were more sensitive than 2nd ribs or fibulas for the detection of lesions.

Lameness is defined as impaired movement or deviation from normal gait. There are many factors that can contribute to lameness, including but not limited to: infectious disease, genetic and conformational anomaly, and toxicity that affects the bone, muscle, and nervous systems. Metabolic bone disease is another cause of lameness in swine production and can be caused by inappropriate levels of essential vitamins or minerals. To understand and evaluate bone mineralization, it is important to understand the differences in diagnostic results between different bones and analytical techniques. Historically, percentage bone ash has been used as one of the procedures to assess metabolic bone disease as it measures the level of bone mineralization; however, procedures and results vary depending on the methodology and type of bone measured. Differences in bone density and ash in response to dietary P and vitamin D were most apparent in the fibulas and second ribs. There were apparent differences in the percentage of bone ash between defatted and non-defatted bone; however, the differences between the treatments remain consistent regardless of the analytic procedure. For histopathology, 10th ribs were more sensitive than 2nd ribs or fibulas for detection of lesions associated with metabolic bone disease.

Assessment of ruminal hydrogen sulfide or urine thiosulfate as diagnostic tools for sulfur induced polioencephalomalacia in cattle.

To determine if ruminal hydrogen sulfide, urine thiosulfate, or blood sulfhemoglobin could be used as diagnostic indicators for sulfur-induced polioencephalomalacia, 16 steers (8 cannulated, 368 ± 12 kg; 8 unmodified, 388 ± 10 kg; mean ± standard error) were fed 1 of 2 dietary treatments. Diets consisted of a low sulfate (0.24% S; control) wheat midd-based pellet or the control pellet with sodium sulfate added to achieve a high-sulfate (0.68% S) pellet. As designed, intake did not differ (P = 0.80) between treatments. At 8 hr postfeeding, ruminal hydrogen sulfide was not affected by cannulation (P = 0.35) but was greater (P < 0.01) in high S (6,005 ± 475 mg/l) than control (1,639 ± 472 mg/l) steers. Time of day of sampling affected (P = 0.01) ruminal hydrogen sulfide, with peak concentrations occurring 4-12 hr after feeding. Urine was collected prefeeding (AM) and 7-9 hr postfeeding (PM). Urine thiosulfate concentrations of high S steers sampled in the PM were greater (P > 0.01) than in the AM. However, there was no difference due to time of sampling for control. In both the AM and PM, urine thiosulfate concentrations of high S were greater (P > 0.01) than control. Although hydrogen sulfide and thiosulfate were elevated by increased dietary S intake, a concentration at which polioencephalomalacia is likely to occur could not be determined. Sampling urine for thiosulfate or rumen gas for hydrogen sulfide of nonsymptomatic pen mates 4-8 hr after feeding may be useful to assess sulfur exposure and differentiate between causes of polioencephalomalacia.