Literature review and discussion

In 1931, Marek & Wellmann published their historical data on the effects of Ca and P supply in growing dogs. They summarised their findings about the detrimental effects of excess Ca, concluding that the symptoms such as lameness or deviation of limb axes were more detrimental when the P content in the diet was not increased concurrently. It has been reported that two German Shepherd puppies developed severe clinical signs of skeletal problems, confirmed by radiological and histological findings, as well as hypophosphataemia after being fed excess Ca and a normal amount of P (calculated: 2·2 % Ca; 0·9 % P⁽Reference Marek and Wellmann¹⁰⁾). Severe clinical signs of DOD were observed in a Fox Terrier puppy after adding CaCO₃ to its diet, and these signs disappeared after CaCO₃ was exchanged with bone meal, which led to an increase in the P supply and a balanced Ca:P ratio. The underlying reason for these clinical signs might be the decreased availability of P in cases with a wide Ca:P ratio caused by a high Ca content of the diet, as described previously⁽Reference Jenkins and Phillips¹⁵⁾. This effect of selective Ca excess on the apparent digestibility of P was also observed in Beagles during the own experiments⁽Reference Dobenecker¹⁶⁾. The results of Nap et al. ⁽Reference Nap, Hazewinkel and van den Brom¹¹⁾ can help explain the sometimes inconsistent findings published more recently by various laboratories (Table 1).

Table 1

Effects of excess calcium on growing dogs

n.e., not examined; n.m., not mentioned.

* In one sentence, severe skeletal abnormalities were mentioned.

† Constant supplementation of 2·3 g Ca/d per dog.

‡ Clinical symptoms disappeared when one of the dogs received P in addition to excess Ca.

§ Supply with low P and normal Ca for comparison.

Hazewinkel and his colleagues⁽Reference Goodman, Montgomery, Titch, Reinhart and Carey^4–Reference Hazewinkel, Brom and Van't Kloster^7, Reference Schoenmakers, Hazewinkel and Voorhout¹²⁾ also observed detrimental effects in Great Danes (GD) after feeding the animals excess Ca in a diet with a P supply that fulfilled the minimum requirements (0·9 % DM; wide Ca:P ratio)⁽¹⁷⁾. In some studies of Fox Terrier, German Shepherd, and GD puppies fed an excess amount of Ca, clinically severe symptoms were observed⁽Reference Hazewinkel, Goedegebuure and Poulos^5, Reference Hazewinkel, Brom and Van't Kloster^7, Reference Marek and Wellmann^10, Reference Schoenmakers, Hazewinkel and Voorhout¹²⁾. In other studies, mild symptoms have been reported in puppies fed excess Ca, and only subclinical effects were measured in radiographs or through histology⁽Reference Goedegebuure and Hazewinkel³⁾, or no symptoms have been observed or reported⁽Reference Hazewinkel, Hackeng and Bosch^6, Reference Voorhout and Hazewinkel¹⁴⁾. In another trial using Miniature Poodles (MP), the combination of excess Ca and a marginal P supply did not cause signs of DOD⁽Reference Nap, Hazewinkel and van den Brom¹¹⁾. Therefore, excess Ca alone without a concomitant increase in the P supply (i.e. a wide Ca:P ratio >2/1) seems to trigger signs of DOD in growing dogs of certain breeds, especially GD, and increase the number of severely affected puppies. In dogs with severe clinical symptoms, some authors have reported hypophosphataemia⁽Reference Hazewinkel, Brom and Van't Kloster^7, Reference Marek and Wellmann¹⁰⁾, which supported the hypothesis that P deficiency is a major co-factor in the development of skeletal problems in puppies fed excess Ca. Accordingly, trials were performed where P levels were elevated approximately 25 % or more above the minimum requirements or were provided at 0·9 % of the DM to ensure a more balanced Ca:P ratio. These trials led to less severe skeletal changes or, more frequently, to no clinical symptoms at all (GD^(4,7,9,12); Beagles⁽Reference Dobenecker, Kasbeitzer and Flinspach^2, Reference Stephens, Norrdin and Benjamin¹³⁾). When Foxhound crossbreeds were fed a P supply above the previously published recommended allowance⁽Reference Meyer and Zentek¹⁸⁾, the animals developed no clinical or subclinical symptoms⁽Reference Dobenecker, Kasbeitzer and Flinspach²⁾. Lauten et al. did not state their clinical findings clearly enough to evaluate their results in this context⁽Reference Lauten, Cox and Brawner⁸⁾.

The hypothesis that DOD in growing dogs is related to the co-factor P supply was reinforced by the results of a study of P deficiency in growing Beagles and Foxhound crossbreeds⁽Reference Dobenecker and Kienzle¹⁹⁾. The puppies received a diet providing approximately 40–50 % of the recommended P allowance (approximately 0·35 % DM⁽Reference Meyer and Zentek¹⁸⁾) while the Ca supply met the requirements, resulting in a Ca:P ratio above the recommended ratio. In this trial, some puppies of both breeds developed severe clinical symptoms of DOD.

Along with evaluating the impact of the nutrient supply, especially the supply of Ca and P, it is important to consider other factors in the study of complex nutritionally triggered DOD. The adult body weight alone might influence the effects of excess Ca through body-weight development or the growth rate, which involves the corresponding hormonal status of the animal. Another potential factor is the susceptibility or sensitivity of the breed to certain nutritional factors. From the literature and from clinical experience, we know that large or giant dog breeds are more likely to develop skeletal problems during growth when they ingest insufficient or excess nutrients. Overall, dogs with an adult body weight of about 30 kg or more are more vulnerable to excess Ca. However, too intensive growth alone can lead to a greater frequency of developmental skeletal disease even when all nutrients are supplied according to the requirements⁽Reference Zentek, Meyer and Daemmrich²⁰⁾. The breeding of some dog varieties seems to be problematic even when the required energy and nutrient supplies are met. For example, in radiographic examinations⁽Reference Zentek, Meyer and Daemmrich²¹⁾, there were diagnosed skeletal changes in GD but not in MP after feeding the animals a balanced diet without an excess of Ca. The authors have reported that the majority of the GD showed abnormally flattened distal ulnar metaphyses with increasing incidence of cartilage cones, and the growth plates were more irregular in the GD than in the MP puppies.

The evidence collected in the present review supports the hypothesis that excess Ca is much more hazardous to growing dogs when it is accompanied by a low or a marginal P supply. Moreover, large and giant dogs are particularly prone to nutritionally triggered developmental skeletal diseases.