Fetal skeletal development

The 3 main organs involved in Ca regulation are: the kidney, the bones and the intestine. Much attention has been given to intestinal and renal regulation of Ca. Bone however, may be of greater importance since a majority of Ca is stored in skeletal tissue (Crenshaw, 2001) with almost 97 % of Ca in skeletal tissue of neonates (Schneider et al., 1997). The primary response to dietary Ca and P therefore would preferentially be evaluated by examining the changes in skeletal tissue such as measurement of total ash content or bone mechanical properties (Crenshaw et al., 1981; Combs et al., 1991; Crenshaw, 2001).

In comparison with adults, there are obvious limitations to studies on mineral and bone homeostasis. In the developing fetus, fetal Ca metabolism is adapted to meets the needs during the developmental period through; 1) maintenance of sufficient Ca for skeletal mineralization and 2) extracellular Ca balance (Kovacs, 2006). Skeletal mineralization reaches a peak during late gestation and the importance of these adaptations becomes more evident as gestation advances. Comparable to adults, bone resorption may occur in the fetal skeleton to help maintain the Ca balance in the blood, which is probably controlled by fetal parathyroid hormone (PTH) and parathyroid hormone-related proteins (Kovacs and Kronenberg, 1997). Studies in sheep have shown that the fetal parathyroid gland is required by the developing skeleton (Aaron et al., 1989; Aaron et al., 1992). Several lines of evidence from animal models such as rats (Miller et al., 1983; Brommage and Deluca, 1984) and ewes (Lima et al., 1993) however, indicated that 1,25- dihydroxy vitamin D may not be required by the fetus for skeletal development. Fetal femur length and mineral ash content was reduced during maternal hypocalcemia (Chalon and Garel,

1985) suggesting a relationship between fetal skeletal development and maternal Ca. However, most of these studies were conducted in rats where differences in body size, gestation period, and litter size may be of concern if extrapolating to pigs. Older studies using radiochemical procedures to study placenta transfer in pigs suggested that sow requirements during gestation influenced Ca movement and transfer to the developing fetuses (Itoh et al., 1967) and selective deposition of Ca occurs at an incremental rate as gestation advances (Hansard et al., 1966). The limited studies in pigs showed fetal bone calcification was reduced in Ca-deficient sows (Itoh et al., 1967). This is consistent with evidence from ewe studies (Lima et al., 1993); however, in both cases, no effect was seen on fetal plasma Ca (Itoh et al., 1967; Lima et al., 1993). During lactation, sows apparently provide a buffer of Ca and P in milk hence, abnormalities in piglet skeletal development will not be seen during lactation even if sows receive inadequate Ca (Mahan and Fetter, 1982).

Since the mid-1900s, nutritionists have been using bone strength to assess the mineral requirements in swine and the bioavailability of the minerals (Crenshaw et al., 1981). The majority of the Ca and P is stored in skeletal tissue, thus changes in skeletal storage will provide information on dietary Ca and P requirements (Crenshaw, 2001). Several studies have shown that increasing dietary Ca and P will increase bone strength in piglets (Miller et al., 1962; Miller et al., 1964) and growing pigs (Libal et al., 1969; Cromwell et al., 1970; Nimmo et al., 1980; Crenshaw et al., 1981; Combs et al., 1991). These studies however, involved feeding diets with different Ca and P concentrations directly to the weanling or growing pigs. At present, there is no strong evidence showing that the sows’ Ca and P status has an effect on fetal or newborn piglet bone development.

In pigs, the response to dietary Ca and P in skeletal tissue in the form of bone ash or mechanical properties depends on the bone used and the pig’s age (Crenshaw et al., 1981). An earlier paper by Tanksley (1979) implied that the femur was a better indicator of bone status than the metacarpals whereas Crenshaw et al. (1981) showed that the femur, humerus and ribs were responsive to Ca and P in younger pigs (approximately 8 wk of age) in terms of bone mechanical properties, making them a better option to assess bone mineralization in young pigs compared to other bones such as the thoracic vertebra or metatarsals that were used in his study. Although results from both studies differ in the type of bone as being the better indicators of bone status,

both authors were in agreement that the type of bone used to assess Ca and P requirements may yield different results.

In summary, although the mechanisms associated with fetal skeletal mineralization are unclear; studies in humans, rats and pigs have suggested the possible influence of maternal bone metabolism in mediating fetal skeletal mineralization particularly at late gestation. Maternal Ca and P deficiencies, or conditions that alter the placenta Ca transfer may affect bone development of the fetuses in utero.

2.3.3 Effects of piglet birth weight and within-litter variation on bone health  

Increasing litter size is one of the goals of swine production. Larger litters however are often associated with low piglet birth weight and piglet mortality (Rutherford et al., 2013). The large litter size of the modern sow means that there is a chance of a reduced proportion of heavy piglets, which have a higher chance of survival compared to the smaller birth-weight piglets (Boulot et al., 2008). Quesnel et al. (2008) reported that 20 % of the birth weight variation is due to litter size, parity, sow birth date and breeding season. Further investigation is required therefore, to identify other factors involved.

Maternal nutrition, which includes dietary energy, and protein, and amino acid ratios and feed intake is one possible factor that has been examined. A review of the literature by Campos et al. (2012) suggested that restrictions to sow feed and protein intake, and inadequate amino acid intake may have a profound effect on the developing fetus and consequently, affect piglet performance postnatally. The large increase in fetal Ca and P content during late gestation indicates a greater nutritional demand for these minerals especially in sows with larger litters (Mahan et al., 2009). As discussed by Lanham et al. (2011), nutrient restrictions in animal models such as rats and ewes during gestation have shown direct alteration to bone ossification (bone tissue formation) in growing fetuses, hence affecting the size, structure and strength of bones in the newborn. Incorrect maternal nutrition, may be associated with a limitation of sows to provide adequate nutrition to all the developing fetuses due to decreased uterine blood flow to each piglet as litter size increases (Père and Etienne, 2012) and this may subsequently lead to fetal growth retardation and decreased uniformity in piglets birth weight (Campos et al., 2012). Current available studies that evaluated maternal nutrition in relation to fetal development and